44° SCIVAC

Transcription

44° SCIVAC

I.C.
44°
congressonazionalescivac
FIERA MILANO
PA D I G L I O N E 1 7 - P O RTA G AT TA M E L ATA
16-19 MAGGIO 2002
in collaborazione con
®
SOCIETÀ CULTURALE ITALIANA VETERINARI
PER ANIMALI DA COMPAGNIA
44°
RELATORI AL
RELATORI STRANIERI
RODNEY BAGLEY
DVM, Dipl ACVIM (Int Med),
Dipl ACVIM (Neur)
Washington State University,
USA
DON HULSE
FRANCESCO ALBANESE
DVM, PhD, Dipl ACVS
Med Vet
Texas A&M University,
USA
Napoli
SILVIA AUXILIA
MARIE-NOËLLE
ISSAUTIER
Med Vet, Dip ECVD, Cert VD
Crema (CR)
Dr Vét
MASSIMO BARONI
AVERY BENNETT
France
DVM, MS, Dipl ACVS
LUC JANSSENS
San Francisco Bay, USA
Med Vet, Dipl ECVN
DVM, PhD, Dipl ECVS
SUSAN E. BUNCH
Antwerpen, Belgio
DVM, PhD, Dipl ACVIM
DOUGLAS MADER
North Carolina State
University, Raleigh, USA
LAURENT CAUZINILLE
Dr Vét, Dipl ACVIM,
Dipl ECVN
Monsummano Terme (PT)
MARCO BERNARDINI
Med Vet, Dipl ECVN
MS, DVM, Dipl ABVP (Exotic)
Big Pine Key, Florida,
USA
Bologna
ALESSANDRO BONIOLI
Med Vet
Torino
DENIS J.
MARCELLIN-LITTLE
UGO BONFANTI
Dr Vét, Dipl ACVS, Dipl ECVS
Med Vet
Milano
Management University
of Nantes, France
YVES MOENS
Med Vet
DVM, Phd, Dipl ECVA
Padova
DOUGLAS J. DeBOER
University of Berne,
Svizzera
ROSARIO CERUNDOLO
Paris, France
FABRICE CLERFEUILLE
Dr Vét, PhD, MBA
DVM, Dipl ACVD
MARCO CALDIN
Med Vet, Dipl ECVD
University of Wisconsin,
USA
PATRICK PAGEAT
GERALDINE DIETHELM
Apt, France
Dr Med Vet
MARK G. PAPICH
Roma
DVM, MS, Dipl ACVCP
DAVIDE DE LORENZI
Marathon Veterinary
Hospital, Florida, USA
KENNETH J. DROBATZ
DVM, Dipl ACVIM,
Dipl ACVECC
University of Pennsylvania,
USA
Dr Vét, PhD
Napoli
DANIELE CORLAZZOLI
Med Vet
CLAUDIA REUSCH
Dr Med Vet, Dipl ECVIM-CA
University of Zurich,
Svizzera
Med Vet
Forlì
FABRIZIO FABBRINI
Med Vet, Dipl CES Derm
Milano
GILLES DUPRÈ
EMILIO FELTRI
Dr Vét, Dipl ECVS
Med Vet
Arcueil, France
RELATORI ITALIANI
ELIZABETH HARDIE
Tortona (AL)
ALESSANDRA FONDATI
DVM, Dipl ACVS, PhD
FRANCESCA ABRAMO
Med Vet, Dipl ECVD
North Caroline State
Med Vet
Universidad Autonoma
de Barcelona, Spagna
Università di Pisa
4
44°
CONGRESSO
PAOLO FRANCI
ERSILIA PAPPALARDO
Med Vet
Med Vet
Firenze
Cannizzaro (CT)
TOMMASO FURLANELLO
ALESSANDRO PIRAS
Med Vet
Med Vet, MRCVS, Spec Chir Vet
Padova
FRANCA GALEOTTI
Med Vet
Impruneta (FI)
RELATORI A TEMA
GIUSEPPE BARILLARO
Newry, Irlanda del Nord,
UK
Med Vet
Reggio Calabria
MATTIA BIELLI
Med Vet
Novara
GIANNI RE
FRANCESCA COZZI
Med Vet
GIOVANNI GHIBAUDO
Università di Torino
Med Vet, Dipl ECVN
Med Vet
GIORGIO ROMANELLI
DONATELLA LOTTI
Med Vet, Dipl ECVS
Med Vet
Vittuone (MI)
Milano
OSCAR GRAZIOLI
Milano
Med Vet
FABIA SCARAMPELLA
ALESSANDRO MELILLO
Med Vet, Dipl ECVD
Med Vet
Milano
Roma
ENRICO STEFANELLI
GIAN LUCA ROVESTI
Reggio Emilia
UGO LOTTI
Med Vet
Monsummano Terme (PT)
MASSIMO MARISCOLI
Revigliasco (TO)
Med Vet, Dipl ECVS
Med Vet
Portomaggiore (FE)
Med Vet, Dipl ECVS
Università di Teramo
LUCA MECHELLI
Med Vet
ALESSANDRO SPADARI
CHIARA TIEGHI
Med Vet
Med Vet
Università di Bologna
Varese
GIUSEPPE VISIGALLI
Università di Perugia
ANTONELLA VERCELLI
CHIARA NOLI
Med Vet, Dipl CES Derm
Med Vet, Dipl ECVD
Milano
Cavriago (RE)
Torino
FABIO VIGANÒ
LORENZO NOVELLO
Med Vet
Med Vet
Padova
San Giorgio Legnano
(Milano)
CRISTINA OSELLA
ALDO VEZZONI
Med Vet
Med Vet, Dipl ECVS
Torino
Cremona
5
Med Vet
Varedo (MI)
ATTI
DELLE RELAZIONI
Gli atti sono elencati in ordine alfabetico secondo il cognome del relatore.
Le relazioni di uno stesso autore sono elencate secondo l’ordine cronologico di presentazione.
44° Congresso Nazionale SCIVAC
3
Impiego delle tetracicline
in dermatologia veterinaria
Silvia Auxilia
Med Vet, Dipl ECVD
Libero Professionista, Londra
INTRODUZIONE
EFFETTI COLLATERALI
Le tetracicline (TTC) in dermatologia veterinaria vengono utilizzate principalmente per la loro attivita` immunomodulatrice ed antinfiammatoria e nel cane sono spesso somministrate in associazione a niacinamide (amide
della niacina). I quadri clinici in cui si fa uso di TTC nel
cane, e talvolta nel gatto, sono: penfigo foliaceo ed eritematoso, penfigoide bolloso, penfigo volgare, lupus eritematoso discoide, onicodistrofia lupoide, dermatite sterile
granulomatosa o piogranulomatosa, istiocitosi cutanea,
vasculite, pannicolite sterile, fistole metatarsali, dermatosi ulcerativa idiopatica dei Pastori scozzesi e dello Shetland e pododermatite plasmacellulare (PDP) del gatto.
Le TTC vengono inoltre usate con azione antibiotica in
rare infezioni cutanee, quali micoplasmosi ed infezioni da
forme L nel gatto ed alcune rickeziosi tra cui l’erlichiosi
nel cane.
Sono rari nel cane e piu` frequenti nel gatto, ed includono
disturbi gastro-enterici, discrasie ematiche e tossicità epatica e
renale. In soggetti in crescita si puo` manifestare alterazione
del colore dentale e riduzione dello sviluppo scheletrico.
MODALITÀ D’AZIONE
Le TTC esercitano azione batteriostatica inibendo la sintesi proteica batterica e svolgono attivita` immunomodulatrice ed antinfiammatoria sopprimendo la trasformazione
blastogenica dei linfociti, la produzione di anticorpi e la chemotassi dei leucociti. Inoltre inibiscono l’attivazione del
complemento, delle lipasi e delle collagenasi e della sintesi
di prostaglandine.
PROTOCOLLI
Se la tetraciclina e` associata a niacinamide, si utilizza
una dose iniziale di 500 mg PO tid in cani con peso maggiore di 10 kg; di 250 mg PO tid in cani di peso minore di 10 kg
di entrambi i farmaci. La somministrazione puo` essere ridotta a bid e in seguito a sid. Questo protocollo puo` essere
associato ad altre terapie immunomodulatrici quali glucocorticoidi, vitamina E ed azatioprina. Nel gatto (saltuariamente
nel cane) le TTC si somministrano come unico farmaco, e in
particolare nella PDP si utilizza la doxiciclina a 5-10 mg/kg
PO sid. Per il trattamento delle infezioni il dosaggio varia da
5-10 mg/kg PO bid o sid (doxiciclina) a 20 mg/kg PO tid (tetraciclina e ossitetraciclina). Le TTC come immunomodulatore dimostrano un’efficacia sovente parziale e occasionalmente totale, presentano ridotti effetti collaterali, costi contenuti e di solito sono accettate favorevolmente dai proprietari
rispetto ad altre terapie immunomodulatrici.
Bibliografia disponibile su richiesta.
5
Clinical Evaluation of Dogs with Tremor
Rodney S. Bagley
DVM, Dipl. ACVIM - Washington State University, College of Veterinary Medicine
Tremor is the most common involuntary movement disorder in human beings, and is surprisingly common as a clinical abnormality in dogs. This review will discuss the pathophysiological events resulting in tremor, differential diagnosis of diseases with tremor as a predominant clinical sign,
and specific and symptomatic treatment of these diseases.
DEFINITION
Tremor is a rhythmic, oscillatory, involuntary disorder of
movement resulting from alternate or synchronous contraction of reciprocally innervated, antagonistic muscles. Electromyographically, tremor is characterized by rhythmic
bursts of motor neuron activity occurring in opposing muscle
groups. The contraction of muscles with opposing function
gives tremor a biphasic nature. This biphasic character differentiates tremor from other abnormalities of movement.
While seen during the awake state, true tremor should cease
with sleep.
Many abnormalities of movement may be confused with
true tremor. These include shivering, shuddering, myoclonus,
tetany, weakness, myotonia, and seizure.
CLASSIFICATION OF TREMOR
IN HUMAN BEINGS
Tremor in human beings can either be normal (physiological) or abnormal (pathological). Physiological tremor is
present in all muscle groups in the waking state. This tremor
may partially result from passive vibration of body tissues
produced by mechanical activity of the heart, however, its
true origin is not yey known.
Tremor is considered pathological when it impairs normal function. Pathological tremor is thought to result from
imbalances of neurotransmitters such as dopamine, acetylcholine, and gamma-aminobutyric acid. Various pathological tremor syndromes exist in human beings including resting (Parkinsonian) tremor, intention or ataxic tremor, action
tremor, hysterical tremor and a mixed tremor having components of various types of tremor.
CLASSIFICATION OF TREMOR IN DOGS
Tremors are classified in dogs depending upon whether
the tremor is localized to one body area or is generalized.
PATHOPHYSIOLOGY OF TREMOR
Localized tremor
Tremor is a disorder of movement. Therefore, areas of
the nervous system primarily responsible for normal movement, when abnormal, may generate a tremor. In human beings, these areas include the basal nuclei and other components of the extrapyramidal system, cerebellum, diffuse neuronal cell bodies involved in segmental and supraspinal reflex mechanisms, other components of the lower motor neuron, and the interconnecting pathways. Additionally, abnormalities of mechanical components of the limbs (e.g. bones,
joints and tendons) may also result in tremor. Species differences exist as to which anatomical areas within the nervous
system, when abnormal, result in tremor. For example, lesions involving the basal nuclei and substantia nigra commonly result in tremor in human beings but not in dogs. Caution should be exercised when attempting to directly correlate tremor-producing lesions in human beings with similar
lesions in non-primates.
Localized tremors are confined to one limb or body area.
For example, tremor restricted to only the pelvic limbs may
be seen in dogs with lumbar and sacral disease. This tremor
may result in part to muscle weakness from spinal cord or
peripheral nerve impingement, or possible occurs as the result of pain. Pain in the limbs from musculoskeletal disease
may also result in tremor. Compressive spinal or nerve lesions such as stenosis, intervertebral disk disease, neoplasia
and diskospondilytis are also possible. A senile tremor, primarily involving the pelvic limbs has also been reported, the
etiology and pathogenesis of which remains unknown.
Dogs occasionally are admitted with tremor involving
only the head. This type of tremor most likely results from
tremor of the neck muscles. It direction can be eihter in an
up-down (affirmation tremor) or in a side to side plane.
Some refer to this as a head bob. This head tremor appears
to occur without definable cause in some breeds such as the
6
Dobermans and Bulldogs. Head tremors or bobs have been
reported in a dog undergoing peritoneal dialysis for renal
failure and in a dog with iatrogenic hypoparathyroidism. The
author and others have seen dogs with a variety of systemic
illness receiving multiple drugs therapies have similar
tremors. Additionally, a dog evaluated at Washington State
University with syncope due to third degree heart block had
intermittent affirmation head tremor.
In human beings, a nodding of the head can occur with lesions of the thalamus. A head tremor in an anterior-posterior
direction also may accompany midline cerebellar lesions.
Generalized tremor
Generalized tremor is more common than localized tremor.
This type of tremor can result secondary to intoxications, drug
therapies, congenital myelin abnormalities, storage diseases,
encephalitis, or may arise without a definable cause.
Almost any toxicity may result in tremor as a component
of its induced body dysfunction. Tremor is common with
organophosphate, hexachlorophene and bromethalin toxicity. Metaldehyde and strychnine usually cause tetany, however, tremor may also be seen. Mycotoxins such as pentitremA have been associated with tremor in a dog.
The generating mechanism of tremor with many of these
toxic substances is not known. Pathological alterations in the
nervous system such as intramyelinic edema caused by
agents such as hexachlorophene and bromethalin could possibly alter nerve impulse conduction to result in tremor. Other substances most likely result in imbalances in neurotransmitter concentrations as a tremor-producing mechanism.
Numerous drug therapies may cause tremor as a side effect,
possibly through alterations in the normal function of the extrapyramidal system and alterations in the balance of normal
neurotransmitter levels. Examples include fentanyl/droperidol,
epinephrine, isoproterenol, and 5-flurouracil.
Abnormal myelination of the central nervous system can
affect nerve impulse conduction and cause tremor. Many
breeds are affected including the chow chow, springer
spaniel, samoyed, and weimaraner. Tremor in these animals
is worse with excitement and stops during sleep. It is possible that altered impulse conduction or spontaneous discharge
of non-myelinated axons may generate the tremor.
Storage diseases and primary degenerative diseases of
the nervous system may also have tremor as a presenting abnormality.
Generalized tremor may also occur secondary to inflammatory brain disease. This is seen commonly in dogs with
white hair coats, however, dogs with various other hair coat
colors may be similarly affected. An increased incidence of
this disease may be seen in Minature pinshcers. Most affected dogs are usually less than two years of age when a generalized tremor begins. This tremor is worse with excitement
and lessens with sleep, however, the author has seen some
dogs with this type of tremor that had a persistent thoracic
limb myoclonus while under general anesthesia. Other clinical signs may suggest a diffuse central nervous system
problem. These include menace deficits, nystagmus, conscious proprioception deficits, and seizures. Six of seven
Maltese terriers evaluated with generalized tremor by the author had a mild, lymphocytic pleocytosis upon cerebrospinal
fluid analysis. Ventricular dilation was an associated abnormality found in four of four of the affected Maltese terriers
upon computed tomography evaluation of the brain. To date,
no infectious agents have been isolated from any of the affected dogs, but extensive laboratory evaluations for infectious agents have not always been performed.
Histological examination of similarly affected dogs revealed a mild, non-suppurative meningoencephalomyelitis
in most. Not all dogs examined histologically have pathological changes in the central nervous system. Speculation as
to the pathogenesis of this disease has focused on a possible
autoimmunological reaction. A definitive cause for this disease has not been established.
TREATMENT
Treatment of tremor depends upon the inciting underlying cause. Localized tremor in the pelvic limbs may warrant
evaluation for possible compressive spinal cord or peripheral nerve abnormalities. Surgical correction of the compression may result in resolution of this tremor.
When generalized tremor is seen, toxicity should be
eliminated if possible. Offending drug therapies should be
discontinued. While there is no specific treatment for congenital myelin abnormalities, the tremor in some of these
dogs such as the chow chow and the weimaraner may improve as they mature.
Generalized tremor secondary to nervous system inflammation usually improves with administration of glucocorticoids at immunosuppressive dosages. The tremor usually
lessens or resolves within 1 to 3 weeks with this therapy. The
dosage of corticosteroid can then be slowly decreased. If the
drug is decreased too rapidly, tremor may recur. If recurrence is seen, a prolonged taper of corticosteroid over 4 to 6
months may be necessary. Occasionally, a dog may require
corticosteroid treatment indefinitely to control the tremor.
Other drugs used in human beings with tremor such as
propranolol, phenobarbital and primidone have either been
used to infrequently to assess therapeutic response on are not
affective at controlling generalized tremor in dogs.
Further Reading
1.
2.
3.
4.
5.
6.
7.
Bagley RS. Tremor syndromes in dogs:Diagnosis and Treatment. J
Small Anim Pract 1992; 33:485-490.
Bagley RS, Kornegay JN, Wheeler SJ, Plummer SB, et al. Generalized tremors in Maltese terriers:Clinical Findings in seven cases. Accepted for publication, J Am Animal Hosp Assoc 1993, (In Press).
Cuddon PA. Tremor syndromes. Progress Vet Neurol 1990;1:285299.
deLahunta A. Upper Motor Neuron. In: Veterinary Neuroanatomy
and Clinical Neurology, 2nd edn, Philadelphia, WB Saunders Co,
1983, 145-151.
Farrow BH. Generalized tremor syndrome. In: Kirk RW, ed, Current
Veterinary Therapy IX, Philadelphia, WB Saunders Co, 1986, 800801.
Jankovic J, Fahnn S. Physiologic and pathologic tremors. Annals of
Internal Medicine 1980; 93:460-465.
Kornegay JN. The trembling dog. Proceedings of the Americian Animal Hospital Association Annual Meeting 1986, 406-409.
7
Disorders of balance:
vestibular and cerebellar disease
Rodney S. Bagley
VESTIBULAR DISEASE
CLINICAL SIGNS OF VESTIBULAR DISEASE
Disease of the vestibular system results in some of the
most dramatic clinical presentations seen in clinical neurology. The vestibular system is largely responsible for
keeping the animal oriented with respect to gravity.
Vestibular dysfunction is reflected, therefore, in mal positioning of the body including the head, limbs, and eyes.
Falling, incoordination, head titling, nystagmus, and ataxia
are often seen.
Clinical signs of vestibular dysfunction reflect abnormal
orientation of the head, limbs, and eyes. A head tilt, nystagmus, and ataxia are common, regardless of whether the disease involves the peripheral receptors (peripheral vestibular
disease) or the central nuclei, cerebellum, or projection
pathways (central vestibular disease). The head is usually
tilted in the direction of the lesion. With lesions of the caudal cerebellar peduncle, however, the head may be tilted
away from the side of the lesion. An associated ipsilateral
hemiparesis is often helpful in lesion localization as to the
side of the lesion.
Nystagmus, a characteristic eye movement with a quick
and slow phase, is commonly associated with vestibular dysfunction. Nystagmus can be induced normally (oculovestibular response) by turning the head from side to side. The fast
phase of eye movement is in the direction that the head is
moved. This slow drift and quick reset during sideways
movement of the head is normal. In animals with bilateral
vestibular disease, the oculovestibular response is absent.
When the vestibular system is dysfunctional, the eyes have
a tendency to spontaneously drift in the direction of the lesion (slow phase), and, through a brain stem reset mechanism, the eyes are quickly returned to their initial location
(fast phase).
Abnormal nystagmus can occur spontaneously (present
at rest) or with abnormal head positions (i.e. positional nystagmus). This nystagmus is only present when the head is
forced in an abnormal orientation by the examiner. A positional nystagmus is most easily elicited by placing the animal upside down on its back. The direction of the nystagmus
is described in relation to the horizontal axis through the
palpebral fissure. With a horizontal nystagmus, eye movement is in the direction of this axis. A vertical nystagmus is
in the direction perpendicular to this axis. With a rotatory
nystagmus, the eye moves around the parasagittal axis in either a clock-wise or counterclock-wise direction.
By convention, the direction of the nystagmus is described according to the direction of its fast phase. This can
be confusing, as the lesion is present on the side of the slow
phase of the nystagmus. With peripheral lesions, the fast
ANATOMY
The vestibular system is made up of receptor organs
within the ear. These receptor organs sense the static position and movement of the head in relation to the ground
(gravity). For integration of static posture, small, weighted bodies (statconia) of the vestibular receptors (macula
utiricule and sacularis) within the inner ear are acted upon
by gravity.
Statconia lie within a gelatinous covering. Cilia from the
vestibular receptor cells protrude into this gelatinous covering. The force exerted on these statconia results in deflection
of the ciliated receptor, thus providing positional information which is integrated centrally.
For detection of head motion, movement of fluid (endolymph) in small tubular structures (semicircular canals)
results in motion of cilia on additional receptor cells
within terminal dilations (crista ampullaris). This movement of cilia excites the receptor cell which conveys information, through the vestibular nerve, to the central
components of the vestibular system. Thus, the vestibular
receptors collect information regarding the movement of
the head in space.
Nerve fibers coursing from these peripheral receptors
form the vestibular nerve proper. The nerve itself is relatively short. Nerve fibers can then terminate in the vestibular nuclei or within parts of the cerebellum (flocculonodular lobe)
associated with vestibular functions, providing the anatomic
reason that vestibular-type signs can be seen with cerebellar
diseases.
8
phase of the nystagmus is directed away from the side of lesion. With central lesions, the direction of the slow phase in
relation to the side of the lesion can vary.
The vestibular system affects limb movement, normally
being facilatatory to ipsilateral limb extension. A lack of
vestibular input can result in ataxia or falling, and rolling.
The laterally recumbent animal will prefer to lie on the side
of the body ipsilateral to the lesion. The ipsilateral limb often will have decreased extensor tone compared with the
contralateral limbs having increased extension tone. The animal may circle, usually towards side of the lesion. Central
lesions affecting the vestibular system often involve ascending and descending motor and sensory pathways to the limb.
Paresis, therefore, is common. As the vestibular influence
over limb function is ipsilateral, a unilateral brain stem lesion will affect the ipsilateral limbs.
Normal vestibular control is also important for maintenance of the eye in a normal position within the orbit.
Vestibular information is projected through the medial longitudinal fasiculus to cranial nerves III, IV, and VI. If the
vestibular input is abnormal, an abnormal eye position (strabismus) may be seen when the examiner moves the head into an aberrant position. This is most readily seen as the animal’s head is extended dorsally. When viewed from above, a
ventral or ventrolateral strabismus is present in the eye on
the affected side. The dorsal sclera of this affected eye is
more exposed than in the unaffected eye.
Vomiting and nausea are common in humans, more often
associated with peripheral vestibular disease. Vomiting is also recognized in animals, more often with acute vestibular
dysfunction. Nausea is difficult to assess in animals but may
contribute to the anorexia often seen with acute vestibular
dysfunction.
NEUROANATOMICAL LOCALIZATION
Differentiation as to whether the lesion is central (within
the brain stem) or peripheral (within CN VIII proper or its
peripheral receptors) is important for selection of appropriate diagnostic tests (Table 1). The presence of certain clinical signs are associated with a central vestibular lesion. If
these signs are not present, however, a central lesion cannot
be excluded. A head tilt, horizontal or rotatory nystagmus,
and ataxia can occur with both peripheral and central
vestibular disease. A positional vertical nystagmus and limb
paresis are the most consistent signs of central vestibular disease. With unilateral central vestibular lesions, hemiparesis
may be seen ipsilateral to the lesion. Occasionally, a hemiparesis is present on the side of the body opposite to the direction of the head tilt (paradoxical vestibular syndrome). In
this situation, the lesion occurs on the side of the body ipsilateral to the hemiparesis.
In dogs with bilateral peripheral vestibular abnormalities, no oculovestibular response is elicited upon head movement. The animal often has a wide-based stance. The head is
held closer to the ground and may be swung in wide excursions from side to side.
Once the lesion has been localized, appropriate differential diagnoses can be formulated. Unfortunately, intracranial
Table 1 - Differentiation of Peripheral Versus Central
Vestibular Disease
(Important differences in clinical signs that suggest central
vestibular disease are underlined)
Clinical Sign
Central
Peripheral
Horizontal
Rotatory
Vertical
Horizontal
Rotatory
(positional)
Changing
Constant
Head tilt
Present
Present
Cranial Nerve
Deficits
Any other than VII
VII
Horner’s
+/-
+/-
Conscious
Proprioceptive
Abnormalites
Present
Absent
Nystagmus
(spontaneous)
lesions occasionally result in signs indicative of a peripheral
lesion. Conversely, animals with acute, severe peripheral
vestibular dysfunction, may be so incapacitated that accurate
interpretation of neurologic examination findings may not
be possible. Because of these nuances, if the examiner is unsure of location of the lesion, an evaluation for central
vestibular disease should occur concurrently with an evaluation for peripheral disease.
PERIPHERAL VESTIBULAR DISEASES
Idiopathic peripheral vestibular disease occurs in both
dogs and cats (Schunk 1990). Older dogs (canine geriatric
vestibular disease) and young to middle aged cats are most
commonly affected. Cats in the northeast are often affected
in late summer and early fall. No cause is defined. In the
southeast, a similar syndrome is suspected to be caused in
cats by eating of the tail of the blue tail lizard.
Clinical signs are of an acute peripheral vestibular disorder with nystagmus (horizontal or rotary), head tilt (toward the side of the lesion), rolling and falling. Often
these animals are initially so incapacitated that their are
misdiagnosed with cerebrovascular accidents. Clinical
signs, while initially severe, are restricted to the vestibular
system. If Horner’s syndrome or facial nerve paresis are
also present, other differentials should be considered. Differential diagnosis of peripheral vestibular disease includes otitis interna in dogs and cats, middle ear polyps in
cats, trauma, and neoplasia (squamous cell carcinoma of
the middle ear) in both species. Otoscopic examination,
bulla radiographs, and other advanced imaging studies
(computed tomography (CT), magnetic resonance (MR)
imaging) are normal.
Clinical signs of idiopathic vestibular disease usually improve dramatically in 3 to 5 and are resolved by 2 to 4
weeks. The nystagmus usually resolves quickly (within the
first few days). Improvements in posture and walking occurs
within 5 to 7 days, whereas a mild head tilt may remain persistent. While most animals compensate well, some may
have episodic ataxia when performing task such as jumping
up on furniture. No treatment has proved beneficial and recurrence is possible.
Otitis media/interna is a common cause of vestibular
dysfunction. Most often this is due to a bacteria infection, either from extension from the external ear or auditory tube, or
less commonly, from hematogenous spread. Foreign bodies
such as grass awn migration may predispose to severe ear infections.
Clinical signs may reflect either primary ear, vestibular,
or auditory dysfunction. A painful external ear and or pain
on opening the mouth is often present. It has been suggested that up to 50% of animals with otitis media/interna have
associated facial nerve involvement. Otoscopic examination should be used to examine the tympanic membrane.
This may be difficult in animals with severe otitis externa
prior to cleansing. The tympanic membrane is often discolored (hyperemic), opaque, and bulging outward with
middle ear disease. Clear to yellow fluid may be seen behind the membrane. Diagnosis may also be supported by
bulla radiographs or advanced imaging studies (Remedios
and others 1991). Definitive diagnosis is made through culture of the organism via a myringotomy or at surgical exploration.
Tumors of the ear more often occur in older animals.
Squamous cell carcinoma and adenocarcinoma are most
common. Inflammatory polyps occur in cats. Tumors that
extend through the tympanic membrane may be seen during otoscopic examination. Skull radiographs or advanced
imaging is necessary to assess the middle and inner ear.
Abnormalities seen with these studies, however, are not always definitive for neoplasia, and tissue diagnosis at surgery
is often necessary to accurate assessment. Destruction (lysis) of the bone of the bulla is more often associated with
neoplasia as compared to inflammation. Treatment options
include surgical resection/debulking, radiation, and
chemotherapies.
Congenital peripheral vestibular disease is seen in German shepherds, Doberman pinschers, English cocker
spaniels, Siamese and Burmese cats. While often this is an
idiopathic condition, congenital peripheral vestibular disease has been associated with lymphocytic labyrinthitis in
young Doberman pinschers (Forbes and Cook 1991). Bilateral congenital vestibular disease is seen in beagles and Akitas. Clinical signs include head tilt, ataxia and, in some,
deafness. Signs may remain persistent throughout life or
may improve spontaneously. There is no treatment.
Toxicity with metronidazole may result in central
vestibular signs in both dogs and cats (Dow and others
1989, Saxon and Magne 1993). Usually, this is associated
with high doses of the drug. As metronidazole is metabolized by the liver, however, toxic serum levels can occur
9
with appropriate doses in animals with liver dysfunction.
Ataxia is usually the initial clinical sign, progressing to
nystagmus and more severe vestibular dysfunction. Clinical signs often reflect central vestibular dysfunction and
morphological lesions have been found in the brain stem
of some affected dogs. Serum concentrations of metronidazole will be in the toxic range if measured soon after
clinical signs begin. If there is a delay in collecting blood
for drug concentrations after the initiation of clinical
signs, serum concentrations of methronidazole may be
decreased into the normal range even as the clinical signs
remain persistent.
There is no specific treatment for methronidazole toxicity. Discontinuation of the drug is imperative. If clinical signs
are initially severe, some dogs may die. Other dogs will recovery completely, usually over 1 to 2 weeks.
Aminoglycosides, administered either systemically or
topically, may cause deafness and vestibular signs. Streptomycin and gentamicin have the most pronounced effects on
the vestibular receptors, while neomycin, kanamycin, and
amikacin preferentially damage auditory receptors.
Chlorhexidine solution used to clean the external ear may result in vestibular abnormalities.
Other idiopathic or inflammatory neuropathies may affect the vestibular nerve. Overall, these diseases are poorly
described and difficult to definitively diagnose. Similarly, a
possible relationship exists between some metabolic diseases such as hypothyroidism and a vestibular neuropathy.
A cause and effect relationship, however, is not always established.
CENTRAL VESTIBULAR DISEASES
Tumor of the infratentorial space such as meningiomas
and choroid plexus tumors may cause vestibular signs due to
infiltration or compression of the vestibular nerve. Meningiomas may form a mass or grow in a sheet-like configuration (“en plaque”). Choroid plexus tumors arise around the
fourth ventricle, often at the level of the lateral apertures. Diagnosis of a intracranial mass is made with advanced imaging studies. Lesions and associated brain structures are often
better seen with MR imaging as compared to CT as beamhardening artifact with the latter commonly obscures structural detail in this area. Surgical debulking or resection of
these tumors is ideal, but is often hindered by lack of surgical exposure and intimate association with vital brain structures. Irradiation may provide some benefit by slowing tumor growth. Choroid plexus tumors, however, are relatively
radiation-resistant.
Thiamine deficiency is the most common nutritional deficiency affecting the central nervous system. This deficiency most often affects cats and results in lesions in the oculomotor and vestibular nuclei, the caudal colliculus and lateral geniculate. The earliest clinical sign is vestibular ataxia,
progressing to seizures with ventral neck flexion and dilated,
non-responsive pupils. Treatment in administration of thiamine, with paternally or intravenously.
Inflammatory disease can affect the brain stem as well as
other areas of the nervous system. These include both infec-
10
tious and non-infectious etiologies. The incidence of infectious diseases associated with meningitis varies with geographic location. Most meningitis syndromes (~60%) in
small animals do not have a definable infectious cause. Infectious agents causing brain disease include viral (distemper, parvovirus, parainfluenza, herpes, feline infectious peritonitis, pseudorabies, rabies), bacterial, rickettsial (Rocky
Mountain spotted fever, Ehrlichia), spirochetes (Lyme disease, leptospirosis), fungal (blastomycosis, histoplasmosis,
cryptococcosis, coccidioidomycosis, aspergillosis), protozoal (toxoplasmosis, neosporosis), and unclassified organisms (protothecosis).
Specifically, the rickettsia associated with Rocky Mountain spotted fever commonly involves the brain stem, particularly the vestibular system (Greene and others 1985). Usually there is a history of systemic illness (usually with
thrombocytopenia) 5 to 10 days prior to development of neurological signs. As the animal’s fever is decreasing, neurological signs appear. There is no mass lesion present on intracranial advanced imaging studies. Occasionally, increased
contrast enhancement is noted in the choroid plexus area in
affected dogs. This must be differentiated from the degree of
contrast enhancement normally seen in these structures.
Cerebrospinal fluid usually contains milder increases in nucleated cells (<50 nucleated cells/µl; normal <5 nucleated
cells/µl) and milder increases in protein concentration (< 50
mg/dl; normal < 25 mg/dl). Diagnosis is supported by increasing serum titers to the organism, but results often are
available after the disease has progressed. Prognosis is dependent primarily on the severity of clinical signs prior to
treatment. Dogs that are severely obtunded prior to treatment
are less likely to recover. Therefore, dogs with clinical features of vestibular disease after a systemic febrile illness associated with thrombocytopenia should be treated with tetracycline or doxocycline prior to establishing a definitive diagnosis with titers.
Brain stem trauma usually occurs secondary to being hit
by a car. Brain stem function can be assessed by evaluation
of cranial nerve function, particularly the oculovestibular
response. Occasionally, dogs have brain stem signs with
cranial cervical lesions, therefore, manipulation for the
oculovestibular response should be made only after assessing for unstable cervical fracture or luxations. Also, an
otoscoptic examination may reveal hemorrhage in the ear
canals.
Diagnosis is supported by a history of a witnessed traumatic event. Skull fractures may be seen with skull radiography. Because of the complexities of the skull, however,
subtle fractures are easily missed. Advanced imaging studies
are used to assess for intracranial hemorrhage and edema.
With acute trauma (within the first 12 hours), CT may be
better at delineating intracranial hemorrhage. Treatments
center around recognizing and treating the pathophysiologic
sequelae to brain trauma such as brain edema. Surgical removal of debris or hemorrhage is occasionally necessary to
stabilize intracranial pressure.
Vascular diseases which involve the central vestibular areas and associated cerebellum are uncommon. With the advent of advanced imaging studies, however, antemortem diagnosis should be improved.
DIAGNOSTIC TESTING
If a lesion is suspected to involve the central vestibular
structures (supratentorial, brain stem or cerebellum) in small
animals, an advanced imaging study such as CT or MR
imaging is used to assess the structural integrity of these areas. These studies are non-invasive but do require anesthesia
in all but the comatose animal. One disadvantage of CT is
the significant beaming-hardening artifacts that often occur
in the posterior fossa of animals hindering evaluation of the
vestibular area. Survey radiographs of the skull are useful in
instances of skull fracture or middle ear (bulla) disease,
however, do not allow for assessment of nervous system
parenchyma. If peripheral disease is suspected, a through
otoscopic examination, preferably while the animal is anesthetized, is mandatory.
Cerebrospinal fluid (CSF) analysis is helpful primarily
to determine the presence of inflammatory diseases. In
general, collection of spinal fluid caudal to the level of the
lesion is most accurate for diagnosis.
Fluid is analyzed for cellularity, protein content, and
cell morphology. While CSF analysis is often helpful in determining the presence of nervous system disease, used
alone, it does not often lend for a specific etiologic diagnosis. Titers to specific infectious agents can be measured
in CSF to assess for intrathecal production of antibody. In
the presence of blood-brain-barrier breakdown, however,
antibodies may non-specifically cross into the CSF from
the systemic circulation. In this instance, correlation of the
CSF to serum titer may be necessary. An increased antibody titer in the CSF relative to the serum antibody titer
suggests local production of antibodies within the CNS
suggestive of actual CNS infection. Protein electrophoresis
on CSF can give additional information concerning integrity of the blood-brain barrier and local production of immunoglobulins.
Recording the brain stem auditory potential (BAEP or
BAER) may be helpful in determining the presence of intact
hearing pathways and may also provide some information
about the integrity of central (brain stem) projection pathways associated with hearing (Steiss and others 1994, Fischer and Obermaier 1994). BSEP testing requires availability of the equipment and expertise in performing and evaluating the tests.
Surgical biopsy is often necessary for definitive antemortem diagnosis of structural intracranial disease. This is
more difficult in the infratentorial space as surgical exposure, especially of ventrally-located lesions, is often incomplete. Surgical exposure of lesions at the cerebellopontine
angle area may be increased by occlusion of the overlying
transverse sinus and removal of the overlying bone in this
area. The limited access to this area often hinders complete
lesion resection.
For lesions of the ear canal and bulla, lateral ear canal
resection and bulla osteotomy, receptively or in combination are useful for biopsy, lesion resection and drainage of
infected tissue. If these procedures are performed for ear exploration in animals without vestibular signs, head tilts, ataxia and nystagmus may result from damage of the vestibular
structures during the surgical procedure itself.
TREATMENT
Specific treatments can best be recommended after a definitive diagnosis is made.
If intracranial tumors are diagnosed, specific treatments
such as surgical debulking/resection and radiation therapy
may be helpful. With primary inflammatory diseases, the etiological organism should be determined, if possible, and
specific treatments directed toward killing the organism.
With Rocky Mountain spotted fever, tetracycline and doxocycline can eliminate the vestibular signs. With toxoplasmosis, a combination of clindamycin and trimethoprim/sulfadiazine will often improve or eliminate clinical signs. Non-infectious, inflammatory CNS disease will initially be responsive to corticosteroids. Granulomatous meningoencephalitis
has also been treated with irradiation.
Non-specific treatments include protecting the eyes
from damage, especially if there is an associated facial
nerve deficit or if the animal is lateral recumbent and rolling
into the ground. Antihistamines, such as diphenhydramine,
have been useful in decreasing anixety and anorexia and, in
some instances, the severity of the associated head tilt and
nystagmus.
CEREBELLAR DISORDERS
Normal Anatomy and Function
of the Cerebellum
The cerebellum is located dorsal to the fourth ventricle in
the intratentorial area of the intracranial space. It contains
groups of cell bodies and interconnecting fibers that influence to “smoothness” and coordination of movement. The
cerebellum receives information through multiple afferent
pathways. There are two main collection of afferent fibers to
the cerebellum. the mossy fibers, which carry fibers from the
pontine nuclei, tectum, red nucleus, reticular formation,
vestibular nuclei, and the spinocerebellar tracts, and the
climbing fibers, incoming fibers from the olivary nuclei.
The spinal projections to the cerebellum come primarily
from the spinocerebellar pathways. These pathways transmit
proprioceptive (unconscious) information from the muscle
spindles and Golgi tendon organs to the cerebellum
Axons of the cell bodies in the vestibular nuclei project
to the cerebellum via the ipsilateral caudal cerebellar peduncle. These terminate mostly in the flocculus of the hemisphere and the nodulus of the caudal vermis (the flocculonodular lobe) and the fastigial nucleus.
The efferent fibers for the cerebellum include fibers coming from the Purkinje cells and the cerebellar nuclei. Efferents influence motor activity by modifying activity initiated
by other nervous system areas. Because of this, no cerebellar efferents descend the spinal cord.
The Purkinje cells, derived mostly from the flocculonodular lobe, project directly to the vestibular nuclei via the
caudal cerebellar peduncle.
Axons from the fastigial nucleus project to the vestibular
nuclei and the reticular formation via the caudal cerebellar
peduncle. The interpositus nuclei neurons project to the red
11
nucleus and reticular formation via the rostral cerebellar peduncle. The neurons from the dentate nucleus project to the
red nucleus, reticular formation, the pallidum, and the ventral lateral nucleus of the thalamus through the rostral cerebellar peduncle.
Clinical Evaluation
The cerebellum can be divided into functional areas in
two ways. The first, on a phylogenetic basis, divides the
cerebellum into the archicerebellum (the flocculonodular
lobe - vestibular functions), the paleocerebellum which include the vermis of the rostral lobe and the adjacent hemisphere (concerned mostly with spinal cord function and postural tone), and the neocerebellum which includes the vermis
of the caudal lobe and most of the cerebellar hemispheres
(regulation of skilled movement)
The cerebellum can also be divided functionally along its
sagittal axis. The medial zone includes the vermis and fastigial n., important for regulation of tone for posture, locomotion and equilibrium. The intermediate zone includes the
paravermal cortex and interposital n. and is important for adjusting tone and posture for more skilled movement. The lateral zone includes the lateral hemispheres and the dentate n,
which is important for regulation of skilled movement.
Because of its unique function, clinical signs of cerebellar disease are often characteristic and include:
Ataxia and Dysmetria
Intention tremor
Vestibular signs
Menace deficits with normal vision
and normal CN VII function
Decerebellate rigidity
Pupillary abnormalities
Increased frequency of urination
Unilateral lesions of the cerebellum result in ipsilateral
clinical signs.
Ataxia and dysmetria are commonly, but not exclusively, seen with disease of the cerebellum. The animal’s
strength is normal with pure cerebellar disease, however,
movements may be somewhat delayed or compensations
may be exaggerated. If the head is extended and dropped,
it may descend further ventrally than normal (rebound phenomenon).
Intention tremor may involve the whole body but is
usually most obvious in the head. The head usually moves in
an up and down (“Yes”) direction at a frequency of 2 - 4 Hz.
This type of tremor is exaggerated by goal-oriented movement such as eating. This is most likely a dysmetria of head
movement.
Involvement of the flocculonodular lobe or fastigial
area may result in a vestibular disturbance characterized by
lack of balance, nystagmus, and a broad-based stance.
The nystagmus may only be seen when the head is flexed to
one side, with the fast phase directed toward the side in
which the head is tilted. A pendulous eye movement (eyes
oscillate from side to side) may also be seen with cerebellar
disease.
12
A menace deficit with normal vision and normal CN
VII function can be seen ipsilateral to a unilateral cerebellar
lesion as cerebellar influence is needed for performance of
this response.
Occasionally, animals with cerebellar disease may have
abnormal posture. The rostral cerebellar lobe is inhibitory to
stretch in the antigravity muscles, and lesions here may result in opisthotonus with the thoracic limbs extended (Decerebellate posture). The pelvic limbs are usually flexed
forward under the body by the hypertonia of the hypaxial
muscles that flex the coxofemoral joints. If the lesion also
involves the ventral lobules, the pelvic limbs may be in rigid
extension. Reflexes are usually exaggerated.
With unilateral lesions of the fastigial or interposital nuclei, a pupillary dilation which is slowly responsive to light
may be seen (Holliday 1979/1980). Occasionally, the third
eyelid may protrude and the palpebral fissure may be enlarged.
The pupillary dilation occurs in the eye ipsilateral to an
interposital nuclear lesion and contralateral to a fastigial nuclear lesion. Overall, pupillary abnormalities secondary to
cerebellar disease are uncommon.
The cerebellum normally has an inhibitory influence on
urination. Rarely, a cerebellar lesion will result in frequent
urination due to loss of this inhibitory input.
PARADOXICAL VESTIBULAR SYNDROME
Cerebellar lesion of the caudal cerebellar peduncle or
flocculonodular lobules may cause clinical signs of vestibular disease (delahunta 1983, Holliday 1979/1980). The head
tilt, however, is to the side away from the lesion. Postural reaction deficits ipsilateral to the lesion will localize the lesion
to the correct side.
DISEASES OF THE CEREBELLUM:
Cerebellar abiotrophies result from loss of a vital substance necessary for continued life of the neuron. These
diseases are seen most notably in the Kerry blue terrier,
Gordon setter, Rough-coated Collie, Border Collie, Bull
Mastiff and rarely in Samoyeds, Airedales, Finnish harriers, Labrador retrievers, Golden retrievers, beagles, Cocker Spaniels, Cairn terriers and Great Danes (deLahunta1980). In Gordon setters, a late onset cerebellar degeneration has been described (Steinberg and others 1983).
Similarly, storage diseases can result in cerebellum degeneration. Clinical signs are of a progressive cerebellar disease. Diagnosis is based upon biopsy or necropsy. No treatment is effective.
Hypomyelination or dysmyelination of the CNS is seen
in many breeds including the Chow Chow, Springer spaniel,
Samoyed, Weimaraner, and Bernese mountain dogs. This
disease is inherited in an X-linked manner is springers. Individual cases are reported in a dalmatian and a mixed breed
dog. Clinical signs consist of tremor which may appear to be
cerebellar in origin. This tremor usually worsens with excitement.
Abnormal oligodendrocyte numbers or function is the
suggested pathogenic mechanism.
Tremor usually begins in these dogs by weeks of age. It
is most commonly a generalized tremor, which may distinguish itself from the predominent intention tremor of the
head seen with cerebellar disease.
Diagnosis is based upon clinical signs and signalment.
Antemortem diagnosis requires brain biopsy. No treatment
is helpful, however, oligodendrocyte transplant studies are
ongoing. Chow chows and weimaraners may become normal with maturity.
Neuroaxonal Dystrophy is a disease of Rottweiler dogs
(Chrisman 1986), but also collies, chihuahuas, and a family of
domestic cats. In Rottweilers, this is charaterized by cerbellar
signs (ataxia, hypermetria, loss of meance, head tremor) begining at 1 to 2 years (ataxia) and progressing over the next 2
to 4 years (menace deficits, intention tremor). Conscious proprioception remains intact. The cell bodies in the grey matter
are affected (axonal spheroids) throughout the nervous sytem
except the cerebral cortex. The most severe lesions are in the
spinocerebellar tracts and the Purkinje cells. Diagnosis is usually postmortem, however, antemortem biopsy of these areas
may show pathological changes. No treatment is known.
Leukoencephalomyelopathy has been seen in two young
Rottweilers (Chrisman 1986) with progressive ataxia and
weakness. No head signs are seen, even though pathologically the deep cerebellar white matter is abnormal (demyelination). Clinical signs suggest a pure spinal cord problem.
Congenital malformations of the cerebellum are occasionally seen. Caudal vermian hypoplasia is described, with
some dogs having associated ventricular dilation (Dandy
Walker malformation) (Kornegay 1986). Cerebellar hypoplasia has been recognized in chow chows, Irish setters
and wire-haired fox terriers. The latter two breeds may have
concurrent lissencephaly. Cerebellar aplasia has been reported in Siberian huskies.
Feline cerebellar hypoplasia is caused by inutero infection with the panleukopenia virus (parvovirus), which affects the external germinal layer of the cerebellum and prevents the formation of the granular layer. Some affected cats
have a concurrent hydrocephalus and hydranencephaly.
The clinical signs are of a diffuse cerebellar disease. The
course is nonprogressive. Diagnosis can be aided by history
and clinical signs. Magnetic resonance imaging may help to
define the nature of the lesion. No treatment is helpful.
Primary or secondary neoplasia involving the cerebellum
is uncommon. Medulloblastoma is a primary brain tumor
that rarely involves the cerebellum in dogs. Embryonal cysts
such as dermoid and epidermoids coomnly affect this area.
Intracranial injury from a traumatic incidence may affect
the cerebellum as with other intracranial structures. Rarely,
thromboembolic and vascular disease involves the cerebellum (Bagley and others 1988).
Hydrocephalus that involves the fourth ventricle may result in brain stem and cerebellar compression. This may occur as a component of a more generalized hydroecephalus or
be isolated stirctly the fourth ventricle, possibly due to obstruction of CSF outflow at either the lateral aperatures or
foramen magnum. Syringo- and hydromyelia may be an associated consequence.
Hydrocephalus can result from obstruction of the ventricular system, irritation of the ventricle (from inflammation or hemorrhage), increased size of the ventricles due to
loss of brain parenchyma (hydrocephalus ex vacuo), be present without an obvious cause (congenital), or rarely, be the
result of overproduction of CSF associated with a choroid
plexus tumor. Ventricular obstruction can occur due to intraventricular or extraventricular obstruction.
Hydrocephalus can result in clinical signs due to loss of
neurons or neuronal function, alterations in intracranial pressure, associated pathophysiological effects of intracranial
disease. Some breeds predisposed to congenital hydrocephalus include the Chihuahua, Pomeranian, Yorkshire terrier, English Bulldog, Lhasa apso, toy poodle, cairn terrier,
Boston terrier, pug, pekingese, and Maltese terrier. In young
bullmastiffs, hydrocephalus has been described in association with cerebellar ataxia. In siamese cats hereditary hydrocephalus in transmitted as a autosomal recessive trait.
Clinical signs of hydrocephalus reflect the anatomical
level of disease involvement. Forebrain, vestibular, and cerebellar signs are most common. Severity of clinical signs is
not necessarily dependent upon the degree of ventricular dilation, but rather on a host of concurrent abnormalities including the underlying disease process, associated intracranial pressure changes, intraventricular hemorrhage, and the
acuity of ventricular obstruction.
The diagnosis of hydrocephalus can be aided by information obtained for a variety of imaging and electrophysiologic modalities. Historical, invasive techniques such as
pneumo- or contrast ventriculography have been replaced by
non-invasive evaluations.
Magnetic resonance imaging also affords evaluation of
the ventricular system. This modality provides better for better parenchyma resolution than CT, an is especially useful
for evaluation of the infratentorial structures.
Although the prognosis for resolution of hydrocephalus
is generally poor, there are several medical and surgical
treatment options which may be beneficial. The choice of
treatments is generally dictated by physical status, age of the
animal, and cause of the hydrocephalus if known. Medical
treatment may include general supportive care, and medications to limit CSF production and reduce intracranial pressure. Surgical treatment is designed to provide drainage of
CSF from the brain to another site for absorption.
13
References
Vestibular disease
deLahunta A: In:Veterinary Neuroanatomy and Clinical Neurology, 2nd
edn, Philadelphia:WB Saunders, 1983.
Dow SW, LeCouteur RA, Poss ML, Beadleston D: Central nervous system
toxicosis associated with metronidazole treatment of dogs: Five cases
(1984-1987). J Am Vet Med Assoc 3:365, 1989.
Fischer A, Obermaier G: Brainstem auditory-evoked potentials and neuropathologic correlates in 26 dogs with brain tumor. J Vet Int Med
8:363, 1994
Forbes S, Cook Jr JR: Congenital peripheral vestibular disease attributed to
lymphocytic labyrinthitis in two related litters of Doberman Pinscher
pups. J Am Vet Med Assoc 198:447, 1991.
Greene CE, Burgdorfer W, Cavagnolo R, et al: Rocky Mountain spotted fever in dogs and its differentiation from canine ehrlichiosis. J Am Vet
MedAssoc 186: 465, 1985.
(A description of the central nervous system affects associated with Rocky
Mountain spotted fever)
Mansfield PD. Ototoxicity in dogs and cats. Comp Contin Ed 12:331, 1990
Remedios AM, Fowler JD, Pharr JW: A comparison of radiographic versus
surgical diagnosis of otitis media. J Am Anim Hosp Assoc 27:183,
1991.
Saxon B, Magne ML: Reversible central nervous system toxicosis associated with metronidazole therapy in three cats. Prog Vet Neuro 4:25,
1993.
Schunk KL: Disease of the vestibular system. Prog Vet Neurol 1990;1:247254.
Steiss JE, Cox NR, Hathcock JT: Brain stem auditory-evoked response abnormalities in 14 dogs with confirmed central nervous system lesions.
J Vet Int Med 8:293, 1994
Cerebellar Disease
Chrisman CL. Neuroaxonal dystrophy and leukoencephalomyelopathy of
Rottweiler dogs. In: Kirk RW, ed, Current Veterinary Therapy, 9th
edition, Philadelphia:WB Saunders. 1986:805.
Chrisman CL. Problems in Small Animal Neurology. Philadelphia, Lea &
Fabiger 1991, 62.
deLahunta A. Comparative cerebellar disease in domestic animals. The
Compendium on Continuing Education 1980; 2: 8.
deLahunta, A. In: Veterinary Neuroanatomy and Clinical Neurology, 2nd
edn, Philadelphia:WB Saunders. 1983.
Holliday TA. Clinical signs of acute and chronic experimental lesions of
the cerebellum. Veterinary Science Communications 1979/1980;
3:259.
King AS. Physiological and Clinical Anatomy of the Domestic Mammals
Oxford:Oxford Univeristy Press 1987.
McCormick DA, Thompson RF. Cerebellum: Essential involvement.
15
Intracranial surgery
Rodney S. Bagley
Intracranial surgery has developed into a viable therapy
for an increasing spectrum of intracranial diseases. Improved intracranial surgical techniques and outcomes have
followed two main advances: improvements in critical care
patient management and advancement and widespread use
of non-invasive imaging modalities such as magnetic resonance (MR) imaging. While initially limited by concerns
about patient morbidity and mortality and financial restrictions of the owners, intracranial surgery is now a necessity to
improve quality of life and life expectancy in animals with
certain intracranial disease.
PREOPERATIVE EVALUATION
AND MANAGEMENT
Accurate clinical assessment, neuroanatomical localization, accurate interpretation of diagnostic imaging, and understanding intracranial pathophysiological derangements
are imperitive in the overall management of animals with intracranial disease. The most successful surgeons will be very
competent in clinical evaluation (neuroanatomical diagnosis) and in interpretation of diagnostic testing (especially
magnetic resonance imaging) in addition to having the necessary manual surgical skills. Aspects of neurologic evaluation and interpretation of diagnostic images should be reviewed as needed to gain this expertise.
INDICATIONS FOR INTRACRANIAL
SURGERY
Intracranial surgery is most commonly employed for
removal of intracranial masses, biopsy of intracranial lesions, placement of ventricular shunts, decompression and
debridement of intracranial tissues following exogenous
trauma, and treatment of increased ICP. Intracranial
surgery has less frequently been used in the treatment of
seizures in animals but certainly has a role in this area in
humans. Surgery may include removal of sizable portions
of the skull (craniotomy or craniectomy) or be limited to
smaller burr holes for decompression of hematoma evacuation or stereotactic biopsy.
IMMEDIATE PREOPERATIVE
MANAGEMENT
A consensus on the most appropriate preoperative
management of animals for intracranial surgery is lacking.
Many preoperative procedures are taken from similar experiences in humans, and based on information available regarding pathophysiologic alterations in the CNS and their
treatments.
ANESTHESIA
PATHOPHYSIOLOGY
As with all diseases, and understanding of the pathophysiology associated with the disease is often helpful when
determining the most appropriate treatment. A variety of intracranial diseases affect dogs and cats.
Clinical signs often result not only from mechanical destruction of normal brain but also from associated pathophysiologic alterations induced secondary to the primary
disease process. Effective management of intracranial disease requires recognition and treatment of the primary as
well as of many of these secondary pathophysiological sequelae. (Bagley RS: Intracranial pressure in dogs and
cats. 1996, Bagley RS Vet Clin North Am 1996, Kornegay
JN. Pathogenesis of diseases of the central nervous system.1993)
Anesthetic agents and their effects on the nervous has
been reviewed elsewhere (Shores A. Neuroanesthesia
1985; Cornick JL. 1992, Fenner WR. Neuroanesthesia.
1992). The choice of anesthetic agents depends upon many
factors including ease of administration, rapidity and ease of
recovery, effects on cerebral metabolism and blood flow, alterations in ICP, and familiarity of the anesthetist with the
agent. Specific effects of anesthetic agents on ICP have been
reviewed elsewhere. Most inhalant anesthetics increase ICP
due to their vasodilatory effects on cerebral vessels and subsequent increase in cerebral blood flow. Halothane, for example, causes the largest degree of cerebral vasodilatation.
Increases in cerebral blood flow can increase.(Todd M M
1984). Isoflurane is the most commonly used maintenance
anesthetic agent used for intracranial surgery. (Adams RW
1981, Grosslight K 1985). It has been used safely in both
16
clinical and experimental studies involving intracranial
surgery in dogs and cats. Premedication with benzodiazepenes may help with a smooth induction and provide
short-term seizure control.
Barbiturates can be used during induction to decrease
cerebral metabolism, cerebral blood flow, and subsequently
ICP. (Nordström 1986) Barbiturates may benefit brain
blood flow by causing vasoconstriction in normal tissue;
shunting blood to underperfused or ischemia areas. Other
suggested benefits include decreases in vasogenic edema,
decreased oxygen metabolism, decreases in intracellular
calcium and free radical scavenging. (Nordström 1986) Arterial blood pressure should be monitored closely, as barbiturates can result in hypotension which may decrease cerebral blood flow and increase cerebral ischemia. (Lobato
RD 1988)
HYPERVENTILATION
Once the animal is anesthetized and intubated, hyperventilation can be used to decrease ICP due to the established effects of PaCO2 concentrations on cerebral blood
flow. (Shapiro HM 1975; Lyons MK, 1990. Rosner 1990)
Cerebral vessels are directly responsive to PaCO2 concentrations, with cerebral blood flow coupled to cerebral metabolic rate. The cerebral vessels have the ability to change diameter in response to PaCO2 (chemical autoregulation) as well
as blood pressure (pressure autoregulation) in order to maintain a relatively constant cerebral blood flow. Cerebral vessels change diameter through perivascular changes in pH as
a direct result of PaCO2 concentrations similar to what occurs in the chemosensative area of the medulla oblongata for
stimulation of respiration.
As PaCO2 concentrations increase, cerebral vessels dilate
to increase blood flow to the brain. Poor ventilation and increasing PaCO2 such as with obstruction or kinking of the
endotracheal tube can lead to disastrous increases in brain
volume. This can lead to terminal brain swelling and subsequent herniation. (Kornegay JN, Clinicopathologic features of brain herniation in 1983) If autoregulation is intact, hyperventilation to decrease PaCO2 will cause cerebral
vasoconstriction, decreased cerebral blood volume, and subsequently decreased ICP. Unfortunately, cerebrovascular autoregulatory capability is affected by a variety of intracranial
processes. For example, local acidosis, common in many hypoxic and ischemic areas, will disruption local autoregulatory functions. (Enevoldsen EM1979) If chemical autoregulation is absent in the area of diseased brain, hyperventilation
will not alter the vascular diameter in the affected area. In
this instance, two situations are possible, both dependent upon the premise that cerebrovascular autoregulatory capacity
is absent due to local disease.
Animals should be hyperventilated during intracranial
procedures to maintain PaCO2 in the range between 30 and
35 mm Hg to prevent associated cerebral hypoxia from poor
ventilation. Endotracheal intubation and ventilator support
can be performed under the influence of barbiturate anesthesia or neuromuscular blockade. Appropriate ventilator management is mandatory.
HEAD ELEVATION
Reccommendations for position of the head for intracranial surgery suggest a horizontal or neutral position may
maintain cerebral perfusion. Head elevation to 30o above heart
level, however, has been shown to decrease ICP primarily by
facilitating venous drainage. (Feldman 1992), Schneider GH
1993) In humans it has been shown that cerebral perfusion
pressure and cerebral blood flow is maintained in the 30o head
elevation position and ICP is concurrently decreased. (Feldman Z 1992)
It is helpful to place the animal’s head in holding device
that allows the head to be positioned above the level of the
heart and does not impede venous return by occluding the
jugular veins. If the surgical approach involves the supratentorial areas, then the head is placed in a neutral position parallel the surface of the operating table. The head can be tilted toward one side or the other if needed for adequate exposure. Blood, debris, and saline flush will tend to pool dependently, and this should be kept in mind when positioning the
head. If the lesion will tend to be in the most dependent position of the approach, this debris and fluids may impair visualization for lesion resection. If an approach to the suboccipitial area is planned, then the nose can be pointed downward slightly toward the operating table to facilitate access
to the foramen magnum area.
During surgical preparation of the skin, depending upon
the animal’s position, the possibility exists that the eyes may
be contaminated with surgical scrub solution. This can result
in significant superficial keratitis and possibly corneal ulceration. During skin preparation, the eyes should be aggressively shielded from preparation solution to avoid such contamination.
DIURETICS
Diuretics will help to decrease ICP and improve cerebral
perfusion primarily through their effects on blood viscosity
and intracranial water content. Mannitol and furosemide are
useful in this role. (Ravussion P, 1986; Ravussin P 1985;
Ravussin P 1988; Mendelow AD1985; Shackford 1992;
Abou-Madi M 1987; Cottrell JE 1977; Albright 1984)
These drugs are given immediately prior to performing the
craniotomy in an attempt to decrease the brain size and provide more space between the skull and the brain. In some instances, however, by improving cerebral blood flow it is possible that the risks of hemorrhage are increased.
ANTICONVULSANTS
Many animals requiring intracranial surgery have
seizures as a clinical problem. These animals are often receiving anticonvulsants prior to surgery, which should be
continued in the preoperative period. If animals are not receiving anticonvulsants, and if the risks of seizures after
surgery are significant, then anticonvulsants should be begun
prior to surgery. Ideally, phenobarbital should be begun 1 to
2 weeks prior to surgery to allow for some stabilization of
therapeutic levels prior to the actual surgery. If potassium
bromide is to be used, a longer period of time between initiation of the drug and surgery may be needed. Often, however, surgery may need to be performed in a more expeditious
manner and the ability to achieve steady state therapeutic
levels may not be possible. Loading doses may be useful in
this situation.
CORTICOSTEROIDS
Corticosteroids have received much use in the treatment
of spinal trauma, and have been recommended as a treatment
for elevated ICP. (Hall ED1992; Hall ED 1985) While corticosteroids have shown benefit by reducing cerebral edema
in brain tumor patients, caution has been suggested when using corticosteroids for brain injury. One study in rats has
suggested that corticosteroids may be advantageous in brain
injury, however, corticosteroids may not be efficacious in
head trauma and are known to perpetuate neuronal damage
if ischemia is present. (Braakman R 1983; Sapolsky RM,
1985) Corticosteroid administration may increase blood glucose, a factor that may negatively influence outcome after
head injury. (Lam 1991) Also, the onset of beneficial effects
of decreasing cerebral edema may be delayed too long to be
helpful in acute elevations of ICP.
Whether corticosteroids have the same a potential adverse effects in animals during intracranial surgery is not established. Methylprednisolone sodium succinate (30 mg/kg
IV bolus slowly) is often used immediately preoperatively in
animals receiving intracranial surgery, however, controlled
studies proving benefit of this treatment have not been performed.
ANTIBIOTICS
The necessity for preoperative and intraoperative antibiotics has been debated in human neurosurgery, however,
there is support for the prophylactic antibiotics. (Dempsey
1988; Djindjian 1990) Similar to the reasons supporting
prophylactic antibiotic use for clean surgical procedures, antibiotics are most often given for prolonged (>1.5 hour) procedures, if contaminated body cavities are to be opened (i.e.
the nasal cavity), or if contamination is more likely (excessive number of individuals involved in surgery or traffic in
the OR). Prophylactic antibiotics given are usually first generation cephalosporins (cephalathin 22 mg/kg IV q 1.5 h)
until the end of the surgical procedure.
INTRAOPERATIVE MONITORING
AND TREATMENT
During surgery, standard anesthetic and physiologic
monitoring should occur on a regular basis. This commonly
includes monitoring of heart rate and rhythm, blood pressure, blood gases, urine production, and in some instances,
ICP through objective means. The goal of such monitoring
is to maintain adequate cerebral blood flow without com-
17
promising other systemic organs. These parameters are
maintained through maintenance of systemic blood pressure
through the use of fluid therapy and vasopressive drugs if
needed. Blood gas measurements aid in controlling respiration to avoid increases in PaCO2 and subsequent cerebrovasodilation.
Cerebral perfusion is dependent upon systemic blood
flow and intracranial pressure expressed via the formula
CPP = MABP - ICP (CPP - cerebral perfusion pressure,
MABP - mean arterial blood pressure). (Shapiro 1975;
Germon 1988) For CPP to remain constant, the effects of
increased ICP on blood flow to the brain must be reciprocated for by increases in systemic blood pressure. Cerebral
perfusion pressure is a determinant of cerebral blood flow
(CBF) but is not always equivalent; in many instances, however, as CPP is a reflection of CBF.
Intracranial pressures are monitored objectively in some
situations, however, this type of measurement is not routinely performed in animals. Intracranial pressure monitoring
for dogs and cats has been described. Advantages to ICP
monitoring are that with this measure, trends toward increasing ICP can be recognized early and treated prior to
having life-threatening increases. An objective measure of
ICP and blood pressure also allows for calculation of CPP.
Disadvantages to ICP monitoring included added surgery
time or implantation of the monitoring system, expense, and
the potential for iatrogenic brain damage from the monitoring system. Until some of these disadvantages are overcome,
ICP monitoring will probably not become routine for animals undergoing intracranial surgery. (Crutchfield 1990;
Narayan 1982)
Newer, non-invasive techniques for measurement of the
cerebral blood flow with Doppler may give an indirect measure of ICP. In humans with increasing ICP, transcranial
doppler ultrasound waveforms showed low, then zero, and
finally reversed diastolic blood flow velocities correlated to
increasing ICP. (Hassler 1988; Tucker 1996; Tucker 1997)
SURGICAL PROCEDURES
Surgical anatomical approaches to intracranial lesions
are based upon lesion location, the extent of the lesion, the
anticipated consistency of the lesion, the nature of the lesion
(inflammatory versus neoplastic versus hemorrhage), and
the goal of the surgery (removal versus biopsy versus decompression). More limited approaches are used for biopsy,
decompression of hematomas, and intraventricular shunt
placement. The size and extent of skull removal is also limited by normal anatomical components of the skull, surrounding soft tissues, and the associated vasculature.
A craniotomy is removal of a portion of the skull for access to the intracranial space, with subsequent replacement
of bone. A craniectomy is removal of a portion of the skull
for access to the intracranial space, without subsequent replacement of bone. These procedures are adequate for access
to the intracranial structures for lesion removal or biopsy. As
much exposure as possible of the lesion to be manipulated is
a key aspect of a successful intracranial surgical outcome.
Limited approaches make lesion visualization difficult and
18
increase the risk of iatrogenic brain disease from excessive
brain manipulation. Often, when the intracranial nervous tissues are manipulated, brain swelling ensues. Adequate skull
removal will provide a decompressive effect for this swollen
brain. Conversely, however, over zealous skull removal increases the risk of post-operative scarring (craniectomy
membrane formation) and allows for significant shifts of
brain parenchyma which, in itself, may lead to further brain
damage from vascular compromise.
SURGICAL APPROACHES
AND TECHNIQUES
Multiple surgical approaches to intracranial structures
have been used in dogs. Some of the more standard approaches are summarized.
LATERAL ROSTROTENTORIAL
CRANIOTOMY/CRANIECTOMY
(Oliver JE Jr 1968, Oliver 1966, Sorjonen 1991)
A lateral rostrotentorial craniotomy/craniectomy is used
for exposure of the lateral parietal, temporal, and occipital
cortices. Many of the same basic surgical techniques described are used with other intracranial surgical approaches
differing only in the anatomical site of the surgery.
The animal is positioned in sternal recumbency. The
head is ideally positioned in a head-holding device so as to
avoid compression on the jugular veins (which will subsequently result in increased venous pressure, decreased venous return from the brain, and possibly, increased intracranial pressure). A dorsal skin incision is made on midline extending from just caudal to the level of the eyes to ~2-4 cm
caudal to the external occipital protuberance. Alternatively, a
horseshoe-shaped incision is made beginning ventrally at the
level of the lateral canthus of the eye. The incision is begun
approximately 2-4 cm lateral to the lateral canthus to avoid
damage to the facial nerve and other periorbital structures.
The incision is extended in an arc to dorsal midline, and then
ventrally again in a arc to end caudal to the ear. While this
latter incision may improve access ventrolaterally, because
the skin the head in dogs is relatively movable, similar exposure can be accomplished with a dorsal midline incision.
This avoids iatrogenic damage to the peripheral nerves of the
head, primarily cranial nerve VII.
Dissection is continued through the subcutaneous tissues
and fat. Dissection is continued until the interscutularis muscle is encountered. This muscle is divided ipsilaterally with
an electroscalpel usually as close to midline as possible but
allowing 2-4 mms of dorsal muscle end for reattachment
during closure. The white, smooth, fibrous temporalis fascia
is next encountered. The fascia of the temporalis muscle is
incised from its rostral, dorsal, and caudal attachment to the
skull with a scalpel or electroscalpel 2-4 mms ipsilateral to
midline towards the surgeon. The rostral extent of this incision is usually the zygomatic process of the frontal bone extending caudally along the temporal line, the external sagittal crest, the external occiptial protuberance, and down the
nuchal line to the level of the caudal attachment of the zygomatic arch. The temporalis muscle is then reflected laterally and ventrally from the skull using an electroscalpel or
periosteal elevator. This muscle can be reflected ventrally to
the level of the zygomatic arch. This exposes the frontal,
parietal, temporal, and basisphenoid wing bones.
Four burr holes are placed in a rectangular fashion over
the area of interest using a high-speed air drill. A large round
bit is used when establishing these burr holes. The bone of
the skull is thicker dorsally compared to ventrally and the inner surface of the skull is irregular having thicker and thinner sections. During drilling of the skull it is not uncommon
to encounter bleeding from the dipolic cavities within the
skull. Bone wax (Bone Wax, Ethicon Inc., Johnson and
Johnson Co, Somerville, New Jersey) is used to control
this hemorrhage.
The burr holes are placed at the peripheral extent of
the proposed craniotomy deep to the level of the dura.
The temporal line is the rostral landmark of the caudal
frontal sinus; the nuchal line is the caudal border designating the underlying transverse sinus and tentorium; the
external sagittal crest is the dorsal border marking the
underlying dorsal sagittal sinus. The area is irrigated
with saline during drilling and debris is removed with
suction. Bleeding from medullary bone is controlled with
bone wax (Bone Wax, Ethicon Inc., Johnson and Johnson Co, Somerville, New Jersey).
The burr holes can then be connected with a high-speed
air drill or craniotome to the level of the dura. The dura in
older dogs and cats is often firmly attached to the inner surface of the skull. Drilling should procedure cautiously to
avoid laceration of the underlying dura.
The skull is removed to the level of the dura at the dorsal, rostral, and caudal edges. Again, caution should be exercised when removing the cranial bone, especially in older animals, as the dura is often firmly attached to the overlying skull and can be torn during skull removal. It may be
possible to avoid dura tearing and traumatic removal at the
time the craniotomy bone is removed by levering and prying the bone outwards with a Addson periosteal elevator or
similar instrument while separating the bone from the dura
with a Freer periosteal elevator. After the bone is removed
it is placed in saline if it may be reapposed in during closure. Dipolic bone hemorrhage is controlled with bone
wax. Dural vessel hemorrhage is controlled with bipolar
electrocautery. If necessary, the craniotomy edges can be
enlarged with rongeurs or with a house curette. If there is
bleeding from the edge of the craniotomy that cannot be
controlled easily, it often helps to remove the overlying
bone with rongeurs at the edge to allow direct viewing of
the area of hemorrhage. There are often dural arteries and,
more commonly, veins that traverse from the skull to the
dura that are disrupted during bone removal that will require cauterizing. Using suction to decrease blood volume
in the area and a drop of saline in the area of hemorrhage
between the ends of the bipolar cautery often helps in cauterizing smaller vessels.
After removal of skull, the dura will be exposed. The dura can be incised with a #11 Bard Parker blade after cauterizing the limits of the incision. In some instances, small
veins course from the bone to the dura, and from the dura to
the brain. These can be easily damaged and result in hemorrhage. Control of this hemorrhage is usually accomplished
with bipolar electocautery. Venous hemorrhage can also be
controlled Gel foam (Gel Foam, The Upjohn Co., Kalamazoo, MI) or similar material (autogenous muscle). If the
dura is to be saved to repair, it should be stretched to maintain its length and kept moist. This can be performed by suturing it muscle surrounding the incision.
Extraaxial lesions are removed via blunt dissection
with microdissectors and lintless sponges (Cotton paddies). Gentle abaxial retraction on the lesion aids in removal. Establishing a plane of dissection is very helpful
in lesion removal, but is not always easily accomplished.
The brain parenchyma is the consistency of chilled pudding and does not tolerate significant manipulation.
Therefore, caution should be exercised when dissecting
or manipulating intracranial masses as the pressure exerted on the mass may be distributed to the relatively softer
brain. Brain parenchyma becomes even softer when edematous. This combined with the fact that brain at the
edges of the lesion are often grossly abnormal due the lesion itself make the gross distinction between lesion and
brain parenchyma difficult.
Intraaxial lesions often require incision of a cortex. An
incision is made through a gyrus rather than a sulcus to
avoid larger vessels that tend to lie within the sulci. The
superficial pia and cortical vessels can be cauterized with
bipolar cautery. If intraventricular exposure in needed,
cortical dissection is continued to the level of the ventricle. The outer aspect of the ventricle appears darker (often bluish) in color compared to the surrounding white
matter, and CSF will flow out of the incision when this
layer is penetrated. If previous bleeding has occurred in
the ventricule, the CSF will be yellow to brown (tea-colored) in color. The interior of the ventricle is white in color smooth in texture.
When closing, as the dura has often been damaged or removed during surgery, a dural graft is collected and placed
over the exposed brain. This is most critical when the frontal
sinus has been entered. A temporalis fascia graft is often
used as an autogenous dural substitute. The fascia graft is
placed over the craniotomy defect with the fascia side placed
in contact with the brain. The edges of the fascia are placed
under the edges of the bone to create a seal or in some instances may be sutured in place.
For a lateral rostrotentorial craniectomy, the removed
skull is not replaced as this may help with control of intracranial pressure and brain swelling after surgery. If the
brain is not swollen and the risk of further brain swelling is
minimal then the removed bone may be replaced. The bone
is fitted into place and sutured in place using 2/0 nylon to
avoid metal artifact on postoperative MR studies that can occur with wire sutures. Small holes are drilled in the skull and
mirrored on the bone flap to achieve this purpose.
The cut edge of the temporalis muscle (fascia) is sutured
to the opposite edge of the temporalis fascia that remained
attached to the skull. The interscutularis muscle is reapposed
and sutured, as the subcutaneous and subcuticular tissues.
The skin is then apposed.
19
RADICAL ROSTROTENTORIAL
An extension of the lateral rostrotentorial craniotomy/
craniectomy has been described for access to more rostral
and lateral cortical lesions. (De Wet 1982) A lateral rostrotentorial craniotomy/craniectomy is performed as described,
however, bone removal is extended rostrally and laterally to
open the ipslateral frontal sinus. The outer cortical bone over
the lateral frontal sinus is penetrated to access the air-filled
frontal sinus. The bone over the medial wall of the frontal sinus (lateral to the frontal and olfactory areas) is then removed. This bone is usually removed with a high-speed air
drill. This approach is most appropriate for lateral and rostral superficial dura or cortical lesions.
SUBOCCIPITAL CRANIOTOMY/
CRANIECTOMY
(Oliver 1968)
A suboccipital craniotomy/craniectomy is used for exposure of the caudal cerebellum, caudal medulla oblongata
(obex), and cranial cervical spinal cord (foramen magnum
area). The animal is positioned in sternal recumbency. A dorsal skin incision is made on midline extending from the middle of the skull caudally to ~4-6 cm caudal to the external
occipital protuberance in the dorsal cervical area. Dissection
is continued until the interscutularis, occipitalis, cervicoscutularis, and the cervicoauricularis superficial muscles are encountered. These muscles are divided on midline with an
electroscalpel. The dorsal cervical muscles are divided on
midline to the level of the dorsal arch of C1 and C2, and elevated off of the occipital bone and occipital condyle to the
level of the nuchal line (transverse ridge) using a periosteal
elevator. Brisk bleeding can occur from the occipital emissory vein caudal to the nuchal line.
Using a high-speed air drill, the occipital bone is removed as with a laminectomy by burring the bone away to
the level of the dura. This essentially enlarges the foramen
magnum to the level of the occipital protuberance and
nuchal line. Any bleeding from the medullary bone is controlled with bone wax. Bleeding from the occipital emissary
vein at its exit from the skull (mastoid foramen) can be brisk.
Gel foam, bone wax, or muscle placed in area is often necessary for control of this hemorrhage. The occipital bone
overlying the cerebellar area is relatively thin and often does
not have a medullary area except in larger dogs. The cranial
bone forming the dorsal foramen magnum, however, is
thicker and tends to curve dorsally at the caudal edge (rostral to the formen magnum). With more ventrolateral bone
removal in the foramen magnum area it is not uncommon to
damage the condyloid vein in the condyloid canal. Bleeding
from this vein can be brisk and require pressure from
Gelfoam or muscle to be controlled.
After removal of skull, the dura will be exposed. The dura can be incised with a #11 Bard Parker blade or microscissors after cauterizing the limits of the incision. The suboccipital approach, however, provides for a limited view of the
caudal cerebellum, obex, and dorsal brain stem. Lateral
20
brain stem lesions are often not well seen in a circumferential manner. Over the dorsal foramen magnum area there is
often thin, semi-transparent tissue that covers the obex area.
This tissue is cautiously incised to expose the dorsal medulla oblongata and fourth ventricle.
COMBINED ROSTROTENTORIAL/
SUBOCCIPITAL CRANIECTOMY WITH
TRANSVERSE SINUS OCCLUSION
(Pluhar 1996; Bagley RS Vet Surg1997)
traverse from the skull to the dorsal sagittal sinus and may
bleed during drilling. This hemorrhage is controlled with
bone wax or electrocautery.
When closing, it is important to replace the bone flap to
decrease post-operative scarring. The bone is fitted into
place and sutured using 2/0 nylon.
COMBINATION DORSAL, BILATERAL
FRONTAL, AND TRANSFRONTAL
(Oliver 1968; Oliver 1966; Kostolich 1987)
A combined rostrotentorial/suboccipital craniectomy
with transverse sinus occlusion is used for exposure of the
dorsolateral cerebellopontine medullary angle and unilateral
tentorial area. The animal is positioned in sternal recumbency. A dorsal skin incision is made on midline extending caudally from just caudal to the level of the eyes to ~4-6 cm caudal to the external occipital protuberance, basically combining the skin incisions used for both the lateral rostrotentorial and the suboccipital craniectomies. A rostrotentorial and
suboccpital craniectomies are performed as previously described. The bone encircling the transverse sinus is next
burred cautiously away to expose the vein. After the lateral
bone is removed to this thin cortical layer circumferentially
as far as possible (usually somewhere between 180o and 270o
around the vein). Ventral burring may expose the connections between the transverse sinus and the occipital diploic
vein, the temporal sinus, and the dorsal petrosal sinus.
The thin cortical layer overlying the transverse sinus is
removed with rongeurs. Bone wax is used to occlude the
canal for the transverse sinus (transverse groove) dorsally
and ventrally. After removal of skull, the dura will be exposed. The dura can be incised with a #11 Bard Parker blade
or microscissors after cauterizing the limits of the incision.
BILATERAL ROSTROTENTORIAL (DORSAL)
(Oliver 1968; Bagley RS callosotomy 1995)
A bilateral rostrotentorial (dorsal) craniotomy/craniectomy is used for exposure of the dorsal olfactory, frontal, parietal, temporal, and occipital cortices. The animal is positioned in sternal recumbency. A dorsal skin incision is made
on midline extending caudally from just caudal to the level
of the eyes to ~2-4 cm caudal to the external occipital protuberance. Dissection is continued through the subcutaneous
tissues and fat, the interscutularis muscle, and the temporalis
fascia. Four burr holes are placed in a rectangular fashion,
two on either side of the external sagittal ridge in the
frontal/parietal bone using a high speed air drill. The temporal line is the rostral landmark marking caudal the frontal sinus; the nuchal line is the caudal border designating the underlying transverse sinus and tentorium; the external sagittal
crest is the dorsal border marking the underlying dorsal
sagittal sinus. The burr holes can then be connected with a
high-speed air drill or craniotome to the level of the dura.
Drilling over the dorsal sagittal sinus should be performed
with caution to avoid iatrogenic rupture of this sinus. Veins
A more radical extension of the dorsal and transfrontal
rostrotentorial craniotomy/craniectomy is used for exposure
of the dorsal frontal cortices, olfactory bulbs, and ethmodial
areas. We have modified this approach and remove the cranium over the frontal sinus and dorsal skull bilaterally for
greater access to this area. This is basically an extension of
the bifrontal craniotomy to involve the area over the frontal
sinus area, however, provides more exposure that either the
transfrontal or radical lateral rostrotentorial craniotomy
alone. A modified bilateral transfrontal approach has been
described for access to the dorsal frontal and olfactory bulbs.
This approach may be useful for smaller dorsal lesions in
this area, however, access to the ventral cranial area is limited. (Glass 2000)
Six burr holes are placed in a rectangular fashion, one on
either side of the external sagittal ridge in the frontal/parietal
bone using a high speed air drill, two over the dorsal frontal
sinus area, and two over the lateral frontal sinus area. The
burr holes can then be connected with a high-speed air drill
or craniotome to the level of the dura. Drilling over the rostral dorsal sagittal sinus should be performed with caution to
avoid iatrogenic rupture of this sinus. After removal of skull,
the dura will be exposed as for the bilateral rostrotentorial
approach.
When closing, the frontal sinus is lavaged and packed
with autogenous fat or Gelfoam. Temporalis fascia grafts are
collected bilaterally. One of the grafts is placed over the
brain and the edges of the graft are tucked under (between
the skull edge and the underlying brain) to the limits of the
craniotomy to form a seal over the exposed brain. The bone
previously removed is replaced to decrease scarring over the
area. Sutures (2/0 nylon) can be placed spanning from the
rostral to caudal edges of the craniectomy to be used as a
scaffolding so as when the bone is replaced it does not fall
ventrally onto the brain. The bone is then replaced and sutured to skull by drilling small holes at the limits of the craniotomy edge and mirrored in the bone to be replaced.
As the frontal sinuses are entered during this procedure,
epistaxis is common both during the procedure and in the recovery period. This hemorrhage is self-limiting and is rarely
persistent beyond 24 hours after surgery.
PITUITARY SURGERY
Surgical approaches to the pituitary gland have been described mostly through a transsphenoidal incision. (Niebauer
1988; Niebauer 1990; Meij BP 1997). Dogs were initially
positioned in dorsal recumbency, however, more recently are
positioned in sternal recumbency. The palatine mucosa and
mucoperiosteum is incision with an electroscapel. The bony
landmarks are inconsistent therefore preoperative computed
tomography is used for localization of the pituitary relative
to bony landmarks of the skull.
The bone over this area is drilled with a high-speed drill
until the bone is paper thin. This final layer of bone is removed bluntly with a small curette or similar instrument.
The dura is incised and the pituitary is visualized and can
subsequently be removed.
This approach works best for small (<1.0 cm) pituitary
tumors. As large macroadenomas enlarge dorsally, limited
resection of these tumors can be performed through this approach. Additional complications include electrolyte imbalances such as hypernatremia, iatrogenic hypopituitarism requiring life-long replacement therapy, pneumonia, lack of
resolution of clinical signs, decreases in tear production, soft
palate dehiscence, diabetes insipidus, and secondary hypothyroidism.
APPROACH TO THE TRIGEMINAL NERVE
(Bagley RS Tigeminal nerve sheath tumor in
10 dogs 1998)
In dogs, a lateral rostrotentorial craniectomy or a transzygomatic craniectomy has been used to provide exposure of the ventral and ipsilateral floor of the skull in the
area of the trigeminial nerve. Most often, the trigeminal
mass is surgically approached via a rostrotentorial lateral
craniectomy. The temporalis muscle is often atrophied
which was beneficial during ventral exposure as the atrophied muscle is less of an obstacle to skull exposure. In
addition, the dorsal ramus of the mandible may be an obstruction, and opening the mouth slightly may ventrally
displace the ramus and provide extra room for the approach. The jaw should not be opened excessively or
maintain opened under excessive force as this may lead to
subsequent muscle damage and ultimately, fibrosis that restricts jaw mobility. The trigeminal nerve can be found
just lateral and rostral to the level of the attachment of the
zygomatic arch. The nerve is then traced medially to the
level at which it enters the skull through a foramen. A
high-speed air drill is used to enlarge the foramen medially and caudally following the path of the nerve.
ALTERNATIVES
Each of these major craniotomies/craniectomies can be
modified to achieve improved exposure. The major obstacles
to increasing skull removal are vascular structures and exiting cranial nerves. In general, ventral exposure of the skull
below the level of the zygomatic arch is difficult and the exposure is less than adequate for mass removal. With increasing skull removal, the risk of postoperative scarring and
stricture of intracranial structures increases. As stated previously, if the dorsal skull bone is removed bilaterally, the
21
bone over midline needs to be replaced, a bone graft needs
to be added, or a cranioplasty needs to be performed to avoid
scarring over midline and subsequent brain damage. This
type of bone replacement will also help with the cosmetic
appearance of the head.
Significant amounts of skull often need to be resected
when there is tumor involving the skull such as multilobular
osteochondrosarcoma. (Straw 1989; Dernell 1998) In these
instances, if the amount of resection requires bilateral dorsal
skull removal, a skull allograph is used to cover the dorsal
defect. Chemical sterilization techniques are used to prepared the graft to so that osteogenic potential is retained.
(Dahners 1989)
POSTOPERATIVE MANAGEMENT
After surgery, a repeat imaging study (MR) is performed
if possible to assess the degree of lesion or tumor resection,
cerebral edema, and hemorrhage (hematoma). Immediate
decompression is indicated if there is an expanding
hematoma or if brain compression is significant.
Animals are recovered from anesthesia and placed in a
neutral or head elevated position.
After intracranial surgery, animals are usually monitored
in a critical care or intensive care area for signs of neurologic deterioration as cerebral edema may evolve up 24 and 48
hours after injury and persist for a week or more. (Shapiro
1975) Parameters commonly monitored include heart rate
and rhythm, respiratory rate and pattern, blood pressure,
urine production, and pain. Neurologic parameters monitored include pupil size and responsiveness to light, level of
consciousness, behavior, and the ability to move and walk.
Intravenous fluid therapy is given to maintain normal hydration and perfusion. Both dehydration and overhydration
should be avoided. Cortisosteroids and anticonvulsants are
continued as needed.
A stockenette is placed over the head. Holes are cut in
the stockenette to allow for the ears to protrude. Gauze
sponges may be placed under the stockenette to collect and
discharge from the wound. Incisions are examined daily for
evidence of the cardinal signs of inflammation. Rarely, if an
animal is excessively violent in its movements, a protective
helmet or similar device can be used to avoid additional head
injury. Animals with excessive or violent movements should
also be sedated with valium.
Oral food and water are withheld until the animal is fully alert. Unless the animal is normal and walking, we do not
give postoperative intracranial surgery animals anything
orally for up to 5 days to decrease the risk of aspiration
pneumonia if the animal it not alert and walking.
Pain control is instituted with narcotics for at least 72
hours after surgery. Fentanyl patches are used for this purpose in our hospital. While morphine has been shown to increase ICP, this narcotic is given in our hospital routinely for
pain control within the first 24 hours after surgery until the
fentanyl patch is effective. Some animals are delirious after
surgery and vocalize, which may be mistaken for a painful
response. Sound and light stimulation of the animals should
be kept to a minimum.
22
More rigorous physical therapy is begun when the animal is alert. Massage and passive range of motion of the
limbs is reasonable even in stuporus or comatose animals.
As severely impaired animals have little control over their
movements they may be predisposed to secondary musculoskeletal injuries primarily to joints, ligaments, tendons and
muscles. Cautious manipulation of comatose and stuporus
animals is necessary to avoid iatrogenic injury in the postoperative period
be effectively swallowing during accumulation of saliva or
administered food and water. Finally, the role of early feeding probably plays a role.
While all of the potential causes of pneumonia have not
be clarified, this complication is the most common non-neurologic complication is dogs following intracranial surgery.
NPO status for up to 5 days following surgery may be the
best way to decrease this development of pneumonia in these
dogs balanced against the nutrition needs of the animal.
POSTOPERATIVE COMPLICATIONS
REHABILITATION OF THE BRAIN
INJURED ANIMAL
Postoperative complications following intracranial surgery
include those involving damage or injury to the intracranial
nervous system and systemic abnormalities. Iatrogenic injury to the brain often results in intracranial signs that are
present immediately upon recovery from anesthesia or
evolve within the following 48 hours. Intracranial hemorrhage, increasing cerebral edema, increasing ICP, and ischemia due to cerebrovascular disease are most often the
causes of neurologic deterioration following surgery. As
with all surgery, infectious complications are possible, but
overall, are rare.
Seizures occurring in the immediate postoperative period
are managed as in dogs without surgery. Intravenous diazepam bolus doses are used acutely if seizures occur, and
previously administered maintenance doses of anticonvulsants are adjusted as necessary. If recurrent seizure activity
ensues, a constant infusion of diazepam may be needed for
seizure control.(Parent 1996) Seizures may suggest increasing intracranial pressure or poor cerebral perfusion.
With definitive surgical therapy we have noted dogs that,
after surgery, seem overtly sedated considering their serum
concentration of phenobarbital. This suggests that, either
due to alterations in brain blood flow or cellular concentration of the antiepileptic medication, the effects of phenobarbital may be relatively more potent after surgery. Seemingly
excessive sedation from a similar dosage of phenobarbital
may last for 3-5 days, but usually is self-limiting. Occasionally, if the sedative effects are excessive, the phenobarbital
dose may need to be decreased for a few days.
Of the non-neurologic complications following intracranial surgery, pneumonia is the most common. (Fransson Vet
Surg 2001) Numerous factors may contribute to the development of pneumonia however is probably the result of aspiration of food or other digestive material. Megaesophagus
seems to be an associated risk factor for the development of
pneumonia in dogs following intracranial surgery. Many of
these dogs are also chronically ill and in overall debilitated
states. Many dogs are receiving multiple drugs including
corticosteroids and anticonvulsants. The use of corticosteroids due to their immmunosuppresive effects may contributed to development of pneumonia. Often, these dogs
have dry mouths and other oral changes that may have predisposed to alterations in the microorganisms present in the
mouth. Some dogs have received or were receiving antibiotics which could have altered the normal flora of the mouth
and pharynx or predisposed to superinfection. Some animals, while apparently being able to reflexly gag, may not
In general, lesions of supratentorial structures or the
cerebellum have a better overall prognosis for recovery than
lesions involving the brain stem. After the acute effects of
brain injury are controlled (usually within 7 days), the goal
is to allow time for brain healing and recovery of function to
occur. Smaller animals are often better candidates for prolonged nursing care in comparison to larger animals due to
the ease of manipulation. Good nursing care includes the
prevention of decubital ulcers in the recumbent animal and
monitoring for secondary infections primarily of the pulmonary and urogenital systems. Recumbent animals should
be placed on clean, soft bedding and turned frequently (at
least every 4 hours). Physical therapy can begin as soon as
possible if there are no unstable vertebral injuries. Physical
therapy is individualized to the animal’s needs, but may include supported or non-supported walking, passive flexion
and extension of the limbs, massage, or swimming. Cats
may be more reluctant than dogs to perform the latter physiotherapy. A daily record of physical therapy will ensure that
this therapy is not overlooked, and allows for multiple individuals, including the owner, to become involved in the healing process.
In general, clinical signs of unilateral supratentorial surgical injury improve within the first two weeks following
trauma. Usually the animal is ambulatory by 4 weeks post
injury, although, residual paresis and blindness may continue. A tendency to circle may also persist, being especially
prominent when the animal is distressed or excited.
Recovery from brain stem surgical injury may be less
complete, and residual signs commonly remain. Recovery
form cerebellar injury often occurs in a similar time frame as
for supratentorial injury. If the secondary effects of brain injury are controlled, many animals can recover from the primary brain insult associated with trauma.
Selected References
Abou-Madi M, Trop D, Abou-Madi N, Ravussin P. Does a bolus of mannitol initially aggravate intracranial hypertension. Br J anaesth 59:630639, 1987.
Adams RD, Victor M: In Principles of Neurology, 4th edn. New York:McGraw-Hill, 1989.
Adams RW, Cucchiara RF, Gronet GA, et al. Isoflurane and cerebrospinal
fluid pressure in neurosurgical patients. Anesthesiology 1981; 54:97-99.
Albanese J, Viviand X, Potie F, et al. Sufentanil, fentanyl, and alfentanil in
head trauma patients:a study on cerebral hemodynamics. Crit Care
Med 1999, 27:407-411.
Albright AL, Latchaw RE, Robinson AG. Intracranial and systemic effects
of osmotic and oncotic therapy in experimental cerebral edema. J
Neurosurg 60:481-489, 1984.
Allen R. Intracranial pressure: a review of clinical problems, measurement
techniques and monitoring methods. J Med Eng Tech 1986; 10:299320.
Bagley RS: Intracranial pressure in dogs and cats. Physiology and treatment. Comp Contin Ed Pract Vet 18:605-621, 1996.
Bagley RS: Pathophysiologic sequelae of intracranial disease. Vet Clin
North Am 26:711-734, 1996.
Bagley RS, Baszler TV, Harrington ML, Pluhar GE, Moore MP, Keegan
RD, Greene SA. Clinical effects of longitudinal division of the corpus callosum in dogs. Vet Surg 24:122-127, 1995.
Bagley RS, Gavin PR, Moore MP, et al: Comparison of BNCT alone or in
combination with surgery for spontaneous brain tumors in dogs. Proceedings Eighth International Symposium on Neutron Capture Therapy for Cancer. La Jolla, California. Sept 1998, 34-35.
Bagley RS, Harrington ML, Gay JM, Silver GM. Effect of changing ultrasonic aspirator power on the cerebral cortex of healthy dogs. AVJR
Feb 2000.
Bagley RS, Harrington ML, Pluhar GE, Gavin PR, Moore MP. Acute, unilateral transverse sinus occlusion during craniectomy in 7 dogs with
space-occupying intracranial disease. Vet Surg, 26:195-201, 1997.
Bagley RS, Harrington ML, Pluhar GE, Keegan RD, Greene SA, Moore
MP, Gavin PR: Effect of craniectomy/durotomy alone or in combination with hyperventilation, diuretics, and corticosteroids on intracranial pressure in normal dogs. Am J Vet Res 57:116-119, 1996.
Bagley RS, Keegan RD, Greene SA, Harrington ML, Moore MP: Pathologic effects in brain following intracranial pressure monitoring in normal dogs using a fiberoptic monitoring system. Am J Vet Res
56:1475-1478, 1995.
Bagley RS, Keegan RD, Greene SA, Moore MP, Gavin PR. Intraoperative
intracranial pressure monitoring in five dogs with structural brain disease. J Am Vet Med Assoc 5:588-591, 1995.
Bagley RS, Kornegay JN, Page RL, et al:Central nervous system neoplasia.
In: Slatter DH, ed, Textbook of Small Animal Surgery, 3rd edition
Philadelphia: WB Saunders, 1992, p 2137.
Bagley RS, Silver GM, Gavin PR. Cerebellar cystic meningioma in a dog.
JAAHA 2000, 36:413-415.
Bagley RS, Wheeler SJ, Klopp L, Sorjonen DC, Thomas WB, Wilkens BE,
Gavin PR, Dennis R. Tigeminal nerve sheath tumor in 10 dogs.
JAAHA 34:19-25, 1998.
Bagley RS, Gavin PR, Moore MP, Silver GM, Harrington ML, Connor R.
Clinical signs associated with brain tumor in dogs: 97 cases (19921997). JAVMA 1999, 215:818-819.
Bansal BS, Mittal SC, Gupta RB, et al. Experimental evaluation of neurological disorders following ligation of the dorsal sagittal sinus in
dogs. Indian Vet J 1976, 53:213-215.
Barker J. Epilepsy in the dog-a comparative approach. J Small Anim Pract
14:281-289, 1973.
Beck DJK, Russell DS. Experiments on thrombosis of the superior longitudinal sinus. J Neurosrug 1946, 3:337-347.
Bindal RK, Sawaya R, Leavens M, et al: Surgical treatment of multiple
brain metastasis. J Neurosurg 79:210, 1993.
Bouma GJ, Muizelaar JP, Bandoh K, Marmarou A. Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow. J Neurosurg 77:15-19, 1992.
Braakman R, Schouten HJA, Dishoeck MB, Minderhound JM. Megadose
steroid in severe head injury. J Neurosurg 58:326-330, 1983.
Brinker T, Seifert V, Dietz H. Cerebral blood flow and intracranial pressure
during experimental subaarchnoid haemorrhage. Acta Neurochir
Wien 115;47-52, 1992.
Caruselli G, Recchioni MA, Occhipinti C, Bernardini M, et al. The role of
CSF ventricular drainage in controlling intracranial hypertension in
patients with brain lesions. Comparison of three methods. Preliminary results. J Neurosurg Sci 36;219-25, 1992.
Cardoso ER, Rowan JO, Galbraith S. Analysis of the cerebrospinal fluid
pulse wave in intracranial pressure. J Neurosurg 59:817-821,
1983.
Chozick BS, Reinert SE, Greenblatt SH. Incidence of seizure after surgery
for supratentorial meningiomas: a modern analysis. J Neurosurg
84:382-386, 1996.
23
Cornick JL. Anesthetic management of patients with neurologic abnormalities. Comp Contin Ed Pract Vet 1992; 14:163-172.
Cottrell JE, Robustelli A, Post K, Turndorf H. Furosemide- and mannitolinduced changes in intracranial pressure and serum osmolality and
electrolytes. Anesthesiology 47:28-30, 1977.
Coulter DM, Gooch WM. Falling intracranial pressure: an important element in the genesis of intracranial hemorrhage in the beagle. Biol
Neonate 63:316-26, 1993.
Cordy DR. Tumors of the nervous system and eye. In:Moulton JE, ed, Tumors of Domestic Animals, 3rd ed, Berkeley, University of California Press,1990, 640-665.
Crutchfield JS, Narayan RK, Robertson CS, Michael LH. Evaluation of a fiberoptic intracranial pressure monitor. J Neurosurg 1990; 72:482487.
Cunnigham JG. Canine seizure disorders. J Am Vet Med Assoc 158:589597, 1971.
Dempsey R, Rapp PR, Young B, et al. Prophylactic parenteral antibiotics in
clean neurosurgical procedures: a review. J Neurosurg 1988, 69:5257,
Dahners LE, Hoyle M. Chemical sterilization of bacterially contaminated
bone without destruction of osteogenic potential. J Orthop Trauma
1989, 3:241-243.
Dernell WS, Straw RC, Cooper MF, et al. Multilobular osteochondrosacrcoma in 39 dogs: 1979-1993. JAAHA 1998, 34:11-18.
Dewey CW. Emergency management of the head trauma patient. Principles
and practice. Vet Clin North Am Small Anim Pract 2000, 30:207-225.
de Nadal M, Ausina A, Sahuquillo J, et al. Effects on intracranial pressure
of fentanyl in severe head injured patients. Acta Neurochir Suppl
(Wein) 1998, 71:10-12.
De Wet PD, Ali II, Peters DN. Surgical approach to the rostral cranial fossa by radical transfrontal craniotomy in the dog. J South African Vet
Assoc 53:140-151, 1982.
Djindjian M, Lepresle E, Homs JB. Antibiotic prophylaxis during prolonged clean neurosurgery. J Neurosrug 1990, 73:383-386.
Duffy GP. Lumbar puncture in the presence of raised intracranial pressure.
Br Med J 1:407-409, 1969.
Dunbar PJ, Visco E, Lam AM. Craniotomy procedures are associated with
less analgesic requirements than other surgical procedures. Anesth
Analg 1999, 88:335-340.
Enevoldsen EM, Jensen FT. Autoregulation and CO2 responses of cerebral
blood flow in patients with acute severe head injury. J Neurosurg
48:689-703, 1979.
Feldman Z, Kanter MJ, Robertson CS, Contant CF, et al. Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients. J Neurosurg 76:207-211,
1992.
Fenner WR: Metastatic neoplasms of the central nervous system. Seminars
Vet Med Surg 5:253, 1990.
Fenner WR. Neuroanesthesia. Proc ACVIM Forum, 10:722-24, 1992.
Findlay SR, Dvorak AM, Kagey-Sobotka A, Lichtenstein LM. Hyperosmolar triggering of histamine release from human basophils. J Clin Invest 67:1604-1613, 1981.
Fisher CM, Ojemann RG. Bilateral decompressive craniectomy for worsening coma in acute subarachnoid hemorrhage. Observations in support of the procedure. Surg Neurol 1994;41:65-74.
Fishman RA:Brain Edema. N Eng J Med 293:706-711, 1975.
Foley PL, Takenaka K, Kassell NF, Lee KS. Cytotoxic effects of bloody cerebrospinal fluid on cerebral endothelial cells in culture. J Neurosurg
81;87-92, 1994.
Foster ES, Carrillo JM, Patnaik AK:Clinical signs of tumors affecting the
rostral cerebrum in 43 dogs. J Vet Int Med 2:71, 1988.
Fransson BA, Bagley RS, Gay JM, Silver GM, Gokhale S, Sanders S, Connors RL, Gavin PR. Pneumonia following intracranial surgery in
dogs. Vet Surg 2001, 30: 432-439.
Gaab MR, Rittierodt M, Lorenz M, Heissler HE. Traumatic brain swelling
and operative decompression: a prospective investigation. Acta Neurochirurgica Suppl 1990; 51:326-328.
Gaab MR, Schroeder HWS. Neuroendoscopic approach to intraventricular
lesions. J Neurosurg 1998, 88:496-505.
Gallagher JG, Berg J, Knowles KE, et al: Prognosis after surgical excision
of cerebral meningiomas in cats: 17 cases (1986-1992). J Am Vet
Med Assoc 203:1437, 1993.
24
Gavin PR, Fike JR, Hoopes PJ: Central nervous system tumors. Seminars
Vet Med Surg 10:180, 1995.
Geib LW: Ossifying meningioma with extracranial metastasis in a dog.
Pathol Vet 3:247, 1966.
Germon K. Interpretation of ICP pulse waves to determine intracerebral
compliance. J Neurosci Nurs 20:344-349, 1988.
Glass EN, Kapatkin A, Vite C, et al. A modified bilateral transfrontal sinus
appraoch to the canine frontal lobe and olfactory bulb:Surgical technique and five cases. JAAHA 2000, 36:43-50.
Goldsack C, Scuplak SM, Smith M. A double-blind comparison of codeint
and morphine for postoperative analgesia following intracranial surgery. Anaesthesia 1996, 51:1029-1032.
Gordon LE, Thacher C, Matthiesen DT, et al: Results of craniotomy for
treatment of cerebral meningioma in 42 cats. Vet Surg 23:94, 1994.
Graf CJ, Rossi NP. Catecholamine response to intracranial hypertension. J
Neurosurg 49:862-868, 1978.
Greenberg MS: Treatment of Hydrocephalus. In: Handbook of Neurosurgery. Lakeland, FL, Greenberg Graphics, 1991, p.200-218.
Grosslight K, Foster R, Colohan AR, Bedford RF. Isoflurane for neuroanesthesia:Risk factors for increases in intracranial pressure. Anesthesiology 1985; 63:533-536.
Guyton AC: Nervous regulation of circulation, and rapid control of arterial
pressure, In Textbook of Medical Physiology, 9th ed,Philadelphia,
W.B. Saunders, 1996, pp 209-219.
Hall ED. High-dose glucocorticoid treatment improves neurological recovery in head-injured mice. J Neurosurg 62:882-887, 1985.
Hall ED. The neuroprotective pharmacology of methylprednisolone. J Neurosurg 76:13-22, 1992.
Hassler W, Steinmetz H, Gawlowski J. Transcranial doppler ultrasonography in raised intracranial pressure and in intracranial circulatory
arrest. J Neurosurg 68:745-751, 1988.
Heidner GL, Kornegay JN, Page RL, et al: Analysis of survival in a retrospective study of 86 dogs with brain tumors. J Vet Int Med 5:219,
1991.
Hermann BP, Wyler AR, Ackerman B, Rosenthal T. Short-term psychological outcome of anterior temporal lobectomy. J Neurosurg 71:327334, 1989.
Holliday TA. Clinical signs of acute and chronic experimental lesions of the
cerebellum. Veterinary Science Communications 1979/1980; 3:259.
Hopkins AL, Wheeler SJ. Subdural hematoma in a dog. Vet Surg 20, 413,
1991.
Jay V, Becker LE, Otsubo H, Hwang PA, et al. Pathology of temporal lobectomy for refractory seizures in children. J Neurosurg 79:53-61,
1993.
Jeffery N, Brearley MJ. Brain tumours in the dog: Treatment of 10 cases
and review of recent literature. J Small Anim Pract 1993, 34, 367372.
Jourdan C, Convert J, Mottolese C, Bachour E, Gharbi S, Artru F. [Evaluation of the clinical benefit of decompression hemicraniectomy in intracranial hypertension not controlled by medical treatment]. Neuro
Chirurgie 1993;39:304-310.
King JM, Roth L, Haschek WM: Myocardial necrosis secondary to neural lesions in domestic animals. J Am Vet Med Assoc 180:144-148,
1982.
King RB, Schell GR. Cortical localization and monitoring during cerebral
operations. J Neurosurg 67:210-217, 1987.
Kornegay JN. Pathogenesis of diseases of the central nervous system. In
Textbook of Small Animal Surgery, 2nd ed., Slatter D, ed., Philadelphia, W.B. Saunders, 1993, 1022-1037.
Kornegay JN, Oliver JE, Gorgacz EJ. Clinicopathologic features of brain
herniation in animals. J Am Vet Med Assoc 182:1111-1116, 1983.
Kostolich M, Dulisch ML. A surgical approach to the canine olfactory bulb
for meningioma removal. Vet Surg 1987, 16:273-277.
Kriebel RM, Shah AB, McAllister JP 2d.: The microstructure of cortical
neuropil before and after decompression in experimental infantile hydrocephalus. Exp Neurol 119(1):89-98, 1993.
Lam AM, Winn HR, Cullen BF, Sundling N. Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg 75:545-551,
1991.
Lauer KK, Connolly LA, Schmeling WT. Opoid sedation does not alter intracranial pressure in head injured patients. Can J Anaesth 1997,
44:929-33.
LeCouteur RA. Tumors of the Nervous System. In: Withrow SJ, MacEwen
EG, eds, Clinical Veterinary Oncology, Philadelphia, Lippincott,
1989, 325-350.
Lobato RD, Sarabia R, Cordobes F, Rivas JJ, et al. Posttraumatic cerebral
hemispheric swelling. J Neurosurg 68:417-423, 1988.
Lovell AT, Marshall AC, Elwell CE, et al. Changes in cerebral blood volume with changes in position in awake and anesthetized subjects. Anesth Analg 2000, 90:372-376.
Lyons MK, Meyer FB. Cerebrospinal fluid physiology and the management
of increased intracranial pressure. Mayo Clinic Proc 65:684-707,
1990.
Mavrocordatos P, Bissonnette B, Ravussion P. Effects of neck position and
head elevation on intracranial pressure in anesthetized neurosurgical
patients: preliminary results. J Neurosurg Anesthesiol 2000, 12:1014.
McAllister JP 2d., Cohen MI, O’Mara KA, et al: Progression of experimental infantile hydrocephalus and effects of ventriculoperitoneal
shunts: an analysis correlating magnetic resonance imaging with
gross morphology. Neurosurgery 29(3):329-40 1991.
Meij BP, Voorhout G, van den Ingh TSGAM, et al. Transsphenoidal hypohysectomy in beagle dogs: evalation of a microsurgical technique.Vet Surg 1997, 26:295-309.
Mendelow AD, Teasdale GM, Russell T, et al. Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury.
J Neurosurg 63:43-48, 1985.
Moore MP, Bagley RS, Harrington ML, et al: Intracranial tumors. Vet Clinic North Am 26:759, 1996.
Mursch K, Buhre W, Behnke-Mursch J, et al. Peroperative cardiovascular
stability during brainstem surgery. The use of high-dose methylprednisolone compared to dexamethasome. A retrospective analysis. Acta
Anaesthesiol Scan 2000, 44:378-382.
Narayan RK, Kishore PR, Becker DP, Ward JD, et al. Intracranial pressure:to monitor or not to monitor? J Neurosurg 56:650-659, 1982.
Niebauer GW, Dayrell-Hart BL, Speciale J. Evaluation of craniotomy in
dogs and cats. JAVMA 1991, 198:89-95.
Niebauer GW, Eigenmann JE, Van Winkle TJ. Study of long-term survival
after transsphenoidal hypophyscetomy in clinical normal dogs. Am J
Vet Res 1990, 51:677-681.
Niebauer GW, Evans SM. Transsphenoidal hypophysectomy in the dog. Vet
Surg 1988, 17:296-303.
Nordström CH, Messeter K, Sundbärg G, Schalén W, et al. Cerebral blood
flow, vasoreactivity, and oxygen consumption during barbiturate therapy in severe traumatic brain lesions. J Neurosurg 64:231-237, 1986.
Oliver JE Jr. Principles of Canine Brain Surgery. Animal Hospital 2:73-88,
1966.
Oliver JE Jr: Surgical approaches to the canine brain. American Journal of
Veterinary Research, 1968, 29:353-378.
Oliver JE Jr. Seizure disorders in companion animals. Comp Cont Ed 2:7785, 1980.
Oliver JE, Hoerlein BF: Cranial Surgery. In: Oliver JE, Hoerlein BF,
Mayhew IG, eds: Veterinary Neurology. Philadelphia, WB Saunders,
1987, p 486-88.
Ojemann GA. Surgical therapy for medically intractable epilepsy. J Neurosurg, 1987, 66:489- 499.
Owens G, Stahlman G, Capps JM, et al. experimental occlusion of dural sinuses. Surg Forum 1958, 8:521-524.
Palmer AC, Malinowski W, Barnet KC: Clinical signs including papilloedema associated with brain tumors in twenty-one dogs. J Small Anim
Pract 15:359, 1974.
Parent JML, Quesnel AD. Seizures in Cats. Vet Clin North Am, Small Animal, 1996; 26:811-826.
Patchell RA, Tibbs PA, Walsh JW, et al: A randomized trial of surgery in the
treatment of single brain metastases to the brain. New Engl J Med
322:494, 1990.
Perneczky A, Fries G. Endoscope-assisted brain surgery: part 1- evolution,
basic concept, and current technique. Neurosurgery 1998, 42:219224.
Piatt JH Jr: Peritoneal cerebrospinal fluid shunt insertion: a technique for
protection of the abdominal catheter. J Neurosurg 82:305-306 1995.
Pluhar GE, Bagley RS, Keegan RD, Moore MP: The effect of acute, unilateral transverse venous sinus occlusion on intracranial pressure in
normal beagles. Vet Surg 23:425, 1994.
Polkey CE, Binnie CD. Assessment and selection of candidates for surgical
treatment of epilepsy. Epilepsia 36(Suppl 1):S41-45, 1995.
Pollack IF, Sekhar LN, Jannetta PJ, Janecka IP. Neurilemomas of the trigeminal nerve. J Neurosurg 1989;70:737-745.
Pomeranz S, Safar P, Radovsky A, Tisherman SA, et al. The effect of resuscitative moderate hypothermia following epidural brain compression
on cerebral damage in a canine outcome model. J Neurosurg 79:241251, 1993.
Quesney LF, Gloor P. Localization of epileptic foci. In:Long-Term monitoring in Epilepsy, Gotman J, Ives JR, Gloor P, eds, Amsterdam:Elsevier, 1985, 165-200.
Rasmussen T. Results of Cortical Resection in Focal Epilepsy. In: Roger J.
Porter et al, eds. Raven Press, New York. Advances in Epileptology:
XVth Epilepsy International Symposium, 449-455, 1984.
Ravussin P, Abou-Madi M, Archer D, et al. Changes in CSF pressure after
mannitol in patients with and without elevated CSF pressure. J Neurosurg 69:869-876, 1988.
Ravussin P, Archer DP, Meyer E, et al. The effects of rapid infusions of saline and mannitol on cerebral blood volume and intracranial pressure
in dogs. Can Anaesth Soc J 32:506-515, 1985.
Ravussion P, Archer DP, Tyler JL, et al. Effects of rapid mannitol infusion
on cerebral blood volume. J Neurosurg 64:104-113, 1986.
Recht LD, Glantz M. Neoplastic diseases. In: Engel J, Pedley TA, eds, Epilepsy: A Comprehensive Textbook, Philadelphia:Lippincott-Ravin,
1997, 2579-2585.
Regan RF, Panter SS. Neurotoxicity of hemoglobin in cortical cell culture.
Neurosci Lett 153;219-222, 1993.
Reulen HJ. Vasogenic Brain Oedema, New aspects in its formation, resolution and therapy. Br J Anaesth 48:741-752, 1976.
Ribas JL, Mena H, Braund KG, et al: A histologic and immunocytochemical study of choroid plexus tumors in the dog. Vet Path 26:55-64,
1989.
Rinaldi A, Mangiola A, Anile C, Maira G, Amante P, Ferraresi A. Hemodynamic effects of decompressive craniectomy in cold induced brain
oedema. Acta Neurochirurgica Suppl 1990;51:394-396.
Roberts DW. Corpus Callosum Section. In Surgery for Epilepsy, Spencer
SS, Spencer DD eds, Boston, Blackwell Scientific Publications,
1991, pgs. 168-178.
Rosner MJ, Daughton S. Cerebral perfusion pressure management in head
injury. J Trauma 30:933-941, 1990.
Russo ME. The pathophysiology of epilepsy. Cornel Vet 71:221-224, 1981.
Sarfaty D, Carillo JM, Peterson M.E: Neurologic, endocrinologic and
pathologic findings associated with large pituitary tumors in dogs: Eight cases (1976-1984). J Am Vet Med Assoc 143:854, 1988.
Salvati M, Cosentino F, Artico M, Ferrari M, et al. Electrocardiographic
changes in subarchnoid hemorrhage secondary to cerebral aneurysm.
Report of 70 cases. Ital J neurol Sci 13;409-13, 1992.
Samii M, Migliori MM, Tatagiba M, Babu R. Surgical treatment of trigeminal schwanomas. J Neurosurg 1995;82:711-718.
Sapolsky RM, Pulsinelli WA. Glucocorticoids potentiate ischemic injury to
neurons: Therapeutic implications. Science 1397-1400, 1985.
Sarwar M, Virapongse C, Crbo P/ Experimental production of superior sagittal sinus thrombosis in the dog. Am J Neurol Res 1985, 6:19-22.
Schmidek HH. Operative Neurosurgical Techniques. Schmidek HH, Sweet
WH, eds, 4th ed, Philadelphia, WB Saunders, 2000.
Schneider GH, von-Helden GH, Franke R, Lanksch WR, et al. Influence of
body position on jugular venous oxygen saturation, intracranial pressure and cerebral perfusion pressure. Acta Neurochir Suppl Wien
59;107-12, 1993.
Schulman FY, Ribas JL, Carpenter JL et al: Intracranial meningioma with
pulmonary metastasis in three dogs. Vet Path 29:196, 1992.
Segal DH, Oppenheim JS, Murovic JA. Neurological recovery after cranioplasty. Neurosurg 34:729-31, 1994.
25
Shackford SR, Zhuang J, Schmoker J. Intravenous fluid tonicity: Effect on
intracranial pressure, cerebral blood flow, and cerebral oxygen delivery in focal brain injury. J Neurosurg 76:91-98, 1992.
Shapiro HM. Intracranial hypertension:Therapeutic and anesthetic considerations. Anesthesiology 1975; 43:445-471.
Shiozaki T, Sugimoto H, Taneda M, Yoshida H, et al. Effect of mild hypothermia on uncontrollable intracranial hypertension after severe
head injury. J Neurosurg 79:363-368, 1993.
Shores A. Neuroanesthesia:A review of the effects of anesthetic agents on
cerebral blood flow and intracranial pressure in the dog. Vet Surg
1985; 14:257-263.
Shores A, Jevens D, DeCamp CE. Intraoperative brain pressure monitoring
in the dog. Proceedings 9th ACVIM, New Orleans, LA, May 1991,
831-833.
Sakatani K, Ohtaki M, Morimoto S, Hashi K. Isotonic mannitol and prevention of local heat generation and tissue adherence to bipolar
diathermy forceps tips during electrical coagulation. J Neurosurg
82:669-671, 1995.
Smith HP, Challa VR, Moody DM, Kelly DL: Biological features of meningiomas that determine the production of cerebral edema. Neurosurgery 8:428-433, 1981.
Spencer SS, Gates JR, Reeves AR, Spencer DD, et al. Corpus callosum section. In Surgical Treatment of the Epilepsies, Engel J, Jr ed, New
York, Raven Press, 1987, pgs. 425-444.
Sperry RJ, Bailey PL, Reichman MV, et al. Fentanyl and sufentanil increase intracranial pressure in head trauma. Anesthesiology 1992, 77:416420.
Sorjonen DC, Thomas WB, Myers LJ, et al. Radical cerebral cortical resection in dogs. Prog Vet Neurol 1991, 2:225.
Speciale J, Steinberg SA, Van Winkle T. Morbidity and mortality related to
cerebellomedullary spinal tap in dogs and cats. J Vet Int Med 9:208,
1995.
Straw RC, LeCouteur RA, Powers BA, et al. Multilobular osteochondrosacroma of the canine skull: 16 cases (1978-1988). JAVMA 1989,
195:1764-1769.
Todd M M, Drummond JC. A comparison of the cerebrovascular and metabolic effects of halothane and isoflurane in the cat. Anesthesiology
60:276-282, 1984.
Tucker RT, Bagley RS, Gavin PR, Greene SA,Keegan RD. Technical considerations in transcranial doppler ultrasound. J Vet Int Med 11:119,
1997.
Tucker RL, Gavin PR: Brain imaging. Vet Clinic North Am 26:735, 1996.
Tucker RL, Gavin PR, Bagley RS, Greene SA, Britt L. Transcranial doppler
in normal dogs. Vet Rad US, 1996:37; 473.
van Loon J, Shivalkar B, Plets C, Goffin J, et al. Catecholamine response to
a gradual increase of intracranial pressure. J Neurosurg 79:705-709,
1993.
Venes Jl, Collins WF. Bifrontal decompressive craniectomy in the management of head trauma. J Neurosurg 1975;42:429-433.
Waters DJ, Hayden DW, Walter PA. Intracranial lesions in dogs with hemangiosarcoma. J Vet Int Med 3:222, 1989.
Yasui T, Hakuba A, Kin SH, Nishimura S. Trigeminal neurinomas: operative approach in eight cases. J Neurosurg 1989;71:506-511.
Yokoh A, Sugita K, Kobayashi S. Intermittent versus continuous brain retraction. J Neurosrug 1983, 58:918-923.
a
Olm Intracranial Pressure Monitoring Kit- Model 110-4B. Camino Laboratories, San Diego, California.
b
Digital Pressure Monitor, Model 420, Camino Laboratories, San Diego,
California.
27
Surgery in the avian patient:
special considerations
R. Avery Bennett
DVM, MS, Diplomate ACVS, Associate Professor of Surgery, University of Pennsylvania
Most avian patients are either pets or falconry birds. These
birds are highly intelligent and have a strong will to live making them good patients. They seem to be very annoyed by bandages and topical medications but tolerate sutures very well. In
some cases the relationship between the owner and the bird is
tenuous and care must be taken to protect that trust.
The integument of birds is thin - approximately 10 cells
thick in feathered regions - and devoid of glands. It has little attachment to underlying muscle but is often firmly adhered to
bone especially at the distal extremities. Contour and covert
(body feathers) feathers grow in tracts separated by areas of
skin without feathers. The large flight feathers (remiges and retrices) are attached to periosteum. Body feathers are easily
plucked in the direction of their growth, however, flight feathers are difficult and painful to remove.
The stomach of most birds is divided into 2 parts. The glandular portion (proventriculus) is orad and separated from the
muscular gizzard (ventriculus) by the isthmus. Carnivorous
birds usually do not have a crop for storage of food and the stomach is large, sac-like, and thin-walled with little distinction between parts. Insectivorous, herbivorous, and granivorous birds
have a heavily muscled ventriculus with a distinct isthmus.
Psittacines fall into this category. The proventriculus is very
glandular and does not hold sutures well. Only the left side of the
female reproductive tract is functional. The left ovary produces
large follicles (yolks) that pass into the oviduct where a complex
system adds membranes, albumen, and the shell to the egg.
Prior to performing surgery on an avian patient it is important to establish a clinical data base. A complete history including diet, housing and furniture, and exposure to other birds
should be taken. The physical examination should be complete
and include auscultation and palpation. Whole body radiographs are often very valuable for evaluating the surgical condition as well as screening for concomitant disease processes. A
blood chemistry panel and a CBC should be performed. Contaminated or infected wounds should be cultured and appropriate antibiotic therapy initiated preoperatively.
If the hematocrit is <30% surgery should be delayed or a
whole blood transfusion should be considered. A PCV of >60%
is an indication of dehydration and fluid therapy should be instituted. Blood transfusions are best made from donors of the
same species, however, heterologous transfusions with chicken
or pigeon blood appear to be safe and efficacious. Blood substitutes also appear to be beneficial.
Serum uric acid of >30 mg/dl is an indication of dehydration or renal disease. PCV and total solids (TS) can help determine which. Patients with a TS of <2 mg/dl are usually severely debilitated and should be stabilized before considering
surgery.
Respiratory recovery time is the time it takes a bird to return
to a prestressed respiratory rate following restraint and 2 min of
handling. A return to normal respiration in 3-5 min indicates
respiratory stability sufficient for most anesthetic and surgical
procedures.
The patient’s nitrogen balance must also be addressed.
Changes in body weight can be used to monitor nutritional status. In adequately hydrated birds, increasing body weight is a
good indication that the nutritional status of the bird is appropriate. A short fast of 1-3 hr will help decrease the probability
of aspiration and will have minimal effect on intraoperative
blood glucose. Patients with blood glucose of <200 mg/dl
should receive 5% dextrose IV as supportive therapy during
surgery.
Intraoperative IV fluid therapy should be provided using a
balanced electrolyte solution or 5% dextrose at 10 ml/kg/hr. Perioperative antibiotics should be administered if indicated because of anticipated contamination, but high-potency, very
broad spectrum antibiotics should not be used for prophylaxis.
Loss of body heat must be minimized during anesthesia.
Some form of supplemental heat should be provided to the patient. Standard aseptic technique is essential with avian patients.
Patient preparation with excessive amounts of water or alcohol
can predispose the patient to hypothermia. Because it has a
broader spectrum of activity and residual effects, chlorhexidine
is generally preferred over povidone iodine as a patient preparation solution.
Feathers should be plucked to a distance of 2-3 cm around
the surgical site. Plucking large feathers such as flight feathers
should be avoided. This can damage the follicle resulting in the
growth of malformed feathers. The skin of birds is very fragile
and tears easily. In areas where the skin has been damaged, the
feathers may be cut to avoid further damage to the skin. Water
soluble gel, masking tape, and stockinette may be used to keep
down and contour feathers under control.
Patient drapes may be fashioned of cloth, paper, or plastic.
Clear plastic drapes provide the advantage of allowing more
precise patient monitoring as respiratory movements can be assessed.
29
Instrumentation and materials
in avian surgery
R. Avery Bennett
Some form of magnification is recommended for surgery
in birds. Relatively small amounts of hemorrhage can be disastrous and strict attention to hemostasis is vital. The average
cotton tipped applicator holds approximately 0.1 cc blood.
Loss of more than 3 cotton tipped applicators of blood in a
budgie is potentially dangerous. Individual vessels are much
more easily identified for coagulation under magnification.
The dexterity and manipulation of fingers and hands is far
greater than can be achieved using unaided vision. For patients less than 50 g an operating microscope may be needed.
Various styles of binocular loupes are available with the hobby loupe being the least expensive and simplest. These cost
$20-50 but have several disadvantages. They have a set focal
distance such that only object that distance from the lenses are
in focus. The surgeon must hold their head at that distance
from the patient and any movement of the head results in blurring and dizziness. The lenses are located in front of the eyes
such that the surgeon is obligated to look through them. If the
surgeon tries to pick up an instrument or suture that is not at
the correct focal distance, it will be blurry. Hobby loupes do
not have an attached light source making it difficult to see
within body cavities.
A modification of the hobby loupe is marketed with interchangeable lenses and a cool halogen focal light source
(MDS, Inc., Brandon, FL, 813-653-1180). This type of loupe
still has a set focal length and the surgeon is committed to
looking through the lens. It is important to emphasize that the
higher the magnification, the shorter the focal distance.
SurgiTelR (General Scientific Corp. Ann Arbor, MI, 800959-0153) eliminates many of the problems associated with
the hobby loupes. It has a halogen focal light that attaches to
the lenses. The lenses are attached to either a pair of glasses or
a head set. The surgeon is not committed to look through the
lenses as they function like bifocals. The lenses also have a focal range which varies with the lens but is generally 25-75 cm.
With this system, any objects within that focal range will be
in focus. Though the cost may seem high, these loupes have
application for surgery in other species as well.
Microsurgical instruments are constructed such that only
the tips are miniaturized. The handles should be of normal
length to help provide stability to the tips. The handles should
be round to facilitate the required rolling action. This is most
important for the needle holders where the curved needle must
be rolled through the tissue
The microsurgical pack should include micro-scissors, micro-needle holders, and micro-forceps. Many prefer needle
holders without a clasp or box lock as the motion which occurs when the lock is set and released may be enough to cause
the needle to tear tissues. Micro-mosquito hemostats and other small instruments should also be included in the small exotic animal surgery pack.
Electrosurgery employs high frequency alternating current
to generate energy. There are 2 electrodes (an active electrode
and an indifferent electrode) with concentration of current
density at the tip of the smaller (active) electrode. Burns can
result if the ground plate (indifferent electrode) contacts only
a small area. A variety of active electrode tips are available including wire or fine tip electrodes which are useful for skin incision and removal of fine, delicate tissues for biopsy. Loop
electrodes are useful for contouring and removing heavier tissues. Ball electrodes should only be used for coagulation and
fulguration. The power setting will vary with the type and size
of the electrode, the area of electrode surface in contact with
tissue, the nature of the tissue, the operation performed (cut or
coagulation), and the depth of the incision desired.
The SurgitronR (Ellman International, Inc. Hewlett, NY,
516-569-1482) uses radio frequency current which is received
by the indifferent electrode acting as an antenna. As a result,
if only a small area of the patient is over the electrode it will
not burn the patient.
Bipolar electrosurgical forceps have a broader surface to
disperse the current and may be used at a lower setting.
They contain both electrodes in the forceps so there is no
need for a ground plate. They are most useful for hemostasis within body cavities. The forceps are insulated except
for the tips. If a non-insulated portion of the forceps contact
tissue, the current will pass from one electrode, through the
tissue, and to the other electrode without accomplishing the
required function at the tips.
Hemostatic clips are also very useful but each size clip requires a different applier. These are marketed by a variety of
companies. Sterile cotton tipped applicators should also be
available. These are useful for absorption of fluid as well as
gentle tissue dissection and manipulation. Absorbable gelatin
sponges (Gelfoam, Upjohn Co., Kalamazoo, MI) and oxidized regenerated cellulose (Surgicel, Johnson and Johnson,
Sommerville, NJ) are valuable for controlling hemorrhage.
31
Avian biopsy techniques
R. Avery Bennett
Clinical evaluation helps define the historical behavior
and clinical characteristics of the tumor, identify intercurrent
diseases, establish a differential diagnosis, and develop a rational diagnostic plan. Signalment provides valuable clues
for differential diagnoses. Many tumors have a greater tendency to affect animals of a particular age, gender, or
breed/species (e.g. renal carcinoma in male budgies > 2yrs).
History is used to define tumor behavior and identify signs
of intercurrent diseases. Owners should be questioned
specifically about the onset, duration, growth rate, and prior
treatments of a mass. Physical examination is performed to
define the extent of tumor burden and characterize intercurrent disease processes. Tumors are assessed for size, location, and invasiveness. A differential diagnosis list is made
for the mass and a diagnostic plan developed to rule in/out
each potential tumor type. The purpose of the diagnostic
evaluation is to identify the specific tumor type, determine
the clinical stage of disease, and define the presence, type
and extent of intercurrent diseases to decide on a safe and effective treatment plan.
General health status is assessed to identify intercurrent disease processes that may adversely affect prognosis
and limit or alter planned treatments of the neoplasm.
Screening includes a CBC, chemistry panel, and survey radiographs. Other diagnostic tests (e.g. ultrasound) are performed as indicated.
Biopsy is always performed prior to initiating therapy or
condemning an animal to euthanasia, to confirm the mass is
neoplastic and to identify the tumor type. The goal of biopsy is to safely and simply procure an adequate tissue sample
to provide a proper diagnosis. Biopsies can be excisional or
nonexcisional. Careful planning of the biopsy is essential
since improper technique can alter an animal’s therapy and
adversely affect the prognosis.
Excisional biopsy is seldom recommended, as it is not
possible to determine the specific goals of tumor removal
without knowing the type of tumor first. A skin lesion could
be a squamous cell carcinoma requiring wide margins or it
could be a feather cyst requiring minimal tissue margins. Excisional biopsy is most often performed when the client does
not want to pursue treatment of a mass and only wants the
mass removed. They must be properly informed so they understand with certain tumor types, a second surgery might be
indicated to obtain wider margins.
Fine needle aspirate (FNA) cytology is easy to perform
and may provide a definitive diagnosis. Mast cell tumors,
lymphoma, and lipomas are easily diagnosed using FNA.
However, many tumors do not exfoliate cells well making it
difficult to obtain a diagnosis using cytology. Brush samples are generally obtained through an endoscope in hollow
viscera. The limitations are similar to those of FNA. Impression smears are usually obtained from ulcerated masses. A glass slide is gently pressed onto the surface of the
mass to obtain cells for cytologic examination. If the number of cells and their morphology is not adequate, a diagnosis may not be obtainable with this method.
Surface biting instruments are used to obtain a tissue
sample, not just cells, either through an endoscope or of a
mass that is not easily accessible, such as an oral or cloacal
mass. These come in various sizes and many are made to
pass through a biopsy channel in an endoscope. They allow
collection of a piece of tissue which is more likely to provide
a definitive diagnosis than a cytologic sample.
Cutting needle core biopsy instruments are used to obtain a core of tissue through the mass. The tip of the needle
is inserted into the surface of the mass, the needle is advanced into the tumor and tissue drops into its sample chamber. The sleeve comes over the needle cutting the core of tissue in the sample chamber from the tumor. These are available in various sizes and lengths. They are used commonly
with the aid of ultrasound to obtain samples of intracoelomic masses. Ultrasound helps avoid major vessels and other
vital structures.
Punch biopsy instruments are typically used for skin
biopsies or surface lesions. They are small circular cutting
instruments placed on the surface of the tumor and rotated to
cut a cylindrical core of tissue. Their depth of penetration is
not far and the sample must be cut free from the deep tissues.
An incisional biopsy involves using a scalpel to cut a
section of the tumor for histologic analysis. Mainly used for
surface tumors, the location of the incision is carefully
planned so that is can be easily excised during the definitive
surgery for tumor removal.
Staging is done to determine the extent of disease, provide a framework for treatment planning, facilitate communication between clinicians, facilitate evaluation of treatment results, and aid prognostication. The most widely used
system in veterinary medicine is the TNM system. This system is based on assessment of the extent of local (T-tumor),
regional (N-lymph node), and distant disease (M-metastasis). Other information may be used to modify staging (clinical signs, histologic grade, tumor location, etc.).
33
Wound management in birds
R. Avery Bennett
A number of substances and systems are used for wound
irrigation. A system that produces a reliable pressure that
will not damage tissues or cause dissection through tissue
planes uses a 30 cc syringe and an 18 ga needle. An apparatus is constructed using a bag of irrigation solution with an
IV tube set up. A 3-way stopcock is attached to the tube and
a 30 cc syringe attached to one port. The needle is broken off
an 18 ga needle and attached to the 3-way stopcock. This set
up produces a stream of irrigation solution at 7-8 psi. Irrigation solutions function to removed debris and provide a topical antibiotic.
Dilute povidone-iodine is acidic with only short residual
activity. It should be made as a 1% solution (1 part of a 10%
stock solution in 9 parts LRS) as stronger concentrations are
less effective and kill fibroblasts. Povidone-iodine is inactivated by organic material which is frequently present in
open wounds. Dilute chlorhexidine should be made as a
0.05% solution (1:40 dilution of the 2% stock solution).
Stronger concentrations have a negative effect on wound
healing.
Chlorhexidine is broad spectrum with long residual activity and it is not inactivated by organic material. The diacetate form precipitates with saline. Hydrogen peroxide has
little effect on bacteria but is an effective sporicidal agent.
The bubbles can dissect between tissue planes. It is most
useful as a first time cleanser.
TOPICAL TREATMENTS
Triple antibiotic ointments typically contain bacitracin,
polymyxin, and neomycin in a petrolatum base. Petrolatum
products inhibit wound healing; however, the zinc bacitracin
component has been shown to enhance epithelialization. Silver sulfadiazine cream (1%) is a water miscible cream that
is among the best at promoting epithelialization. Its action
comes from the effects of the silver molecules on bacteria. It
is broad spectrum, nontoxic, painless, and nonstaining. It is
able to penetrate an eschar providing antimicrobial action to
tissues below. Nitrofurazone is broad spectrum and watersoluble. It is most applicable for wounds in the repair stage
of healing as a non-adherent semi-occlusive dressing. It is
hydrophilic and pulls fluids from deeper tissues to soften the
exudates and increases the capillarity of the bandage to help
pull exudates into the intermediate layer. It does appear to
slow epithelialization. Enzymes (Granulex, SmithKline
Beecham) contains trypsin which digests necrotic tissues
and crusts. Balsam of Peru stimulates capillary growth and
improved blood flow. Castor oil improves epithelialization
and is analgesic. It is most useful early in wound management to help debride the wound.
Substances that enhance epithelialization include silver
sulfadiazine (best), bacitracin zinc (second), capsaicin, scarlet red, Preparation H, allantoin, and acemannan. Those with
little effect on epithelialization include 1% povidone-iodine,
0.05% chlorhexidine, hydrogen peroxide, mupirocin, benzoyl peroxide, aloe vera. Those substances that retard epithelialization include nitrofurazone, gentamicin ointment,
tretinoin, acetic acid (0.25%), Dakin’s solution (0.1%) and
petrolatum.
BANDAGING
The bandage is composed of three layers - contact, absorbant, and outer. Adherent contact layers are generally
used in the early stages of wound management to aid in
debridement. The most familiar of these is the Wet-to-Dry
bandage which is put onto the wound wet and allowed to
stay in contact with the wound while it dries. Necrotic debris adheres to it and is removed when the bandage is
changed.
Nonadherent semiocclusive materials and nonadherent
occlusive materials are used after the tissue bed is healthy.
Semiocclusive materials retain enough moisture to prevent
drying, promote epithelialization, and allow excess fluid to
be absorbed.
Examples include Telfa pads and petrolatum impregnated gauze. They provide a good envirionment for healing and
removal does not damage tissues.
Nonadherent occlusive dressings (Dermaheal, Duoderm, BioDress) promote more rapid epithelialization.
They have a hydrocolloid on one surface which sticks to
surrounding normal skin. It does not stick to the wound as
it absorbs fluids forming a nonadherent occlusive gel.
These are also recommended for the repair stage of healing and are left in place 1-3 days until they feel like a fluid filled blister. In some birds, it will not stick well to the
skin. A thin line of Super Glue can be applied to the skin
to improve adherence.
34
The intermediate absorbent layer is composed of a material with good capillary action such as cotton or cast
padding. It provides a protective pad and absorbs exudates
pulling them away from the wound. The outer layer holds
the bandage in place and protects it from the environment. A
porous material (Vetrap, Elasticon, porous tape) is most
commonly used as it allows evaporation.
In locations where it is not feasible to apply a bandage in the traditional manner a tie on bandage can be
used. Loops of suture are placed in the skin around the
wound.
The wound is dressed with a contact and an absorbent
layer. Then, umbilical tape is used to tie the bandage on by
passing it across the wound from loop to loop.
35
Surgery of the avian beak
R. Avery Bennett
ANATOMY AND PHYSIOLOGY
The beak is composed of the upper and lower jaws
with their horny sheaths. The horny sheaths only partially
cover the jaws and are called the maxillary rhamphotheca
(rhinotheca) and the mandibular rhamphotheca (gnathotheca).
The cutting edges of the beak are called the tomia. Histologically, the beak resembles skin with the dermis closely
attached to the periosteum of the underlying bone. The stratum corneum is very thick and the cells contain free calcium
phosphate and hydroxyapatite crystals giving it the characteristic hardness.
The horny tissue is constantly turning over with the surface keratin lost by normal wear. Keratin is produced from
the stratum germinativum at all sites and migrates to the surface. Keratin also migrates as a result of underlying transitional cells directed at various angles in columns toward the
tomia creating distinct growth patterns from the base of the
beak to the tip.
The upper jaw is formed primarily by the premaxilla and
nasal bones. These are hollow as they contain the rostral diverticulum of the infraorbital sinus making the bony wall of
both the upper and lower beaks very thin. The craniofacial
hinge is located caudal to the nasal bone where it attaches to
the frontal bone. In most psittacines this is a synovial articulation.
Psittacine birds generate high pressures when they bite.
It is reported that macaws generate pressures over 200 psi.
This makes stable repair of fractures challenging.
and an acrylic patch is placed over the fracture. Similarly,
fractures with bony defects are covered with an acrylic
patch. If the defect is small, it may be covered with acrylic
alone. Larger defects (>2cm) usually require a steel or
polypropylene mesh to cover the defect prior to applying
the patch. The beak will granulate under the patch which
will slough with normal keratin turn over in a couple of
months. Simple but unstable fractures heal with variable
success.
In larger birds with bigger bones the chance of bone
healing is greater. In smaller birds it can be very difficult
to obtain bone healing. Various methods of fracture stabilization have been used. Interfragmentary wires with
acrylic covering on the lateral and lingual sides may afford
the best chance for healing. In order to neutralize the compression forces, placement of an esophageal feeding tube
and bridging the upper and lower beaks for 2-3 weeks
should be considered. Splitting of the mandible occurs in
small birds and rarely heal; however, these birds function
very well.
Similarly, birds missing a portion of either the upper or
lower beak will generally adapt and function quite well.
They may require tube feeding until they develop new
techniques to prehend food.
Hyperextension of the premaxilla has been reported primarily in macaws. Reduction involves placing a pin through
the base of the beak to lever the premaxilla over the vomer
bones allowing it to drop into its normal position.
GROWTH DEFORMITIES
TRAUMA
Traumatic injuries to the beak may cause simple fractures, depression fractures, fractures with bone defects, or
avulsion fractures. Because of the tenuous blood supply,
the contaminated location, and the high stresses applied by
the awake bird, fracture repair is challenging. Traumatic
wounds may be closed primarily if the tissues are minimally contaminated and appear healthy. Necrotic, infected, or seriously contaminated wounds are managed open
until the tissues are healthy. As with any crush injury, it
will take several days for the extent of the vascular injury
to be evident. Once the tissues are healthy, depressed fracture fragments are pulled up flush with the beak surface
Scissor beak is characterized by the lateral deviation
of the premaxilla and can be to the right or left. Various
etiologies have been implicated and it is most commonly
diagnosed in macaws. If detected early (before the premaxilla has ossified) it may be corrected by beak trimming and physical therapy. If the cartilage has ossified, an
acrylic ramp or pin and rubber band technique is generally required.
Mandibular prognathism is mainly seen in cockatoos. As with scissor beak, if detected early, conservative
management may be effective. Two techniques have met
with success in managing beak deformities in juvenile
psittacines. The acrylic ramp technique involves the ap-
36
plication of acrylic polymer to build a ramp onto the
mandible (for scissor beak) or maxilla (for mandibular
prognathism) to train the beak to grow in the proper direction. The pin and rubber band technique involves inserting a pin into the upper beak at its base and attaching a rubber band to the pin and to the diverted section
of beak to train the beak to grow in the proper direction.
In either case, frequent recheck for adjustments are required.
PROSTHESES
Beak prostheses can be used to reconstruct a damaged
or missing beak. They are temporary appliances. Realize
that any metal implants will eventually lyse surrounding
bone and come out. Prosthetics applied to the outside
come off when the keratin surface sloughs. Once a prosthesis has failed, application of a second prosthesis is
more difficult as there is less tissue to work with.
37
Reproductive surgery in birds
R. Avery Bennett
SALPINGOHYSTERECTOMY
Salpingohysterectomy is performed through a left lateral celiotomy. There is a ventral suspensory ligament that is
nonvascular and throws the oviduct and uterus into folds. It
is broken down allowing the oviduct to be stretched into a
linear configuration providing exposure to the vessels in
the dorsal suspensory ligament. The cranial oviductal vessels are identified at the infundibulum emerging from the
ovary. Two hemostatic clips are applied to the vessels as
they emerge from behind the ovary. The dorsal suspensory
ligament of the uterus extends from the dorsal body wall to
the oviduct and uterus containing numerous vessels supplying the oviduct and uterus. Each is coagulated with the
bipolar forceps as close to the oviduct and uterus as possible. Clips may be applied to larger vessels.
The uterus and oviduct are exteriorized completely
such that only its junction with the cloaca is within the
coelom. This is where the clips will be applied prior to the
transection. A cotton-tipped applicator is inserted through
the vent into the cloaca to help delineate its boundaries.
Clips are applied to the uterus near its junction with the
cloaca. The uterus is transected distal to the clips. Prior to
closure, the abdominal cavity is extensively evaluated for
hemorrhage
ORCHIDECTOMY
The indications for orchidectomy in birds remain anecdotal. In male birds with chronic cloacal prolapse, straining
and masturbation may be contributing factors. Castration
may prevent these behaviors which may decrease the
chances of recurrence following cloacopexy. In aggressive
male birds, castration may ameliorate their behavior.
Birds have two testicles that lie on the caudal vena cava. They are attached by a short ligament with numerous
small vessels providing blood supply to the testicle. The
testicles are approached through a left lateral celiotomy.
The caudal pole of the testicle is gently grasped with fine
forceps and elevated exposing the short ligament. A vascular clip is applied between the testis and the vessel. Fine
scissors are used to cut the ligament along the clip. In most
cases it will take more than one clip to be able to remove
the testis. Once the ligament is cut, the testis can be elevat-
ed farther allowing a second clip to be placed cranial to the
first one. The ligament is then cut along the second clip.
This procedure is continued until the testis is removed. The
site is inspected for testicular tissue which must be removed. The right testicle is adjacent to the left but separated by an air sac membrane. This membrane is opened to
create a window through which the right testicle can be removed. It is somewhat more difficult to remove the right
testicle because it is deeper. A right-angled hemostatic clip
applier is advantageous. In addition to controlling hemorrhage, the clips provide a barrier to help protect the fragile
caudal vena cava. If the vein is damaged during dissection,
gentle pressure is applied and a hemostatic agent is used to
control hemorrhage.
VASECTOMY
Vasectomy is indicated to control reproduction in birds
especially in situations where flock size has become a
problem. The vasa deferentia are approached through a
ventral midline celiotomy. The viscera are retracted to allow visualization of the cloaca and the structures dorsal to
it. On each side, lateral to the colon the vasa deferentia are
located. Be sure that it is not the ureter. Hemostatic clips
are placed in two sites approximately 5 mm apart. The section of vas between the ligatures is excised. This tissue may
be submitted for histologic examination.
ABDOMINAL HERNIORRAPHY
Acquired abdominal hernias appear to occur primarily
in egg laying females. The main problem seen in birds with
abdominal hernias is herniation of the cloaca with resultant
entrapment of eggs, urates, or feces. An incision is made in
the skin over the hernia. It is vital to identify the borders of
the body wall surrounding the hernia. Dissect the skin from
the midline incision laterally until the body wall can be
identified. The hernial sac is usually adhered to the hernial
ring in the body wall making it challenging to determine
the margins of the hernia. Once the border of the hernial
ring in the body wall is identified, dissect around the hernial ring to isolate the entire ring.. Simple interrupted sutures are used to close the defect along ventral midline.
38
One of the major complications associated with closure of
an abdominal hernia in birds is compression of the air sacs.
Removing abdominal fat will help prevent this. If it appears that the patient has difficulty breathing after reduction of the hernia, a mesh may be needed.
Plastic mesh may be used to repair body wall defects. The
mesh is not absorbable making aseptic technique critical. The
hernial ring must be isolated as previously described. The
mesh is placed inside the body wall. Sutures pass through
body wall into the mesh and into the coelomic cavity, then,
out the mesh and through the body wall again, then tied. Also note there is very little subcutaneous tissue in birds to support the skin laying over the mesh. Because of this, the skin
to may become devitalized exposing the mesh.
39
Surgery of the avian gastrointestinal tract
R. Avery Bennett
CELIOTOMY
The bird is positioned in right lateral recumbency with
the left leg retracted caudally for a left lateral celiotomy. The
skin incision is made from the pubis to the second to the last
rib dorsal to its uncinate process. A branch of the femoral
artery must be coagulated before the abdominal musculature
is incised. The muscle is incised through the mid-lateral
body wall. To gain exposure to the gonad and proventriculus, the last 2 ribs often must be transected. The intercostal
vessels are located cranial to each rib. They are coagulated,
then transected just dorsal to the junction between the sternal and vertebral ribs. A retractor is placed between the cut
ends providing exposure to the more cranial organs. Closure
involves apposition of the abdominal and intercostal muscles. No effort is made to unite the cut ends of the ribs.
For a transverse abdominal approach, with the bird in
dorsal recumbency, a transverse incision is made midway
between the vent and the caudal extent of the sternum. The
body wall is lifted and incised. The duodenal loop and pancreas lie immediately under the body wall. The body wall incision is closed in a simple continuous pattern.
A flap approach is also made with the bird in dorsal recumbency. A ventral midline celiotomy incision is made and
extended along one side of the caudal border of the sternum
leaving 2-3 mm of muscle into which sutures may be placed.
A Y-shaped incision may be performed by creating bilateral
flaps. The approach should be limited to minimize tissue exposure, compromise of blood supply, and disruption of air
sacs
CROP SURGERY
For an ingluviotomy, the head is elevated to prevent liquid in the crop from being aspirated. The skin incision is
made in the left lateral cervical region. The incision in the
crop is made to a length approximately 1/2 the length of the
skin incision. Closure is accomplished using a continuous
appositional or inverting pattern. The skin is closed over the
ingluviotomy incision.
Crop biopsy is indicated for diagnosing proventricular
dilation syndrome. The biopsy must be taken in a location
where there are blood vessels to obtain nerves demonstrating
the histologic changes.
In acute burns, it may be difficult to distinguish viable
from devitalized tissues. It is best to wait 3-5 days for a line
of demarcation between necrotic and viable tissue to develop. The wound edges are debrided until the skin can be separated from the crop wall. The skin and crop are sutured separately.
PROVENTRICULOTOMY
AND VENTRICULOTOMY
Ventriculotomy is considered more likely to leak postoperatively as it is difficult to seal the incision with sutures and
birds do not have an omentum. A left lateral approach is
used. The suspensory tissues surrounding the ventriculus are
dissected and stay sutures placed in the white tendinous portion of the ventriculus to allow the isthmus to be elevated. A
stab incision is made in an avascular area of the isthmus
(electrosurgery is not used). The incsions is extended orad
using scissors for a proventriculotomy or aborad for a ventriculotomy. The incision is closed with a fine monofilament
absorbable material on a small atraumatic needle using a
simple continuous, oversewn with a Cushing pattern. For a
ventriculotomy, the incision is closed in a simple interrupted
pattern.
ENTEROTOMY
Enterotomy is usually indicated as the result of trauma or
accidental incision during celiotomy. Historically enterotomy has carried a poor prognosis. With the use of magnification and fine sutures, accurate closure is more easily accomplished with a much better prognosis.
CLOACOTOMY
Through a cloacotomy you will be able to visualize the
coprourodeal fold and the uroproctodeal fold as well as the
ureteral and oviductal openings. Insert a moistened cotton
tipped applicator stick into the cloaca. Incise through the
skin, the muscle of the cloacal sphincter, and the mucosa of
the cloaca from the vent to the cranial extent of the cotton
tipped applicator. You should not enter the coelomic cavity.
40
Closure is accomplished using 6-0 monofilament absorbable
material in a simple continuous pattern. The vent sphincter
muscle is closed with a single mattress suture.
CLOACOPEXY
Cloacopexy is indicated for treatment of chronic cloacal
prolapse. It is important to excise the fat on the cloaca which
can prevent adhesion formation. The circumcostal cloacopexy uses the last rib to which the cloaca is sutured. Two
sutures are passed around each rib at the junction of the ster-
nal and vertebral portions. The ventral midline body wall incision is closed to incorporate the cloaca. The suture passes
through one side of the body wall incision, full thickness
through the cloaca, and through the other side of the body
wall. This encourages the cloaca to heal within the body wall
forming permanent adhesions.
Ventplasty is indicated in birds where the vent sphincter
has become dilated. The skin at the lateral commissures of
the vent lips is excised. Fine suture is placed transversely in
the mucosa of the cloaca. The vent sphincter is apposed in a
mattress pattern between the cranial and caudal aspects of
the sphincter. The skin edges are apposed cranial to caudal.
41
Respiratory surgery in birds
R. Avery Bennett
Choanal atresia is characterized by a failure of the
choana to form during development. Patients present at an
early age with a mucoid nasal discharge. To create a permanent choanal opening, a 1/8th or 7/64th inch pin is passed into each naris through any bone entering the choanal slit. An
8 Fr red rubber catheter is passed through the openings created with one end into each. Openings are cut into the side
of the tube to allow mucus to drain. The ends of the tube are
tied behind the head and a chin-strap is made. The tubes are
left in place for 4-6 weeks. Once the tubes are removed, the
nares are flushed daily to help keep the openings free of debris.
Effective treatment of infraorbital sinusitis depends on
a definitive diagnosis of the etiology. Left untreated, sinusitis may progress to an abscess requiring surgical exploration
and curettage.
Trephination may be used to gain access to areas of the
sinus that are not accessible to sinus flushing. Holes are
drilled into the frontal bone about _-2/5 the distance from
the rostral plane of the eye to the naris. Drilling continues into the sinus, widening the hole to an appropriate diameter.
Following the collection of samples, the sinus is irrigated.
After surgery, the trephination sites may be irrigated with an
appropriate antimicrobial solution.
Sinusotomy is performed to curette caseous material, remove a mass, or debride a granuloma. MRI or CT is useful
in localizing the lesion. The infraorbital sinus is the only
paranasal sinus of birds and has numerous diverticula (rostral, preorbital, infraorbital, postorbital, preauditory, and
mandibular diverticula and maxillary and suborbital chambers). It communicates caudally with the cervicocephalic air
sac and opens dorsally into the middle and caudal nasal conchae. The surgical approach varies with the location of the
lesion. Samples are submitted for microbiologic, cytologic,
and histologic evaluation. Appropriate topical and systemic
therapies are instituted. Flushing drains are usually left in
place days to weeks.
Tracheotomy is performed to relieve a tracheal obstruction. The patient is positioned in dorsal recumbency with the
shoulders elevated 45o. The skin is incised along ventral
midline. Over the caudal portion of the trachea the crop must
be dissected free and retracted to the right. The tracheotomy
is made through the ventral half of the annular ligament between rings. Once the object is removed, the tracheotomy is
closed by preplacing a fine, monofilament, absorbable suture using as few sutures as possible with knots external.
If the object is located at the syrinx, a thoracic inlet approach is used. The interclavicular air sac is broken down
and fat is removed. Sternotrachealis muscles are transected
to allow the trachea to be retracted. Stay sutures are placed
around tracheal rings orad to the obstruction. A transverse
tracheotomy is created 3-5 rings orad from the syrinx. An
endoscope is a valuable aid. Jeweler’s forceps and alligator
forceps are useful for grasping the obstruction. Once the tracheotomy is closed, an endoscope is used to assure patency
of the trachea and that the entire obstruction has been removed. No effort is made to reattach the sternotrachealis
muscles and the remaining soft tissues are closed in a routine manner.
Lateral thoracotomy is indicated for management of
diseases of the syrinx, bronchi, lung, pericardium, or thoracic air sacs. The approach will vary with the location of the
disease process. The patient is positioned in lateral recumbency with the wings positioned dorsally over the back and
the legs retracted caudally. The caudodorsal border of the superficial pectoral muscle is palpated and the skin is incised
along this muscle border. The second and third ribs are identified and the intercostal muscles are coagulated using bipolar. They are then transected with scissors ventral to the uncinate process and as close to the junction of the sternal and
vertebral ribs as possible. The section of ribs is removed allowing access to the thoracic cavity. Following removal of
the obstruction, the syrinx is not sutured and the ribs are not
replace. The pectoral muscle is sutured to the epaxial muscles to cover the thoracic wall defect. Subcutaneous and skin
closure is routine.
Idiopathic pericardial effusion may be treated by partial
pericardiectomy. The fluid is drained from the pericardial
sac prior to making an incision into the pericardium. A large
window is surgically created in the pericardium at the apex
of the heart. The heart base is avoided as the phrenic nerve
and the great vessels are located in this region.
Bifid sternum is characterized by a failure of the two
halves of the sternum to closure during embryonic development. The bird’s heart is visualized beating just under the
skin. The skin is incised along the ventral midline. The pectoral muscles are elevated from the sternum laterally until
the entire muscle is freed from the sternum and ribs. The existing portions of the keel are cut off using scissors. The pectoral muscles are advanced to midline and suture in a simple
interrupted pattern. This provides a thick pectoral muscle
pad to protect the heart.
43
Miscellaneous surgical techniques in birds
R. Avery Bennett
CONSTRICTED TOE SYNDROME
CATARACT REMOVAL
Circumferential constriction caused by fibers, scabs, or
necrotic tissue may result in avascular necrosis of the digit distal to the constriction. Treatment must reestablish circulation to the digit by removing the constriction and preventing circumferential scabs from forming using a hydroactive dressing.
Constricting fibers are best visualized with the aid of magnifying loupes. The tip of a 25ga needle is bent and used to elevate the fiber which is cut by rolling the needle. Microsurgical forceps are useful for untangling encircling fibers. A hydroactive dressing is applied to keep the tissues moist and protected. In most cases healing will proceed without incident.
In neonates, proposed causes for necrosis of digits include low humidity, egg related strictures, and ergot-like intoxication. A circular indentation may be identified and carefully excised using magnification. A circumferential skin
anastomosis performed and release incisions are made on
the medial and lateral aspects of the digit longitudinally
across the anastomosis to allow swelling to occur without
compromising circulation.
Birds are less prone to developing lens-induced anterior
uveitis. The cataractous lens is easily fragmented and phacoemulsification is not usually necessary. Cataract removal
requires an operating microscope and microsurgical instruments. A small incision is made in the cornea near the limbus. A needle with a bent tip is inserted into the anterior
chamber and used to tear the anterior lens capsule. Irrigation
floats the lens material out of the anterior chamber. Once all
of the lens material is gone, the incision in the cornea is
closed with fine absorbable suture. The anterior chamber is
filled with saline.
Nonsteroidal antiinflammatory and antibiotic ophthalmic
medications are used pre and postoperative to minimize anterior uveitis.
FEATHER CYSTS
Feather follicle cysts are the result of trauma or abnormal
development. Norwich and Gloucester canaries breeds are
predisposed to this syndrome. Blade excision of the affected
follicle appears to be the treatment of choice. Isolated cysts
on the body are easily removed using fusiform excision. If
an entire feather tract (pteryla) is involved the entire pteryla
is removed using fusiform excision. Removal of one or more
pterylae does not seriously affect cosmesis.
On the wing, a tourniquet may be used for hemostasis.
The entire follicle including any attachments to bone is removed being careful to preserve the integrity of adjacent follicles. Following surgery the wing is immobilized and the
wound allowed to heal by second intention.
With large feathers, the follicle may be saved by marsupializing the lining of the follicle cyst to the surrounding
skin. An incision is made in the center of the cyst parallel to
the direction of the feather’s normal growth. The feather debris is removed and redundant tissue is excised. A simple
continuous pattern of a monofilament suture is used to appose the cyst lining to the skin.
ENUCLEATION
This procedure is more difficult in birds than mammals
because the eye is bigger with respect to the orbit and the
optic nerve is short. Excessive traction can result in contralateral blindness. Suture the lids together. Make a circumferential incision 1-2 mm from the lid margins. Be careful at the medial canthus where the ligamentous attachments are firm. Dissection is continued between the palpebral conjunctiva and the bony orbit. Once the only remaining structure is the optic stalk, a hemostatic clip is applied.
It is critical to apply minimal traction to the globe when
placing the clip blindly on the stalk. The stalk is transected
distal to the clip and the eye removed. The eyelids are sutured in a simple interrupted pattern. In some birds with a
large globe, it may be necessary to collapse the globe prior
to enucleation. This will distort structures making histologic examination more difficult and it may release infectious
agents contained with the globe.
DUODENOSTOMY FEEDING TUBE
A duodenostomy tube is place to bypass the upper gastrointestinal tract. Through a ventral midline incision the
duodenal loop is immediately inside the body wall. It is exteriorized and a through-the-needle catheter (less than 1/3
the diameter of the intestine) is placed. The needle is first
44
passed through the left body wall, then into the descending
loop of the duodenum. The catheter is advanced through the
needle into the ascending loop. The needle is withdrawn from
the intestine and body wall. Two sutures are placed between
the peritoneal surface of the body wall and the intestine to
maintain them in apposition while a seal forms preventing
leakage. The catheter is secured to the outside skin using a
finger trap suture. The needle is protected in the “snap guard”
which may be bent to conform to the body. The catheter is directed caudal to the leg, under the wing and may be bandaged
or sutured in place. The tube should not be used for 24 hr. It
must be maintain at least 10 days to allow a seal to form.
When no longer needed, the catheter is pulled and the wound
is allowed to heal by second intention.
45
Surgery of the ferret adrenal glands
R. Avery Bennett
At least 95% of generalized alopecia in neutered ferrets 2
years of age or older is caused by neoplasia or hyperplasia of
the adrenal glands. Histologically, adrenal cortical hyperplasia,
adrenal cortical adenoma or cortical adenocarcinoma is diagnosed. Metastasis is uncommon. Clinical signs are related to
overproduction of sex hormones and consist primarily of bilaterally symmetrical alopecia, beginning at the hindquarters and
progressing cranially along the body. Behavior changes consistent with resurgence of sex hormones also occur. Spayed females frequently present with vulvar enlargement with or without alopecia. Males may present with prostatic or paraprostatic cysts with or without alopecia.
The diagnosis is suspected on physical examination and
history. Confirmation is obtained using ultrasound evaluation
of the adrenal glands. In some situations, exploratory surgery
confirms the diagnosis.
Surgery is considered the treatment of choice. A standard
ventral midline celiotomy is performed. Because adrenal neoplasias frequently occur coincidentally with insulinoma and
lymphoma, the lymph nodes, liver, spleen, and pancreas must
be evaluated. It is also important to evaluate the ovarian and
uterine stumps and the mesentery for any evidence of ectopic
or residual ovarian tissue.
The left adrenal gland is found within the sublumbar fat
just cranial and medial to the cranial pole of the left kidney.
Only the ventral surface of the gland can be visualized through
the peritoneum. This surface may appear grossly normal while
the abnormal portion may be deeper and not readily visible. It
is important to open the peritoneum and explore the entire
gland before declaring it normal.
The right adrenal gland is located by elevating the caudal
pole of the caudate lobe of the liver. A thin membrane extends
from the caudal tip of this liver lobe to the kidney (hepatorenal
ligament). This is incised to allow the lobe to be elevated exposing the adrenal. The gland is visualized on the dorsal aspect
of the caudal vena cava attached tightly to it. Frequently it appears more dorsal than strictly on the right side. Because of its
intimate association with the vena cava, removal of the right
adrenal gland is more difficult. The adrenal glands should be 24 mm wide, 4-6 mm long, and appear light pink and homogenous. Lumps, hard spots, discolorations, cysts or gross enlargement are indications for removal
It is generally easy to remove the left adrenal. The adrenolumbar vein courses over the left adrenal gland and is ligated
on each side of the gland prior to its removal. Hemostatic clips
are very valuable in controlling hemorrhage. Once the vessels
have been ligated, the adrenal gland is removed using sharp or
blunt dissection. Cotton-tipped applicators are valuable in this
dissection.
For right adrenalectomy, the gland is dissected from both
the right and left sides of the vena cava to isolate the tumor as
much as possible prior to placing vascular clamps. When the
adrenal is free from surrounding tissues and only attached to
the vena cava, the clamps are applied, one cranial to the mass
and one caudal to the mass. With the aid of magnifying loupes,
a plane of dissection between the adrenal and the vena cava is
identified. Dissection is continued until the adrenal is removed
from the surface of the vena cava. When the clamp is removed,
hemorrhage will be noted from small holes in the wall of the
vena cava. Surgicel is quickly placed on the vena cava where
the adrenal was dissected free and gentle pressure is applied for
approximately 5 minutes. This will allow the holes to seal. The
Surgicel is left in place and not disturbed during closure. If a
defect is created in the vena cava during dissection it is closed
with 8-0 to 10-0 monofilament suture on an atraumatic needle
with the aide of magnification.
Another technique described for partial excision of the
right adrenal involves the use of hemostatic clips. Once the
gland is freed from surrounding tissues, hemostatic clips are
applied between the gland and the vena cava. The tissue is then
transected along the clips which provide hemostasis of vessels
between the adrenal and the vena cava. More of the diseased
adrenal tissue remains in the ferret increasing the chances for
recurrence.
Dexamethasone at 1 mg/kg is administered as the gland is
removed. In 24 hours the ferret is given 0.1mg/kg prednisone
orally daily for 3 days followed by the same dose every other
day for 3 treatments. Although postoperative steroids are not
required it appears that many ferrets suffer less depression and
have a more rapid return to their normal state when glucocorticoids are administered for a short period of time. Following
bilateral adrenalectomy, ferrets often require glucocorticoid
therapy for a longer period of time. Rarely they require mineralocorticoid supplementation as well. Patients are returned to a
normal diet within 6-12 hours postoperatively. Following adequate removal of the adrenal neoplasia, the swollen vulva will
generally return to normal within 2 weeks and hair loss will begin to resolve in 1-4 months.
47
Non abdominal surgery in ferrets
R. Avery Bennett
ANAL SACCULECTOMY
MAST CELL TUMORS
The anal sacs collect secretions for many of the anal
glands. It is important to realize that it is not possible to remove all of the anal glands and skin glands which produce
odor. Following this procedure, ferrets will still have some
odor. Some feel castration is all that is necessary as this will
decrease the odor to roughly the same level as anal sacculectomy. However, the anal sacs will still accumulate secretions and if the ferret is stressed or defensive, it will express the sacs and a very pungent odor will occur. Antibiotic therapy is indicated as the site is considered contaminated
due to its proximity to the anus.
The duct openings at the 4 and 8 o’clock positions are
identified. A fine hemostat is place across the duct to prevent
the contents of the sac from escaping during dissection. A
circumferential incision is made around the duct in the mucosa using a #11 blade. The flat portion of the blade is used
to scrap the anal sphincter muscle off the duct and sac. Care
is taken to preserve the anal sphincter. Dissection is continued until the base of the sac is identified and the sac is removed. The wounds are left to heal by second intention. If
the sac is ruptured during dissection, the site should be irrigated.
Mast cell tumors usually affect the skin in ferrets and
are considered benign. They are usually found on the
neck, shoulders, or trunk as single or multiple raised, hairless, well-circumscribed nodules. Cytology reveals mature
mast cells. Surgical removal is curative with relatively narrow margins (0.5 cm). Pretreatment with histamine blocking agents is not necessary.
CHORDOMAS
Chordomas usually arise at the tip of the tail in relatively young ferrets, but can affect the thoracic or cervical
spine as well. They are formed from remnants of notochord tissue. Immunohistopathology is necessary to distinguish between chordoma and chondrosarcoma, an important distinction to make. Tail chordomas do not cause
neurologic dysfunction due to their location. Amputation
is recommended at the second disc space cranial to the
cranial extent of the mass. Chordomas of the thoracic or
cervical spine often grow to a point where they cause neurologic dysfunction. CT or MRI is useful for determining
the extent of the lesion and the potential for surgical removal. Surgery is performed to debulk the mass and potentially decompress the spinal cord. Resolution of clinical signs following surgery is dependent on the length of
time and severity of the compression.
MAMMARY TUMORS AND PREPUTIAL
ADENOMAS/ADENOCARCINOMAS
Neoplasia of the mammary glands is rare in ferrets.
Mammary adenomas occur most frequently in male ferrets often in conjunction with preputial masses. Mastectomy or lumpectomy is usually curative. Masses at the
preputial orifice in ferrets are either adenomas or adenocarcinomas. They can cause partial urinary obstruction.
Preoperative biopsy is indicated to determine the degree
of resection required. Adenomas are removed with narrow
margins and carry a better prognosis. Following removal
of the mass, reconstruction of the prepuce is necessary.
For large masses, penile amputation and perineal urethrostomy may be the best option. Most ferrets tolerate
exposure of the distal end of the penis if adequate penile
coverage cannot be achieved.
PERINEAL URETHROSTOMY
Performing a perineal urethrostomy can palliate crystalluria in hobs that are refractory to medical management
and have recurrent cystitis. The stoma is created about 12 cm ventral to the anus between the os penis and the
pelvic urethra. A 1-1.5 cm incision is made in the perineal
urethra along the midline avoiding the cavernous tissues
on the lateral aspects. The subcutaneous tissues are apposed to take tension off the stoma. The urethral mucosa
is sutured to the skin with 5-0 or 6-0 monofilament suture. The final stoma should be at least 1 cm long. Postoperative care includes antibiotic therapy, fluids, analgesics, and a collar if necessary.
48
THORACOTOMY
Thoracotomy is infrequently required in ferrets. Approaches (intercostals or sternotomy) are analogous to
those used in cats. Controlled ventilation and perioperative analgesia are very important. The ribcage is easily
opened and relatively elastic. A lateral thoracotomy is indicated for most pulmonary surgery. A sternotomy is used
primarily for cranial mediastinal masses. When performing a sternotomy is it best not to cut all of the sternebrae.
Closure is accomplished with 0 or 2-0 monofilament absorbable suture to appose the ribs or sternebrae. A 5 fr
catheter is used as a chest drain to monitor for pneumoth-
orax or blood or other fluid in the thoracic cavity. Ferrets
generally tolerate chest tubes well.
OTHER SURGERIES
Ferrets present for a variety of surgical diseases including spinal cord injury, salivary mucocoeles, and orthopedic
injuries. In general, application of basic surgical principles
and techniques apply to ferrets. Their small size makes
surgery more challenging but most procedures performed in
cats can be performed in ferrets if the appropriate instruments are utilized.
49
Abdominal surgery in ferrets and anal sacculectomy
R. Avery Bennett
GASTROINTESTINAL FOREIGN BODIES
Foreign body ingestion is particularly a problem in ferrets less than one year of age. In older ferrets obstruction or
partial obstruction with trichobezoars becomes a relatively
frequent problem. Clinical signs are often vague including
intermittent anorexia, dark tarry stool and depression. Gradual weight loss and potentially severe wasting may occur.
With acute, complete gastrointestinal obstruction signs include severe depression and dehydration, vomiting, and crying in pain. Vomiting in ferrets is an inconsistent clinical
sign even with complete obstruction.
Diagnosis of gastrointestinal foreign body is made based
on physical examination and radiography. Most ferrets have
are easy to palpate. Small trichobezoars may be difficult to
palpate as they compress easily and may go undetected. Radiography may reveal a foreign object or gas pattern consistent with ileus. A gas distended stomach is consistent with
gastric outflow obstruction and is an indication for surgery
as soon as possible.
A complete abdominal exploratory is performed and
the entire GI tract evaluated for the presence of multiple
foreign bodies. The techniques for gastrotomy and enterotomy in ferrets are analogous to those used in other species.
The gastrotomy incision is made in a relatively avascular
region of the stomach after isolating the stomach with
saline moistened sponges. A two layer closure is recommended using 4-0 monofilament absorbable material with
the first layer being a simple continuous appositional pattern and the second layer being an inverting pattern such as
a Cushing’s or Lembert.
The diameter of the small intestine of ferrets is quite narrow and there are reports of intestinal stricture following
routine enterotomy in ferrets. The enterotomy be made on
the antimesenteric border of the intestine in the aborad portion as this is the more healthy portion. In order to minimize
the likelihood of postoperative stricture formation, the enterotomy is closed transversely. The prognosis following
surgery is generally good; however, clients must take steps
to prevent recurrence.
INSULINOMAS
Hypoglycemia in ferrets is usually caused by insulinoma
(pancreatic beta cell tumors). The tumor produces high levels of insulin driving glucose out of the circulation and into
the cells. Clinical signs generally consist of weakness and
depression. Frequently, ferrets salivate and paw at the mouth
as if experiencing nausea. As the disease progresses the periods of weakness and lethargy become more pronounced
and persistent. Some animals eventually develop seizures,
coma and may die. Definitive diagnosis is made based on a
fasting (4-6 hr) blood glucose of less than 70 mg/dl (normal
is 90-100 mg/dl). Generally insulinomas are too small to detect with ultrasonography.
The recommended treatment for insulinoma is surgical
excision. Patients should receive 2.5 % dextrose + 0.45%
NaCl or 5% dextrose during the procedure. Insulinoma may
metastasize to the liver and spleen indicating the need for
biopsy of these tissues during the exploratory celiotomy.
The free border of the greater omentum is pulled out of
the abdomen and wrapped in saline moistened sponges. The
proximal portion of the duodenum is exteriorized while the
colon is retracted caudally. The left lobe of the pancreas is
visualized in the deep leaf of the greater omentum. The right
lobe is visualized within the mesoduodenum. The body of
the pancreas is along the pyloroduodenal junction. By moving the duodenum toward midline the dorsal aspect of the
right lobe can be seen. Moving the duodenum laterally allows visualization of the ventral surface of the pancreas.
These manipulations will allow inspection of the lymph
nodes as well.
Insulinomas can be visualized within the pancreas as
small firm masses (0.5-2 mm). These small masses can be
removed by blunt dissection. Hemorrhage is minimal and is
controlled using gentle digital pressure and a hemostatic
agents. Small pancreatic ducts will generally seal and leakage of pancreatic enzymes in small amounts may not be associated with pancreatitis because enzyme activation has not
occurred and the peritoneum will absorb pancreatic enzymes.
The presence of multiple masses may be an indication
for partial pancreatectomy. It has also been recommended
that if no masses are palpable, a section of pancreas should
be removed and submitted for histologic examination because tumors may be microscopic and diffusely disseminated within the pancreas. There are two methods for performing partial pancreatectomy - dissection and ligation of ductules and vessels, or suture fracture technique. The suture
fracture technique requires less time but is associated with
more inflammation. In dogs, removal of 80-90% of the pancreas will not alter exocrine or endocrine pancreatic function
as long as the common duct is maintained.
50
Postoperatively an IV catheter should be maintained for
24-48 hours and the patient should be maintained on 2.5%
dextrose + 0.45% saline or 5% dextrose in water at 10% of
the body weight for 24 hours. The patient is given a bland diet in small but frequent meals 24 hrs after surgery and fluids
are continued converting to lactated Ringer’s solution. The
third day following surgery the patient is returned to its normal diet and generally requires no additional medication.
Blood glucose is monitored every 12-24 hrs and may take 23 days to return to normal.
Surgical removal of insulinomas is frequently considered
a debulking procedure as insulinomas have a high rate of recurrence and metastatic potential. Fasting blood glucose level should be evaluated two weeks postoperatively and then
every 1-3 months to detect if insulinoma is recurring. Subsequent surgeries may be performed; however, in many cases the patient is managed with diet and medications following the first surgery.
SPLENOMEGALY
Splenomegaly is relatively common in ferrets 2 years of
age or older. Splenomegaly in ferrets is usually due to extramedullary hematopoiesis, a benign condition and routine
removal of the spleen is not recommended. Conditions associated with splenomegaly in ferrets include lymphoma, insulinoma, cardiomegaly, adrenal neoplasia, systemic mast
cell tumors, Aleutian disease, eosinophilic gastritis, hemangiosarcoma, primary splenic neoplasia, hypersplenism and
splenitis. A spleen that increases rapidly in size over a very
short period of time or one that is irregular in shape, painful
or so large that it interferes with abdominal viscera function
is cause for concern. In cases where the spleen is excessively large, when the spleen is interfering with normal abdominal function, or if it is lumpy or irregular in shape, splenectomy or partial splenectomy should be performed.
Preoperative biopsy or fine needle aspirate of the spleen
is recommended as partial splenectomy is preferred over
complete removal if possible. Ultrasound will help determine the safety and efficacy of percutaneous biopsy.
Partial splenectomy is indicated as treatment of non-neoplastic conditions such as extramedullary hematopoiesis as it
allows for retention of normal splenic function. The vessels
supplying the portion of the spleen to be removed are double ligated, and transected at the hilus. In most cases the caudal portion of the spleen is removed as it is less likely to result in vascular compromise to the stomach. After several
minutes, a line of demarcation will be visible between the viable portion of the spleen and the section that has been deprived of its blood supply. The splenic tissue is pinched between the thumb and forefinger milking the pulp toward the
ischemic tissue. Forceps are placed along the flattened portion and the spleen is transected distal to the clamp. The cut
surface along the clamp is sutured with an absorbable material in a continuous pattern. Automatic stapling devices, if
available, are excellent for performing partial splenectomy.
Total splenectomy is performed beginning at the free end
of the spleen by double ligating the vessels at the hilus of the
spleen and transecting the vessels between the ligatures.
LIVER BIOPSY
The liver of ferrets has six lobes; left lateral, left medial,
quadrate, right medial, right lateral, and caudate. Liver biopsy is indicated during most exploratory celiotomies. Diagnosis of hepatic lipidosis, lymphoma, metastatic insulinoma,
and other hepatic diseases may be obtained using hepatic
biopsy. A suture fracture technique is appropriate for liver
biopsy when a protruding point of liver is identified. If all
lobes have a rounded configuration, a transfixation suture
fracture technique is used.
CYSTOTOMY
Urolithiasis occurs in both male and female ferrets of any
age. The calculi are generally composed of magnesium ammonium phosphate. They are frequently secondary to bacterial infection. Clinical signs associated with urolithiasis include dysuria, hematuria and painful urination. Diagnosis is
based on clinical signs, palpation of a large bladder, palpation of calculi, and radiographic or ultrasonographic evidence of calculi or crystals within the bladder. A tom cat
catheter can be placed in male ferrets with urinary obstruction; however, it can be quite challenging. Infusing lidocaine
into the urethra and administering diazepam may help dilate
the urethra to allow passage of the urinary catheter. A 3 fr
urethral catheter is produced by Cook Veterinary Products.
Cystotomy is indicated for removal of calculi and irrigation of the urethra. Standard approach and technique for cystotomy are used in ferrets. The apex of the bladder is inspected for a diverticulum which have been reported in ferrets. Culture of the bladder wall and the calculi is performed
and appropriate antibiotic therapy administered. The bladder
is closed in two layers - a simple continuous and an inverting pattern. Postsurgically the patient is placed on systemic
antibiotics pending the results of urine culture. IV fluid diuresis is maintained for 24-48 hr posoperatively. The patient
should be placed on a diet of primarily meat protein and no
plant material. Urinary acidifiers are not recommended.
PARAURETHRAL OR PROSTATIC CYSTS
Male ferrets with adrenal neoplasia may develop prostatic enlargement, prostatitis, paraprostatic cysts, or paraurethral cysts as a result of excessive quantities of hormones
produced by the adrenal tumor. Following removal of the
adrenal neoplasia the prostate rapidly decreases in size within 1 or 2 days. These cysts frequently contain a tenacious
green, often odoriferous material. This material is removed
at the time of surgery. Omentalization hastens resolution of
the prostatic disease especially in the presence of infection.
OVARIOHYSTERECTOMY
Ferrets are induced ovulators and remain in estrus until
they are stimulated to ovulate by breeding or artificial
means. This chronic hyperestrogenemia results in bone mar-
row suppression and potentially fatal aplastic anemia. CBC
reveals a severe nonregenerative, normocytic anemia. Additionally, a CBC frequently demonstrates the presence of nucleated RBCs, a neutropenia and a thrombocytopenia. Clinical signs include lethargy, depression, anorexia, hindlimb
weakness, pale mucus membranes, and petechial and ecchymotic hemorrhages of the mucous membranes and skin.
Ovariohysterectomy is performed as soon as the patient is
stable. Prevention by spaying females at 4-6 months of age
51
or within the first two weeks of the first estrus is best. Ovariohysterectomy in ferrets is analogous to that in cats with the
ventral midline incision centered midway between the umbilicus and pubis. The uterus is bicornuate and the suspensory ligament is loose and easily torn.
Pyometra is uncommon. Polyuria and polydypsia are not
common in ferrets with pyometra. Hyperestrogenism may
occur concurrently. The CBC may be normal though pancytopenia and neutrophilic leukocytosis may be evident.
53
Inconvenienti e sorprese nell’esame
del liquido cefalorachidiano
Marco Bernardini
Med. Vet., dipl. ECVN - Via Montebello 7, 40121 Bologna
Davide De Lorenzi
Med. Vet., SCMPA - Via Corelli 16, 47100 Forlì
Il prelievo e l’esame del liquido cefalorachidiano (LCR)
costituiscono un’importante tappa del protocollo diagnostico di molte patologie del sistema nervoso centrale (SNC) e,
talvolta, anche di quello periferico (SNP).
Sebbene venga effettuata sempre più di routine, specialmente da parte di chi si occupa di malattie neurologiche, deve essere sempre considerata una prova invasiva. Infatti, durante la sua effettuazione, possono comparire improvvisi inconvenienti, alcuni dei quali necessitano un intervento immediato poiché possono costituire un pericolo di vita per il
paziente.
Le modalità di prelievo e di esame del LCR non costituiscono materia di questa presentazione e possono essere consultate altrove1,2. In questa sede verranno presi in considerazione alcuni imprevisti e la maniera di minimizzarne la frequenza e l’incidenza sul risultato finale.
Il paziente ideale per il prelievo del LCR non presenta
controindicazioni cardiorespiratorie o metaboliche per l’anestesia, né masse intracraniche che provochino variazioni
significative della pressione intracranica (PIC).
La variazione della PIC causata dal prelievo di LCR è
causa potenziale di crisi convulsive, anche se l’evenienza di
una crisi al momento del risveglio è molto rara. L’uso di
preanestetici della famiglia delle fenotiazine è quindi controindicato, al pari della ketamina per l’induzione dell’anestesia. Si consiglia l’uso di diazepam e propofol o diazepam
e tiopenthal, avendo l’avvertenza di monitorare il respiro ed
aspettando la scomparsa dell’apnea eventualmente indotta
dagli anestetici. In caso di crisi deve essere seguito il protocollo usato per gli stati di male epilettico.
Dopo aver posizionato il capo per il prelievo dalla cisterna magna (flessione di 90° dell’asse nasooccipitale rispetto
al rachide cervicale), bisogna controllare che la respirazione
rimanga normale, osservandola per alcune decine di secondi. Alcuni cani tendono all’apnea in questa posizione. Assicurarsi che ciò non sia dovuto ad un inginocchiamento del
tubo endotracheale. In altre situazioni l’arresto respiratorio
può essere dovuto ad un transitorio aumento della PIC per la
riduzione del flusso del LCR a livello della cerniera occipi-
tale. In entrambi i casi è sufficiente diminuire di qualche grado l’angolazione del capo.
Il paziente, che va sempre intubato, deve ricevere ossigeno per tutta la durata dell’anestesia. Il piano dell’anestesia deve essere sufficientemente profondo da assicurare
l’insensibilità delle strutture attraversate dall’ago spinale
durante il prelievo. Bisogna ricordare che le meningi sono
strutture riccamente innervate e che eventuali stati infiammatori a loro carico possono aumentare la loro sensibilità.
Qualsiasi movimento dell’animale durante l’infissione dell’ago o, ancor peggio, mentre la bietta dall’ago si trova nello spazio subaracnoideo, è potenzialmente lesivo per il SNC.
Si ricorda che, a causa della posizione del capo, durante il
prelievo del LCR dalla cisterna magna si hanno delle modificazioni delle relazioni anatomiche tra i vari apparati, per
cui la parte più aborale del midollo allungato viene a trovarsi a livello di cisterna magna ed è quindi a rischio di lesioni, le cui conseguenze cliniche sono più gravi rispetto alle lesioni midollari. Nei gatti, specialmente se cuccioli, la
cisterna magna è situata in posizione relativamente superficiale. La pelle sovrastante, come in tutto il dorso dell’animale, può presentare un notevole spessore ed opporre resistenza all’entrata dell’ago. La forza necessaria per vincere
tale resistenza può portare ad un eccessivo approfondimento dell’ago ed a lesioni del SNC.
Nelle razze toy, specialmente nei volpini, sarebbe corretto far precedere al prelievo una radiografia del cranio in
proiezione frontooccipitale per evidenziare un’eventuale displasia occipitale. Questi casi sono nella maggior parte dei
casi clinicamente silenti, per la presenza di un setto fibroso
che chiude il difetto osseo e funzionalmente contiene il cervelletto, impedendone l’erniazione. Durante il prelievo direzionare troppo cranialmente l’ago potrebbe portare alla
perforazione del setto e all’infissione dell’ago nel parenchima cerebellare.
L’ago spinale, una volta che la bietta ha raggiunto lo spazio subaracnoideo, non andrebbe mai abbandonato dalla presa dell’operatore fino alla sua estrazione. Se, infatti, nelle
razze medio-grandi la quantità di tessuti attraversati è suffi-
54
ciente a mantenere l’ago in una posizione mediana e stabile,
nelle razze toy e nei gatti c’è il rischio che il cono, che è dotato di un certo peso, lasciato libero dall’operatore, tenda a
spostarsi verso il basso, causando un conseguente pericoloso movimento della bietta nello spazio subaracnoideo. Ciò
raramente causa lesioni del SNC, ma aumenta notevolmente
le possibilità di una contaminazione ematica.
L’infissione dell’ago lungo la linea mediana del corpo è
la conditio sine qua non per evitare la contaminazione ematica del campione. La prima regola sta nel mantenere l’asse
nasooccipitale parallelo alla tavola, compensando la differenza di diametro tra neurocranio e splancnocranio con spessori (molto spesso è sufficiente la mano dell’aiuto che afferra il capo durante il prelievo). Ciò risulta agevole nella razze dolicocefale, mentre può essere più difficile da conseguire nei soggetti brachicefali e soprattutto nei gatti.
A volte, nonostante vengano seguite alla perfezione tutte
le manualità, è possibile una piccola contaminazione ematica iniziale. Per evitare che questa ostacoli l’interpretazione
del campione è sufficiente scartare le prime gocce che fuoriescono. Può succedere che la goccia di sangue iniziale si
depositi nella parte più bassa del cono dell’ago, contaminando il LCR mano a mano che fuoriesce. In questi casi è
consigliabile aspirare la goccia con un ago e una siringa da
insulina per “pulire” il cono, prima di raccogliere il LCR in
una provetta.
Altra frequente causa di contaminazione ematica consegue alla connessione di una siringa all’ago spinale. Con l’aspirazione si crea infatti un’eccessiva pressione negativa che
favorisce la rottura di vasi. Inoltre aumenta la possibilità di
pericolosi movimenti della punta dell’ago.
Classicamente viene detto che il raggiungimento dello
spazio subaracnoideo viene avvertito dall’operatore come la
sensazione di forare un foglio di carta molto spessa. In un
buon numero di casi questa sensazione non si avverte e può
essere molto pericoloso approfondire la posizione dell’ago
nella speranza di avvertirla. Sempre è consigliabile controllare l’eventuale fuoriuscita di LCR, togliendo il mandrino,
ad ogni approfondimento di pochi millimetri dell’ago. Penetrare con la punta dell’ago nel midollo spinale provoca
emorragie intraparenchimatose che sono di solito clinicamente silenti, a meno che questa manualità errata non venga
ripetuta più volte.
A volte si ha la chiara sensazione di essere entrati nello
spazio subaracnoideo, ma il LCR non fuoriesce. Ciò può essere dovuto ad una nostra sensazione sbagliata, ma in realtà
l’ago non è correttamente posizionato. In questi casi è consigliabile estrarre l’ago e ritentare, piuttosto che approfondire la posizione e rischiare di entrare nel midollo. In altri casi la PIC è troppo bassa: in questi casi è consigliabile comprimere gentilmente entrambe le vene giugulari, per diminuire il deflusso venoso dal capo e conseguentemente aumentare la PIC. Se si vuole prelevare il LCR dalla cisterna
lombare, ma non fuoriesce nulla (evenienza non rara nel gatto e nelle razze toy), la compressione delle vene giugulari è
inutile se esiste un ostacolo al deflusso del LCR lungo il midollo. La compressione dovrà essere effettuata sulla vena cava caudale, tramite compressione addominale, in un punto
immediatamente caudale alla compressione stessa, se è stata
localizzata. Una mancata fuoriuscita di LCR nel gatto può
essere dovuta ad infezione con il virus della peritonite infettiva (FIP).
Si ricorda che la quantità prelevabile in tutta sicurezza è
pari a 1 ml / 5 Kg p.v. e che è assolutamente sbagliato prelevare LCR con tutti i rischi connessi (manualità, anestesia)
se non si hanno tutte le possibilità per analizzare il campione in maniera completa.
I tre esami ai quali il liquido cefalorachidiano (LCR)
deve essere routinariamente sottoposto sono la stima delle
proteine presenti, la conta delle cellule nucleate e la valutazione citopatologica. In realtà sono numerosi gli esami
effettuabili su campioni di liquor, tuttavia nella grande
maggioranza dei problemi neurologici per i quali si è ritenuto opportuno eseguire il prelievo, la valutazione di questi tre soli parametri permette un adeguato inquadramento
della patologia.
La valutazione citopatologica del liquor rappresenta senza dubbio una sfida, non tanto per le difficoltà interpretative
che questo può presentare, quanto per la difficoltà nell’ottenere campioni di eccellente, o almeno soddisfacente, qualità.
La meta principale che il laboratorio di citologia deve
porsi nell’allestimento di preparati da liquor è quella di ottenere sul vetrino portaoggetti un elevato recupero di cellule
ben conservate a partire da piccole quantità di liquido che
difficilmente potrà essere riprelevato; se a questo si aggiunge che il campione di liquor non può essere conservato che
per pochi minuti e che non può essere spedito si comprende
facilmente perché chiunque si appresti a prelevare un campione di questo materiale debba necessariamente essere a
conoscenza delle tecniche che permettono l’allestimento di
vetrini di buona qualità .
Esistono due soli metodi accettabili per allestire campioni citologici a partire da campioni di liquor: il sedimentatore o camera di Sayk e la citocentrifuga, che può essere considerata una evoluzione del sedimentatore stesso.
Risultano assolutamente inadeguati sia la centrifugazione che l’impiego di rudimentali sistemi di sedimentazione
che prevedono l’adesione del cilindro di sedimentazione direttamente sul vetrino, sia questa ottenuta con vaselina oppure con colla; con la prima tecnica si causa la rottura o la
grave deformazione di tutte le cellule in sospensione, mentre con la seconda tecnica si ottengono campioni inquinati in
partenza da materiale estraneo ed insufficiente conservazione delle caratteristiche citomorfologiche. In aggiunta questi
ultimi campioni non possono essere fissati con balsamo e
coprioggetto, per cui non possono essere archiviati, caratteristica fondamentale per tutti i campioni citologici.
Una volta raccolte le cellule sul vetrino con le tecniche
già descritte, queste devono essere colorate; a questo scopo si possono usare le colorazioni c.d. di Romanowsky, fra
le quali ricordiamo Diff Quik , Hemacolor , May
Grunwald-Giemsa, etc.
Qualunque sia la tecnica di colorazione usata, è molto
importante impiegare coloranti freschi o appena filtrati e
questo allo scopo di evitare accidentali contaminazioni da
parte di cellule od agenti eziologici derivati da cicli di colorazioni precedenti.
Le caratteristiche citologiche del liquor derivante da animali sani sono state descritte in numerosi articoli, da parte di
Autori diversi nel corso di questi ultimi venti anni3-7. Pur non
essendoci una assoluta uniformità di pareri viene uniformemente accettato che le componenti cellulari normalmente
presenti nel LCR sia nel cane che nel gatto sono date da
linfociti e cellule monocitoidi, in percentuali variabili a seconda delle tecniche di concentrazione utilizzate; i granulociti neutrofili rinvenuti nel liquor, considerati in un primo
momento sempre cellule patologiche, non vengono attualmente considerate tali se presenti in piccolo numero e comunque mai in numero superiore al 10%. Un analogo discorso vale anche per i granulociti eosinofili che possono essere presenti in liquor di animali sani in numero ancora inferiore rispetto ai neutrofili e comunque mai in numero superiore all’1% delle cellule presenti.
La più frequente anomalia riscontrabile nel LCR di animali con patologie neurologiche è data dall’aumento percentuale e/o assoluto di una o più delle linee cellulari normalmente presenti.
Difficilmente un quadro di pleocitosi corrisponde ad una
specifica patologia: più generalmente queste alterazioni sono comuni ad un gruppo di patologie che devono essere più
precisamente individuate sulla base di tutti i dati clinici a disposizione.
Un completo elenco delle possibili patologie neurologiche collegate alle diverse anomalie citologiche del liquor è
presente in un recente testo di citologia veterinaria8.
Il rilievo di agenti eziologici nel liquor, se associato a
corrispondente flogosi, ha sempre enorme significato diagnostico: questa evenienza è da considerarsi estremamente
55
rara in medicina veterinaria anche se sono stati identificati
vari tipi di batteri e miceti.
Fra le alterazioni più rare ed anche più significative che si
possono riscontrare nell’esame citologico del liquor ricordiamo la presenza di cellule neoplastiche. Se la sensibilità di questo esame è molto bassa nell’individuare cellule da neoplasie
primarie del SNC esso risulta estremamente utile in corso di
metastasi meningee di neoplasie maligne altrove localizzate.
Bibliografia
1.
2.
3.
4.
5.
6.
7.
8.
Chrisman CL, (1992), Cerebrospinal Fluid Analysis, Vet Clin North
Am Small Anim Pract, 22 (4):781-810
Oliver JE, Lorenz MD, Kornegay JN, (1997), Handbook of Veterinary Neurology, WB Saunders, Philadelphia, 89-92
Coles EH, (1986) Veterinary Clinical Pathology, 4th ed., WB Saunders, Philadelphia, 267-278
Cook JR, DeNicola DB, (1988), Cerebrospinal fluid, Vet Clin North
Am Small Anim Pract, 18: 475-499
Christopher MM, Perman V, Hardy RM, (1988) Reassessment of cytologic values in canine cerebrospinal fluid by use of cytocentrifugation. J Am Vet Med Assoc, 192:1726-1729
Rand JS, Parent J, Jacobs R et al, (1990) Reference intervals for feline cerebrospinal fluid: cell counts and cytological features, Am J Vet
Res, 51: 1044-1048
Parent JM, Rand JS (1994) Cerebrospinal fluid collection and analysis. In August JR (ed): Consultations in Feline Internal Medicine 2,
WB Saunders, Philadelphia, 385-393
Raskin RE, Meyer DJ, (2001),Atlas of canine and feline cytology,
WB Saunders, Philadelphia, 325- 365.
57
Esame citologico del fegato
Ugo Bonfanti
DVM, Clinica Veterinaria Gran Sasso - Via Donatello 26, 20131, Milano
La biopsia citologica del fegato rappresenta un esame collaterale utile, semplice ed economico. Non necessita solitamente di anestesia e, a differenza della biopsia istologica ecoguidata o di quella “a cielo aperto”, presenta meno rischi ed
una minore percentuale di complicanze. In questi ultimi anni,
la progressiva diffusione della biopsia citologica ecoguidata
ha permesso di ottenere campioni mirati da porzioni di parenchima epatico alterato, o da lesioni di dimensioni ridotte.
morali lungo il tratto di entrata dell’ago, evenienza comunque, assolutamente occasionale.
*****
Le patologie comunemente diagnosticate sono rappresentate da lipidosi epatica, epatopatia steroido-indotta, amiloidosi, gravi condizioni infiammatorie, neoplasie maligne
primarie, neoplasie infiltrative (ad es. linfoma, mastocitoma,
istiocitosi maligna, leucemie) e neoplasie metastatiche.
MATERIALE E TECNICHE
—————
Il materiale comunemente impiegato consiste in aghi spinali, muniti quindi di stiletto, di lunghezza e gauge variabili
(da 23 a 27 gauge), in siringhe da 5 – 10 ml (nel caso in cui
si scelga la tecnica ago-aspirativa) e vetrini sui quali strisciare il materiale ottenuto. Le tecniche impiegate consistono in ago aspirazione ed ago infissione (“capillary action technique”). In particolare, l’ago infissione prevede l’esclusivo utilizzo dell’ago senza che venga effettuata alcuna manovra aspirativa: in tal caso, il materiale entra nell’ago per
azione della capillarità, effettuando veloci movimenti di “va
e vieni” e di rotazione sull’asse dell’ago stesso.
In generale, il consiglio potrebbe essere quello di approntare dapprima la manovra “non aspirativa”, che dovrebbe fornire campioni meno contaminati da sangue e meglio
conservati; se il campione non fosse diagnostico per materiale insufficiente, si procederebbe all’esecuzione dell’ago
aspirazione.
Gli epatociti normali sono cellule ovali o poligonali, di
diametro da 25 a 35 µm contenenti un nucleo singolo, centrale o eccentrico, ed uno più nucleoli spesso prominenti; il
citoplasma è basofilo, finemente granuloso e punteggiato;
gli epatociti possono essere occasionalmente binucleati, con
nucleoli multipli e possono contenere corpi inclusi cristallini intranucleari, che non rivestono comunque alcun significato patologico. Solo raramente si evidenziano cellule epiteliali dei dotti biliari, sotto forma di piccoli aggregati di cellule cuboidali o colonnari ad elevato, ma costante, rapporto
nucleo-citoplasma, cromatina compatta ed omogenea e nucleoli non visibili. Le cellule dei dotti biliari non devono essere confuse con cellule mesoteliali normali, di origine contaminante, spesso raccolte in aggregati regolari con architettura mosaiciforme. Dal fegato normale possono essere infine prelevati occasionali mastociti.
—————
INDICAZIONI E CONTROINDICAZIONI
Le principali indicazioni sono rappresentate da epatomegalia diffusa, da gravi alterazione dell’ecogenicità (rilevate
in corso di esame ecografico) e dalla presenza di lesioni nodulari o focali, solide o cistiche.
Tra le principali controindicazioni si ricordano le alterazioni dei parametri coagulativi, le trombocitopenie e le
trombocitopatie; inoltre, nelle razze e in età a rischio per
emangiosarcoma, lesioni cistiche, singole o multiple, di
grosse dimensioni, non dovrebbero essere campionate, per
l’alta probabilità di causare sanguinamenti e di ottenere
campioni non diagnostici; infine a seguito del campionamento di forme neoplastiche, viene riportata, in particolare
in letteratura umana, la possibilità di impianto di cellule tu-
La lipidosi epatica si manifesta sotto forma di vacuoli a
margini netti di differenti dimensioni, otticamente vuoti,
conseguenti alla coalescenza di lipidi accumulatisi all’interno dell’epatocita, che si sono sciolti durante la procedura di
colorazione; la stessa cellula epatica può talora assumere l’aspetto di cellula “ad anello con castone”: un voluminoso singolo vacuolo spinge alla periferia il nucleo picnotico; nel
gatto la lipidosi epatica rappresenta un’evenienza estremamente frequente: può essere idiopatica o primaria (spesso associata ad epatomegalia), oppure secondaria ad altre patologie che provocano inappetenza: in tal caso le dimensioni del
fegato sono sovrapponibili a quelle di un fegato normale.
—————
58
L’epatopatia indotta da steroidi è la conseguenza della
somministrazione esogena di corticosteroidi, oppure dell’aumento della produzione di steroidi da parte dell’organismo
(sindrome di Cushing); il quadro citologico è caratterizzata
dalla presenza di epatociti voluminosi con rarefazione del citoplasma che assume aspetto schiumoso, simile a quello che
si reperta in corso di degenerazione idropica; in corso di epatopatia indotta da steroidi il citoplasma contiene glicogeno;
gli epatociti, di maggiori dimensioni, hanno nucleo centrale
(sono occasionalmente binucleati) e non contengono vacuoli a margini netti.
—————
L’amiloidosi consiste nell’accumulo di materiale amorfo,
eosinofilo, extracellulare. La deposizione di amiloide, proteina prodotta da parte degli stessi epatociti, rappresenta un’infrequente condizione correlata a patologie infiammatorie croniche sistemiche, extraepatiche. Può inoltre essere di origine
familiare nei cani Shar-pei e nei gatti Abissini.
—————
In riferimento ai quadri infiammatori, è necessario sottolineare come la citologia possa fornire indicazioni utili per
definire la componente cellulare responsabile della flogosi,
ma non sia in grado di chiarire la localizzazione iniziale o
prevalente delle cellule stesse. Non è quindi possibile definire con precisione se l’infiammazione abbia origine dal parenchima epatico (epatite) o dai dotti biliari (colangite), e
quindi quale componente del lobulo epatico sia primariamente coinvolta. Inoltre, è necessario ricordare come la contaminazione ematica che si può verificare in corso di prelievo citologico in un paziente con neutrofilia o linfocitosi,
possa rendere difficile la corretta interpretazione del campione. In tal caso, ad esempio, la presenza in corso di epatite suppurativa di neutrofili a contatto diretto con gli epatociti (frammisti o attorno), ed eventualmente contenenti batteri
fagocitati, possono supportare l’ipotesi flogistica. Ricordiamo inoltre come un modesto aumento delle cellule infiammatorie all’interno del parenchima epatico possa verificarsi
in corso di iperplasia nodulare epatica o in corso di condizioni tossiche aspecifiche (farmaci, tossine……).
Infiammazioni neutrofiliche, settiche o asettiche, possono derivare da pancreatiti, da malattie infiammatorie del
piccolo intestino (IBD), da infezioni batteriche - ascendenti dall’apparato gastroenterico attraverso i dotti biliari o a
seguito di diffusione ematogena -, e da peritonite infettiva
(FIP) nel gatto.
La presenza di numerosi piccoli linfociti ed eventualmente di plasmacellule, è frequentemente correlata a colangioepatite linfocitaria, reperto non infrequente nei gatti, primaria o secondaria ad altre malattie extraepatiche (IBD, pancreatiti); a differenza dell’infiltrazione del fegato conseguente a leucemia linfocitica cronica, in questo tipo di infiammazione non si rileva linfocitosi nel sangue periferico.
Infiammazioni croniche o miste sono caratterizzate dalla
presenza di una consistente percentuale di macrofagi accanto a un numero variabile di neutrofili, linfociti, eosinofili,
plasmacellule ed eventualmente istiociti. Si rilevano spesso
in corso di FIP, micosi sistemiche (istoplasmosi, aspergillosi), infezioni da micobatteri ed infezioni protozoarie (leishmaniosi, hepatozoonosi, toxoplasmosi). L’infiltrazione del
fegato da parte di numerosi eosinofili è spesso associata ad
enteriti eosinofiliche, e a sindrome ipereosinofilica nel gatto.
—————
Le forme neoplastiche che coinvolgono il fegato possono
essere tumori primari (epatocellulari e colangiocellulari),
tumori neuroendocrini, neoplasie mesenchimali, neoplasie
emolinfatiche e neoplasie metastatiche.
L’adenoma epatocellulare, che spesso coinvolge un lobo epatico come massa singola, è caratterizzato dalla presenza di epatociti quasi normali che possono manifestare
lievi anisocitosi ed anisocariosi; può essere impossibile distinguere un adenoma epatocellulare da un quadro di iperplasia nodulare.
Il carcinoma epatocellulare rappresenta la neoplasia
epatica più frequente. Se ben differenziato, il quadro citologico è sovrapponibile a quello di fegato normale o iperplastico; più spesso, comunque, le cellule manifestano caratteri di evidente atipia: anisomacrocariosi, elevato rapporto nucleo-citoplasma, alterazioni nucleolari, iperbasofilia del citoplasma.
Le neoplasie che hanno origine dalle cellule dei dotti biliari sono più frequenti nei gatti. L’adenoma colangiocellulare, tipico della specie felina, è caratterizzato dalla formazione di strutture cistiche contenenti liquido mucinoso. Il colangiocarcinoma, invece, è caratterizzato dalla presenza di
cellule simili alle cellule dei dotti biliari normali; esse esfoliano in aggregati di differenti dimensioni, estremamente
coesi, che formano talora strutture acinari o tubulari; le cellule sono di forma cuboidale o colonnare, più piccole degli
epatociti, con anisocariosi moderata ed elevato rapporto nucleo-citoplasma.
I carcinoidi o tumori neuroendocrini, rare neoplasie che
derivano dalle cellule APUD localizzate nella parete dei dotti biliari, sono citologicamente caratterizzati da elevata cellularità, margini citoplasmatici indistinti, nucleo tondeggiante, cromatina moderatamente addensata e citoplasma chiaro;
frequente è il riscontro di nuclei nudi.
Tra le neoplasie emolinfatiche il linfoma “a grandi cellule” rappresenta il tumore che con maggiore frequenza infiltra il parenchima epatico: accanto ad epatociti normali sono
presenti grosse cellule linfoidi immature con grosso nucleo,
cromatina finemente o grossolanamente reticolare e scarso
citoplasma iperbasofilo; raramente il citoplasma può contenere granuli rossastri (LGL o Large Granular Lymphoma).
Raramente, i linfomi che infiltrano il fegato sono costituti
da piccoli linfociti maturi: in tal caso può essere difficile differenziare il linfoma da una colangioepatite linfocitica o da
infiltrazione epatica in corso di leucemia linfocitica cronica:
a tale proposito si rende necessaria una biopsia epatica o l’esame del midollo osseo. Il fegato, inoltre, può essere sede di
infiltrazione in corso di altre forme leucemiche (in particolare acute, linfoblastica o mieloide) per la cui diagnosi definitiva possono essere necessarie colorazioni citochimiche
specifiche, oltre all’esame di uno striscio di sangue periferico e del midollo osseo.
Il coinvolgimento epatico da parte di mastociti neoplastici (cellule tondeggianti con ampio citoplasma spesso ben
granulato) si verifica più spesso nel gatto rispetto al cane, in
cui invece è più frequente l’infiltrazione epatica in corso di
istiocitosi maligna: in quest’ ultimo caso le cellule possono
manifestare sia caratteri di evidente atipia (multinucleazione, macrocariosi, anomalie nucleolari), sia risultare perfettamente sovrapponibili a macrofagi ed istiociti normali. Le
neoplasie mesenchimali primarie sono molto rare: tra queste, l’emangiosarcoma, più spesso metastatico, ed il leiomiosarcoma. I sarcomi che coinvolgono il fegato si caratterizzano per la presenza di cellule fusate o stellate dai margini indistinti, pleomorfe, con atipie nucleari più o meno pronunciate e nucleoli da inapparenti a multipli e voluminosi.
Le neoplasie metastatiche sono caratterizzate dalla presenza, accanto ad epatociti normali, di cellule non appartenenti al parenchima: esempi tipici sono le metastasi da tumori epiteliali intestinali, pancreatici o mesenchimali
(emangiosarcomi).
—————
È necessario infine sottolineare come, in una percentuale variabile di casi, sia possibile ottenere campioni ematici o acellulari, e quindi non diagnostici; in altri casi, inoltre, è possibile solo effettuare un’accurata descrizione citologica del campione in esame, senza poter giungere alla
diagnosi della patologia sottostante talvolta anche extraepatica. In particolare, con una certa frequenza si possono
diagnosticare:
1 - degenerazione idropica o balloniforme: espressione
di tossicità aspecifica e caratterizzata da rarefazione del citoplasma che assume aspetto simile a quello rinvenibile in
corso di epatopatia da steroidi;
2 - colestasi: rappresentata dalla presenza di pigmento
biliare all’interno degli epatociti sotto forma di piccoli granuli di colore verde scuro, oppure all’esterno, nei canalicoli
biliari tra epatociti contigui, sotto forma di cilindri verde
scuro-nerastri: tappi o trombi biliari;
3 - ematopoiesi extramidollare: caratterizzata dalla presenza di cellule ematopoietiche di aspetto normale a diffe-
59
renti stadi di maturazione; spesso la linea eritroide risulta essere quella maggiormente rappresentata; tale processo parafisiologico si verifica spesso in corso di aumentata richiesta
di cellule ematiche in pazienti con midollo osseo ipoplastico
e a seguito di altre condizioni patologiche; può essere talora
associato ad iperplasia nodulare nel cane.
Iperplasia nodulare, neoplasie benigne, alcune forme flogistiche (ad es. epatite cronica, colangite, colangioepatite),
fibrosi, cirrosi rappresentano entità patologiche non sempre
indagabili in modo approfondito mediante esame citologico,
per la cui diagnosi definitiva è spesso quindi necessaria l’esecuzione di una biopsia istologica.
Bibliografia
Alleman AR, (1997), Cytologic evaluation of the liver, Proceedings 15th
ACVIM congress, Lake Buena Vista, Florida, USA, 4-6.
Baker B, Lumsden JH, (2000), Color atlas of cytology of the dog and cat.
Mosby, Inc., St. Louis, Missouri, 177-197.
Bolliger AP, (1996), Cytology of the liver. Proceedings 6th ESVIM congress, Veldhoven, the Netherlands, 68-69.
Burkhard MJ, Meyer DJ, (1996), Invasive cytology of internal organs – Cytology of the thorax and abdomen, Vet Clin North Am Small Anim
Pract 26 (5): 1203-1222.
Cowell RL, Tyler RD, Meinkoth J.H., (1999), Diagnostic cytology and hematology of the dog and cat, Mosby, Inc., St. Louis, Missouri, 183194
De May
Kristensen AT, Weiss DJ, Klausner JS, Hardy RM, (1990), Liver cytology
in cases of canine and feline hepatic disease, Compend Contin Educ
Pract Vet 12 (6): 797-804.
Léveillé R, Partington BP, Biller DS, et al., (1993), Complications after ultrasound-guided biopsy of abdominal structures in dogs and cats: 246
cases (1984-1991), J Am Vet Med Assoc 203 (3): 413-415.
Raskin RE, (2000), Liver cytology: interpreting needle biopsy samples, Vet
Med 95 (3): 244-249.
Raskin RE, Meyer DJ, (2001), Atlas of canine and feline cytology, W.B.
Saunders company, Philadelphia, 231-252.
Roth L., (2001), Comparison of liver cytology and biopsy diagnoses in dogs
and cats: 56 cases, Vet Clin Path 30 (1): 35-38.
Teske E, (1992), Fine needle aspiration biopsy of the liver, a new tool in the
diagnosis of liver disease, Tijdschr Diergeneeskd 117 (4): 13S-14S.
Teske E, Stockhaus C, Van den Ingh T, Rothuizen J, (2001), Evaluation of
cytological criteria for the evaluation of diagnosis of hepatobiliary diseases in dogs, Proceedings 7th FECAVA, Berlin, 114-116.
61
Feline exocrine pancreatic disease
Susan E. Bunch
DVM, PhD, Diplomate ACVIM - Professor of Medicine, College of Veterinary Medicine
North Carolina State University, Raleigh, NC USA
WHAT ARE THE CLINICALLY
SIGNIFICANT PANCREATIC DISEASES
OF CATS?
Results of several retrospective analyses of post mortem
findings indicate that pancreatic disease in cats may not be
as unusual as has traditionally been thought. There isn’t always uniform agreement, however, as to the relationship between histopathologic findings and their clinical importance.
Studies that have taken into consideration clinical as well as
biopsy or post mortem findings have consistently identified
several clinically important diseases of the feline exocrine
pancreas (in order of commonness): acute and chronic pancreatitis, adenocarcinoma, and exocrine insufficiency.
Acute Pancreatitis
Lack of distinctive clinical signs and clinicopathologic
test results probably account for the low index of suspicion
clinicians have for pancreatitis in cats. Similar to dogs with
pancreatitis, cats with pancreatitis are examined most often
for signs common to many illnesses: lethargy, anorexia, and
dehydration. Vomiting is observed infrequently. Unlike the
stereotypic aged, overweight, neutered, nonsporting breed
dog, a cat with pancreatitis is more likely to be a middleaged, thin domestic shorthair cat. Signs observed commonly
in dogs such as persistent vomiting, abdominal pain, and diarrhea, are noted much less often in cats. The welcome sight
of laboratory test abnormalities including inflammatory
leukon, high liver enzyme activities, hyperbilirubinemia,
azotemia, mild hyperglycemia, hyperamylasemia and hyperlipasemia in a dog suspected of having pancreatitis is virtually unknown in feline pancreatitis. Serum trypsin-like immunoreactivity (TLI) is consistently elevated (> 82 ug/L,
ELISA). Low ionized serum calcium concentration has recently been reported to be associated with a poorer outcome.
Abdominal effusion, consisting of a nonseptic inflammatory
exudate, is found more frequently in cats than in dogs. Diagnostic imaging results (survey abdominal radiography and
ultrasonography) are consistent between species.
Causes of pancreatitis in cats are even less well recognized and understood than in dogs. Risk factors such as
those determined for dogs (increasing age, certain breeds,
neutered gender; possibly certain intercurrent diseases, exposure to drugs, anesthesia, and surgery) have not been
identified in cats. In fact, the experimental model used to
consistently create pancreatitis in dogs (infusion of oleic
acid into the pancreatic duct, to mimic the clinical syndrome of pancreatitis that follows ingestion of a high-fat
meal), unpredictably induces clinical signs of illness and
laboratory evidence of pancreatitis in cats. Pancreatic
flukes (Eutrema procyonis, Amphimerus pseudofelineus)
can cause signs of acute or chronic pancreatic inflammation, but most often are found incidentally during routine
examination of fecal specimens. The pancreas can also be
involved in certain systemic disorders including toxoplasmosis, feline infectious peritonitis, herpes virus, blunt trauma, and organophosphate toxicity.
Histopathologic changes mostly resemble those of canine pancreatitis. Pancreatic acinar necrosis, with or without fibrosis, and peripancreatic fat necrosis are the consistent features. Less often, moderate to severe suppurative
pancreatitis is found, characterized by nodular lesions that
exude pus when incised. About 50% of cats have mild hepatic lipidosis.
Treatment is similar to that for canine pancreatitis: nothing per os (NPO; controversial), fluid and electrolyte therapy, and plasma transfusion to supplement depleted circulating antiprotease activity. If the period of NPO exceeds 3 to 4
days, and clinical improvement is not seen, more aggressive
nutritional therapy is instituted (operative tube jejunostomy
would be ideal). Analgesia may also be needed (butorphanol
- 0.2 to 0.4 mg/kg SQ q 6 to 8 hr, or 5 µg/kg/hour, continuous infusion IV).
An especially discouraging condition is the combination
of acute pancreatitis and hepatic lipidosis. Presenting signs
are indistinguishable from those of lipidosis alone, except
that cats are more likely to be cachectic and have coagulation abnormalities. The prognosis is guarded.
Possible complications of severe pancreatitis include abscess or pseudocyst formation. Translocating enteric bacteria may infect either of these collections of fluid. Each of
these complications is addressed surgically if there is inadequate resolution with medical management (i.e., ultrasoundguided percutaneous aspiration for cytology, and microbial
culture and sensitivity testing, and appropriate antibiotic
therapy).
62
Chronic Pancreatitis
Clinical signs in over 50% of cats reported to have chronic pancreatitis include anorexia, weight loss, and vomiting.
Diagnosis is made primarily by the findings of high serum
TLI and characteristic microscopic features in pancreatic
biopsy specimens. Typical histologic findings include acinar
cell atrophy, interstitial fibrosis, and lymphocytic inflammation. No specific treatment suggestions have been published.
Diabetes mellitus and exocrine pancreatic insufficiency may
result if a majority of functional tissue has been destroyed.
Pancreatic Adenocarcinoma
Signs of adenocarcinoma, evident only late in the course
of the disease, mimic those of pancreatitis: anorexia, weight
loss and vomiting. Occasionally, the neoplasm is large
enough to compress the bile duct and cause jaundice. Aged
cats (> 12 years) are affected most often. A mass is readily
palpable in the cranioventral abdomen. Though abdominal
effusion has been noted in about 30% of cases, malignant
cells are rarely identified, and fluid analysis results are consistent with a modified transudate. There are no unique
hematologic or serum biochemical test results. Diagnosis is
usually made by ultrasound-guided aspiration biopsy or at
surgery. There is no predilection for a particular site within
the pancreas. The prognosis for cats with adenocarcinoma is
poor because metastases are usually evident at the time of diagnosis.
low-fiber diet is recommended (e.g., Hill’s c/d® or Purina
CNM EN-Formula®), as well as vitamin B12 supplementation (250 ug IM or SQ once weekly until serum concentration is normal, then every 3 months). Cats with vitamin K
deficiency should also be supplemented initially (1-2 mg/kg
of vitamin K1 SQ once daily for 3 days).
Miscellaneous conditions
Pancreatic bladder is a term describing a dilated sacculation of the pancreatic duct. First described in the human
medical literature in 1925, this condition has been described
in a few individual case reports in cats presented for signs of
bile duct obstruction. We have seen two cats with this condition recently, both of which were managed successfully
with surgery.
WHAT IS THE BEST WAY TO IDENTIFY
PANCREATIC DISEASE IN CATS?
The recommended diagnostic package for cats showing
signs suggestive of pancreatic disease is: CBC, chemistry
profile, urinalysis, serum TLI, and abdominal ultrasonography. If pancreatitis is suspected, a coagulation profile
(platelet count, prothrombin time, activated partial thromboplastin time, fibrin degradation products, and fibrinogen
concentration) is also recommended. Measurement of serum
trypsin-like immunoreactivity is available through: Dr.
David Williams, The Gastroenterology Laboratory, College
of Veterinary Medicine, Texas A&M University, USA
Exocrine Pancreatic Insufficiency
Lack of adequate secretion of digestive enzymes into the
duodenum results in a constellation of signs identical to
those seen in dogs with exocrine pancreatic insufficiency
(EPI): polyphagia, weight loss and voluminous, steatorrheic
stools. Progressive destruction of exocrine tissue by chronic
pancreatitis or acinar cell atrophy are now believed to be
equally responsible for the development of EPI in cats. Obstruction of the pancreatic duct by an abdominal mass or by
pancreatic flukes (Eutrema procyonis) can also yield the
same result, but is very unusual. Thin body stature, poor
haircoat, and bright alert disposition are typical physical examination findings. The haircoat in the perineal region is
greasy in some cats. Results of CBC, serum biochemical
profile and urinalysis are usually normal. Subtle increases in
liver enzyme activities may be seen. Some cats have severe
fat malabsorption that results in vitamin-K dependent coagulopathy. Most cats are deficient in vitamin B12 and about
50% are folate-deficient, consistent with concurrent primary
small intestinal disease. Serum TLI is low (_8 ug/L). Treatment consists of supplementing each meal with one teaspoon of pancreatic enzyme powder (e.g., Pancrezyme Powder®, Daniels Pharmaceuticals Inc, or Viokase-V®, Fort
Dodge Laboratories Inc). Primary small intestinal diseases
are pursued if response to treatment (gradual weight gain
and resolution of physical examination changes, rapid return
to normal fecal character) is suboptimal. A highly digestible,
Bibliography
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Akol KG, Washabau RJ, Saunders HM, et al: Acute pancreatitis in
cats with hepatic lipidosis. J Vet Intern Med 1993;7:205-209. [5 of 13
cats]
Andrews LK: Tumors of the exocrine pancreas, in Holzworth J (ed):
Diseases of the Cat. Philadelphia, WB Saunders Co, 1987, pp 505507. [58 cats with adenocarcinoma]
Bruner JM, Steiner JM, Williams DA, et al: High feline trypsin-like
immunoreactivity in a cat with pancreatitis and hepatic lipidosis. J
Am Vet Med Assoc 1997;210:1757-1760.
Cortese L, Papparella S, Ciaramella P, et al: Pancreatic diseases associated with high serum trypsin-like immunoreactivity in two cats. Eur
J Comp Gastro 2000;5:11-16.
Dill-Macky E: Pancreatic diseases of cats. Compend Contin Educ
Pract Vet 1993; 15: 589-596.
Duffell SJ: Some aspects of pancreatic disease in the cat. J Small
Anim Pract 1975;16:365-374. [17 cats; 3 with diabetes mellitus, 11
with pancreatitis, 3 with cancer]
Gerhardt A, Steiner JM, Williams, DA, et al: Comparison of the sensitivity of different diagnostic tests for pancreatitis in cats. J Vet Intern Med 2001;15: 329-333.
Hill RC, Van Winkle TJ: Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. J Vet Intern Med 1993;7:25-33. [40 cats]
Hines BL, Salisbury SK, Jakovljevic S, et al: Pancreatic pseudocyst
associated with chronic-active necrotizing pancreatitis in a cat. J Am
Anim Hosp Assoc 1996;32:147-152.
Kimmel SE, Washabau RJ, Drobatz KJ: Incidence and prognostic value of low plasma ionized calcium concentration in cats with acute
pancreatitis: 46 cases (1996-1998). J Am Vet Med Assoc
2001;219:1105-1109.
11.
12.
13.
14.
15.
16.
17.
Kitchell BE, Strombeck DR, Cullen JM, et al: Clinical and pathologic changes in experimentally induced acute pancreatitis in cats. Am
J Vet Res 1986;47:1170-1173. [6 cats]
Owens JM, Drazner FH, Gilbertson SR: Pancreatic disease in the cat.
J Am Anim Hosp Assoc 1975;11:83-89. [28 cats; 19 with pancreatitis, 3 with cancer, 6 with benign nodular disease]
Parent C, Washabau RJ, Williams DA, et al: Serum trypsin-like immunoreactivity, amylase and lipase in the diagnosis of feline acute
pancreatitis. Proceedings, 13th Annual Forum, American College of
Veterinary Internal Medicine, Lake Buena Vista FL, 1995, p 1009.
[12 cats]
Perry LA, Williams DA, Pidgeon GL, et al: Exocrine pancreatic insufficiency with associated coagulopathy in a cat. J Am Anim Hosp
Assoc 1991;27:109-114.
Simpson KW: Current concepts of the pathogenesis and pathophysiology of acute pancreatitis in the dog and cat. Compend Contin
Educ Pract Vet 1993;15:247-253.
Steiner JM, Williams DA: Feline pancreatitis. Compend Contin Educ
Pract Vet 1997;19:590-602.
Steiner JM, Williams DA: Feline exocrine pancreatic disorders: in-
63
18.
19.
20.
21.
22.
23.
sufficiency, neoplasia, and uncommon disorders. Compend Contin
Educ Pract Vet 1997;19:836-848.
Steiner JM, Williams DA: Feline exocrine pancreatic disease, in Bonagura KD and Kirk RW (eds): Kirk’s Current Veterinary Therapy
XIII, Philadelphia, WB Saunders Co, 2000, pp 701-705.
Steiner JM, Williams DA, Moeller EM, et al: Development and validation of an enzyme-liked immunosorbent assay for feline trypsinlike immunoreactivity. Am J Vet Res 2000;61:620-623.
Swift NC, Marks SL, MacLachlan NJ, et al: Evaluation of serum feline trypsin-like immunoreactivity for the diagnosis of pancreatitis in
cats. J Am Vet Med Assoc 2000;217:37-42.
Weiss DJ, Gagne JM, Armstrong PJ: Relationship between inflammatory
hepatic disease and inflammatory bowel disease, pancreatitis and nephritis
in cats. J Am Vet Med Assoc 1996;209:1114-1116. [120 cats examined]
Williams DA: Feline exocrine pancreatic insufficiency, in Bonagura
KD and Kirk RW (eds): Kirk’s Current Veterinary Therapy XII, Philadelphia, WB Saunders Co, 1995, pp 732-735.
Williams DA: Feline pancreatic disease. Proceedings, 15th Annual
Forum, American College of Veterinary Internal Medicine, Lake Buena Vista FL, 1997, pp 407-408.
65
When and how I would make a liver biopsy
Susan E. Bunch
INDICATIONS
Microscopic examination of liver tissue is essential
for definitive diagnosis and optimal treatment planning of
primary hepatobiliary diseases of cats and dogs. Bile
evaluation (cytology and microbial culture) is also needed for some icteric patients. Liver tissue is also obtained
at the time of surgery, to complete the diagnostic evaluation, in animals with classic presentations. For certain
conditions repeat biopsy provides objective information
about response to therapy.
PATIENT PREPARATION
All cats and dogs undergoing hepatic biopsy, regardless of the approach, are fasted at least 12 hours, and their
coagulation status is assessed. Ideally a complete coagulation profile (one-stage prothrombin time, [OSPT] activated partial thromboplastin time [APTT], fibrin degradation products, fibrinogen content, and platelet count) is
done. A minimum slate of tests would be platelet count,
buccal mucosal bleeding time test (platelet function), OSPT (extrinsic pathway), and activated clotting time (intrinsic and common pathways). If possible, von Willebrand’s factor is measured in susceptible breeds well in
advance of biopsy, since results of standard coagulation
tests are usually normal in affected dogs. Animals with
von Willebrand’s disease are given desmopressin acetate
(DDAVP, USV Laboratories; 1 mg/kg intranasal preparation SC) before surgery to enhance shift of von Willebrand factor activity from endothelial cells to the plasma.
Mild abnormalities in coagulation test results do not
preclude liver biopsy. Liver biopsy is delayed if there is
clinical evidence of bleeding or marked abnormalities in
results of coagulation tests. Bleeding is more likely if the
platelet count is below 80,000 cells/_l,. Because animals
with complete EBDO may be vitamin K-deficient (manifested by prolongation of both OSPT and APTT), treatment with vitamin K1 (5 mg SC QD or BID) is indicated
for 1-2 days before corrective surgery. Repeating the OSPT and APTT after vitamin K1 administration should
demonstrate normal or near normal values. Some animals
with severe hepatic disease and relatively unremarkable
coagulation test results have serum high activity of proteins induced by vitamin K antagonism (PIVKA) that
could impart bleeding tendencies. These patients would
also benefit from vitamin K1 administration. If there has
been minimal improvement in coagulation test results after vitamin K1 has been given, fresh frozen plasma is administered just before biopsy. If bleeding is excessive
during or after biopsy and cannot be controlled locally
with direct pressure or application of clot-promoting substances, fresh whole blood is given.
Biopsy is delayed in patients with clinically apparent
complications of severe hepatobiliary disease and portal
hypertension, e.g., encephalopathy and/or ascites, until
these are controlled. This may take 1-2 weeks.
CHOICES OF APPROACHES
Procedures that yield material for cytologic evaluation (fine needle aspirates) are chosen for conditions in
which it is not essential to preserve architecture in the
specimen. A 12 ml syringe attached to a 1.5-inch long 22
g needle or a 2.5-inch spinal needle without stylet usually suffices for this purpose. The traditional method relies
on creation of vacuum to remove some cells that can then
be expelled onto a glass slide. Another method uses the
same needle and syringe, which is preloaded with 3-5 ml
of air, with a short length of extension tubing between
them. The needle is passed several times into the liver, the
action of which forces cells into the needle. After the needle is withdrawn from the liver, air in the syringe is expelled, and the cytologic material is discharged onto the
slide. Evidence for certain disorders such as vacuolar hepatopathy (e.g., lipidosis, steroid hepatopathy) and lymphoid neoplasia can be presumptively identified by one of
these methods. Cytologic sampling of a single cavitary or
solid lesion highly likely to be nonlymphoid cancer is
avoided unless the owner is unwilling to permit surgery
for complete resection.
Percutaneous needle biopsy techniques can be used in
animals with hepatomegaly and ultrasonographic evidence of diffuse, uniform hepatic parenchymal disease. A
specimen procured from any area of the liver is considered representative of the disease. Since only a small stab
66
incision large enough to accommodate the biopsy needle
is needed (a #11 blade is the perfect choice), healing in
hypoalbuminemic animals is not compromised. If the operator is confident with the biopsy procedure, there is little time involved, and only heavy sedation is required. If
the results are nondiagnostic, a larger specimen is obtained using an operative technique (e.g., laparoscopy or
laparotomy). An especially small and/or firm, fibrotic liver is difficult to biopsy by percutaneous needle methods;
small, fragmented specimens that are challenging to interpret are often the result. If a percutaneous technique is
selected, the largest available needle is used (preferably
14g; minimum 16 g) to ensure samples adequate for examination.
Biopsy can be done blindly if the operator is confident
of path of the needle. The most common needle biopsy instruments used rely on the tissue falling into a specimen
trough (about 2 cm in length), then being severed by the
sharp outer cannula. One-handed operable versions of
this instrument are now available (e.g., TEMNO [Bauer
Medical, Inc., Clearwater, FL] in 14, 15 and 16 g and 6 or
9 cm in length, and ANCHOR TRU-CUT [Anchor Products Co., Addison, IL], 14 g, 6-inch length), and are easier to use than the standard, older generation TRU-CUT
device. All of these biopsy needles are intended for single
use, and cost in the range of 20USD-30 USD each.
Care is taken to angle the needle to avoid puncturing
the gallbladder. Most often, the animal is placed in right
lateral recumbency for this purpose, and the left lateral
lobe is biopsied. Elevating the head and thorax slightly
may assist in “presenting” the liver to the operator. Regardless of the approach (visualized with ultrasound, or
blind), a minimum of three complete cores is obtained; if
indicated, one core is placed in a sterile container for culture and sensitivity testing. Gently rolling a specimen on
a slide for cytologic evaluation is a good way to attempt
to identify the disease process quickly and inexpensively.
Each of the remaining cores is laid on a piece of stiff paper (such as filter paper) in correct orientation before immersion in fixative for histologic examination and/or special testing.
After biopsy, a small bandage is applied to keep the
site clean during recovery, and the animal is placed in a
position to allow body weight to compress the region of
the biopsy sites in the liver, e.g., left lateral recumbency.
As long as biopsy proceeded smoothly and without unpleasant surprises, only basic monitoring of mucous
membrane color and the skin puncture site is needed. Naturally, if there is excessive bleeding or damage to other
organs with this blind technique, detection and treatment
are delayed.
In animals with diffuse hepatobiliary disease and a
normal-sized liver, or in animals with multifocal hepatobiliary disease, percutaneous biopsy with the aid of ultrasound guidance (US) is preferred. This allows selection of
the site(s) and inspection for bleeding post biopsy. Properly performed, serious complications associated with
this procedure are few, and multiple biopsies can be obtained safely. With the same apparatus described previously for obtaining hepatic cytology specimens (needle
plus tubing plus syringe) and with US guidance, bile is
aspirated from the gallbladder for cytology and culture in
animals suspected of having bacterial cholangitis/cholangiohepatitis. A cavitary mass believed to be an abscess is
sampled similarly, and can even be drained as a component of treatment.
A surgical approach is preferred for liver biopsy if the
liver is small, or if larger specimens are needed for special analysis (e.g., measurement of copper concentration).
Multiple specimens are obtained by use of laparoscopy or
laparotomy. Both are perfectly acceptable for animals of
low anesthetic risk, and allow thorough examination of
the liver, biliary tract, and portal vasculature, as well as
other abdominal structures such as lymph nodes. The visual appearance of the organs is valuable information, and
is an important contribution to the diagnostic evaluation.
Bile can be acquired easily and safely. Bleeding can be
arrested directly. Special equipment is needed for laparoscopy (insufflation system, telescope for examination, instruments), and skill in the procedure is critical to
performing the study successfully and efficiently. Laparotomy is a potentially more lengthy procedure, but is the
approach of choice for surgically correctable conditions;
a liver biopsy is taken concurrently. The advantages of
these surgical techniques generally outweigh the drawbacks of the need for general anesthesia and time required.
PROCESSING THE SPECIMENS
Liver and bile specimens for microbiologic culture
and impression smears are processed first. Samples for
special stains or quantitative analyses (e.g., copper) are
preserved according to the specifications of the pathology
laboratory selected to do the assays. Lastly, specimens are
submerged in buffered 10% formalin at a ratio of at least
10 parts formalin to 1 part tissue for routine processing
and histopathologic examination.
It is the attending clinician who bears the responsibility of putting the biopsy results into perspective by use of
all information that has been gathered, not the cytologist
or pathologist.
Bibliography
1.
2.
3.
4.
Bigge LA, Brown DJ, Penninck DG: Correlation between coagulation profile findings and bleeding complications after ultrasound-guided biopsies: 434 cases (1993-1996). Comp Contin
Educ 2001;37:228-233.
Bunch SE, Polak DM, Hornbuckle WE. A modified laparoscopic
approach for liver biopsy in dogs. J Am Vet Med Assoc
1985;187:1032-1035.
Cole T, Flood S, Center S, et al: Diagnostic accuracy of Tru Cut
needle biopsy compared to wedge biopsy of the liver. Proceedings, 18th Annual Forum, American College of Veterinary Internal Medicine, Seattle WA, 2000, pp 734.
Fondacaro JV, Gulpin VO, Powers BE, et al: Diagnostic correlation of liver aspiration cytology with histopathology in dogs and
cats with liver disease. Proceedings, 17th Annual Forum, American College of Veterinary Internal Medicine, Chicago IL, 1999, pp
719.
5.
6.
7.
8.
9.
Hardy RM. Hepatic biopsy. In Kirk RW, editor: Current Veterinary
Therapy VIII, Philadelphia, 1983, WB Saunders, pp 813-817.
Kerwin SC. Hepatic aspiration and biopsy techniques. Vet Clin
North Am: Small Anim Pract 1995;25:275-291.
Klaus E. Bleeding after liver biopsy does not correlate with indices of peripheral coagulation. Dig Dis Sci 1981;26:388-393
Kristensen AT, Weiss DJ, Klausner JS, et al. Liver cytology in cases of canine and feline hepatic disease. Compend Cont Ed
1990;12:797-808.
Léveillé R, Partington BP, Biller DS, et al. Complications after
ultrasound-guided biopsy of abdominal structures in dogs and
67
10.
11.
12.
cats: 246 cases (1984-1991). J Am Vet Med Assoc 1993; 203:
413-415.
Menard M, Papageorges M: Fine needle biopsies: how to increase
diagnostic yield. Proceedings, 16th Annual Forum, American College of Veterinary Internal Medicine, San Diego CA, 1998, pp
595-597.
Roth L, Meyer DJ. Interpretation of liver biopsies. Vet Clin North
Am: Small Anim Pract 1995;25:293-303.
Withrow SJ. Risks associated with biopsies for cancer., in Bonagura JD and Kirk RW (eds): Kirk’s Current Veterinary Therapy
XII, Philadelphia, 1995, WB Saunders, pp 24-25.
69
Microvascular hepatic dysplasia
Susan E. Bunch
WHAT IS HEPATIC MICROVASCULAR
DYSPLASIA?
Hepatic microvascular dysplasia (HMD) is a congenital
portovascular disorder of dogs and cats that was first described in 1991. Animals were presented with signs consistent with a congenital portosystemic shunt (cPSS), and
in 63%, a single anomalous vessel was found. Because a
PSS could not be documented in 37%, the anomaly was
presumed to be microscopic.
HOW IS THE DIAGNOSIS MADE?
Several reports of the signs, clinicopathologic and
histopathologic abnormalities, and outcome in dogs with
HMD have been published since 1991. It appears to exist
in a spectrum of severity, since some affected dogs are
asymptomatic, and some have signs of hepatic encephalopathy (HE). Regardless, most dogs with HMD are
small purebred dogs (Maltese, Cairn terrier, Yorkshire terrier, dachshund, poodle), most of which are the same
breeds affected with cPSS. Most dogs with HMD are older
than dogs with cPSS, Some studies have shown a female
gender predisposition, but none has reported stunted
growth. In asymptomatic dogs, the only clinicopathologic
abnormality is high serum bile acid concentrations. Symptomatic HMD dogs may have neurologic and/or gastrointestinal signs, and prolonged anesthetic recovery time, but
much milder than dogs with cPSS. Clinicopathologic abnormalities that are considered classic in dogs with cPSS
(i.e., microcytosis, low blood urea nitrogen concentration,
hypoalbuminemia, hypocholesterolemia, hypoglycemia,
hyperammonemia, variable liver enzyme activities), occur
much less frequently and are less dramatic in dogs with
HMD. Via ultrasonography, liver size can be normal or
small, and intrahepatic portal vascular is normal to slightly
reduced.
There is no evidence of portosystemic shunting by use
of per-rectal portal scintigraphy or portography. Histologic
changes in liver biopsy specimens from dogs with cPSS,
HMD, noncirrhotic portal hypertension, intrahepatic portal
vein hypoplasia and surgically created portocaval shunt are
indistinguishable, and consist of random small-caliber ves-
sels, hepatic venule mural hypertrophy, dilation of pericentral vascular spaces, arteriolar proliferation in portal triads,
and inconspicuous portal venules.
The exact defect in HMD is a subject of controversy
among academic clinicians. There appears to be no evidence that there is a direct connection between the terminal portal venules and terminal hepatic venules that could
account for microscopic intrahepatic portosystemic shunting. Several believe that the defect relates to decreased intrahepatic portal vasculature, which can occur in differing
degrees (e.g., mild, moderate, severe), accounting for the
varying clinical presentations. All agree that HMD can occur alone, or combined with cPSS.
WHAT IS THE RECOMMENDED
TREATMENT AND PROGNOSIS?
Because this is a diffuse, intrahepatic congenital (and
probably inherited) vascular condition, there is no specific
treatment at this time. Symptomatic treatment is not necessary for animals identified incidentally during routine
screening, but consists of management of HE for animals
with clinical signs (i.e., protein restricted diet alone, or
with other ammonia-lowering strategies). Dogs that have
been followed for up to 5 years appear to have good to excellent quality lives. More severe consequences, such as recurrent urate urolithiasis or uncontrollable HE, are rare.
Bibliography
1.
2.
3.
4.
Baer KE, Patnaik AK, MacDonald JM: Hepatic vascular dysplasia
in dogs and cats (105 cases). Proceedings, 42nd Annual Meeting,
American College of Veterinary Pathologists, Orlando, FL 1991, p.
71.
Bunch SE, Johnson SE, Cullen JM: Idiopathic noncirrhotic portal
hypertension in dogs: 33 cases (1982-1998). J Am Vet Med Assoc
2000;218:392-399.
Center SA, Schermerhorn T, Lyman R, et al: Hepatoportal microvascular dysplasia. In Bonagura JD (ed), Kirks’ Current Veterinary
Therapy XIII, WB Saunders Co, Philadelphia, 2000, pp 682-686.
Tisdall PLC, Hunt GE, Tsoukalas G, et al: Post-prandial serum bile
acid concentrations and ammonia tolerance in Maltese dogs with
and without hepatic vascular anomalies. Aust Vet J 1995;72:121126.
70
5.
6.
7.
Phillips L, Tappe J, Lyman R: Hepatic microvascular dysplasia
without demonstrable macroscopic shunts. Proceedings, 11th Annual Forum, American College of Veterinary Internal Medicine,
Washington DC, May 1993, pp 438 – 439.
Phillips L, Tappe J, Lyman R, et al: Hepatic microvascular dysplasia in dogs. Progress Vet Neurol 1996;7:88-96.
Schermerhorn T, Center SA, Dykes NL, et al: Characterization of
hepatoportal microvascular dysplasia in a kindred of Cairn terriers.
J Vet Intern Med 1996;10:219-230.
8.
9.
10.
Allen L, Stobie D, Mauldin GN, et al: Clinicopathologic features of dogs
with hepatic microvascular dysplasia with and without portosystemic
shunts: 42 cases (1991-1996). J Am Vet Med Assoc 1999;214:218-220.
Christiansen JS, Hottinger JA, Allen L, et al: Hepatic microvascular
dysplasia in dogs: a retrospective study of 24 cases (1987-1995). J
Am Anim Hosp Assoc 2000;36:385-389.
van den Ingh TSGAM, Rothuizen J, Meyer HP: Portal hypertension
associated with primary hypoplasia of the portal vein. Vet Rec
1995;137:424-427.
71
Copper-associated hepatopathy in dogs
Susan E. Bunch
LIVER INJURY ASSOCIATED
WITH COPPER EXCESS
Copper (Cu) accumulation in the liver may be the primary cause or the secondary effect of chronic hepatitis. Affected dogs may have similar historic and clinical features
and, possibly, liver biopsy abnormalities. Animals that are
examined when their disease is well established have been ill
for weeks to months with combinations of anorexia, weight
loss, lethargy, polyuria and polydipsia. Animals with advanced disease may also have jaundice, abdominal effusion,
signs of hepatic encephalopathy (HE), and hemorrhagic tendency. Persistently high serum alanine aminotransferase
(ALT) activity, with less strikingly abnormal serum alkaline
phosphatase (AP) and gamma-glutamyltransferase (GGT)
activities early in the course of the disease, followed by evidence of multiple hepatocyte function loss late in the course
(e.g., hypoalbuminemia, low blood urea nitrogen [BUN]
content) are typical laboratory findings. Occasionally, abnormal serum liver enzyme activities or other evidence of serious hepatic disease are detected during routine evaluation
before elective surgery in asymptomatic animals. Liver biopsy is crucial for accurate diagnosis and prognosis, although
there are few pathognomonic changes. Typical changes in
routinely stained (i.e., hematoxylin-eosin; H&E) specimens
include hepatocellular necrosis, mixed inflammatory cell infiltrates, fibrosis, biliary hyperplasia, and nodular regeneration. These changes involve primarily the portal and periportal regions, with extension into the parenchyma in some
dogs. Copper granules appear reddish-brown and are usually seen early in the course of disease in the pericentral (centrilobular) region. Use of special stains (e.g., Timm’s silver
sulfide, rubeanic acid, or rhodanine) confirms that these
granules within lysosomes contain Cu.
Familial chronic hepatitis in Bedlington terriers was first
recognized in 1975. The fundamental metabolic error is progressive Cu accumulation resulting from impaired biliary excretion. It is inherited as an autosomal recessive trait, and signs
of illness generally become evident in middle age. Severity of
clinical signs, clinicopathologic test results, and hepatic
histopathologic findings are related to the degree of hepatic Cu
accumulation. Illness does not usually until there is marked Cu
accumulation in hepatocytes (approximately 2000 ppm, dry
weight [DW]) after which lysosomes rupture and release Cu.
Liver Cu content in normal juvenile and adult Bedlington
Terriers is 91 to 358 ppm DW. Most affected (homozygous)
dogs have liver Cu concentrations greater than 850 ppm, regardless of age at the time of biopsy. Heterozygotes may also have similar liver Cu concentration. If quantitative methods are not available, histochemical staining of biopsy or cytology specimens can be used as a semi-quantitative measure of liver Cu content. Results of studies examining biopsy and cytology specimens agree that affected dogs can be
reliably identified. Heterozygous and normal dogs cannot be
differentiated by these methods.
Previously, methods to identify affected dogs early consisted of serial hepatic Cu determinations, or test matings (for
dogs intended for breeding). Progressive hepatic Cu quantitation identified by liver biopsy at 6 months of age and if necessary, at least 6 months later. Carrier dogs have hepatic Cu
concentrations in both specimens that are normal or slightly
higher than normal (range: 400 to 700 ppm DW; grades 1,2
and possibly 3 by cytologic methods) but similar to one another. In affected dogs, hepatic Cu content of the second
specimen is much greater than that of the first, confirming
progressive Cu retention. If there still is uncertainty, especially about dogs intended for breeding, test matings between
known affected dogs and dogs in question, with liver specimens for hepatic Cu measurement obtained from all offspring, are necessary. If the dog in question is heterozygous
for this trait, 50% of the offspring of such a test mating would
be affected. Carrier and affected dogs should be neutered.
More recently, genetic analysis has been the focus of
considerable interest. Several investigators have evaluated
the use of a microsatellite marker in identifying affected
dogs in the USA, UK, and Europe. As long as several related dogs are available for testing, this method will identify affected, heterozygous and normal dogs. Researchers in The
Netherlands have made considerable progress in identifying
the putative gene causing Cu hepatotoxicosis, which will be
very useful as a single diagnostic test.
Chronic hepatopathy characterized by Cu accumulation
is also known to occur in other breeds, particularly Doberman Pinscher (predominantly middle-aged females), West
Highland White terrier, and possibly Skye terrier. Some dogs
of these breeds have hepatic Cu accumulation but no clinical
signs or histopathologic abnormalities, and some affected
dogs have normal Cu concentration, but have microscopic
72
evidence of chronic hepatitis. Although the genetics are yet
to be clarified, a familial basis is strongly suspected.
The Doberman Pinscher was first identified as having a
breed-associated hepatopathy in 1982. Some investigators
have attempted to equate this disease with the autoimmune
type of chronic active hepatitis in human patients to which it
bears weak resemblance. To reach a diagnosis of autoimmune CAH in a human patient, there must be strong evidence of autoantibody production directed at nuclear protein, smooth muscle, mitochondria, and several liver cell
membrane antigens. Immune-mediated reactions are directed toward altered hepatocytes, which may cause self-perpetuated injury. Preliminary immunologic analysis of affected
Doberman Pinschers has failed to reveal evidence of these
markers. In addition to parenchymal, portal and periportal
inflammation, there is also pericentral inflammation in some
dogs. Two studies of affected asymptomatic dogs (dogs with
high serum ALT activity and biopsy evidence of chronic hepatitis) agree that Doberman hepatopathy is progressive.
The role of Cu in Doberman Pinscher hepatopathy is less
well understood than in Bedlington Terrier Cu hepatotoxicosis. Liver Cu concentrations in affected Dobermans are lower in general than those in affected Bedlingtons. Whether the
specific error in Cu metabolism is a primary or secondary
event in affected Dobermans is currently not known. Unexplained excessive hepatic iron has also been observed in
both Bedlington Terrier and Doberman Pinscher Cu-associated hepatopathies.
On the basis of one study of 70 adult dogs and one puppy, hepatic disease associated with Cu retention in West
Highland White Terriers appears to differ from other familial hepatopathies. Liver Cu content does not increase progressively with age, but similar to Doberman hepatopathy,
the reason for variable liver Cu content in affected dogs is
not understood. The range of hepatic Cu content in affected
dogs is 450 to 3500 ppm DW. Further information regarding
the inheritance pattern, clinical course, and mechanism of
Cu retention is not currently available.
Familial hepatopathy in nine Skye Terriers of varying
ages has been described as mild to moderate periportal and
pericentral inflammation with intracanalicular cholestasis
and Cu accumulation. Regenerative parenchymal nodules
surrounded by fibrous connective tissue bands are seen in
more chronic cases. The degree of Cu retention seems to
correlate with the degree and duration of cholestasis. The
cause is unknown but might relate to disturbed membrane
bile transfer and transport systems.
Treatment
Prevention Administration of zinc (Zn) salts (preferably
acetate or sulfate; 100 mg of elemental zinc PO twice daily)
has recently been found to be of benefit in the management
of affected dogs early in life before massive accumulation of
hepatic Cu occurs. Zinc discourages absorption of Cu by
stimulating the formation of metallothionein by the intestinal mucosa. Swallowed Cu (from dietary and gastrointestinal secretions) binds more avidly than Zn to this protein, sequestering it in mucosal cells that are eventually shed. The
goal of treatment is to maintain serum Zn concentrations
(measured every 2 to 3 months) in the range of 200-300
_g/dl; a single blood sample is drawn before the morning
dose. The dose may be reduced to 50 mg twice daily after
about 3 months of treatment, assuming the plasma Zn concentration remains in the target range.
Diet Decreasing Cu in the diet does not remove excess
hepatic Cu but helps to slow further accumulation. Completely eliminating Cu from the diet is impossible. Most
commercial diets contain much greater quantities of Cu than
the National Research Council recommends for dogs (i.e., 2
mg/g of dog food). A homemade diet that does not contain
organ meats, shellfish, or cereals could be used. Commercial
prescription diets made by Waltham or Hill’s are also an option. Snacks with high Cu content such as chocolate, nuts,
dried fruit, legumes, and mushrooms are avoided.
Chelation In Bedlington Terriers, progressive liver injury
will occur unless hepatic Cu is mobilized for urinary excretion. In older dogs that have marked Cu accumulation, maximal benefit is derived from use of drugs that chelate Cu and
promote its extraction from the liver, although studies of
large numbers of affected dogs have not been conducted. Dpenicillamine (10 to 15 mg/kg PO twice daily 30 minutes before meals) is the drug most often recommended; it also has
weak antifibrotic and anti-inflammatory properties. Starting
at the lower end of the dose range and increasing the dose after 1 week, or dividing the dose and giving it more frequently reduces adverse gastrointestinal effects. Chelation treatment is recommended for affected dogs if the liver Cu content is 2000 ppm DW or higher. A decrease in liver Cu content of 900 to 1000 ppm DW per year is typical. Trientine (10
to 15 mg/kg PO twice daily 30 minutes before meals) may be
also be used in dogs that cannot tolerate d-penicillamine.
LIVER INJURY ASSOCIATED
WITH COPPER DEFICIENCY
Copper deficiency has been described in many animals,
including humans, sheep, guinea pigs, cattle, rabbits, rats,
and pigs. Congenital Cu deficiency similar to Menke’s syndrome, an inherited defect in Cu absorption in humans, has
been reported in dogs, but is rare. Acquired Cu deficiency is
best understood in humans and ruminants. In humans, it has
been associated with long-term use of unsupplemented total
parenteral nutrition, malabsorption syndromes, and Zn therapy. Ruminants acquire Cu deficiency by eating a low Cu or
high molybdenum forage. Naturally acquired Cu deficiency
has not been reported in dogs until recently. Microcytic anemia, clinicopathologic evidence of hepatic insufficiency, and
liver biopsy changes including lobular disorganization, hepatocyte regeneration, and glycogen accumulation were attributed to Cu deficiency in an aged Bedlington terrier that
had been diagnosed 8 years earlier as affected with Cu hepatotoxicosis. Aggressive treatment with dietary Cu restriction and Cu chelation was recommended and instituted.
Considering newer information about Bedlington terrier Cu
hepatopathy that had been discovered since the original diagnosis, it appeared that the dog was a carrier, and did not
need treatment.
Bibliography
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Brewer NR: Comparative metabolism of copper. J Am Vet Med Assoc 1987;190: 654-658.
Crawford MA, Schall WD, Jensen RK, et al: Chronic active hepatitis
in 26 Doberman Pinschers. J Am Vet Med Assoc 1985;187:13431350.
Danks DM: Copper deficiency in humans. Ann Rev Nutr 1988;8:235257.
van den Ingh TSGAM, Rothuizen J, Cupery R: Chronic active hepatitis with cirrhosis in the Doberman Pinscher. Vet Quart
1988;10:84-89.
Hardy RM, Stevens JB: Chronic progressive hepatitis in Bedlington
terriers (Bedlington liver disease). In Kirk RW (ed), Current Veterinary Therapy VI, WB Saunders Co, Philadelphia, 1977, pp 995-998.
Haywood S, Rutgers HC, Christian MK: Hepatitis and copper accumulation in Skye terriers. Vet Pathol 1988;25:408-414.
Holmes NG, Herrtage ME, Ryder EJ, et al: DNA marker C04107 for
copper toxicosis in a population of Bedlington terriers in the United
Kingdom. Vet Rec 1998;142:351-352.
Hultgren BD, Stevens JB, Hardy RM: Inherited, chronic progressive
hepatic degeneration in Bedlington terriers with increased liver copper concentrations: Clinical and pathologic observations and comparison with other copper-associated liver disease. Am J Vet Res
1986;47:365-377.
Johnson GF, Zawie DA, Gilbertson SR, et al: Chronic active hepatitis in Doberman Pinschers. J Am Vet Med Assoc 1982;180:14381442.
Prohaska JR: Genetic disease of copper metabolism. Clin Physiol
Biochem 1986;4:87-93.
Proschowsky JF, Jepsen B, Jensen HE, et al: Microsatellite marker
C04107 as a diagnostic marker for copper toxicosis in the Danish population of Bedlington terriers. Acta Vet Scand 2000;41:3450350.
Rolfe DS, Twedt DC: Copper-associated hepatopathies in dogs. Vet
Clin North Am 1995;25: 399-417.
73
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
Seguin MA, Bunch, SE: Iatrogenic copper deficiency in a Bedlington
terrier associated with long-term copper chelation treatment for copper storage disease. J Am Vet Med Assoc 218;1593-1597, 2001.
van de Sluis B, Rothuizen J, van Oost BA, et al: The gene causing defective biliary copper excretion in Bedlington terriers. Proceedings,
11th Annual Congress, European Society of Veterinary Internal Medicine, Dublin, Ireland, 2001, p. 82.
Speeti M, Ihantola M, Westermarck E: Subclinical versus clinical hepatitis in the Doberman: evaluation of changes in blood parameters. J
Small Anim Pract 1996;37:465-470.
Speeti M, Eriksson J, Saari S, et al: Lesions of subclinical Doberman
hepatitis. Vet Pathol 1998;35:361-369.
Teske E, Brinkhuis BGAM, Bode P, et al: Cytological detection of
copper for the diagnosis of inherited copper toxicosis in Bedlington
terriers. Vet Rec 1992;131:30-32.
Thornburg LP, Shaw D, Dolan M, et al: Hereditary copper toxicosis
in West Highland White terriers. Vet Pathol 1986;23: 148-154.
Thornburg LP, Rottinghaus G, McGowan M, et al: Hepatic copper concentrations in purebred and mixed-breed dogs. Vet Pathol 1990;27:81-88.
Thornburg LP, Rottinghaus G, Dennis G, et al: The relationship
between hepatic copper content and morphologic changes in the liver
of West Highland White terriers. Vet Pathol 1996;33:656-661.
Thornburg LP: Histomorphological and immunohistochemical studies of chronic active hepatitis in Doberman Pinschers. Vet Pathol
1998;35:380-385.
Thornburg LP: A perspective on copper and liver disease in the dog.
J Vet Diagn Invest 2000;12:101-110.
Twedt DC, Sternleib I, Gilbertson SR: Clinical, morphologic, and
chemical studies on copper toxicosis of Bedlington terriers. J Am Vet
Med Assoc 1979;175:269-275.
Ubbink GJ, van den Ingh TSGAM, Yuzbasiyan-Gurkan V, et al: Population dynamics of inherited copper toxicosis in Dutch Bedlington
terriers. J Vet Intern Med 2000;14:172-176.
Yuzbasiyan-Gurkan V, Blanton SH, Cao Y, et al: Linkage of a miocrosatellite marker to the canine copper toxicosis locus in Bedlington
terriers. Am J Vet Res 1997;58:23-27.
75
Chronic hepatobiliary diseases in dogs and cats
Susan E. Bunch
HOW CAN I BE SURE THAT I AM
PURSUING THE CORRECT CONDITION
(A PRIMARY CHRONIC HEPATOBILIARY
DISORDER VS. HEPATIC CONSEQUENCES
OF AN EXTRAHEPATIC DISORDER)?
ed with bacterial infection arising from nonhepatic sites consist only of canalicular bile plugs. Vacuolar change can be
the result of metabolic product accumulation or a nonspecific reactive change.
Clinicopathologic abnormalities in hepatic status and
function and liver biopsy changes associated with extrahepatic disorders can be identical to those of primary hepatobiliary diseases. This is related to the integral role of the liver
in normal function of many organ systems, and the anatomic proximity and direct connection (via the portal vein) of
the liver to many other organs. In most cases, hepatobiliary
consequences resolve with appropriate treatment of the primary illness, and there is no evidence of persistent hepatic
disturbance. In some conditions, liver involvement may provide an avenue for diagnosis through histologic confirmation
of the cause, such as histoplasmosis in cats. In other conditions, such as cholestasis associated with extrahepatic infection, and glucocorticoid deficient hypoadrenocorticism, the
liver component of the illness can be rather dramatic, potentially leading to misdiagnosis.
On the basis of a complete history, thorough physical examination, and results of a minimum data base (CBC, chemistry profile, urinalysis, and fasting and postprandial bile
acids or plasma ammonia measurement), sufficient information should be available to conclude whether the liver is the
source of illness, or just one of the organs affected by it. If
there are clinical signs that could be interpreted as those of
hepatic encephalopathy (HE), a treatment trial for HE (see
below) of 1-2 week’s duration is reasonable. Extraheptobiliary disorders do not cause development of portosystemic
shunting or sufficient hepatocellular dysfunction to result in
HE. If the signs do not improve dramatically, a secondary
(or extra-) hepatobiliary disorder is likely. If the signs resolve, then additional diagnostic testing for a primary hepatobiliary disorder is indicated.
Common histopathologic changes in the liver attributed
to extrahepatobiliary disorders include mild periportal lymphocytic infiltrates, multifocal single-cell hepatocyte necrosis or clusters of macrophages or inflammatory cells, and
stellate macrophage proliferation. These changes are believed to be mediated by cytokines released in inflammatory
and neoplastic conditions. Histopathologic changes associat-
WHAT ARE THE COMMON PRIMARY
CHRONIC HEPATOBILIARY DISORDERS
OF DOGS AND CATS, AND HOW IS THE
DIAGNOSIS MADE?
Dogs. The most common primary hepatopathies are
chronic hepatitis (CH) complex and various kinds of congenital portovascular anomaly. The chronic hepatitis complex includes diseases that share similar signs, clinicopathologic abnormalities, and, in many cases, liver histopathologic changes (degrees of necrosis and mononuclear inflammation), but may originate differently. Several breeds are predisposed to chronic hepatic injury and copper (Cu) retention). In Bedlington terriers, Cu accumulates progressively
because of a genetic defect in copper excretion. Little to no
progress has been made in our understanding of the mechanism for Cu retention in other breeds, such as the West Highland white terrier, female Doberman pinscher, Cocker
spaniel, Skye terrier, and others. Liver injury occurs as Cu
accumulation exceeds 2000 ppm on a dry weight (DW) basis. Because the predominant inflammatory cell is the lymphocyte, investigators have explored immunologic injury as
the basis for the pathologic consequences. Results have been
conflicting, and have failed to convincingly establish an immune-mediated pathogenesis in the affected dogs studied.
Some drugs can cause CH in susceptible individuals, usually in the form of an idiosyncratic reaction. Anticonvulsants
(phenytoin and phenobarbital, or phenobarbital or primidone
alone) and antiinfectives (trimethoprim-sulfa, ketoconazole)
are the most commonly implicated. Certain infectious agents
can cause liver-specific injury, such as adenovirus type-1,
leptospira serovar grippotyphosa, and the acidophil cell
agent described only in Britain.
Common types of congenital portovascular anomaly include portal or left gastric vein and the caudal vena cava, and
ductus venosus. The preferred treatment for these anomalies
is surgical occlusion of the aberrant vessel, in an attempt to
restore normal portal blood flow and hepatic perfusion. Gen-
76
eralized malformation of the intrahepatic vasculature, such
as intrahepatic portal vein hypoplasia, cannot be corrected
surgically.
Nodular hyperplasia is a common benign finding in older dogs, and must be distinguished from cancer and cirrhosis. Modest increase in serum AP activity is a consistent laboratory finding; there is no serum biochemical evidence of
hepatic dysfunction. Illness has not been ascribed to this
condition, and treatment is not necessary.
Cats. As is observed in dogs, the clinical signs of the
major hepatobiliary diseases in adult cats are similar. The
most consistent clinical findings are jaundice, vomiting, diarrhea, and a normal-sized to enlarged liver. Results of basic
and specialized laboratory testing are often very similar also. Unlike in dogs, in which most of the important hepatic
diseases are primarily hepatocellular, acquired hepatobiliary
disease in cats tends to have a more biliary distribution.
Cholangitis/cholangiohepatitis (CCH) is a group of diseases
involving primarily the biliary tract (cholangitis), with possible extension into peribiliary hepatocytes (cholangiohepatitis). The pathogenesis of this group of diseases is poorly
understood. Because the common bile duct and the major
pancreatic duct join to form a common duct that enters the
duodenum, it has been proposed that ascension of bacteria or
other substances from the duodenum or digestive enzymes
from a subclinically inflamed pancreas may account for the
frequency of CCH compared with that in dogs. In a recent
retrospective study of 78 cats, liver, intestinal, pancreatic,
and renal tissues were examined for evidence of concurrent
disease of these organs. Over 80% of cats with CCH also
had histologic findings of inflammatory bowel disease, and
about half had changes consistent with mild pancreatitis, implying that the source or result of CCH in some cats might
be extension of inflammation to or from these organs. Recently, several investigators reviewed the histologic classification of feline inflammatory hepatic disease, and defined
another group: cats with lymphocytic portal hepatitis (LPH).
There are several types of CCH, based on histopathologic findings; a name is ascribed according to the predominant
inflammatory cell type and it’s distribution. It is tempting to
speculate that they represent phases of a progressive biliary
tract disease that begins with acute inflammation in the extrahepatic bile ducts (neutrophilic CCH), changes in cytologic character from neutrophilic to lymphoplasmacytic or
pleomorphic as the disease progresses (chronic lymphoplasmacytic CCH), extends into the hepatic parenchyma, and
possibly culminates in biliary cirrhosis (rare in cats). Large
studies including serial liver biopsy have not been done in
cats with acute CCH to confirm this suspicion, though two
reports included necropsy results of cats with LPH or lymphocytic CCH, which demonstrated evidence of progression
(more severe lymphocytic infiltrates, fibrosis and biliary hyperplasia). Cats with chronic CCH or LPH are usually males
over 7 years old; over half are purebred, especially those
with LPH. Concurrent diseases were noted in many cats, and
may have been responsible for death in those surviving less
than 1 year.
Fecal sedimentation is recommended in cats living in areas where trematode (fluke) infection is prevalent, obviating
the need for liver biopsy. In all other cats, and dogs, liver
biopsy is essential for accurate diagnosis of primary hepatobiliary disease. Microbial culture of the bile is indicated in
cats and in dogs that have a predominantly biliary distribution to their diagnostic test results (e.g., hyperbilirubinemia,
moderate to marked increase in serum alkaline phosphatase
activity, abnormal biliary tract on ultrasonography ). Liver
Cu quantitation (preferably using DW methods) or at least
special stains for semi-quantitative assessment, may be
needed in dogs suspected of having Cu retention.
HOW DO I TREAT EACH OF THESE
CONDITIONS (SPECIFIC VS. SYMPTOMATIC
TREATMENT)?
Dogs. Specific treatment involves addressing the underlying cause if possible. All drugs that could be considered
causative should be discontinued. Treatment for dogs with
familial Cu-associated hepatopathy depends on the stage at
which they are diagnosed. For affected Bedlington terriers
that are identified at an early age and for other predisposed
breeds with secondary Cu retention (West Highland white
terriers with liver Cu content greater than 2000 ppm DW,
Doberman pinscher, Cocker spaniel, and Skye terrier), prevention of Cu accumulation is indicated. This includes restricting intake (distilled water to drink, diet low in Cu such
as Hill’s u/d or l/d, or home-cooked equivalent that does not
contain organ meats, shellfish or cereals, supplemented with
a vitamin without Cu), and discouraging intestinal absorption (zinc acetate, gluconate, sulfate or methionine; 25-50
mg of elemental zinc PO q 12 hr, 1 hour before feeding).
Measuring serum zinc concentration to be sure that there is
no evidence of toxicity (serum value over 800 mg/ml) is recommended. Vitamin E (400-500 IU/day PO) has also been
shown to prevent oxidative injury associated with Cu excess.
For affected Bedlingtons that have evidence of liver injury
and liver Cu content over 2000 ppm DW, more aggressive
treatment is needed. Penicillamine or trientine (10-15 mg/kg
PO q 12 hr) is given to hasten Cu excretion. Each promotes
removal of about 900 ppm liver Cu yearly. Liver biopsy is
repeated 1 year later, to assure that preventive or chelation
treatment is effective. The goal is to return liver Cu content
to normal (300-400 ppm). Once this has occurred, the chelation regimen may be changed to a preventive regimen.
For dogs with CH of unknown origin, or for dogs with
drug-associated CH that improved after drug discontinuation
but have evidence of ongoing CH, treatment is given to modulate the pathologic processes identified by liver biopsy. If
the predominant change is inflammation, prednisone (0.5-1
mg/kg PO q 12 hr initially) is usually the drug of first choice.
The dosage is controversial, but with proper monitoring,
complications are minimized. Azathioprine (2 mg/kg PO q
24 hr initially) has also been suggested as a sole agent, or for
dogs with unacceptable side effects of prednisone treatment.
Colchicine (0.03 mg/kg PO q 24 hr) is effective when there
is substantial fibrosis. Other medications that are considered
adjunctive for dogs with CH include ursodiol (10-15 mg/kg
PO q 24 hr), for its hepatoprotective and immune-modulating effects, vitamin E (400-500 IU/day PO) for its antioxi-
dant properties and S-adenosylmethionine (20 mg/kg PO q
24 hr, after an overnight fast) for it’s ability to restore glutathione stores and free-radical scavenging capacity. None of
these treatments has been systemically evaluated with a
prospective, controlled clinical trial.
Symptomatic treatment is given to control complications
of severe CH. Hepatic encephalopathy occurs when there is
marked loss of functional hepatic mass, or sustained portal
hypertension resulting in portosystemic shunting. Because
the neurologic signs are associated with encephalotoxins
generated, in part, from ingested protein, signs will markedly improve with moderate dietary protein restriction (Hills
l/d or k/d, Purina CNM-NF, Waltham Hepatic Support Diet,
or home-cooked equivalent). If neurologic signs have not resolved completely, additional medications are given to reduce formation of and inhibit absorption of encephalotoxins.
Lactulose (3-15 ml PO q 8-12 hr), which acidifies intestinal
contents and hastens their transport, or metronidazole (7.510 mg/kg PO q 12 hr), which reduces anaerobic bacterial
populations that generate encephalotoxins, is added. Ascites
forms subsequent to development of portal hypertension and
hypoalbuminemia. Moderate dietary sodium restriction provided by the diets mentioned previously may be sufficient to
limit formation of ascites. If not, judicious use of diuretics
such as spironolactone (0.5-1 mg/kg PO q 12 hr; dosage can
be doubled if there is no response) or furosemide (1 mg/kg
PO q 12 hr initially) may be instituted. The maintenance
dosage should be the lowest needed to relieve signs of discomfort. Occasionally, abdominocentesis may be needed to
relieve tense ascites. Since rapid removal of fluid may be accompanied by sudden vascular derangement in animals with
severe hypoalbuminemia, intravenous infusion of a colloid
(6% hetastarch, 20 ml/kg or 25% albumin, 12.5-25 g) over 6
hours as abdominal fluid is removed is recommended. Dogs
with severe CH and portal hypertension are predisposed to
gastrointestinal bleeding. Famotidine (0.5 mg/kg PO q 12-24
hr) is used for prevention; sucralfate (05.-1 g PO q 8 hr) is
given during active bleeding episodes. Dogs with severe CH
are suspected to have multiple defects in their immune systems, as described in people, which predisposes them to systemic infection. Prophylactic antibiotic treatment is not warranted, but if signs of inflammation are noted (e.g., fever,
band leukocytosis), blood specimens should be collected for
aerobic and anaerobic bacterial culture before starting
broad-spectrum empiric therapy.
Cats. Because the specific causes of chronic CCH in
cats are so poorly understood, treatment is based solely on
liver biopsy and bile culture results. Some investigators advocate use of antibiotics that effectively penetrate bile, such
as amoxicillin or the cephalosporins (20 mg/kg PO q 8-12
hr) for 6-8 weeks, because results of conventional bacterial
cultures are negative, and do not rule out infection with atypical bacteria. This would be reasonable if the liver biopsy results included a suppurative component. Cats with clear evidence of pure mononuclear inflammation, however, require
prednisone (2 mg/kg PO q 12 hr). Metronidazole may be
added, for its immunomodulatory effects. Some cats that
fail to respond to prednisone may respond to other lymphocyte-altering drugs, such as chlorambucil (0.2 mg/kg PO q
77
48 hr). Other possibilities include cyclophosphamide, which
is well tolerated by cats, or methotrexate, which can cause
marked bone marrow suppression at low doses in cats. Ursodiol (10-15 mg/kg PO q 24 hr) is also recommended as a
safe adjunctive treatment. Dietary protein restriction is contraindicated in cats unless they are obviously encephalopathic. For cats that appear to have HE, arginine is added to
the diet (250-500 mg PO 12 hr). The complications observed
so frequently in dogs (ascites, gastrointestinal bleeding) are
rarely observed in cats.
HOW DO I MONITOR A DOG OR CAT
WITH A PRIMARY CHRONIC
HEPATOPATHY?
Regular recheck examinations are needed once treatment
has been started. This may occur every 2-4 weeks, depending upon the severity of the clinical signs. The optimal
means to determine treatment effectiveness is by serial liver
biopsy. Recheck examination should include a complete history, physical examination, and serum biochemistry profile
in all dogs and cats with a chronic hepatopathy. As improvement is seen, repeat examinations may be done less
frequently (every 4-6 months). Improvement in abnormal
liver enzyme activity can be expected within 1-2 weeks,
though serum AP activity may increase in dogs receiving
prednisone. Dosages of all the previously mentioned medications would remain the same, except for prednisone and
azathioprine, which ideally would be changed to an every
other day regimen to avoid serious side effects associated
with long-term daily use. Measurement of fasting and postprandial bile acids may also provide insight into lesion improvement. It is believed that serum bile acid concentrations
may be influenced by administration of ursodiol, which is
absorbed into the animal’s bile acid pool. However, the contribution is probably relatively small, and if the trend is toward improvement (lowering of values), then it is probably
a reasonable way to assess response to therapy.
Bibliography
1.
2.
3.
4.
5.
6.
Bunch SE: Acute hepatobiliary disorders, and systemic disorders that
affect the liver. In Ettinger SJ, Feldman EC (eds), Textbook of Veterinary Internal Medicine, 5th edition, WB Saunders Co, Philadelphia,
1999, pp 1326-1340.
Bunch SE. Diagnostic tests for the hepatobiliary system. In Nelson
RW, Couto CG (eds), Small Animal Internal Medicine, 2nd edition,
CV Mosby, St. Louis, 1998, pp 487-509. [section on liver biopsy].
Center SA. Chronic hepatitis, cirrhosis, breed-specific hepatopathies,
copper storage hepatopathy, suppurative hepatitis, granulomatous hepatitis, and idiopathic hepatic fibrosis. In Guilford WG, Center SA, Strombeck DR, Williams DA, Meyer DJ (eds), Strombeck’s Small Animal
Gastroenterology, 3rd edition, WB Saunders Co, 1996, pp 705-765.
Center SA. Diseases of the gallbladder and biliary tree. In Guilford
WG, Center SA, Strombeck DR, Williams DA, Meyer DJ (eds),
Strombeck’s Small Animal Gastroenterology, 3rd edition, WB Saunders Co, 1996, pp 860-888.
Edwards DF, McCracken MD, Richardson DC. Sclerosing cholangitis in a cat. J Am Vet Med Assoc 1983;182:710-712.
Gagne JM, Armstrong PJ, Weiss DJ, et al. Clinical features of inflammatory liver disease in cats: 41 cases (1983-1993). J Am Vet Med
Assoc 1999; 214:513-516.
78
7.
8.
9.
10.
11.
12.
Gagne JM, Weiss DJ, Armstrong PJ. Histopathologic evaluation of
feline inflammatory liver disease. Vet Pathol 1996;33:521-526.
Hess PR, Bunch SE. Diagnostic approach to hepatobiliary disease. In
Bonagura JD (ed), Kirks’ Current Veterinary Therapy XIII, WB Saunders Co, Philadelphia, 2000, pp 659-664.
Johnson SE. Chronic hepatic disorders. In Ettinger SJ and Feldman
EC (eds), Textbook of Veterinary Internal Medicine, 5th edition, WB
Saunders Co, Philadelphia, 1999, pp 1298-1325.
LaFlamme DP. Nutritional management of liver disease. In Bonagura JD (ed), Kirks’ Current Veterinary Therapy XIII, WB Saunders Co,
Philadelphia, 2000, pp 693-697.
Leveille CR, Arias IM. Pathophysiology and pharmacologic modulation of hepatic fibrosis. J Vet Intern Med 1993;7:73-84.
Lucke VM, Davies JD. Progressive lymphocytic cholangitis in the
cat. J Small Anim Pract 1984;25:249-260.
13.
14.
15.
16.
17.
Meyer DJ, Twedt DC. Effect of extrahepatic disease on the liver. In
Bonagura JD (ed), Kirks’ Current Veterinary Therapy XIII, WB Saunders Co, Philadelphia, 2000, pp 668-671.
Rothuizen J, Meyer HP: History, physical examination, and signs of
liver disease. In Ettinger SJ, Feldman EC (eds), Textbook of Veterinary Internal Medicine, 5th edition, WB Saunders Co, Philadelphia,
1999, pp 1272-1277.
Twedt DC. Treatment of chronic hepatitis: scientific research examines
traditional therapies. Proceedings, 17th Annual Forum, American College of Veterinary Internal Medicine, Chicago IL, May 1999, pp 500-504.
Thornburg LP. A perspective on copper and liver disease in the dog.
J Vet Diagn Invest 2000;12:101-110.
Weiss DJ, Gagne JM, Armstrong PJ: Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis
and nephritis in cats. J Am Vet Med Assoc 1996; 209:1114-1116.
79
Vascular causes of neurologic disorders
Laurent Cauzinille
DMV, Dip. ACVIM(N) & ECVN - Clinique Fregis, Paris - France
There are two reasons why non-traumatic vascular lesions in veterinary neurology are less important or recognised than in human neurology : 1- atherosclerosis is a rare
familial or endocrine finding; 2- recovery of central vascular
disorders in animals is probably more spectacular because
animals have a less prominent pyramidal system.
PHYSIOPATHOLOGY OF VASCULAR CNS
DISORDERS
Non traumatic vascular lesions may be occlusive (embolization) or haemorrhage (rupture of vascular integrity).
They may be difficult to differentiate because the result is often a mixed lesion, both lesions inducing tissue infarction,
mass effect from oedema and various degrees of ischemia.
caused by oedema. Haemorrhage within the lesion will
cause an immediate decrease in density, which becomes
more marked over several days as the clot organises and retracts.
Magnetic resonance imaging is more sensitive than tomodensitometry. An infarct will be hypointense in T1 and
hyperintense in T2. In case of haemorrhage, the intensity of
the image is secondary to the form of haemoglobin present,
its location, and the setting of the machine.
Tomodensitometric and MR images (location, size, density/intensity, mass effect, Blood Brain Barrier disruption) of
vascular lesions are not sensitive enough to exclude with
certainty inflammatory or neoplasic lesions.
The definitive diagnostic means remains the biopsy.
CEREBRAL AND MEDULLAR
NON-TRAUMATIC VASCULAR DISEASE
CLINICAL PRESENTATION
Clinical consequences of vascular disorders depend of
vessel involvement (type and size), degree and duration of
ischemia and parenchyma susceptibility to anoxia. Neurons
are the most sensitive cell type to ischemia. Vascular endothelium is the most resistant. In vascular lesions, oedema
is both vasogenic in origin, because of abnormal
blood/parenchyma barrier permeability, and cytotoxic because of cell hypoxia.
Deficits may vary from simple temporary dysfunction to
death because of cardio-respiratory arrest. Clinical signs
generally appear acutely (“apoplexy”) which is one of the
diagnostic criteria differing from other diseases. Clinical
signs due to vascular impairment usually stabilise and
regress after 24 to 72 hours.
Location of a vascular lesion to the prosencephalon, the
brain stem or the cord explains clinical presentation.
DIAGNOSTIC TOOLS
Blood tests that assess coagulation deficits, specific infectious agents are indicated as well as lipid panel, and thyroid function test.
Tomodensitometry is a non-invasive imaging technique.
Initially, an acute infarct produces a subtle hypodense area
Fibrocartilaginous embolism (FCE) of the spinal cord
is a syndrome of acute spinal cord infarction caused by embolization of extruded intervertebral disc material. Histopathologic evaluation is necessary to establish a definitive
diagnosis. On histo-logically confirmed cases, this acute
non-progressive spinal cord infarction appears to have a
high incidence in large and giant breeds of dogs and a high
predilection for the spinal intumescences. Many suspected
cases of FCE are based on the elimination of other causes
of transverse myelopathy; they have similar clinical signs
of acute non-progressive dysfunction. However the suspected group includes fewer giant breeds and more of these
dogs have upper motor neuron involvement and intact nociception.
Ischaemic neuro-myopathy, secondary to embolism of
the caudal aorta, occurs in cats with cardio-myopathy and
atrial thrombus formation.
Feline ischaemic syndrome is a unilateral cerebral (especially cortical) infarction in cats of any age. The clinical
signs are acute and non-progressive and most of them resolve completely. The middle cerebral artery seems to be
most often involve. The lesion is an ischaemic necrosis
sometimes hemorrhagic, bilateral or multifocal. The cause
of ischemia is unclear.
Vasculitis, adventitial proliferation and perivascular infiltration, are encountered with inflammatory diseases of in-
80
fectious (viral, bacterial, protozoan, rickettsial) or non infectious origin. Non infectious meningo-encephalo-myelitis
(granulomatous, breed specific, arteritis or steroid responsive) may show infarctions due to extreme proliferative vasculitis or spontaneous haemorrhage.
Coagulopathies of diverse origin may induce spontaneous bleeding of the brain or the cord. Immune mediated
thrombocytopenia, hereditary hemophilia and anti-vitamin
K intoxication are the most commonly encountered.
Degenerative vascular diseases are uncommon in pets.
The lipidic form of arteriosclerosis, named atherosclerosis,
common in humans, may be encountered in dogs associated
with hypothyroidism. Arteriosclerosis secondary to systemic
hypertension explains central signs encountered in endocrinopathy (hypo and hyperthyroidism, hyperadrenocorticism, renal insufficiency).
Some congenital or acquired vascular abnormalities may
acutely decompensate and induce large haemorrhages in the
brain or the cord.
Some CNS neoplasm may induce acute deterioration because of large bleeding. Pituitary macroadenoma is one example (pituitary apoplexy)
81
Neurologic consequences of thyroid disorders
Laurent Cauzinille
Among primary thyroid dysfunction, hypothyroidism is a
common endocrine disorder found in dogs; hyperthyroidism
is more common in cats. Neuromuscular signs associated with
thyroid dysfunction have been recognized for years although
central neurological signs have been described only recently.
The more accurate diagnosis of hypothyroidism is based
on low-resting free T4 concentration. The TSH stimulation
test improves the diagnosis in 70% of these cases. A high
TSH measurement may improve the final diagnosis.
In the literature, hypothyroidism is often named as an etiology for numerous diseases. Most of theses studies were
single clinical cases carried out before than modern more
sensitive T4 and TSH assays were available. Since, this idea
has been carried out in the literature without verification until recent Dr A Jaggy’s reviews.
HYPOTHYROIDISM
Primary hypothyroidism is characterized by lethargy,
weight gain, symmetrical alopecia, bradycardia, and generalized weakness. Among clinical signs encountered in hypothyroïd dogs, cranial, laryngeal and appendicular neuropathies have been described. Signs of encephalopathy
have been less observed although hypothyroidism is incriminated in case of peripheral vestibular syndrome. The pathophysiology behind the neurological signs in acquired hypothyroidism is poorly understood.
Large and giant breeds of dogs presenting with generalized weakness have Lower Motor Neurons signs. Clinical
signs usually progress from weakness to non ambulatory
tetraplegia within 4 to 6 weeks. The diagnosis of polyneuropathy is based on electromyographic, electroneurographic,
and histo-pathological findings.
Hypothyroidism has been recognized as a cause of peripheral vestibular syndrome. These dogs are presented with
head tilt, asymmetrical ataxia, nystagmus without postural
reaction deficit. The history and the normal findings of complementary diagnostic procedures rule out middle or internal
ear structural causes. The Brainstem Auditory Evoked Response may show decreased amplitude and latency, consistent with a degenerative neuropathy. Facial paralysis has
been recognized with hypothyroidism in dog.
Megaoesophagus is a common finding in myasthenia
gravis, neuropathy of congenital or metabolic origin, hypoadrenocorticism, LE, …However, a large number of case
have an idiopathic etiology. Some of those have a concomitant hypothyroïd status and their megaoesophagus may be
reversed by thyroid supplementation.
Acquired laryngeal paralysis is a middle-aged to old
large or giant dog condition. The recurrent degenerative
changes may or may not be included in a more generalized
polyneuropathy. In some of them, concomitant hypothyroidism has also been reported and clinical signs reversed by
thyroid supplementation.
Hyper-lipoproteinemia and the lipidic form of arteriosclerosis, named atherosclerosis has been described in
primary hypothyroidism in dogs. Involvement of cerebral arteries may induce hypoxia and spontaneous vascular accidents. Hypothyroidism has also been diagnosed in non structural epileptic dogs. Thyroid supplementation may resolve
the problem and anti-epileptic drugs may be discontinued.
Because of the difficulties encountered to obtain a final
diagnosis of hypothyroidism, a therapeutic diagnosis may
confirm the hypothesis. A T4 supplementation is preferred to
a T3/T4 mix supplementation.
HYPERTHYROIDISM
Hyperthyroidism has been associated with the clinical features of neuromuscular and central nervous system dysfunction. The most common clinical expressions in cats are neck
ventro-flexion, decrease ability to jump, fatigue after physical
activity. Restlessness, hyper-excitability, irritability and aggression are behavior signs that can develop. Seizures are
rarely reported. Most of the neuro-muscular and central nervous system signs resolve with correction of hyperthyroidism.
83
Discospondylitis: diagnostic and therapeutic aspects
Laurent Cauzinille
Discospondylitis is a bacterial infection of the intervertebral disc space and the vertebral plates in contact. The
terminology “spondylitis” is used only when the vertebral
cortices that may have proliferated (spondylosis) are involved. Chronic skin, urogenital (cystitis, pyometra, prostatitis), endocardial and oral infections are usually at the origin of the bacteria which migrate hematogenously toward
the epiphysal vertebral plates. Foreign body migration, extension of paravertebral infections, penetrating wounds or
vertebral surgeries may also be followed by discospondylitis. The most common encountered agents are Staphylococcus sp coagulase positive, Brucella canis, Streptococcus sp,
Aspergillus sp, et Mycobacterium sp. Fungal infections are
rare in Northern Europe.
after the initial clinical signs; this is why radiographs must
be repeated when they are not diagnostic although the suspicion of discospondylitis is high. Scintigraphy or bone scan
(IV radio-isotope injection and gamma-camera imaging) is
diagnostic technique that may sooner reveal a lesion; it allows to detect an abnormal inflammatory “spot” before radiographic signs shows up. However the sensitivity of this test
is poor; a “hot spot” will also be visible in case of neoplasm.
Anyway, discospondylitis may be difficult to distinguish initially from a primary vertebral neoplasm although, generally, a primary neoplasm does not cross the intervertebral
space. Infectious agent may be cultured from fine needle intervertebral space aspiration, but also from urinary or blood
culture. A simple agglutination test with a predictive value of
99% must always be performed to confirm absence of Brucella canis infection in a dog living in a farm.
CLINICAL ASPECT
Discospondylitis are more often described in large or giant breeds of young adults dogs; males are twice more often affected than females. Hyperesthesia is the most common clinical sign. Pain may be so excruciating that the dog
may be reluctant to move or show agressivity. Systemic
signs of infection (weight loss, anorexia, apathy, hyperthermia) is not always present initially. Reactive osseous or discal tissues may protrude in the vertebral canal and induce
spinal cord or nerve roots compression explaining the clinical signs. Vertebral segments the most commonly involved
are the lumbo-sacral junction, the caudal cervical and the
middle thoracic region.
DIAGNOSTIC ASPECT
It is important to radiograph the entire vertebral column
of suspected animal because more than one space may be involved. Radiographic characteristics are : decreased size of
the intervertebral space, lysis of the vertebral plates and sclerosis (increased density) of the adjacent vertebral bodies.
The first radiographic signs may not show up before 6 weeks
THERAPEUTICAL ASPECT
Cephalosporins or clindamycin for 4 to 6 weeks minimum must be used if the culture is negative. Steroids are
sometime necessary to alleviate the pain when non steroid
anti-inflammatory drugs are not improving the condition.
They must be tapered and discontinued as soon as possible.
Radiographs are performed regularly every 3 to 4 weeks to
assess the progression or regression of the lesion. Clinical
improvement must be noticed within one to two weeks
while the steroids are tapered. In case of impossibility to decrease the steroids, culture or review of the tentative diagnosis must be done. Pathological fracture (vertebral body
collapsus) is possible; this is why the patient must be kept
with a reduced physical activity. Surgical exploration must
be considered if the treatment does not improve the dog.
The lesion is biopsied for histopathological analysis and
culture, and the roots and spinal cord are decompressed.
Some internal stabilisation is necessary although the risk is
high to introduce metallic or synthetic foreign bodies in
situ. Patients with neurological deficit rather than only pain
have a poorer prognosis.
85
Impiego del trilostano in dermatologia veterinaria
Rosario Cerundolo
Dept. of Clinical Studies, The School of Veterinary Medicine
University of Pennsylvania, 3900 Delancey Street - Philadelphia, PA 19104-6010
Molecola - (4alfa,5alfa,17beta)-4,5-Epossi-3,17-diidrossiandrost-2-en-2-carbonitrile; C20H27NO3
Meccanismo d’azione - Il trilostano è un’inibitore reversibile dell’enzima 3β-idrossisteroido-deidrogenasi che converte, prevalentemente nella corteccia surrenale, il pregnenolone a progesterone, il 17-idrossipregnenolone a 17-idrossiprogesterone, il diidroepiandrosterone ad androstenodione
e l’androstenediolo a testosterone. Ne consegue, rispettivamente, una riduzione delle concentrazioni ematiche di aldosterone, di cortisolo e degli ormoni sessuali.
Somministrato per via orale è rapidamente assorbito nel
tratto gastrointestinale. Viene metabolizzato nel fegato ed
escreto per via renale
Indicazione - È utilizzato da diversi anni nell’uomo per
il trattamento dell’iperadrenocorticismo, iperaldosteronismo
e del cancro della mammella. In medicina veterinaria è usato per il trattamento dell’iperadrenocorticismo, nel trattamento preparatorio alla surrenalectomia nell’iperadrenocorticismo indotto da neoplasia surrenalica del cane e del gatto
e nell’alopecia X del cane (Hurley, 1999; Cerundolo, 2000;
Cerundolo, 2001; Reush 2002).
ramente riscontrata la comparsa di diarra durante il corso
della terapia. Dosi elevate possono provocare crisi addisoniane e richiedono la somministrazione di corticosteroidi.
Controindicazioni - È da evitare la somministrazione in
animali durante la gravidanza ed in pazienti affetti da disfunzioni epatiche e renali
Visite di controllo - I controlli della cortisolemia vanno
effettuati dopo 7-10 e 30 giorni dall’inizio della terapia eseguendo la prova di stimolo con l’ACTH al fine di valutare
l’adeguata soppressione della funzionalità surrenalica. Modificazioni della dose o dell’intervallo di somministrazione
sono a volte necessarie in alcuni pazienti.
Durante il corso della terapia vanno monitorate le funzionalità epatica e renale e la concentrazione degli elettroliti plasmatici
Bibliografia
1.
2.
Dosaggio - Il dosaggio del trilostano varia dai 5-10
mg/kg per os SID or BID. La singola somministrazione giornaliera è indicata nella maggior parte dei casi. Raramente alcuni pazienti necessitano una doppia somministrazione giornaliera. Ciò è probabilmente dovuto alla breve emivita del
farmaco, ma ciò va valutato effettuando dei test di controllo.
Effetti collaterali - La somministrazione per via orale a
stomaco vuoto può provocare irritazione gastrica. È stata ra-
3.
4.
Cerundolo R., Oliva G., Honour J., Hurley K., Persechino A. Impiego del trilostano nella terapia dell’iperadrenocorticismo del cane. Atti del Congresso SISVET Vol. LIV, Riva del Garda (Italia), 28-30 Settembre 2000, 245-246.
Cerundolo R., Lloyd D. H., Persechino A., Evans, H., Cauvin A. The
use of trilostane for the treatment of Alopecia X in Pomeranians and
miniature poodles. Proceeding of the American Academy Veterinary
Dermatology/American
College
Veterinary
Dermatology
(AAVD/ACVD) annual meeting, Norfolk (USA), 5-8 April 2001.
Hurley K.J. Trilostane in the treatment of canine hyperadrenocorticism. ESVIM Newsletter 1999; 9: 11-12
Ruckstuhl N.S., Nett C.S., Reusch C.E. Results of clinical examinations, laboratory tests, and ultrasonography in dogs with pituitary-dependent hyperadrenocorticism treated with trilostane. Am J Vet Res.
2002; 63(4): 506-12.
87
Search of quality and human resources
Fabrice Clerfeuille
DVM, MBA in Management, MBA in Marketing, PhD in Marketing,
Marketing Professor at the Nantes University (France)
The search of quality is all around us in our society. Well
informed, more active, consumers have now the capacities
and the means to compare differents products or services
which can answer to their needs. To compare the alternatives
offered, they evaluate the quality and the price of the differents options. This tendency is also present in our profession
and the search of quality is increasing more and more.
Our presentation will follow three parts: definition and
clients’expectations about quality, quality through the differents departments of the clinic, and the global management
of quality.
I – QUALITY: DEFINITION AND
CLIENTS’EXPECTATIONS
Quality needs to be define to know exactly what it recovers in a Vet Clinic. We will be able then to study clients’expectations and find the adequation between theirs needs and
the services offered.
1 - Expectations regarding the vet
Pet owners declared the following needs:
-High quality care towards the pet
-A short waiting time and a diagnosis without delay
-Clear explanations
-Confidence in the follow up.
2 - Expectations regarding advice
The vet is perceived as the most competent professional
when a pet is concerned, especially if the pet is a special
companion. Some examples of the types of service for which pet owners may be grateful are:
-Choice of a breed
-Choice of a male or female for the existing pet
-General advice on training
-General advice on show dates, grooming, steps to be taken when an animal is lost, etc.
3 - Expectations concerning the premises
A – Definition
Quality is “ the sum of the properties and characteristics
of a product or a service which can answer to the conscious
ou unconscious needs of the clients ”. It’s a part of a quality
global management destinated to the clients, and the engine
of the economic development of the clinic.
So, the perceived quality by the client means the adequation between his needs and the offered services.
B – Clients’Expectations
A qualitative survey has been carried out among pet owners by Hill’s in 1996 and 1997. This survey in five european
countries shows how their expectations fall into six categories:
-Expectations regarding the vet;
-Expectations regarding advice;
-Expectations concerning the premises;
-Expectations concerning the nurses;
-Expectations concerning payment;
-Expectations about new services.
Clients’expectations regarding the quality of the premises are predictable:
-An accessible parking
-Cleanliness (general aspect, upkeep, unpleasant smells,
etc.)
-Uncluttered public spaces.
4 - Expectations concerning the nurses
Clients expectations towards vet nurses and other staff
are precise:
-They should be identifiable from the others professionnals of the Clinic
-They should be competent technically but also in the area
of communication
-They should be kind with the animals.
5 - Expectations concerning payment
Clients want:
-To be able to consult a list of prices
-To pay reasonable fees
88
-To have the option of different methods of payment (immediate or in instalments).
6 - Expectations about new services
Arising from dicussions on quality with pet owners, some services have been mentionned as desirable:
-Loan of books about pets
-Consultations on diet (obesity)
-Health checks for old animals
-Counselling when a pet companion dies
-Puppy class.
II – QUALITY THROUGH THE DIFFERENT
DEPARTMENTS OF THE CLINIC
To answer to the differents clients’ expectations about
quality, some differents ressources are needed in the Clinic.
Four departments can be arbitrary presented: financial ressources, human ressources, material ressourcse and marketing ressources.
A – Financial ressources
To increase quality, we need at first some material investments, human investments and time investment. These
investments are, at least in the beginning, often consumer of
profit. Choice of quality is a long term strategy, which needs
a good financial health.
A good management is the first condition to develop
quality steps in our clinics. We have not enough time to be
complete in this area but we have to keep in mind two recommandations:
-To have an analytic accountancy which permit to follow
the incomes and expenses of the differents services offered
by the clinic;
-To have some financial indicators to follow the quality
of the clinic.
B – Human ressources
Human ressources are the first indicator of quality for the
clients. We need to motivate our nurses. Motivation is a mix
between the level of perceived competence and the level of
self determination in their job:
High perceived Compétence
Obligation
Revolt
Interest
Selfdétermination
Resignation
Flight
Low perceived Compétence
C – Material ressources
Quality needs material ressources, either technical ones
or commercial ones. Each of them needs to build a forecast
budget and the calculation of a profitable threshold. The indirect incomes need also to be included:
-Clients’ loyalty
-Winnings of clients by the communication developped
-Developments of new services using the investments
-etc.
D – Marketing ressources
Marketing ressources include all the communication
tools used to show the quality of the clinic. Quality is based
on services, so we need to materialize them in order that
clients can see them.
For example we can list:
-a board containing some views of the differents areas of
the clinic with their equipments
-a photograph album showing some funny pictures of the
clients pets
-a newsletters for the clients showing the differents areas
of the clinic
-an information about the new equipments
-etc.
III – TOWARDS A QUALITY
MANAGEMENT
To develop quality in our Clinic needs a global management. We propose below such a management:
Study of the
External Environment
- Threats
- Opportunities
Study of the
Internal Environment
- Strenghts
- Weaknesses
Quality objectives
Plan
Do
Check
Next Action
Such a Quality management can go until the ISO 9000 standard. It’s an international standard which gives the recommandations for quality management in any organization or enterprise
and propose some tools to develop quality between the clients
and the enterprise. A vet clinic in Hambourg has for example the
ISO 9002 standard since 1997. Some countries prefer to develop
their own standard for the vet profession like in the Netherlands
(Koninklijke Nederlandse Maatschappij voor Diergeneeskunde).
To conclude, it appears that all the actors of the vet profession
go towards quality management: the suppliers due to the competition, the vets in front of the technology development and maybe also due to the competition, but also the person in charge of
the vet ethic in the concerned countries. Europe will maybe think
in the next future to elaborate a standard of quality in our profession with some procedures. Are we ready to do this change?
89
Critères de rentabilité d’une clientèle
Fabrice Clerfeuille
Introduction
La rentabilité est définie par le Larousse comme” le caractère de ce qui est rentable”, “qui donne un bénéfice satisfaisant”. En l’absence de normes établies dans la profession,
au contraire d’autres domaines d’activités, et compte tenu du
caractère subjectif de la notion de “bénéfice satisfaisant”,
nous nous tournerons dans cette présentation sur la notion de
taux de rentabilité, plus objective.
Le taux de rentabilité est défini par “le rapport entre les
profits d’une entreprise et les capitaux engagés”.
Ce critère de taux de rentabilité peut donc être défini
dans nos cliniques par:
Bénéfices
Taux de rentabilité = —————————————
Chiffre d’affaires
C’est donc ce taux qui nous servira de fil conducteur tout
au long de cette présentation, qui suivra deux parties:
- la rentabilité: l’existant;
- la rentabilité: les améliorations.
I - LA RENTABILITÉ: L’EXISTANT
La plupart des vétérinaires étant soumis à une comptabilité de type Bénéfices Non Commerciaux, nous partirons de ce
type de comptabilité pour définir la rentabilité de la clinique.
Le document de base sera donc la liste des dépenses, que
l’on doit dans un premier temps retraiter, pour ensuite calculer
des ratios qui permettront des comparaisons.
A - Retraitement des dépenses
Les dépenses doivent être retraitées sur un tableur de type Excel, pour favoriser ensuite les calculs de rentabilité.
Nous suggérons de systématiquement retraiter les
chiffres en pourcentage du chiffre d’affaires. Cela permet de
connaître la part des dépenses pour 100 Lires de chiffre d’affaires effectué.
Il suffit de renoter sur le fichier excel les différentes rubriques de dépenses, et les présenter de cette façon:
2001
Chiffre
RECETTES
2000
Var
% du CA Chiffre % du CA 01/00
100%
100%
Achats
?
?
?
Salaires + charges
?
?
?
Impôts et taxes
?
?
?
Loyers
?
?
?
Locations
?
?
?
TFSE
?
?
?
Transports/
déplacements
?
?
?
Frais réception
?
?
?
Frais divers gestion
?
?
?
Frais financiers
?
?
?
DEPENSES
Ce tableau permet donc d’avoir très rapidement les pourcentages des dépenses par catégorie, et pour 100 Lires de
CA.
La comparaison avec les autres années permet ainsi de
comparer les variations de rentabilité d’une année sur l’autre
et de dépister ses causes.
On va de plus pouvoir calculer des ratios de rentabilité.
B - Le ratio, outil de gestion indispensable
Pour approfondir le taux de rentabilité de sa clinique on
peut utiliser des ratios.
90
1 - Qu’appelle-t-on ratio?
4.1.1 - Evolution de l’activité
Un ratio est un rapport entre deux grandeurs qui exprime
leur importance relative. Les ratios sont uniquement calculés
pour permettre des comparaisons. On peut en créer indéfiniment, mais ils n’offrent d’intérêt que s’ils sont significatifs.
(CA HT) - (CA HT)
————————————————————— x 100
(CA HT)
2 - Intérêt de l’étude des ratios
Etudié isolément, un ratio d’exploitation d’une clinique
donne peu d’informations. Il n’a d’utilité que dans le cadre
d’une comparaison. Deux comparaisons sont alors possibles:
- dans le temps, en comparant le même ratio sur trois ans
par exemple;
- dans l’espace, en le comparant avec des cliniques différentes.
Une comparaison dans le temps et dans l’espace doit permettre au vétérinaire de mesurer sa propre évolution et de se
situer par rapport à la profession. Cette tâche est parfois plus
complexe qu’il n’y paraît car plusieurs phénomènes parasitent souvent les conclusions à tirer.
n
n-1
n-1
L’évolution du CA est toujours considérée comme l’indicateur économique numéro 1 de la clinique. Comparée aux
moyennes de la profession, ce ratio permet au vétérinaire de
mesurer son dynamisme dans son environnement.
4.1.2 - La marge commerciale
Ventes HT - Achats HT revendus
————————————————————— x 100
Ventes HT
avec Achats HT revendus = Achats + Stock initial - Stock
final. Même si les achats sont limités en Italie, les vétérinaires doivent quand même tenir compte des injectables, etc.
Ce ratio nécessite donc de faire un inventaire de stock annuel.
4.1.3 - Autres achats et charges externes
3 - Limites de l’étude des ratios
Il s’agit surtout de charges fixes.
Les moyennes générales (exemple des statistiques
fournies par les services fiscaux) sont avancées comme
étant des normes. Il est donc souhaitable d’obtenir des renseignements statistiques sur une population de cliniques
proches: nombre de vétérinaires, localisation, tranche de
CA, etc.
Attention toutefois dans la mesure où ces chiffres sont
agrégés, rendant impossible toute comparaison.
Des éléments exceptionnels peuvent également fausser
les comparatifs, comme la perte d’un gros éleveur, une création proche, etc. Ces éléments doivent être isolés afin de déterminer avec précision leur impact sur les ratios.
Le mode d’exploitation peut avoir une certaine influence, comme le ratio frais de personnel / CA HT, dépendant de
la stratégie développée par la clinique.
La méthode des ratios doit donc être mise en oeuvre avec
prudence et discernement.
4 - Comment calculer les ratios de la clinique?
Autres Achats + Charges externes
————————————————————— x 100
CA HT
Le poids des charges structurelles par rapport au CA est
un élément d’analyse qui permet au vétérinaire d’apprécier à
leur juste mesure les économies envisageables.
Attention dans la comparaison avec d’autres structures
pour ce ratio qui sera forcément plus faible si le vétérinaire
est propriétaire des murs (absence de loyers).
4.1.4 - Les frais de personnel
Frais de personnel
————————————————————— x 100
CA HT
Ce ratio permet d’estimer la bonne adéquation entre les
moyens mis en oeuvre et les résultats d’activité. Il traduit le
poids de la masse salariale pour 100 Lires de CA HT.
Deux grandes familles de ratios peuvent être définis:
- les ratios de croissance et d’activité, qui influencent la
rentabilité sur le volet CA (numérateur de la rentabilité);
- les ratios de rentabilité sensu stricto, qui influencent la
rentabilité sur le volet Dépenses (dénominateur de la rentabilité).
4.1 - Les ratios de croissance et d’activité
Plusieurs ratios font partie de cette famille, et nous citerons les plus important selon nous.
4.1.5 - Les frais financiers
Frais financiers
————————————————————— x 100
CA HT
Le mode d’acquisition d’une clinique engendre dans les
premières années d’installation des frais financiers extrêmement importants.
Par ailleurs l’évolution de ce poste dans le temps met en
évidence la bonne ou mauvaise santé financière de la cli-
91
nique (mauvais financement de départ, augmentation insuffisante du bénéfice pour couvrir les besoins, etc.).
L’évolution de ce ratio dans le temps est très significative pour une même clinique.
4.2 - Les ratios de rentabilité
Deuxième sous famille de ratios, elle comprend plusieurs
ratios, très souvent calculés par les banquiers, pour s’assurer
de la santé de la clinique, et autoriser de nouveaux emprunts..
4.2.1 - L’Excedent Brut d’Exploitation (EBE)
EBE
————————————————————— x 100
CA HT
Il est mis particulièrement en évidence dans les analyses
faites sur la santé économique des cliniques.
La formation et l’utilisation de l’EBE peuvent se présenter de la façon suivante:
Formation de l’EBE
Utilisation de l’EBE
Du CA à l’EBE
A quoi sert l’EBE?
ventes - achats consommés
- remboursement des emprunts
= marge commerciale
- charges externes
= valeur ajoutée
- impôts
RATIO
1999
2000
2001
(CA HT) n - (CA HT) n-1
——————————— x 100
(CA HT) n-1
5,22%
3,73%
-1,25%
?
?
?
Autres Achats + Charges externes
—————————————— x 100 17,33%
CA HT
18,06%
17,82%
Frais de personnel
———————— x 100
CA HT
19,64%
19,39%
20,94%
Frais financiers
——————— x 100
CA HT
0,21%
0,03%
0,12%
EBE
———— x 100
CA HT
42,88%
42,42%
40,01%
Bénéfice net
—————— x 100
CA HT
34,02%
35,17%
34,09%
Achats
———— x 100
CA HT
23,80%
23,68%
21,17%
Ventes HT - Achats HT revendus
—————————————— x 100
Ventes HT
- train de vie
- impôt sur le revenu
- financement des besoins
en fonds de roulement
- frais de personnel
- autofinancement
- cotisations personnelles
des investissements
Chacun de ces ratios permet donc d’évaluer les variations de rentabilité de la clinique d’une année sur l’autre.
Cela nous amène à nous interroger sur les moyens d’améliorer cette rentabilité au sein d’une clinique.
= EBE
II - LA RENTABILITÉ:
LES AMÉLIORATIONS
L’EBE permet d’appréhender les conditions d’exploitation de la clinique en faisant abstraction du mode de financement des actifs.
Une fois cette rentabilité connue et appréhendée, il reste
à essayer de l’améliorer.
Compte tenu de sa définition, Bénéfices / Chiffre d’affaires,
améliorer le taux de rentabilité nécessite de diminuer les dépenses, d’augmenter le chiffre d’affaires ou les deux à la fois:
4.2.2 - La rentabilité nette
Bénéfices
Taux rentabilité = —————————————Chiffre d’affaires
Bénéfice net
————————————————————— x 100
CA HT
Il exprime dans le temps l’évolution de la capacité de la
clinique à réaliser des bénéfices.
Nous donnerons ci-dessous un exemple de retraitement
pour évaluer les informations que l’on peut en retirer:
Chiffre d’affaires - Dépenses
= —————————————
Dépenses
= 1 - ————————————
92
Nous allons étudier dans un premier temps les moyens
de baisser les dépenses, et, dans un second temps, d’augmenter le chiffre d’affaires, la troisième solution (faire les
deux simultanément) découlant logiquement des deux précédentes.
A - Diminution des dépenses
Les dépenses doivent être appréhendées et comparées
d’une année sur l’autre au moyen des ratios précédemment
présentés.
Une évolution significative d’un ou de plusieurs de ces
ratios doit être étudiée pour essayer de définir des économies
possibles.
Faute de temps, il ne nous sera pas possible d’envisager
tous les moyens de réduction des dépenses, et nous étudierons plus particulièrement celles liées aux achats de matériel, la rentabilité de ces investissements étant souvent mal
maîtrisée.
Il n’est pas de notre propos de conseiller tel ou tel achat
de matériel, et l’on doit toujours avoir à l’esprit que la qualité du travail doit systématiquement primer sur la rentabilité.
Nous voudrions simplement ici conseiller fortement
chaque vétérinaire d’effectuer, avant tout achat de matériel,
un calcul de rentabilité afin de savoir où il s’engage à court
ou moyen terme.
Pour certains matériels, même non rentables mais nécessaires à l’exercice de notre profession (exemple de l’échographe), il sera intéressant de calculer les pertes financières
annuelles.
Ce calcul doit porter sur le point mort, c’est à dire le moment à partir duquel le matériel souhaité va rapporter des bénéfices directs au vétérinaire.
Il doit tenir compte:
- du coût d’achat;
- du coût des consommables pour chaque utilisation de
ce matériel;
- du coût passé par l’ASV à chaque utilisation (ramené
au prorata de son salaire horaire);
- du coût d’une éventuelle garantie supplémentaire;
- de coûts dérivés s’ils existent (exemple de consommables de nettoyage de ce matériel, de produits calibrants,
etc.).
L’idéal est bien entendu de faire des bénéfices le plus tôt
possible!
Dans l’amélioration de la rentabilité par la diminution
des dépenses, chaque secteur doit bien sûr être étudié, en traquant le gaspillage, et la meilleure utilisation de chaque ressource matérielle, mais aussi humaine.
Passons maintenant à l’étude de l’amélioration de la rentabilité par le développement du chiffre d’affaires.
B - Augmentation du Chiffre d’affaires
L’augmentation du chiffre d’affaires d’une clinique peut
se faire par le biais de quatre mécanismes, éventuellement
combinés entre eux:
- l’augmentation des prix;
- l’augmentation de la rotation des clients (chaque client
revient plus souvent à la clinique);
- l’augmentation du panier moyen de chaque client
(chaque client dépense plus à la clinique);
- l’augmentation du nombre de clients.
1 - L’augmentation des prix
L’augmentation des prix amène trois réflexions principales:
- La première est qu’un prix élevé passe d’autant mieux
que le client est satisfait des services qui lui sont proposés.
On doit donc veiller à la qualité des services offerts, ce qui
sort du cadre de cette présentation.
- La seconde est qu’il faut, au minimum, augmenter ses
tarifs du montant de l’inflation annuelle pour éviter une perte de rentabilité mécanique.
- La troisième est qu’il faut une véritable stratégie de
prix, avec un calcul épisodique de la rentabilité de chaque
acte... des surprises sont parfois trouvées !
2 - L’augmentation de la rotation des
clients
Par augmentation de la rotation des clients, nous entendons la mise à leur disposition de produits ou services augmentant leur venue à la clinique.
Il en est ainsi, par exemple, des aliments. Chaque venue
du client entraînant souvent l’achat de produits secondaires
ou d’impulsion.
Ayons à l’esprit que les cliniques vétérinaires développent de plus en plus les soins préventifs, et qu’elles doivent
donc être considérées par les clients comme les interlocuteurs privilégiés pour tout ce qui touche leur animal.
3 - L’augmentation du panier moyen des
clients
Par panier moyen, il faut entendre la division du chiffre
d’affaires sur une période donnée (semaine, mois, année), par
le nombre de contacts à la clinique pendant cette période.
Ce panier moyen peut se calculer tous actes confondus
(prestations médicales et chirurgicales + vente à l’accueil)
ou scindé en deux sous paniers moyens (l’un pour les prestations médicales et chirurgicales), l’autre pour les ventes à
l’accueil.
Il est intéressant de le calculer chaque année pour le relier
au chiffre d’affaires et au bénéfice. On peut en effet avoir une
augmentation de ces deux critères par une augmentation du
panier moyen cachant un nombre de clients en baisse, ce qui
n’est pas une sitauation saine sur le moyen ou long terme.
L’augmentation de ce panier moyen doit être analysé,
dans la mesure où il peut résulter de plusieurs effets tels que
l’augmentation des tarifs, des ventes supérieures, le développement d’une activité coûteuse (exemple de la chirurgie
osseuses), etc. Cela confirme donc la nécessité, si possible,
de réaliser des paniers moyens par secteur d’activité pour
comprendre l’évolution du panier moyen global.
4 - L’augmentation du nombre de clients
Ce critère dépasse le cadre de cette présentation, mais
nous voudrions insister sur quelques points:
- la rentabilité n’existe pas sans client;
- la rentabilité n’est pas une fin en soi, mais simplement
un outil;
- il est plus facile d’augmenter la rentabilité d’une clinique ayant un gros fichier clients, qu’une clinique ayant un
faible fichier clients;
- plus les clients sont nombreux, plus les investissements
sont divisés, plus la rentabilité est meilleure... si elle est menée correctement;
- le nombre de clients doit augmenter la rentabilité de la
clinique, qui permet donc de dégager des fonds pour réinvestir dans de nouveaux investissements, qui permettront à
leur tour de mieux satisfaire les clients, donc d’augmenter
leur nombre, etc.
L’augmentation de ce nombre de clients ne pouvant se
faire que grâce à la seule publicité autorisée par le Code de
déontologie - le bouche à oreille - nous constatons l’importance d’offrir des services irréprochables, ce qui nécessite
dans la plupart des cas des investissements, dont une part
provient de la rentabilité de la structure... la boucle est bouclée et nous amène sur notre conclusion.
93
Conclusion
Cette présentation n’a bien sûr pas la prétention d’avoir
été exhaustive, faute de temps.
Nous avons donc été amenés à privilégier certains aspects au détriment d’autres, ce choix s’étant porté sur l’importance, ou la facilité des moyens correctifs à apporter à
ceux retenus.
Ce calcul de rentabilité ne doit pas être envisagé seul,
mais relié systématiquement à une stratégie claire de la clinique, tenant compte en priorité de la satisfaction des clients
et de la qualité de l’exercice.
Il doit aussi tenir compte d’autres paramètres propres à
chaque vétérinaire, qu’ils soient objectifs (répercussions sur
les autres composantes de la structure, évolution à moyen ou
long terme, etc.), ou subjectifs (préférences de chaque vétérinaire, libéral avant tout).
Nous voudrions enfin, pour terminer, réinsister sur quelques
points majeurs.
1 - La recherche de rentabilité doit être pensée comme un
moyen de développer les services aux clients.
2 - Tout investissement, de quelque nature que ce soit,
n’est pas forcément rentable, la rentabilité ne devant pas
aveugler ni freiner les décisions du vétérinaire.
3 - Le vétérinaire est un chef d’entreprise à part entière... il doit donc veiller à la rentabilité de sa structure.
4 - Certaines décisions stratégiques sont imprévisibles
dans le futur, mais des calculs de rentabilité limitent les
grosses erreurs dans la plupart des cas.
5 - Calculer une rentabilité doit être un réflexe dès qu’un
investissement est fait.
Vous commencez demain?
95
Les 10 indicateurs informatiques qui mesurent
la santé de votre clinique
Fabrice Clerfeuille
Pour étudier la bonne santé de sa clinique, deux grandes
approches sont envisageables:
- une approche comptable consistant à étudier ses bilans
comptables
- une approche stratégique consistant à étudier sa base de
données pour peu que l’on soit informatisé.
C’est cette dernière étude qui sera abordée ici, en proposant quelques indicateurs qu’il est nécessaire de suivre mensuellement pour apprécier l’évolution de son activité.
1 – Le Chiffre d’Affaires mensuel
Cela consiste à suivre le Chiffre d’Affaires du mois en le
comparant à celui du même mois de l’année précédente. Il
est également souhaitable de suivre l’évolution du Chiffre
d’Affaires en cumul mobile.
Cette analyse doit s’accompagner d’autres analyses:
- La comparaison avec un Chiffre d’Affaires prévisionnel
calculé en début d’année
- Le calcul du Chiffre d’Affaires prévisionnel pour l’année en cours à partir du Chiffre d’Affaires réalisé sur les
trois premiers mois de l’année. On constate en effet dans de
nombreuses structures que le Chiffre d’Affaires des trois
premiers mois correspond à une constante proche d’une année sur l’autre par rapport au Chiffre d’Affaires réalisé de
l’année.
Pour les cliniques ayant une activité spécialisée, il est possible de scinder ce Chiffre d’Affaires en fonction des spécialités:
96
Il est même possible de se servir de ces analyses comme
un outil de communication interne en affichant les résultats:
2 – Le Chiffre d’Affaires par jour
Il est nécessaire de ramener le Chiffre d’Affaires du
mois au Chiffre d’Affaires par jour en tenant compte du
nombre de jours ouvrés de travail pour comparer ce qui
est comparable. Dans une structure à plusieurs associés
ou plusieurs collaborateurs, cet outil permet des comparaisons utiles.
3 – Le nombre de contacts par mois
Par nombre de contacts nous entendons le nombre de
paiements du mois.
Pour affiner cette étude il est intéressant de scinder son
activité en plusieurs sous rubriques. Par exemple en activité
de chirurgie, en activité de dermatologie, activité de vaccination, etc.
Dans le cas où il y a plusieurs intervenants dans la clinique, il est possible de rescinder ces contacts par intervenant.
4 – Panier moyen
C’est le rapport entre le Chiffre d’Affaires et le nombre
de contacts. Le panier moyen donne le montant moyen dépensé par consultation. Il est intéressant de suivre la va-
leur du panier moyen d’un mois à un autre, au cours de
l’année. Si la scission du Chiffre d’Affaires le permet
nous pouvons calculer un panier moyen par vétérinaire
ou par type d’activité dans la clinique (chirurgie, dermatologie, etc.).
5 – Ratio Bénéfices / Chiffre d’Affaires
6 – Ratio Dépenses / Chiffre d’Affaires
Il correspond au pourcentage des bénéfices par rapport au Chiffre
d’Affaires. Il permet d’objectiver le niveau des dépenses de la clinique et
de suivre son évolution au cours du temps, mois par mois et année
après année. Il permet d’évaluer les raisons de l’évolution des bénéfices
(augmentation du Chiffre d’Affaires et/ou Baisse des dépenses).
Ratio symétrique au précédent, il correspond au pourcentage des dépenses par rapport au Chiffre d’Affaires. Par
rubrique de dépenses, il donne la répartition des dépenses
pour 100 Lires de Chiffre d’Affaires.
7 – Les impayés
Il convient de savoir quel est le montant des sommes non
rentrées: impayés et montants différés. Là encore il est nécessaire de suivre l’évolution de ces montants dans le temps
pour mettre en place des mesures correctives, si nécessaire
(augmentation des montants des impayés ou paiements différés).
8 – Les 10 plus gros clients
Aucun vétérinaire n’est capable de mémoire de citer ses
10 plus gros clients en termes de somme dépensée au cours
de l’année écoulée. Il est pourtant important de les connaître
pour les traiter au mieux lors de chacune de leurs venues.
Qui plus est, si le vétérinaire est remplacé par un collabora-
10 – Inventaire
Il est important d’étudier son Bénéfice en fonction d’un
sur stockage ou d’un sous-stockage de consommables: injectables, cathéters, fils de sutures, bandes, coapteurs de
fixateurs, broches orthopédiques, etc.
Pour ce faire il est important de réaliser son inventaire selon la méthode ABC qui revient à regrouper les consommables selon le montant qu’ils immobilisent. Reste alors à
97
teur au cours de l’année il est important que ce collaborateur
sache que le client qu’il voit est un des plus gros clients de
la clinique.
9 – Ratio des clients gagnés par rapport
aux clients perdus
Il est nécessaire de connaître sa balance entre les clients gagnés (client venant pour la première fois dans un intervalle de
13 mois) et les clients perdus (clients non venus dans un laps
de temps de 13 mois). Cela permet de mieux comprendre
l’évolution de son Chiffre d’Affaires: est-il lié ou pas à la venue de nouveaux clients, à une augmentation de prix, etc.).
Un exemple de la situation française à partir de trois cliniques (exemples prêtés par Yannick POUBANNE):
suivre particulièrement les consommables qui immobilisent le plus d’argent.
Conclusion
Ces dix critères permettent d’avoir une bonne idée sur la
rentabilité de la clinique et de trouver des modes d’amélioration. Ils nécessitent simplement de la rigueur et un tableur.
99
Miopatie: forme congenite ed acquisite nel cane
Francesca Cozzi
Med Vet, Dipl. ECVN. - Istituto di Patologia Speciale e Clinica Medica Veterinaria
Università degli Studi di Milano
Le patologie muscolari sono affezioni spesso caratterizzate dal punto di vista clinico da intolleranza all’esercizio e
debolezza generalizzata. Possono essere primitive o secondarie ad alterazioni che danneggiano il tessuto muscolare per
via indiretta.
Il muscolo scheletrico è composto da miofibre (elementi cellulari multinucleati) e dai relativi vasi e nervi.
Viene denominato “unità motoria” il complesso di fibre
muscolari innervate da un singolo neurone (motoneurone
alfa); il numero di fibre innervate da un singolo neurone
varia da poche decine (muscoli appendicolari) a migliaia
(muscoli ad attività altamente finalizzata, come i muscoli
extraoculari). In ogni muscolo sono presenti in varia percentuale fibre a diverso metabolismo; tra queste, le fibre di
tipo I, con prevalente metabolismo glicolitico (o fibre “lente”) e quelle di tipo II, con prevalente metabolismo ossidativo (o fibre “veloci”) sono le più rappresentate, in diversa
proporzione a seconda della funzione del muscolo. Le diverse fibre muscolari sono frammiste tra loro. Più fibre sono distribuite in fascicoli muscolari racchiusi da tessuto fibroso (endomisio tra singole fibre, perimisio attorno a più
fascicoli).
I livelli sierici di lattato e piruvato possono essere elevati a riposo o dopo esercizio in miopatie con alterazioni del
metabolismo ossidativo.
Lo studio elettromiografico, comprendente elettromiografia e studio della velocità di conduzione nervosa, è in grado di supportare un sospetto diagnostico di miopatia e indirizzare verso il gruppo muscolare dove eseguire la biopsia.
L’esame bioptico di campioni muscolari, eseguito su
campioni congelati e presso laboratori di riferimento per la
miopatologia, permette di ottenere informazioni riguardo:
- morfologia (diametro delle fibre, presenza di infiltrati,
tessuto connettivo, etc), con colorazioni standard quali Ematossilina-Eosina e TRG.
- metabolismo muscolare, mediante reazioni istoenzimatiche (citocromo-ossidasi, NADH, SDH, diastasi).
- accumulo di lipidi o glicogeno (colorazioni istochimiche specifiche: Oil red-O e PAS).
- tipi istochimici presenti e loro interessamento (ATPasi
a differenti pH).
MIOPATIE SU BASE INFIAMMATORIA
Miosite batterica
Segni clinici
I segni clinici dominanti in corso di miopatia sono la debolezza, non associata a deficit sensitivo, spesso costante ma
che può aggravarsi con l’esercizio; può essere presente atrofia muscolare diffusa, soprattutto nelle forme a carattere cronico. Nelle forme su base infiammatoria possono essere
inoltre presenti segni sistemici (febbre altalenante, depressione) e mialgia.
In alcuni casi specifici, ad esempio nella miotonia, il segno clinico dominante può viceversa essere un’ipertrofia
muscolare.
Diagnosi
La diagnostica delle patologie muscolari è basata su indagini di laboratorio, elettrodiagnostica e biopsia muscolare.
I livelli sierici di creatinchinasi (CK) possono essere elevati in corso di lesione muscolare attiva (necrosi o infiammazione acuta che comporti un danno della fibra muscolare). Nelle forme croniche l’enzima può viceversa essere nella norma.
Forma infrequente, focale, data da infezioni di origine
traumatica (ferite da morso, contaminazione di ferite chirurgiche). È inoltre segnalata in letteratura una miosite da
leptospira, osservata in alcuni soggetti in corso di leptospirosi.
Miosite protozoaria
La polimiosite da Toxoplasma gondii o Neospora caninum può presentarsi autonomamente od accanto ad un
interessamento del sistema nervoso (polineurite, encefalomielite) e/o coinvolgimento di organi interni. La forma
più comune è rappresentata dal complesso polineurite-polimiosite da Neospora caninum che colpisce in prevalenza i cuccioli determinando rigidità ed iperestensione degli
arti posteriori.
La toxoplasmosi è in genere subclinica; le cisti che giungono nel muscolo durante la fase extraintestinale del parassita rimangono in genere quiescenti; possono essere a rischio
100
per un’infezione attiva animali immunodepressi (cimurro
nel cane, FIV nel gatto).
La diagnosi è basata su segni clinici, titolo sierico ed altri riscontri (biopsia, EMG); è necessario per una diagnosi
l’evidenza di sieroconversione. Nel gatto un titolo anticorpale di IgM superiore ad 1:256 può essere considerato indicativo di infezione recente o attiva.
La terapia è basata sull’impiego di farmaci antiprotozoari (clindamicina 10-15 mg/kg BID per 15 gg, talora in associazione a sulfamidici quali la sulfadiazina 30 mg/kg BID).
La prognosi è variabile a seconda dell’estensione dell’infezione.
Polimiosite
La polimiosite è una patologia infiammatoria che colpisce la muscolatura scheletrica del cane, e sporadicamente del gatto. La patogenesi di questa forma è poco conosciuta; nell’uomo la polimiosite, su base immunomediata, viene inquadrata nell’ambito di altre forme autoimmuni o come sindrome paraneoplastica. Nel cane se ne
ipotizza un’origine analoga, che però è scarsamente documentata; sono riportate in letteratura forme di polimiosite canina in corso di lupus eritematoso sistemico, miastenia grave e forme neoplastiche; sono stati inoltre riscontrati autoanticorpi con specificità per il sarcolemma
ed immunocomplessi legati alla membrana; ulteriori studi saranno necessari per chiarire la patogenesi di questa
malattia.
In genere sono colpiti cani di grossa taglia, adulti, che
presentano una sintomatologia acuta o segni gradualmente
progressivi; i segni clinici prevalenti sono rappresentati da
debolezza, iperestesia, talvolta febbre. Rigurgito, disfonia
e zoppie sono presenti in alcuni casi. Nelle fasi croniche si
rende evidente atrofia muscolare diffusa. Gli esami di laboratorio possono evidenziare leucocitosi ed un aumento di
CK, LDH ed AST. L’elettromiografia indica la presenza di
potenziali spontanei; la conferma diagnostica si ottiene con
l’esame bioptico: la biopsia muscolare mostra un’ infiammazione multifocale non suppurativa (infiltrati linfoplasmacellulari, necrosi e rigenerazione) in entrambi i tipi di
fibre. In corso di polimiosite si rende inoltre necessario
eseguire ANA test e ricerca di eventuali neoplasie (radiografia del torace, necessaria inoltre per verificare l’eventuale presenza di megaesofago). L’esclusione di altre patologie concomitanti può far formulare la diagnosi di polimiosite idiopatica.
La terapia è basata sull’impiego di farmaci immunosoppressivi (prednisolone a dosaggio immunosoppressivo
e, se necessario, altri agenti chemioterapici quali l’azatioprina a 50 mg/m2 ogni 24 ore).
scolatura scheletrica (somiti), possiedono proteine di tipo
2M. Queste fibre di tipo 2M presentano nel cane antigeni di
superficie simili ad antigeni batterici, cosicché infezioni intercorrenti (urinarie, cutanee, ecc) sarebbero in grado di innescare una reazione immunologica nei confronti di questo
distretto.
Ne sono conosciute una forma acuta, la cosiddetta
“miosite eosinofilica”, ed una cronica, o “atrofica”; queste
due varianti potrebbero in realtà rappresentare due diversi
stadi della stessa malattia. La presentazione iniziale è data da tumefazione, talora intermittente, della muscolatura
ed algia all’apertura della bocca; gradualmente si instaura
una vistosa atrofia della muscolatura temporale e dei masseteri, ed un trisma mandibolare con impossibilità di aprire la bocca completamente. La diagnosi è basata sull’evidenziazione degli autoanticorpi (anticorpi anti-fibre 2M).
Gli esami di laboratorio possono evidenziare nelle fasi iniziali eosinofilia, un aumento transitorio degli enzimi sierici muscolari ed ipergammaglobulinemia. La terapia è immunosoppressiva, la prognosi favorevole nelle fasi acute
ma riservata quando è già presente un imponente trisma
mandibolare.
Rabdomiolisi da sforzo
È descritta nei levrieri da corsa in seguito a sforzo fisico
e sporadicamente in altre razze canine come conseguenza di
crisi epilettiche prolungate. La sintomatologia è data da debolezza, algia, tachipnea, febbre che compaiono 24-72 ore
dopo l’esercizio. È presente acidosi lattica, aumento imponente della CK e mioglobinuria; può complicarsi per il comparire di insufficienza renale.
Dermatomiosite
È una malattia ereditaria segnalata nel collie e nel pastore delle Shetland, nei quali ha una trasmissione autosomica
dominante.
Miosite da virus dell’Immunodeficienza
felina
In gatti adulti infettati sperimentalmente con il virus
dell’Immunodeficienza felina è stata osservata l’insorgenza di una miopatia infiammatoria; sebbene fossero
presenti alterazioni istopatologiche (necrosi, infiltrati monocellulari) nei muscoli testati ed aumento della CK sierica, i gatti non presentavano sintomatologia clinica apprezzabile.
Miosite dei muscoli masticatori
MIOPATIE DI NATURA DEGENERATIVA
È una forma di miosite su base immunomediata, caratteristicamente confinata ai soli muscoli masticatori (massetere, temporale e pterigoideo). Questi muscoli, di differente
origine embrionale (mesoderma) rispetto al resto della mu-
Queste forme possono essere acquisite, e presentarsi secondariamente a patologie che disturbano il tessuto muscolare, o essere presenti su base congenita, rappresentando l’esito di difetti strutturali o metabolici del muscolo.
FORME ACQUISITE
Miopatie di natura endocrino-metabolica
101
ta) una caratteristica zoppia dell’arto anteriore; non è presente algia e il muscolo infraspinato si presenta atrofico. La
patogenesi è da ricercarsi in traumi di questo distretto, con
graduale sostituzione del muscolo con tessuto fibroso.
Da iperadrenocorticismo
In soggetti con Cushing primitivo o iatrogeno possono
rendersi evidenti i caratteri di una miopatia steroidea; oltre a
debolezza ed atrofia muscolare vengono talvolta osservate
forme di rigidità di alcuni gruppi muscolari (muscolatura posteriore della coscia in uno o entrambi gli arti, e talvolta degli anteriori). Si può avere un aumento della CK e segni elettromiografici riferibili a scariche bizzarre ad alta frequenza.
Contrattura del quadricipite
Da ipotiroidismo
FORME PRIMITIVE
Questa miopatia è caratterizzata da debolezza generalizzata, ed istochimicamente da atrofia selettiva delle fibre di
tipo II. È spesso associata a neuropatia periferica.
Distrofie muscolari
Miopatia ipocaliemica felina
L’ipokaliemia cronica può portare nel gatto a questa patologia; le cause sono da ricercare nella deplezione di potassio, in genere in corso di nefropatie e/o a ridotto apporto alimentare o assorbimento. La sintomatologia è caratterizzata
da intolleranza all’esercizio, mialgia, ventroflessione cervicale. La diagnosi è basata sul rilievo dell’ipokaliemia ed aumento della CK. Elettromiograficamente si può osservare attività spontanea o, in altri casi, assenza di alterazioni. Non
sono presenti segni istologici caratteristici. La terapia è basata sull’integrazione potassica con la dieta.
Miopatie fibrotiche/ossificanti
Miopatia del complesso muscolare
“gracile-semitendinoso” del cane
È causa di zoppia; colpisce prevalentemente il pastore tedesco (88%) e sporadicamente cani di altre razze. Si tratta di
soggetti adulti, spesso maschi; l’insorgenza è in genere insidiosa ed il decorso progressivo. La zoppia derivante dal processo fibrotico dei muscoli è caratteristica, con un movimento
a scatto dell’arto che viene portato in avanti con un’infrarotazione del piede e del ginocchio ed il passo accorciato. Alla palpazione il muscolo interessato appare teso, ingrossato e di consistenza aumentata. Gli esami di laboratorio inclusi gli enzimi
muscolari sono nella norma. L’esame elettromiografico ha riscontri variabili. L’eziologia è sconosciuta, e tra le ipotesi vi
sono i microtraumi ripetuti, disturbi neurogeni o vascolari.
Miopatia dell’infraspinato
(contrattura dell’infraspinato)
Riguarda prevalentemente cani da lavoro, nei quali si
sviluppa cronicamente (spesso in seguito ad insorgenza acu-
Esistono forme congenite o post-traumatiche (secondarie
soprattutto ad infibulazione centromidollare del femore con
accesso prossimale) di contrattura del muscolo quadricipite;
la forma congenita va differenziata dalla polineurite-miosite
da Neospora caninum.
Le distrofie sono un gruppo di patologie muscolari primitive caratterizzate da un progressivo danno della muscolatura scheletrica. La forma meglio conosciuta e più frequente
è la distrofia muscolare legata al cromosoma X; ampiamente descritta nel Golden Retriever e sporadicamente segnalata in altre razze canine, questa patologia è trasmessa da femmine portatrici asintomatiche e manifestata dai cuccioli maschi affetti. Il difetto genetico alla base di questa distrofia interessa il gene che codifica una proteina di membrana muscolare, la distrofina; l’alterazione o l’assenza di questa proteina del citoscheletro porta ad un danno muscolare progressivo ed irreversibile. I cuccioli distrofici mostrano nei primi
mesi di vita una progressiva atrofia muscolare e difficoltà di
movimento; compare disfagia, spesso legata ad un’ipertrofia
della muscolatura linguale. Nel gatto la distrofia muscolare
legata al cromosoma X ha invece caratteri di vera e propria
ipertrofia muscolare diffusa, ed è denominata “distrofia muscolare ipertrofica felina”. La diagnosi è data dal rilievo di
CK estremamente elevata, un quadro elettromiografico di
miopatia diffusa e dalla evidenziazione immunoistochimica
del difetto di distrofina a livello di fibre muscolari.
Altre forme di distrofia sono state descritte: ad esempio
la miopatia ereditaria del Devon Rex, conosciuta tra gli allevatori come “spasticità felina” e legata ad un coinvolgimento muscolare progressivo; i soggetti colpiti mostrano,
da quando iniziano a camminare, una progressiva atrofia
muscolare e debolezza generalizzata con ventroflessione
passiva del collo. Sempre nel gatto è stata descritta una distrofia muscolare da deficit di merosina (laminina alfa-2);
in questi animali, che presentavano anche una neuropatia
demielinizzante, erano presenti gravi alterazioni muscolari
e l’assenza della merosina, glicoproteina di membrana la
cui carenza è responsabile, nell’uomo, di gravi forme di distrofie congenite.
Miopatia distale del Rottweiler - In diversi cuccioli di
Rottweiler è stata osservata l’insorgenza di deficit posturali
e progressiva comparsa di atteggiamento plantigrado e palmigrado associato ad atrofia della muscolatura distale. I livelli di carnitina erano diminuiti in tutti i soggetti. Il sospetto è di una forma di distrofia muscolare, nel quale il deficit di carnitina potrebbe essere secondario.
102
Miopatia del Labrador
Questa patologia è una neuromiopatia ereditaria, a trasmissione autosomica recessiva, che colpisce sporadicamente cani di razza Labrador retriever. I soggetti affetti (in
genere attorno ai 6 mesi di vita) sono ipomiotrofici, presentano debolezza che si accentua con l’esercizio ed il
freddo e segni lentamente progressivi, che successivamente tendono a stabilizzarsi. All’esame neurologico è possibile osservare una riduzione dei riflessi spinali. La CK è
solo lievemente elevata, e gli altri parametri di laboratorio
sono inalterati; la diagnosi è basata sull’esito dell’esame
bioptico muscolare, che evidenzia una carenza selettiva
delle fibre di tipo II associata ad alterazioni neurogene
(denervazione-reinnervazione) e ad alterazioni della citoarchitettura muscolare, variabili a seconda della gravità
del quadro. Non esiste una terapia specifica; l’utilizzo
temporaneo di diazepam può alleviare i sintomi, che in genere si stabilizzano quando il cane raggiunge l’età adulta
e non sono in genere invalidanti.
I riscontri clinici consistono in facile affaticabilità,
crampi muscolari, mialgia e talvolta mioglobinuria. Può
essere presente acidosi lattica dopo esercizio e CK alta. A
livello istologico nelle patologie mitocondriali sio possono mettere in evidenza accumuli di corpuscoli subsarcolemmali (fibre “ragged red”) ed ultrastrutturalmente segni
di sofferenza mitocondriale. La diagnosi di queste affezioni è difficoltosa, e la conferma, difficile da raggiungere, è
basata sull’evidenziazione del difetto genetico alla base,
in quanto le alterazioni dei mitocondri possono essere anche secondarie.
Tra le forme classificate, la malattia da accumulo di glicogeno (tipo VII, o carenza di fosfofruttochinasi) dello
Springer spaniel, la miopatia mitocondriale del Clumber e
Sussex spaniel.
Nel Bobtail è stata segnalata una forma di debolezza, acidosi lattica da esercizio, CK alta, non caratterizzata dal punto di vista biochimico.
Miopatia da accumulo di lipidi
Miotonia
Per miotonia si intende una contrazione attiva ripetuta
che persiste in seguito ad attivazione muscolare. Miopatie
congenite su base ereditaria caratterizzate dalla presenza
di miotonia sono descritte nel Chow-Chow, nello Schnauzer nano ed in segnalazioni isolate in altre razze canine. I
segni clinici catratteristici sono dati da rigidità diffusa,
ipertono ed ipertrofia muscolare. La rigidità può essere
tanto imponente da impedire ai soggetti di correre o sollevarsi dal decubito. Le biopsie muscolari mostrano un ingrandimento delle fibre in assenza di segni di sofferenza
del tessuto, e l’esame elettromiografico evidenzia caratteristici potenziali “miotonici”.
Miopatia nemalinica
Miopatia ereditaria descritta in una famiglia di gatti ed,
in segnalazioni isolate, nel cane. Le descrizioni in letteratura riguardano gatti in età giovanile, presentanti atrofia muscolare e fascicolazioni. La diagnosi è basata sull’evidenza
di alterazioni bioptiche caratteristiche (grave atrofia, corpi
nemalinici).
Sono forme nelle quali si ha un accumulo patologico di
lipidi a livello muscolare; nell’uomo questa alterazione è
legata ad alterazioni del metabolismo della carnitina. Clinicamente si osservano mialgia, debolezza, atrofia muscolare diffusa.
La diagnosi è basata sulle alterazioni istopatologiche
muscolari; il dosaggio della carnitina a livello sierico, muscolare ed urinario può aiutare a comprendere il difetto
biochimico alla base della malattia. La terapia con integrazione dietetica di carnitina (50 mg/kg BID) nei casi riportati in letteratura ha portato a risultati variabili.
Miopatia da ‘central cores’
Descritta nell’alano, si tratta di una miopatia di presunta
origine ereditaria caratterizzata dalla presenza di alterazioni,
date da accumulo di glicogeno e mitocondri, nella regione
centrale delle miofibre (i cosiddetti “central cores”). Non è
stato chiarito il difetto sottostante questa patologia ed una
sua precisa collocazione.
Collasso indotto dall’esercizio fisicoLabrador retrievers
Miopatie metaboliche
Queste patologie derivano da difetti biochimici primitivi
del muscolo, che comportano un disturbo del metabolismo
energetico muscolare.
Si tratta di forme poco caratterizzate nel cane e nel gatto
sia dal punto di vista del difetto biochimico che dei difetti
genetici sottostanti. Le alterazioni possono riguardare il metabolismo glicolitico, come nelle malattie da accumulo di
glicogeno, o derivare da disturbi della catena ossidativa; tra
queste, le miopatie mitocondriali, nelle quali è possibile riscontrare alterazioni ultrastrutturali e biochimiche a carico
di questi organelli.
In giovani Labrador, immediatamente in seguito ad esercizio fisico intenso, è stato osservata la comparsa di debolezza e collasso; dopo 10-20 minuti di riposo i soggetti sono nuovamente in piedi (in rari casi si è invece avuta morte
dell’animale).
È stata osservata in questi soggetti una notevole ipertermia, non dissimile da quanto accade in soggetti normali dopo l’esercizio; è possibile che in questi cani vi sia un ritardo nel ripristinare la normotermia, per un difetto biochimico muscolare.
Tale forma va differenziata dalle altre patologie tipiche
della razza e dalla miastenia grave.
Letture consigliate
Dow SW and Le Couteur RA: Hypokaliemic polymyopathy of cats. In
KIRK RW and Bonagura JD (eds): Current Veterinary Therapy X,
Small Animal Practice. Philadelphia WB Saunders C 1989, pp 812815.
Fuhrer L.: Examens complementaires dans les syndromes neuromusculaires. Electrodiagnostic et biopsies nerveuse et musculaire. Le Point
Veterinaire Vol 27, 172, 1995, pp 15-23.
Gaschen FP, et al: Dystrophin deficiency causes lethal muscle hypertrophy
in cats. J Neurol Sci 110:149,1992
Kornegay JN: The X-linked muscular distrophies. In KIRK RW and
Bonagura JD (eds): Current Veterinary Therapy XI, Small Animal
Practice. Philadelphia WB Saunders C 1992, pp 1042-1047.
Kornegay JN Disorders of skeletal muscles. In Ettinger SJ, Feldman EC
(eds): Textbook of Veterinary Internal Medicine. Diseaseas of the
Dog and Cat. 4th ed. Philadelphia WB Saunders C 1995, pp 727-736.
Le Couteur RA, et al: Metabolic and endocrine myopathies of dogs and
103
cats. Semin vet Med Surg (Small Animal) 4:146, 1989.
Lewis DD: Gracilis-Semitendinosus myopathy. In KIRK RW and Bonagura JD (eds): Current Veterinary Therapy XIII, Small Animal Practice.
Philadelphia WB Saunders C. 2000, pp 989-992
Lewis, RM. Immune-mediated muscle disease. Vet Clin of North America:
Small An Pract vol 24, n. 4.1994 pgg 703- 710.
Mc Kerrell RE and Braund KG: Hereditary myopathy of Labrador retrievers. In KIRK RW and Bonagura JD (eds): Current Veterinary Therapy X, Small Animal Practice. Philadelphia WB Saunders C 1989,
pp 820-821.
Shelton GD Differential diagnosis of muscle diseases in companion animals. Progr Vet neur 2:27, 1991
Shelton GD and Cardinet GH, III. Pathophysiologic basis of canine muscle
disorders. J Vet Int Med 1:36, 1987
Shelton GD et al: canine masticatory muscle disorders: a study of 29 cases.
Muscle Nerve 10:753, 1987
Shelton GD: Canine lipid storage myopathies. In KIRK RW and Bonagura
JD (eds): Current Veterinary Therapy XII, Small Animal Practice.
Philadelphia WB Saunders C.
105
Pododermatitis and claw diseases
Douglas J. DeBoer
DVM, Associate Professor of Dermatology, School of Veterinary Medicine
University of Wisconsin, Madison, Wisconsin USA
The most common diseases affecting this area can be divided into four categories, depending on the specific clinical
signs: (1) diseases mostly involving the footpads; (2) diseases mostly involving the interdigital areas; (3) diseases
mostly involving the claw or nailbed; and (4) diseases mostly involving pedal pruritus.
MOSTLY FOOTPADS: In pemphigus, the lesions typically are found on the bridge of the nose, face, ears, mucocutaneous junctions, and trunk. Many animals (both dogs
and cats) have prominent involvement of the footpads, and
some animals have ONLY footpad lesions. The footpad lesions tend to be peeling, scaling, and crusting lesions in layers. In hepatocutaneous syndrome, distinctive skin lesions
are present along with any type of liver disease. The skin lesions consist of erosions, ulcerations, and fissuring of the
skin of the muzzle, mucocutaneous areas of the face, distal
limbs, and footpads. Differential diagnoses for footpad diseases include other uncommon skin diseases such as canine
distemper, zinc responsive dermatosis, and feline lymphoplasmacytic pododermatitis. Routine laboratory and radiographic evaluations may be of some help in differentiating
these syndromes; in pemphigus they will be abnormal, but in
hepatocutaneous disease, evidence of liver disease will be
found. Skin biopsy is diagnostic, and should always be performed to confirm the diagnosis. Treatment of pemphigus
foliaceus consists of immunosuppressive drugs. Successful
treatment of hepatocutaneous syndrome depends entirely on
resolution of the liver disease. If the liver disease is not treatable, some dogs have made improvement in their skin lesions if their diet is supplemented with egg yolks or by supplementation with intravenous amino acid solutions.
INTERDIGITAL AREA: Interdigital pyoderma is a
deep folliculitis and furunculosis caused by Staphylococcus
intermedius bacteria, but additional factors such as foreign
body reaction to trapped hair, chronic scar tissue, anatomical
predisposition, and hereditary factors also contribute to this
disease. Typically, nodules between the toes rupture and
drain a purulent or bloody exudate. Treatment consists of oral
antibiotic administration for 6 to 12 weeks. Longer term,
pulse-treatment with antibiotics may be necessary; immunostimulant preparations are generally of little use. Pododemodicosis is an infestation and overgrowth of Demodex canis mites in the interdigital areas and skin of the toes and feet.
In a very young dog, an inherited immunologic defect is present. In adult-onset demodicosis, any underlying systemic
disease may be possible. Clinical signs include alopecia, furuncles and draining tracts on the distal limbs and interdigitally. Secondary bacterial infection (usually Staphylococcus)
is always present. One must distinguish this from interdigital
pyoderma without mites; they often look very similar. In diseases of the interdigital area, initial diagnosis is made by examination, skin scrapings, and cytology. In recurrent cases,
biopsy and culture is warranted. The prognosis for pododemodicosis is always somewhat worse than with other cases of
demodicosis. Possible treatments include topical amitraz or
systemic avermectins. It is important to check skin scrapings
once monthly, and to continue treatment until two successive
negative scrapings are obtained.
CLAW OR NAILBED: Paronychia is inflammation of
the proximal nail and nailbed area, and is often caused by
bacterial infection. There is purulent discharge around the
nailbed, or even coming out of the nail. The nails are often
malformed, broken, or may come off. The disease is usually
painful, rather than pruritic. Initial diagnosis based on physical appearance. It is important to distinguish this condition
from nail loss without swelling of the nailbed and exudate. It
is important to identify the primary organism involved with
culture. Treatment of bacterial paronychia involves initial
debridement of the nailbed areas under anesthesia, then antibiotics for 8-12 weeks. When there is breakage, malformation, or loss of nails without paronychia, diagnosis is difficult. Dermatophyte fungi occasionally cause nail infections,
but other causes are poorly understood. In idiopathic cases,
usually a series of medications are tried empirically. No one
drug seems to be uniformly effective. Medications to try include fatty acid (EPA/GLA) supplements; pentoxifylline, or
oral corticosteroids.
PEDAL PRURITUS: Malassezia dermatitis in the interdigital areas or around the nails is relatively common and
can create severe pedal pruritus. This condition often exists
as a part of atopic dermatitis. In this case, it is not always
clear whether clinical signs (pedal pruritus) are related to
yeast overgrowth or to the allergy itself. Diagnosis is
straightforward via cytology. Treatment consists of oral
and/or topical antifungals, such as ketoconazole. In some
cases, staphylococcal infection occurs at the same time, and
must be treated with antibiotics. After the infections are controlled, remaining pedal pruritus is often related to atopic
dermatitis or food allergy, which must be addressed by additional diagnostic investigation.
107
Principles of immunotherapy in atopic dermatitis
Douglas J. DeBoer
Allergen immunotherapy (“hyposensitization” or “desensitization”) is a treatment for atopic dermatitis in dogs and cats
wherein extracts of allergens to which the patient is sensitive
are injected, in gradually increasing amounts, to lessen or reverse the hypersensitivity state. Various theories as to how this
treatment works have been advanced. The “blocking antibody
theory” was popular for many years, but has been largely replaced by the “helper T lymphocyte subset” theory. This theory holds that subsets of T lymphocytes exist, one of which
when stimulated evokes IgG production (Th1 response), and
one of which evokes an IgE response (Th2 response). In an
atopic state, the pro-allergic, Th2 response predominates instead of the more ‘normal’ or appropriate Th1 response. By
administering large doses of the allergen extract, the balance
between Th2 and Th1 is shifted back towards Th1.
Immunotherapy has a strong advantage of being nearly
free of adverse effects in the great majority of dogs and cats,
even with prolonged use. Disadvantages include the fact that
it takes several months or more to begin working, that it does
not always work, and that it may be relatively expensive.
Most effects of immunotherapy are thought to be allergenspecific, rather than nonspecific. Thus, accurate testing to
identify the offending allergens in each patient is of paramount importance to successful immunotherapy. In particular,
the clinician must strive to avoid ‘false positive’ allergy test results, which would result in including an allergen in the patient’s mixture that is not relevant to that individual’s disease.
Selection and formulation of an allergen immunotherapy
mixture is both an art and a science. With regard to the actual production of the extracts, several schemes of standardization have appeared in human allergy to permit more consistent dosing from manufacturer to manufacturer, and from
lot to lot. Unfortunately, these schemes have not yet been applied to veterinary medicine. Nevertheless, the veterinary
profession must encourage extract manufacturers to take all
measures possible to insure reasonably uniform potency and
allergen content in their products. Most often, veterinary extracts are supplied either by protein nitrogen units (1 mg protein = 100,000 PNU) or by weight:volume (1:10 = 1 gram of
raw material extracted in 10 cc buffer. Most veterinary extracts are supplied as aqueous preparations, though alumprecipitated extracts are used in some countries. Each type
of extract has its own recommended protocol of administration, and no one extract type or protocol has been shown to
be superior.
Experimental observations that large doses of allergen
evoke Th1 (IgG) responses and small doses of allergen
evoke Th2 (IgE) responses suggest that there is some minimum, fairly large dose of each allergen necessary in a mixture to achieve benefit. Thus, many allergists limit the number of extracts used in each prescription to between 10 and
15 substances. When a large number of positive reactions are
obtained with allergy testing, choosing the proper 10-15 substances can be based on the following: strength of the positive reaction; degree of possible exposure of the animal to
the substance; consideration of patient characteristics; and
botanical interrelationships of pollen allergen groups. Because proteolytic allergens present in mold extracts can degrade some pollen allergens, some allergists administer
mold allergens my separate injection.
The exact protocol and schedule for injections will vary
according to the allergen preparation; generally, the extract
manufacturer will provide an appropriate schedule. In some
situation, particularly with very small animals or where the
allergen mixture contains larger amounts of only a few allergens, the animal may not be able to tolerate the maximum
specified dosage. In this case, the dosage may have to be reduced to between one-half and one-tenth of the normal full
dose. Injections are given year-round, and the minimum initial trial period should be 12 months. As far as is known,
concurrent treatments with antihistamines, fatty acid supplements, or low-dose glucocorticoids will not interfere with response. Treatment is generally considered to be lifelong,
though it is possible to attempt discontinuation after 2 to 3
years of injections if the animal has responded very well. If
the owner stops giving the injections, then wishes to restart,
the injection amount should be reduced and gradually increased again.
Expected response rate to immunotherapy is approximately 60-70% “good-to-excellent” response (defined as at
least 50% improvement in clinical signs). Response can be
seen as soon as 1 month, but more typically takes 3 to 6
months to occur, and the maximum response may take 1
year or longer. Adverse reactions to allergen immunotherapy
include localized itch at the injection site and transient worsening for 12-24 hours after the injection (~10% of patients).
Generalized anaphylaxis occurs in less than 1% of dogs and
cats; such reactions are generally mild and further reaction
can be prevented by pretreatment with an oral antihistamine
1-2 hours prior to each injection.
109
Clinical update on diagnosis and treatment
of feline dermatophytosis
Douglas J. DeBoer
Feline dermatophytosis can be a challenge to manage,
especially in a cattery situation. Research over the past ten
years has uncovered the following “highlights” that are particularly important when treating this common disease.
Dermatophytosis has many different clinical presentations and can look like almost anything in a cat! Therefore, it is probably never wrong to perform a fungal culture
in feline skin disease. Though the typical presentation may
involve focal areas of alopecia and scaling on the head or extremities, dermatophytosis can also produce more generalized patchy alopecia, “feline acne,” miliary dermatitis, or
even just a few broken hairs, such that the cat appears outwardly normal.
It is clear that diagnosis of dermatophytosis is best
achieved via fungal culture. Direct examination of hair
shafts and Woods’ light examination are not sensitive
enough; many false negative results are possible. The fungal
culture medium must be used correctly to assure best results:
take a sample over a broad area of the cat with a toothbrush
if possible, inoculate the medium, incubate at room temperature, and examine every 2-3 days for growth. A dermatophyte can be suspected if there is a white or off-white colony
with a red color change in the medium at the time the colony
is first visible. Dermatophyte test medium is not infallible –
suspicious colonies should be checked microscopically to
verify that the dermatophyte is present and determine the
species, if possible.
It is widely held that in most healthy animals, dermatophytosis is a self-curing disease that eventually resolves
spontaneously, even without therapy. This might create the
appearance that certain treatments are effective, even if they
are not, and complicates the study of treatments for dermatophytosis. It is clear in both human beings and cats that
a few individuals fail to develop an appropriate cellular immune response to the fungus, and fail to clear the infection
spontaneously. In humans, there is evidence that chronic
dermatophytosis involves hereditary factors, and we suspect
that the same may be true in cats.
The best treatment protocols combine 3 approaches,
including topical treatment, systemic treatment, and environmental treatment. Topical treatment of the cat serves to
inactivate infective material and prevent its spread to other
individuals or to the environment, but probably does not
shorten the course of infection in the individual cat. The best
topical products include lime-sulfur dips, enilconazole dips,
and possibly miconazole, ketoconazole, or chlorhexidine
shampoos. Systemic treatment serves to shorten the time to
recovery; drugs of choice in cats currently include griseofulvin and itraconazole. Recent studies suggest that itraconazole can be used in pulse-treatment regimens (e.g., every
other week), which are just as effective, but easier and less
expensive for the owner. Many common environmental disinfectants are not very active against dermatophyte-infected
hair fragments. Products with an oxidizing action (chlorine,
chlorine dioxide, peroxide) appear to have the best actions.
Enilconazole is a very effective environmental disinfectant,
in countries where approved.
Alternative antifungal treatments are useful for resistant strains or in special cases. Fluconzole has a nearly identical spectrum to itraconazole, but is not well-studied for feline use, and has no particular advantage. Terbinafine, in initial studies, is effective for some strains of M. canis at 10-30
mg/kg once daily, but may induce elevations in liver enzymes. Large series of case studies suggest that lufenuron
may be effective for dermatophytosis, but this has not yet
been confirmed by a controlled, scientific study. The current
collective opinion of veterinary dermatologists is that
lufenuron may be successful for some cases of feline dermatophytosis but unsuccessful in others; it is less successful
in cattery outbreaks than for individual animals; and that
more successes are reported at higher doses (approx. 80
mg/kg orally every 2 weeks). Fungal vaccines have, to date,
not provided substantial benefit in prevention or treatment of
this disease in cats. Their remarkable success in cattle ringworm holds hope that in the future, effective vaccines will be
developed for cats as well.
When working with infected catteries, it is especially
critical that the “3-pronged” approach to treatment be followed. Initially, it is important to isolate obviously-infected
cats from possibly-uninfected cats. During the treatment
process, fungal cultures should be collected from all cats
every 2-4 weeks to monitor the status of the decontamination
effort. Before being released as “infection-free,” each cat
should have no visible lesions at all, and at least two successive negative fungal cultures taken by the toothbrush
method. After cattery decontamination, the cattery should be
advised to construct an isolation area into which each new
cat is introduced. Newly-introduced cats should be lesionfree and culture-negative before introducing them to the
main cat group.
111
Aggressive medical treatment of severe otitis
externa/media
Douglas J. DeBoer
Though surgical treatment is clearly indicated for some
pets with otitis externa, a substantial number of animals with
even very severe, chronic ear disease can be helped with aggressive medical treatment. Aggressive medical treatment is
often desirable immediately prior to ear surgery, to increase
chances for success. This lecture describes one approach to
aggressive medical treatment of severe otitis.
At the preliminary visit, the patient is evaluated by examination, otoscopy, cytology, and culture and sensitivity. In
addition, a list of possible underlying causes must be made;
chronic ear disease most often happens because there is a
predisposing factor that is keeping the pet’s ears inflamed or
otherwise susceptible to growth of microorganisms.
The important objectives of initial treatment are to open
the ear canal, treat the infection, and use response to treatment as a prognostic factor. Opening the ear canal is one of
the most important principles of treatment, as it will allow
increased air circulation, permit exudate to escape, and permit medications to reach the deeper tissues of the canal. If
the ear canal is occluded by edema and/or hyperplasia, these
changes are often reversible by brief (2 weeks) treatment
with corticosteroids (prednisone, 2-3 mg/kd/day); if the
more chronic changes of scarring or calcification are present, these changes are irreversible. Regarding treatment of
the infection itself, initial therapy is based upon cytology
and culture/sensitivity. For many patients, topical treatments
are not appropriate initially; the canal may be to occluded or
painful for this to be effective. Systemic therapy is indicated, with antibiotics and/or antifungal drugs. Thus, for the
initial 2 weeks, the patient is receiving high-dose prednisone, plus systemic antimicrobials.
After 2 weeks, the patient must be rechecked, and the response to initial treatment is a good prognostic indicator.
Hopefully, the pet will be more comfortable, with canal occlusion notably better and less exudate; the pet may permit
examination without struggling. This suggests successful
lessening of the occlusive disease and that continued medical treatment will likely be beneficial. Conversely, if the ear
canals are minimally changed and still very narrowed, these
changes probably involve calcification and scarring, and are
likely not medically reversible. Surgery (bulla osteotomy,
lateral ear resection, and/or ear canal ablation) may be the
best option in this event.
At this 2-week evaluation, re-examination and cytology
are performed. The animal is placed under a general anesthetic, and the external and middle ears are evaluated radiographically, preferably with a CT scan. If the scan demonstrates only fluid and debris in the middle ear, this can effectively be removed using the procedure “middle ear irrigation”. If the scan
demonstrates solid soft tissue in the bulla, bulla osteotomy or
other appropriate surgery is preferred. To perform a middle ear
irrigation, a plastic, open-end tomcat catheter is introduced into the external ear canal through the otoscope, and passed
through the ventral aspect of the tympanic membrane (if present), past the membrane and into the middle ear. One can verify that the catheter is in the middle ear by feeling the end of
the catheter tapping against the bone of the bulla wall. It is best
at this time to obtain additional material from the middle ear
for culture. The middle ear is flushed vigorously with saline
solution until all debris and pus has been eliminated. This may
take from 10 to 30 minutes. After the procedure, the treatment
goals are to kill microorganisms in the middle ear and ear
canal, keep the ear canal open, and reduce inflammation, discomfort, and cerumen production. To accomplish this, the animal is treated with topical and systemic antimicrobials (based
on culture results), topical corticosteroids, and a continuing
declining-dose course of prednisone. A brief course of pain
medication may be desirable after the procedure.
Two weeks later, the animal is examined again, with otoscopy and cytology. The owner should report definite improvement in clinical signs, and the number of organisms
present on cytology should be dramatically reduced. The
same treatment is continued, with recheck examinations approximately every 2 to 4 weeks until the ear appears normal
and asymptomatic.
Following resolution of the current infection, consideration must be again given to underlying causes, especially in
pets with chronic bilateral disease. For example, in young
dogs, underlying atopy or food allergy are common causes
of bilateral inflammatory ear disease. At this point, the owner may elect to pursue diagnostic evaluation for these causes. Alternatively, and especially if the ears are the only clinical signs of the allergy, maintenance treatment (2 to 3 time
weekly) with topical corticosteroid-only ear drops is useful,
along with periodic (every 1-2 weeks) cleaning with an antimicrobial cleaner.
113
Treating Pseudomonas otitis
Douglas J. DeBoer
Infection of the external and middle ear with Pseudomonas
bacteria can be a challenging clinical problem. It is first important to realize that the mere presence of the bacterium is
not generally sufficient to cause infection; the normal ear
canal is quite resistant to growth of such organisms. Additional factors must be present that change the physiology of
the ear canal in order for Pseudomonas infections to occur.
The most common factors include the presence of underlying
inflammatory ear disease, and the presence of notable physical occlusion from masses, edema, or hypertrophic changes
in the ear canal.
Thus, when treating Pseudomonas otitis, it is critical that
ALL of the following factors be considered; your treatment
must be aimed at more than the organism itself!
(1) any occlusive disease of the ear canal MUST be reversed to the extent possible. High-dose oral corticosteroids
will reverse inflammation and hypertrophic changes; if scarring, masses, or calcification are present, surgery may be required. Simply “opening the ear canal up” to increased air circulation generally results in substantial improvement of the
infection.
(2) inflammatory changes in the ear canal must be reversed using systemic and/or topical corticosteroid preparations.
(3) the ear canal must be cleaned of pus and debris as thoroughly as possible. This involves thorough cleansing under
anesthesia, including middle ear irrigation if radiographic
studies indicate there is debris in the middle ear.
(4) the organism must be attacked with topical antibiotics,
and if the infection is especially severe or in any patient with
middle ear disease, systemic antibiotics must be used as well.
It must be emphasized that systemic antibiotic selection
for Pseudomonas ear infections must be based on culture and
sensitivity testing, ideally done by the minimum inhibitory
concentration (MIC) method. In addition, the laboratory
should take care to isolate and identify different strains of the
organism if present, not merely test the predominant isolate. It
is not uncommon for an ear to contain two or more strains of
Pseudomonas, each with a different pattern of antibiotic sensitivity. Aminoglycosides are not ideal choices for systemic
therapy, due to their nephrotoxic effects. Many strains of
Pseudomonas are still sensitive to fluoroquinolones. It is important to realize that the various available fluoroquinolones
vary as far as our ability to uniformly achieve tissue concentrations that are at least 8X MIC, and that when this is possi-
ble, it always requires a dose on the very high end of the
dosage range. For example, enrofloxacin or ciprofloxacin
should be used at 20 mg/kg once daily for Pseudomonas ear
infections; use of dosages less than this may not be effective
and/or may promote development of drug resistance. If the organism is not sensitive to fluoroquinolones, systemic treatment will necessitate subcutaneous injections by the owner at
home, at least 3 times daily. Using injectable antibiotics such
as ticarcillin, ticarcillin-clavulanic acid, ceftazidime, or aztreonam is extremely expensive.
Regarding topical treatment of Pseudomonas ear infections, a few strains are still sensitive to gentamicin, and gentamicin-corticosteroid combination products are useful in this
case. For fluoroquinolone-sensitive strains, enrofloxacin ear
drops (formulated commercially or by dilution of injectable solution) are valuable. Some clinicians have found polymixin E
to be effective in other strains. With strains that are resistant to
gentamicin or enrofloxacin, it is often necessary to formulate
an ear drop using the injectable form of an antibiotic such as
ticarcillin, tobramycin, amikacin, or ceftazidime. Regarding
dilution to use, a general rule is that the injectable solutions,
when diluted 1/20 in saline, will be at a concentration that is at
least 1 to 2 logs above the MIC of the organism. When formulating an ear drop in this manner, one must be careful to pay attention to the stability of the antibiotic once diluted. Most solutions will have to be kept in the refrigerator, or frozen in portions, in order to maintain good activity. The antibiotic package insert generally includes stability information.
Non-antibiotic components of topical ear preparations that
may inhibit growth of Pseudomonas include silver sulfadiazine (the silver ion is responsible for inhibiting bacterial
growth) or buffered EDTA solutions (the EDTA functions to
chelate metals that may be important growth factors, and to
inhibit bacterial efflux pumps – and thus may enhance the effect of antibiotics).
Treatment of Pseudomonas otitis is monitored by examination and cytology, every 2 to 4 weeks. Treatment should be
continued for at least 2 weeks past a negative cytologic finding. At the end of therapy, it is preferable to stop all antibiotic
treatment for 2-3 days, then perform an additional culture to
verify that the organism has been eliminated. Following successful resolution of the infection, the underlying causes must
be corrected to reduce the probability of reinfection. Many
dogs require lifelong maintenance treatment with corticosteroid and/or disinfectant ear cleaning to prevent reinfection.
115
Can we really evaluate immunocompetence
in our patients?
Douglas J. DeBoer
Several skin diseases of companion animals are theorized to involve host immunodeficiency as at least part of the
pathogenesis. Evaluation of immunologic function of the patient seems to be a logical clinical step. “Immunostimulatory” therapy has therefore been proposed for some of these
diseases. However, is it possible to conduct a reasonable
evaluation of a patient’s immune system?
TESTS FOR EVALUATING ANTIBODY PRODUCTION: One of the simplest methods for initial evaluation of
immunologic function is to measure the total concentrations
of Ig in serum. This assay is typically available for IgG, IgM,
and IgA in dogs, cats, and horses. “Normal values” of serum
Ig concentration vary widely between individuals, over time
in the same individual, with the presence of concurrent diseases, and substantial variation has been reported between
results of kits from different manufacturers. Thus, the results
are likely to be important only if they are dramatically and
consistently lower than “normal.” Low serum IgA and/or
IgM have been reported in some dogs with recurrent pyoderma. Selective IgA deficiency has been reported in dogs,
manifesting as chronic, recurrent respiratory and skin infections. Measuring serum total antibody levels is a very crude
and inexact method of evaluating the overall immune system. Importantly, therapy or the disease process itself may
modify serum Ig levels as an incidental effect; the mere finding of a low serum Ig level does not prove cause and effect.
A normal animal, when injected with a routine vaccine
like canine distemper virus, mounts a strong, specific, and
long-lasting antibody titer against the vaccine antigens. This
principle can be used as another crude measure of immunologic function. A serum sample is obtained, and then a dose
of a routine annual “booster” vaccination is given. A second
serum sample is obtained 3 to 6 weeks later, and both samples are tested for specific antibody titer against distemper
virus or parvovirus antigen. In some cases of immunodeficiency disease, the pre-vaccination titer will be low, and will
not rise following the booster vaccination: the animal’s immune system is not responding appropriately to injection of
a foreign antigen. This test provides compelling evidence of
immunologic dysfunction, though not all animals with immunodeficiency will fail to mount vaccine antigen titers; for
example, dogs with generalized demodicosis are reported to
be normal in this regard.
TESTS FOR EVALUATING CELLULAR IMMUNITY: The simplest indication of a possible cell-based immunologic defect is total lymphocyte count on a hemogram.
In general, in an otherwise healthy animal, lymphocyte
counts persistently less than 1000/µl have been taken as evidence for immunologic dysfunction. Lymphocyte blastogenesis is a crude measure of lymphocyte function, is subject to
numerous technical pitfalls, and is not generally available
outside of an institutional setting. Nevertheless, its use has
been reported in numerous canine skin diseases, including
demodicosis and recurrent pyoderma. Exclusively research
tools, various techniques are available to measure aspects of
neutrophil function such as chemotaxis, phagocytosis, and
killing. Neutrophil function has been assessed in early studies of recurrent staphylococcal pyoderma in dogs, with conflicting results. Immunohistology can be a valuable technique to evaluate the cellular response in disease. Histologic
sections are stained using antibodies specific for surface
markers present on cells such as lymphocytes and histiocytes, in an attempt to describe the nature and function of the
infiltrating cells. Perhaps the widest practical use of this
technique is in determining the clonal origin of neoplastic
lymphocytes in canine malignant lymphoma. In veterinary
dermatology, this technique has more recently been used on
a research basis to identify the characteristics of infiltrating
cells in canine demodicosis, in histiocytic diseases, and in
German Shepherd Dog pyoderma. Flow cytometry is an
everyday technique for monitoring immunologic function in
human beings, for example in HIV infection, but is only just
being developed for use in companion animals. The greatest
barriers to its use in veterinary medicine have been availability of specific antibody reagents that identify cell surface
markers, development of standardized instrument protocols,
and equipment availability.
Our ability to assess the many functional aspects of the
tremendously complex immune system of our animal patients is, at present, crude and inexact. From a practical
standpoint, the cost of performing an extensive immunologic evaluation must be balanced against the potential benefit
to the patient. If we can document an immunologic deficiency, is there anything we can do about it? In many, perhaps
most cases the answer is “no” – we cannot with present technology identify the specific immunologic lesion, and even if
we can, we do not have therapies that will correct the lesion.
117
The history of immunomodulation
in veterinary dermatology
Douglas J. DeBoer
A variety of chemical and biological substances have
been used in an attempt to “nonspecifically stimulate” the
immune system in several chronic diseases with suspected
components of immunodeficiency. In the great majority of
cases, such use has been entirely empirical. Many literature
reports of use of immunomodulatory substances are case reports of one or two animals, or uncontrolled studies, such
that the true benefit of the substance cannot be determined.
Levamisole has received the most attention and study of
the immunomodulatory drugs. The mode of action of levamisole is still not known at the biochemical level. The
overall conclusions of the 1000+ studies on its use since
1971 are that (1) it restores depressed immune responses in
animals and humans, but has little to no effects in immunologically competent individuals; (2) its effects are related to its ability to improve deficient activities of
macrophages and T-lymphocytes; (3) numerous “immune
functions” can be augmented by levamisole, including
phagocytosis, chemotaxis, intracellular killing, delayed cutaneous hypersensitivity, and lymphocyte proliferation induced by antigens or mitogens; (4) clinical effects are
achieved only when it is used as an adjunct treatment, along
with some other primary treatment; (5) no one particular
initially-measured immune parameter seems to be predictive for later responsiveness to the drug; and (6) some patients respond, and some don’t. Levamisole has been evaluated as adjunct treatment for neoplastic diseases such as canine mammary cancer and lymphosarcoma, without
demonstrated effect; in cattle dermatophytosis; in dogs with
generalized demodicosis; and in feline eosinophilic granuloma, all with variable results.
The major use of cimetidine as an immunomodulatory
drug has centered on its ability to aid regression of tumors,
and only recently have mechanistic details of this effect been
uncovered. Cimetidine treatment after surgical resection of
human colorectal carcinoma results in a demonstrably higher mitogen-stimulated lymphocyte response in patients,
which strongly correlates with better 3-year survival rates.
This effect may occur by blocking high local histamine concentrations at the tumor site. In dogs, histamine produces a
dose-dependent inhibition of lymphocyte blastogenesis, an
effect that can be blocked by cimetidine (H2 block) but not
by diphenhydramine (H1 block). Cimetidine may block histamine-induced activation of H2-bearing suppressor lymphocytes. Cimetidine has been proposed as an immunostimulatory drug for uses in such conditions as recurrent pyoderma and demodicosis, but its efficacy in such diseases has not
been demonstrated.
Staphage Lysate, a preparation of Staphylococcus aureus
bacteria lysed by bacteriophage, is an immunomodulatory
bacterin originally developed for human use, and later used
for immunomodulation in recurrent canine superficial pyoderma. Its mechanism of action has, in rodent models, been
shown to include both antigen-specific and nonspecific effects, and effects on cell-mediated immunity as well as antibody titers. Propionibacterium acnes bacterin has a substantial number of reports describing its use in human medicine,
mostly under its former name, Corynebacterium parvum.
Early uses centered on possible effects as an anticancer immunotherapeutic treatment, but numerous trials with doubtful or marginal efficacy statistics have seen its use dwindle
over the years. Its use in animals has centered on treatment
of chronic skin infections, but carefully-done studies have
shown inconsistent results.
Miscellaneous biological immunomodulators that have
been proposed for veterinary use include Baypamun, an inactivated ovine parapoxvirus; muramyl dipeptide; and interferon alpha. None of these substances have been subjected to
careful study for treatment of animal skin diseases.
In addition to intentional attempts at therapeutic immunostimulation, it is important to recognize that unintended immunomodulation may occur during the course of treatment with “ordinary” drugs. Antimicrobials, for example,
have been shown in model systems to have multiple effects
on cytokine production, either through a direct action or
through release of bacterial endotoxin from killed organisms. The clinical consequences of these effects remain to be
discovered. Certain clinical conditions (for example, severe
inflammatory disease) may alter measured cytokine profiles
substantially. In addition, caution must be exercised in conducting studies that use multiple-drug treatments, as unintended effects of a concurrently-administered medication
could possibly overwhelm the actions of the actual drug under study.
119
Fluoroquinolone confusion-how to select a drug
Douglas J. DeBoer
Fluoroquinolone drugs inhibit DNA gyrase, an enzyme
necessary for cell replication. There are multiple ways that
an organism can become resistant to fluoroquinolone drugs,
and Pseudomonas seems especially clever in this regard. All
fluoroquinolone drugs are contraindicated in juvenile dogs,
and there is substantial recent concern regarding retinal disease caused by these drugs in cats. Fluoroquinolones are extremely valuable drugs for certain very resistant bacteria,
and it is desirable to preserve their value for such infections.
Thus, to help prevent promotion of fluoroquinolone-resistant
bacterial strains, these drugs should be reserved for infections where they are truly needed and alternatives are not
available.
The dosage of fluoroquinolone drugs is typically given
as a rather wide range. It is up to the veterinarian’s clinical experience, nature and severity of the disease, and type
and sensitivity of the pathogen to determine what the
proper dosage will be for each patient. In particular, the
organism, the tissue of interest, and the pharmacokinetics
of the drug must be known in order to make a correct judgment. Regarding the organism, it is most helpful to know
the minimum inhibitory concentration (MIC) for the antibiotic in question; sensitivity testing based on disk diffusion methods is less valuable. Sensitivity testing by MIC
is becoming increasingly available at commercial laboratories.
Antibiotics may exert their effects on bacteria in either a
time-dependent or a concentration-dependent manner, and
fluoroquinolones fall into the latter category. Thus, when using a fluoroquinolone, an important therapeutic goal is to
have the peak antibiotic concentration in the target tissue be
very high, even if the peak concentration lasts only a short
time. This means that fluoroquinolones should generally be
administered in a single daily dose rather than divided into
two or more doses. Pharmacologists tell us that the best clinical success will be obtained if we can achieve peak tissue
concentrations that are 8-10 times the MIC of the organism
– and that should be our goal if possible.
To evaluate the predicted success of a fluoroquinolone
antibiotic against a given pathogen, start with the following
exercise: determine the MIC of the organism (in ug/ml),
from laboratory testing or from literature supplied by the
drug manufacturer. Multiply this by 8-10; this will give the
desired peak antibiotic concentration. Now examine pharmacokinetic data for the antibiotic, which is supplied by the
manufacturer, and determine what peak concentrations can
be achieved using various dosages within the recommended
range. In addition, examine information on the ability of that
antibiotic to concentrate in various tissues. If you can truly
achieve a tissue concentration of 8-10 times the organism’s
MIC, the chances for success are good.
General rules include the following: coliform bacteria
typically have very low MICs for fluoroquinolones (and thus
are very sensitive); staphylococci are intermediate; and
Pseudomonas aeruginosa has very high MICs (implying it
will be most resistant and/or require the highest doses). Fluoroquinolones are typically excreted in urine; urine concentrations are often 20 or more times those in plasma, meaning
that these drugs are often excellent for urinary infections.
Topical treatment with fluoroquinolones in an otic formulation creates extremely high concentrations in the ear canal,
much higher than the MIC for even many difficult organisms. Thus, these drugs may be effective in uncomplicated
otitis externa (infections not involving bone or soft tissue of
the middle ear) even when a “sensitivity test” says that the
organism is resistant.
Fluoroquinolones vary from drug to drug in their pharmacokinetic properties and attainable plasma concentrations
within the recommended dosage range. Do not assume these
drugs are interchangeable for all infections, and do not assume that a newer drug is necessarily better for a given infection! Manufacturer literature often emphasizes ‘enhanced’ pharmacologic properties of certain fluoroquinolone
drugs, but these properties are often not yet proven to result
in superior clinical effect. Unfortunately, controlled studies
that directly compare efficacy of different fluoroquinolones
currently on the market are uncommon.
It is not always possible to predict in vivo efficacy from
in vitro data. Other factors related to host, disease, or drug
may make the infection more or less clinically responsive to
a drug. However, the above calculations are a useful starting
point in choosing which drug to use, and at which dose.
121
Clinical challenges in veterinary dermatology
Douglas J. DeBoer
This lecture will present several diagnostic and treatment
dilemmas encountered by dermatologists, as illustrated by
cases, and suggested approaches to their resolution.
CHALLENGE #1 – THE DOG THAT WON’T GROW
HAIR. Though the most common endocrine/metabolic diseases that cause alopecia are hypothyroidism and hyperadrenocorticism, a disturbing number of patients with apparently “endocrine alopecia” are not hypothyroid or Cushingoid! In such cases, skin biopsy (and the opinion of an expert dermatopathologist) is useful to insure that the histologic changes are consistent with endocrine disease and not
with diseases such as pattern baldness, flank alopecia, etc. If
the disease appears to be endocrine, spaying or neutering intact animals is recommended, as this manipulation may produce hair regrowth regardless of the underlying endocrine
pathology. In general, measurement of basal serum sex hormone concentrations has little correlation with the presence
of any “sex hormone-related alopecia”. The clinical syndrome known as “Alopecia X” is under intensive investigation, and may represent altered steroid hormone biosynthesis in the adrenal gland. Some authors advise measurement
of various steroid hormone intermediates before and after
ACTH administration as a diagnostic test, but this procedure
is not widely available. Dogs with “Alopecia X” have been
successfully treated with low-dose mitotane protocols, but
the risk of iatrogenic HYPOadrenocorticism may make this
treatment unwise. Recently, oral melatonin has been evaluated for treatment of this syndrome, with some hair regrowth
in 40-50% of patients.
CHALLENGE #2 – THE DOG WITH RECURRENT
SUPERFICIAL STAPHYLOCOCCAL INFECTION. Superficial staphylococcal infections produce lesions and pru-
ritus of varying (but usually moderate to severe) pruritus. In
some cases, the infection and pruritus is completely antibiotic-responsive, but returns within 1-4 weeks after discontinuation of antibiotic treatment. All such patients should be
evaluated thoroughly for parasitisms, underlying systemic
diseases, and allergic diseases such as food allergy and
atopic dermatitis. In the syndrome “idiopathic recurrent superficial pyoderma” all laboratory evaluations will be normal despite the continually recurring infections. To maintain remission, initially consider trying frequent application
of topical products containing chlorhexidine as a preventive
measure. A second alternative is the use of “immunomodulatory” drugs or bacterins. Many such treatments are poorly studied. Administration of levamisole or cimetidine has
not met with much success in maintaining remissions.
Staphylococcal bacterin products, including autogenous
bacterins or commercial products such as Staphage Lysate,
are effective in maintaining remission in 50-70% of dogs.
As a last resort, “pulse-therapy” with antibiotics is effective
for many dogs.
CHALLENGE #3 – THE DOG WITH SEVERE SEBORRHEIC DISEASE. This author has a strong bias towards
performing skin biopsy in dogs with severe seborrheic diseases. It is important first to identify and treat secondary infections that are present, as these may obscure the important
histologic changes. Following resolution of the infection, the
main goal of skin biopsy is to attempt to ascertain if the histologic changes are consistent with primary or secondary seborrhea. In addition, certain less common scaling/crusting
diseases (such as granulomatous sebaceous adenitis, “vitamin A-responsive dermatosis”, zinc-responsive dermatosis,
etc.) are only diagnosable by use of histology.
123
Approach to respiratory distress:
how to see where is the problem how to treat the problem
Kenneth J. Drobatz
DVM, DACVIM, DACVECC - Philadelphia, PA
INTRODUCTION
Respiratory distress is a common presenting complaint
in veterinary emergency medicine. Animals with respiratory
distress represent a diagnostic and therapeutic challenge.
The initial approach to these patients can often make the difference between life and death in this acute phase of their
disease.
SIGNS OF RESPIRATORY DISTRESS
When an animal develops difficulty in oxygenation it
makes attempts to improve oxygenation. This may be manifested simply as an increase in respiratory rate or more severely as extended head and neck posture with abduction of
the elbows, flaring of the nares, and open-mouth breathing.
With severe resistance to movement of air, there may be
paradoxical motion of the chest and abdomen. Normally,
the chest and abdomen move together during respiration.
On inspiration the abdominal wall and chest wall move out
and during expiration they both move in. Paradoxical motion occurs when they move in opposite directions (e.g. the
chest moves in and the abdomen moves out. This suggests
extreme resistance to air movement. Dogs are more demonstrative in manifesting clinical signs of respiratory distress.
Some cats may have severe respiratory dysfunction and only manifest tachypnea at rest. In either species, postural
changes suggest extreme respiratory distress and warrant
immediate attention.
INITIAL APPROACH TO THE PATIENT
At presentation, a patent airway should be assured. If the
airway is not patent, then attempts should be made to clear
the airway and intubate the patient. If an obstruction prevents intubation, then emergency tracheostomy should be
performed if it will by-pass the obstruction and assure a
patent airway. To provide perspective, it is extremely rare
that an emergency tracheostomy is required. Most patients
can be intubated and the tracheostomy then performed in a
more controlled way.
Immediate oxygen supplementation should be provided
while assessing for a patent airway. Our first choice is via
mask. This is convenient, inexpensive, and provides an opportunity to examine the patient as well as do procedures if
necessary. Other modes of oxygen supplementation include
an enriched oxygen environment (oxygen cage or tent),
transtracheal catheter, nasal oxygen, and intubation with
positive pressure ventilation. Each has its advantages and
disadvantages.
The oxygen cage is an excellent method for oxygen supplementation, but has some major disadvantages that should
be considered. The animal is isolated from the caregivers
and physical monitoring and other therapies cannot be applied without interrupting oxygen supply. Each time the
oxygen cage is opened, the animal’s Fi02 will decrease and
compromise the patient. In addition, placing an animal in the
oxygen cage can give one a false sense of security thinking
that the patient is ok. Other disadvantages include the expense, large amounts of oxygen are needed to fill the cage,
large dogs can sometimes overheat smaller cages, and the
large size of the cage itself. Advantages of this method include minimal stress to the patient and carbon dioxide concentration, temperature, and humidity can be controlled. In
addition, many cages allow for nebulization. If used judiciously with recognition of its limitations, oxygen supplementation via an oxygen cage can be advantageous.
Nasal oxygen supplementation is an inexpensive method
of oxygen supplementation and can be done using commonly available equipment. Its major medical advantage is that
oxygen supplementation can be continuously given while
procedures and physical assessments are performed. Inspired oxygen concentration may be as high as 40-60%. Disadvantages include that it can be stressful to place and some
animals will not tolerate the nasal catheter. This is not a
mode of oxygen supplementation that we utilize when the
animal first presents, but it is utilized on hospitalized animals that need ongoing oxygen supplementation.
An oxygen tent, plastic bag, or an E. collar with plastic
wrap over the top with oxygen supplied into this “microenvironment” can be an effective means of oxygen supplementation. Fi02 of nearly 100% can be achieved with high
oxygen flow. Disadvantages include that some animals will
not tolerate this method, condensation can develop inside the
124
plastic cover, the animal can overheat and carbon dioxide
can build up. Leaving an opening at the top for heat, carbon
dioxide and condensation to escape can minimize some of
these complications.
Transtracheal oxygen supplementation is rarely used in
our practice. It can be used to provide oxygen support with
upper airway obstruction if the catheter is placed between
the lungs and the obstruction.
Positive pressure ventilation is the ultimate in control of
ventilation but is more invasive than other methods and requires sedation/anesthesia. One can control nearly all aspects of ventilation with this method. Indications for positive
pressure ventilation include hypoventilation, persistent hypoxemia despite high-inspired oxygen concentration, and
respiratory fatigue.
Once oxygen supplementation has been provided, further
evaluation can be performed if the patient’s condition will
allow it. Animals that are in respiratory distress can be difficult work with. One must provide oxygen and assess the patient while minimizing stress to the patient. Excessive stress
or struggling can be catastrophic in an animal with respiratory distress. Even dorsal recumbency positioning for ventral dorsal radiographs can be devastating. Any stress that
causes the patient to consume more oxygen or decrease inspired oxygen concentration from breath holding while
struggling can severely compromise some patients. This can
be understood by looking at the hemoglobin/oxygen saturation curve below:
clues may be obtained from auscultation of the thorax and
neck, as well as observation of the respiratory pattern.
Respiratory patterns may be helpful in localizing the
problem. Irregular respiratory rhythms are almost invariably
associated with central nervous system abnormalities. Poor
airway compliance due to pulmonary parenchymal disease
or restricted lung expansion often results in rapid and shallow respirations. Airway narrowing or fixed obstruction may
be manifested as very slow and prolonged respirations. Dynamic obstructions result in resistance to airway flow during
inspiration or expiration. If the dynamic obstruction is extrathoracic (e.g. laryngeal paralysis) then respiratory difficulty is mainly on inspiration. If respiratory distress occurs
more severely on expiration, then the obstruction is most
likely intrathoracic (intrathoracic collapsing trachea, feline
asthma, etc.).
It is convenient from a diagnostic point of view to approach respiratory distress in an algorithmic fashion.
Heart Disease
Animals with signs of respiratory distress are often around
a hemoglobin saturation of 90% or less. This is at about the
steep portion of the curve. Any minor changes in Pa02 (x-axis) can result in relatively dramatic changes in the hemoglobin saturation with oxygen and hence a dramatic decrease in
total oxygen content of the blood.
At presentation we also like to place an intravenous
catheter and collect blood for an emergency database
(packed cell volume, total solids, dipstick BUN, blood glucose and a blood smear). This minimal amount of bloodwork
can provide valuable additional information about the patient and sometimes provides a diagnosis of the cause of the
respiratory distress. In addition, intravenous access allows
for the immediate administration of fluids or drugs.
GENERAL DIAGNOSTIC THOUGHTS
During or after assuring a patent airway, providing oxygen supplementation, and acquiring intravenous access, examination of the patient should be done. The most important
If the answer is “yes” to this first question then empirical
therapy for heart failure should be considered if the patient’s
condition will not allow further diagnostic tests (e.g. thoracic radiographs). Intravenous or intramuscular furosemide
(2mg/kg in the dog, 1mg/kg in the cat) should be given. In
severely affected dogs we also use nitroprusside (arterial and
venous vasodilator) and begin a constant rate of infusion at
1ug/kg/min and slowly increase every 15 minutes. In most
dogs, the effective dose is usually between 5 - 10 ug/kg/min.
This is a very potent vasodilator and may cause severe hypotension. Therefore, blood pressure monitoring is warranted when using this drug. If used judiciously, this drug is very
effective in relieving respiratory distress in patients with severe pulmonary edema secondary to heart failure. It is rare
that we use this drug in cats. Most commonly, if vasodilatation is necessary in cats with heart failure, 2% nitroglycerine
paste our first drug of choice. An area on the flank, axilla or
groin is clipped and the _ inch of paste is applied (wear
gloves). In the acute emergency situation, furosemide and
these vasodilators are our first line treatments. In mild to
moderate heart failure patients, oxygen supplementation and
furosemide is often all that is needed for initial stabilization.
Endomyocarditis is an inflammatory condition of the endocardium and the pulmonary vessels and therefore does not
125
fit well into any category but will be discussed here. The typical presentation of this condition is a cat that presents with
respiratory difficulty 1-3 days or so after a stressful event
such a declaw or neutering. These animals can often have severe respiratory compromise with generalized increased
bronchovesicular sounds or crackles. The heart usually
sounds relatively normal. Radiographically, the pulmonary
opacities are predominantly interstitial with a diffuse distribution. Echocardiographically, some appear to have a
“bright” endocardium. The treatment that we have used for
this condition is aggressive diuretic therapy with furosemide
and oxygen supplementation. Resolution of this problem can
sometimes be difficult.
Upper Airway Disease
If the answer to the first question is “no”, then consideration should be directed at pulmonary or extrapulmonary
causes of the respiratory distress. The two main areas of the
pulmonary tree are the airways and the pulmonary parenchyma. Dogs may develop upper or lower airway problems. The
most common is upper airway disease (in contrast to cats).
Upper airway disease may involve the pharynx, larynx, or
trachea. Problems in these areas include edema, infection,
foreign bodies, neoplasia, as well as neuromuscular and degenerative diseases. The most common upper airway diseases we see in dogs are laryngeal paralysis (typically larger breeds) and collapsing trachea (typically smaller breeds).
One of the hallmark clinical signs of upper airway disease is
loud respiration or stridor. These are heard without the
stethoscope. If a patient presents with loud respirations, upper airway disease should be strongly considered. This does
not preclude the existence of other causes of respiratory distress, but does warrant investigation of the upper airway. Patients with extra-thoracic dynamic airway obstruction (e.g.
laryngeal paralysis) will have severe inspiratory difficulty.
Collapsing trachea patients may have both inspiratory and
expiratory difficulty depending upon the location of the collapsing segments of the trachea.
Patients with dynamic airway obstruction such as laryngeal paralysis or collapsing trachea may present in severe respiratory distress. A vicious cycle develops in these
patients in which something places a demand on the respiratory system (e.g. exercise) causing greater pressure
changes within the upper respiratory tree. This results in
greater collapse of the affected area causing inefficient gas
exchange, further stimulating the patient to breath harder.
Pulmonary edema (cardiogenic/noncardiogenic)
This, in turn, worsens the dynamic obstruction and the cycle continues. Because of the interference of gas exchange,
these patients may also develop very high body temperatures causing even greater demands on respiration. It is important to break this cycle. If the patient’s pulses and perfusion is adequate, we sedate with acepromazine (30 - 50
ug/kg intravenously or IM), and continue supplementing
with oxygen. This is very effective and usually within 15 to
30 minutes the respiratory stress is diminished and the patient is breathing relatively comfortably. We also try cooling the animal (spraying water on the fur coat) if the body
temperature is greater then 105F. Some patients may benefit from anti-inflammatory doses of corticosteroids because
of laryngeal or tracheal edema.
It is extremely rare that emergency laryngeal surgery is
required in patients with laryngeal paralysis. The above
medical therapy is generally quite effective. If a patient is in
acute distress, and you are concerned about imminent collapse, anesthesia and intubation will relieve the distress immediately if laryngeal paralysis is the cause. It should be remembered that waking patients (from anesthesia) with dynamic upper airway obstruction is extremely difficult. The
excitement phase of recovery causes dynamic airway pressure changes resulting in collapse of the affected area of the
pulmonary tree, starting the vicious cycle again.
Pulmonary Parenchymal Disease
Pulmonary parenchymal disease may be due to edema
(cardiogenic or noncardiogenic), hemorrhage, infection, or
infiltrative processes. Harsh respiratory sounds (increased
bronchovesicular sounds) or pulmonary crackles are often
heard on auscultation. Crackles are not heard as commonly
in cats compared to dogs. The location of these sounds may
help in the diagnosis. For example, a cranioventral distribution or right middle lung lobe distribution makes aspiration
pneumonia a likely possibility, while a perihilar location
makes a cardiogenic cause a suspicion. Harsh respiratory
sounds or pulmonary crackles in the absence of auscultable
cardiac abnormalities make pulmonary parenchymal disease the most likely cause of the respiratory distress. A thorough clinical history, thoracic radiographs, bloodwork, tracheal wash, bronchoscopy, or even lung biopsy may be required to definitively diagnose the problem so that appropriate therapy can be applied. The following table lists some
of the causes of pulmonary parenchymal disease that we see
in our hospital:
Pneumonia (aspiration, fungal, viral)
Toxin inhalation
Hemorrhage
Pulmonary contusion
Uremic pneumonitis
Pulmonary thromboembolism
Neoplasia
Smoke inhalation
ARDS
PIE
Feline asthma
Heartworm
126
Pulmonary edema due to cardiac disease is usually has a
perihilar distribution in dogs but can be patchy and diffuse in
cats. The majority of dogs will have a loud murmur or persistent cardiac arrhythmia if heart disease is the cause of pulmonary edema. Most cats will have auscultable cardiac abnormalities such as a murmur or gallop rhythm but auscultable cardiac abnormalities are not as consistently noted
in cats with heart disease compared to dogs. Thoracic radiographs generally show some degree of cardiomegaly in
most animals. Cardiac ultrasound often confirms cardiac
disease as the cause of the pulmonary edema but this method
is not commonly or readily available in a general practice or
most emergency clinics. In most instances, cardiac disease
as the cause of the pulmonary edema can be inferred from
the signalment, history, physical examination, and thoracic
radiograph findings.
Noncardiogenic pulmonary edema is fluid accumulation
in the lungs not due to heart disease. A specific cause of noncardiogenic pulmonary edema is neurogenic pulmonary edema. The four most commonly recognized causes of neurogenic pulmonary edema include upper airway obstruction,
head trauma, seizures, and electrocution. This cause of pulmonary edema is characterized by an acute onset (typically
within minutes) of respiratory abnormalities after one of the
four listed insults. The degree of pulmonary edema can very
from mild to severe involving all lungfields. The typical pattern is interstitial to alveolar with the distribution initially
starting in the caudodorsal area. The treatment for this condition is supportive with oxygen supplementation and diuretics (furosemide 2-4 mg/kg IV q6-8h). The animals with
upper airway obstruction or head trauma tend to be more severely affected with pulmonary edema compared to animals
with seizures or electrocution. Some animals require positive pressure ventilation and synthetic colloid support because of the severity of the pulmonary edema and the massive loss of high protein fluid into the lungs. These animals
have a poor prognosis and usually die. Most animals with
neurogenic pulmonary edema are substantially improved or
dead from respiratory compromise within 48 hours of the inciting incident.
Spontaneous pulmonary hemorrhage is most commonly
due to rodenticide anticoagulant intoxication or thrombocytopenia. Supportive care with oxygen supplementation and
specific treatment of the underlying cause are the only options available to treat this problem.
Pulmonary thromboembolism (PTE) is challenging to diagnose as well as treat. Diagnosis in veterinary medicine is
most commonly arrived at using medical history, recognition
of concurrent diseases or drug therapies that are commonly
associated with PTE, a history of sudden onset of respiratory abnormalities, and thoracic radiograph findings. Thoracic
radiograph findings can vary and many times look completely normal. In fact, an animal with severe respiratory distress (not due to upper airway disease) that has normal appearing thoracic radiographs is highly suggestive of PTE.
Other radiographic sometimes seen with PTE include patchy
interstitial pattern, patchy alveolar pattern, and mild pleural.
Depending upon the severity of the PTE, the respiratory
signs can vary from just mild tachypnea to severe distress.
Treatment for PTE is primarily supportive with oxygen sup-
plementation, heparin therapy and specific therapy for the
associated cause. Thrombolytic therapy can be used but we
have had limited experience with this treatment.
ARDS or adult respiratory distress syndrome is recognized in dogs and cats. It is an inflammatory condition of the
lungs resulting in severe respiratory compromise with hypoxemia and decreased pulmonary compliance. It is characterized clinically by bilateral pulmonary infiltrates (on thoracic radiographs) and hypoxemia with normal heart function. There are also certain histological characteristics that
are recognized with ARDS. ARDS can be an end stage
process secondary to almost any inflammatory condition
within the lungs or any inflammatory condition remote from
the lungs such as pancreatitis, sepsis, trauma, etc.... Treatment is primarily supportive while the associated cause
treated.
Feline asthma is an airway hypersensitivity condition in
cats that results in bronchoconstriction, pulmonary air trapping, and increased respiratory secretions. The degree of respiratory distress can be mild to life threatening. Many owners describe that their cat is retching or coughing. Some
owners incorrectly think that their cat is vomiting. Most cats
have a prolonged expiratory phase with end expiratory
wheezes heard on auscultation. Rarely, a cat will present
with a barrel chest secondary to severe airway trapping. You
cannot auscult airway sounds because the animal is moving
so little air. Emergency therapy for cats with asthma and respiratory distress include oxygen supplementation, corticosteroids (Dexamethasone sodium phosphate 0.2mg/kg IV or
IM) and terbutaline (0.01 mg/kg IM or SQ). We generally
see improvement in respiratory rate and effort within 30
minutes to an hour after terbutaline injection.
Inhalation of toxins that affect the respiratory system are
relatively rare and will not be covered in this discussion.
Animals with severe uremia can develop signs of respiratory difficulty due to uremic pneumonitis. A diffuse interstitial pattern is typically noted. Therapy is primarily supportive with oxygen supplementation and treatment to resolve the uremia.
The most common cause of pneumonia in dogs at our
hospital is aspiration pneumonia. This is primarily diagnosed
based on the radiographic appearance of interstitial/alveolar
infiltrates in the cranioventral and right middle lung lobe areas. Treatment includes oxygen supplementation, nebulization and coupage, maintenance of hydration, broad-spectrum
antibiotics (ideally based on culture and sensitivity, and mild
exercise (walking) if possible. In addition, diagnostics and
therapy should also be directed at the underlying cause of
the vomiting.
Pulmonary contusions may vary from mild to severe
causing mild to severe respiratory distress. Increased bronchovesicular sounds and/or crackles are often heard or auscultation. Some dogs with severe contusions will have a soft
cough at presentation and can also have hemoptysis. Pulmonary contusions tend to get worse over the first twelve
hours or so. In addition, radiographic signs will lag behind
clinical signs by several hours. Treatment for pulmonary
contusions is primarily supportive with oxygen supplementation and judicious fluid therapy if resuscitation with fluids
for other problems (e.g. hypovolemia) is necessary. Respira-
tory signs tend to start improving after about 36 - 48 hours
in most cases.
Smoke inhalation is a relatively rare cause of respiratory
distress in dogs and cats. Respiratory changes can vary from
no clinical signs to severe respiratory distress. The majority
of dogs and cats have an increased respiratory rate. Upper
airway sounds may occur as a result of mucosa swelling
from irritation and thermal injury. Lower airway abnormalities are relatively common and are manifested as increased
bronchovesicular sounds and crackles. Expiratory wheezes
may be heard due to small airway narrowing from bronchoconstriction and mucosal swelling. Rarely, localized areas of decreased airway sounds may occur due to small airway obstruction from mucosal swelling, mucosal sloughing
and particulate debris. Thoracic radiographs provide additional assessment and monitoring of the respiratory system.
A variety of radiographic abnormalities may be noted including alveolar, interstitial, and peribronchial patterns.
Rarely, a collapsed lung lobe may occur as result of
bronchial obstruction from mucosal swelling, sloughing and
debris. As with most dynamic disease processes, thoracic radiographic changes lag behind the clinical appearance of the
animal.
Oxygen supplementation should be provided if hypoxemia is detected or signs of respiratory difficulty are noted.
Oxygen supplementation will also shorten the life span of
carboxyhemoglobin if it is present. Corticosteroids are controversial with some studies showing improvement and others showing detriment or no detectable effect. Antibiotics
should be given based on detection of infection and culture
and sensitivity results. Bronchodilators such as phosphodiesterase inhibitors or the beta-2 agonist terbutaline may help
relieve bronchoconstriction if it is present. Most animals
with smoke inhalation that make it to the veterinary hospital
alive tend to do well and survive to discharge. Dogs that are
not worse by the second day and have mild respiratory signs
will likely remain in the hospital approximately two days.
Dogs that have severe signs and have gotten worse by the
second day either die by 72 hours or remain hospitalized for
6-7 days before being discharged. Similarly, in a study on
cats with smoke exposure, the outcome for cats that survived
to be admitted to the veterinary hospital was good with none
of the cats dying spontaneously and only two requiring euthanasia due to severe neurologic or respiratory compromise.2 Overall, the survival rate was 91%. This rate is comparable to the 90% survival rate of humans with smoke inhalation only (no skin burns). When euthanasias were excluded, 100% of the cats survived. As in dogs, it appears that
if a cat can make it to the hospital alive, there is a good
chance that it will survive.
Extrapulmonary Diseases
Thoracic wall abnormalities such as rib fractures or flail
chest are relatively easy to diagnose. Diaphragmatic rupture
and pleural space abnormalities are not as obvious. Diaphragmatic rupture interferes with respiration via diaphragmatic dysfunction as well as producing a pleural space problem secondary to abdominal contents in the pleural space
127
and/or pleural effusion. Clinical findings include diminished
respiratory sounds either unilateral or bilateral as well as
well typical signs consistent with a restrictive pulmonary
disease (e.g. rapid, shallow respirations). Definitive diagnosis of diaphragmatic rupture requires thoracic radiographs,
ultrasound, or contrast radiography (upper GI or intraperitoneal). Definitive treatment of diaphragmatic rupture requires surgery.
Pleural effusion may cause respiratory distress depending upon its severity. Accumulation of fluid within the
pleural space may be due to a variety of causes including
congestive heart failure, neoplasia, empyema, vasculitis,
hepatic disorders, coagulopathy, pulmonary thrombosis,
diaphragmatic hernia, and chylothorax. Clinical signs of a
patient suffering from pleural effusion may be a result of
the underlying disease process as well as the effects of the
effusion itself. Respiratory signs are usually a result of restriction of expansion of the lungs resulting in small, rapid
respirations.
Effusions may be unilateral or bilateral. Diminished
ventral respiratory sounds are detected during auscultation
of the chest. If pleural effusion is suspected, thoracocentesis should be performed. As much fluid should be removed
as possible. Both sides of the thorax should be aspirated if
diminished sounds are detected bilaterally. Fluid analysis
should include PCV (if bloody), total solids, cytology, cell
count, aerobic and anaerobic culture, and measurement of
triglyceride concentration if indicated. Analysis of fluid
may be the most important diagnostic clue in patients with
pleural effusion. The following algorhythm provides a
summary of pleural fluid analysis.
Pneumothorax is a pleural space abnormality that may
occur spontaneously or secondary to trauma. Spontaneous
pneumothorax most commonly occurs in large breed dogs
and is usually secondary to a pulmonary parenchymal abnormality such as a cyst, bullae, bleb, or abscess. These patients often present in severe respiratory distress with bilaterally diminished respiratory sounds dorsally. A large
amount of air is often obtained during thoracocentesis. Both
sides of the thorax should be aspirated. Air should be removed until a negative result is obtained. If a negative result
cannot be obtained then chest tubes should be placed and a
constant vacuum applied.
128
Tension pneumothorax occurs when air continues to accumulate in the pleural space due to a one-way valve effect
at the leak. Air continues to accumulate causing pressures
greater than atmospheric. This causes progressive atelectasis
as well as interference with venous return resulting in poor
cardiac output. Immediate relief of the pneumothorax is required. A small intercostal incision into the pleural space
may rapidly relieve the pneumothorax. After removal of the
air, the incision should be sealed with a sterile dressing and
close monitoring for the reoccurrence of the pneumothorax
should be done. Chest tube placement is usually required in
patients where a negative pressure cannot be achieved during thoracocentesis or when large amounts of air repeatedly
accumulate.
Summary
Respiratory distress is a common presenting complaint
in emergency medicine. These patients, despite some appearing relatively stable, may quickly decompensate. Aggressive, yet judicious therapy should be provided to optimize the outcome. Disease categories causing respiratory
distress in dogs include cardiac disease, airway disease, pulmonary parenchymal disease, pleural space disease, thoracic
wall abnormalities and diaphragmatic rupture. The most
common causes of feline respiratory distress are hypertrophic cardiomyopathy, feline asthma, and pleural effusions. Because many of these patients are so compromised,
diagnostic tests may be limited until initial stabilization is
provided. Auscultation of the pulmonary and cardiovascular
system combined with signalment and a careful medical history may provide important clues to the underlying cause
and allow the clinician to provide judicious empirical therapy until definitive diagnostic procedures may be performed.
Key words
feline asthma
laryngeal paralysis
collapsing trachea
pulmonary thromboembolism
pulmonary hemorrhage
aspiration pneumonia
pneumothorax
pleural effusion
hypoxemia
uremic pneumonitis
neurogenic pulmonary edema
129
Diagnostic approach to the acute abdomen
Kenneth J. Drobatz
DVM, DACVIM, DACVECC - Associate Professor, Section of Critical Care
University of Pennylvania, School of Veterinary Medicine
INTRODUCTION
After initial stabilization of an animal with an acute abdomen, definitive diagnostic evaluation should be performed
to diagnose the underlying cause as soon as possible so that
definitive care can be provided. If the underlying cause can
be identified quickly and treated, the chances for more serious complications such as septic peritonitis or systemic inflammatory response syndrome and multiorgan dysfunction
syndrome can be minimized.
The extended database that includes a packed cell volume (PCV), total solids (TS), dipstick glucose, dipstick
BUN, blood smear, venous blood gas, and electrolytes including sodium, potassium, chloride, and ionized calcium
helps in rapidly providing a relatively well-rounded metabolic assessment of the patient and can sometimes provide
or point towards a diagnosis of the underlying cause.
PCV and TS should always be assessed together. Parallel
increases in both suggest dehydration and anecdotally seems
to be the most common problem in dogs and cats that present with an acute abdomen. A normal or increased PCV
with a normal to low total solids indicates protein loss from
the vasculature. In an animal with an acute abdomen, this
clinicopathologic picture is often associated with protein
loss in animals with peritonitis and should alert the clinician
of this possibility. Hemorrhagic gastroenteritis (HGE) is associated with a very high PCV (60-90%) and normal or low
total solids. An animal with an acute onset of vomiting and
bloody diarrhea with these changes in PCV and TS make
HGE the most likely diagnosis.
Hemorrhage most commonly results in a parallel decrease in the PCV and TS although in acute hemorrhage,
these changes may not be initially recognized until intravenous fluid therapy has been provided. Acute hemorrhage
in dogs can sometimes be recognized with a normal or increased PCV and normal or decreased total solids. Splenic
contraction in dogs makes total solids a more sensitive indicator of acute blood loss compared to PCV. The most common causes of acute hemorrhage in dogs with acute abdomen are splenic rupture (usually secondary to neoplasia)
and severe gastrointestinal hemorrhage from gastrointestinal
ulceration. In cats with an acute abdomen, the most common
cause of acute hemorrhage is abdominal hemorrhage secondary to hepatic neoplasia.
Blood glucose is easily and rapidly obtained by dipstick
methods and a glucometer. It is important to recognize that
the packed cell volume may affect the accuracy of these
methods. High packed cell volume often causes falsely low
glucose measurements and low packed cell volumes may
give falsely increased glucose measurements. This variation
is not consistent from manufacturer to manufacturer; therefore it is best to consult the manufacturer of your dipstick
and glucometer regarding these and other affects. Anecdotally, we think that we can improve the accuracy by measuring blood glucose on the plasma or serum instead of
whole blood. This is most easily done by using the plasma
off of a hematocrit tube after it has been centrifuged to measure PCV.
Increased blood glucose in a dog with an acute abdomen
can be associated with diabetes or transient diabetes associated with severe pancreatitis. Blood glucose can rarely be
quite high in dogs with extreme hypovolemia secondary to
severe abdominal or gastrointestinal hemorrhage. Physical
examination findings of extremely poor tissue perfusion are
evident and it is clear that the animal may die. We some
times call this the “death glucose” and associate it with massive catecholamine release from the extreme poor tissue perfusion. If perfusion is not correctly quickly in these dogs,
they will die. Increased blood glucose in cats may be associated with stress or diabetes. Hyperglycemia in cats is not as
useful diagnostically as compared to dogs.
Decreased blood glucose is often associated with sepsis
and warrants a more aggressive approach to find the underlying cause of the acute abdomen, particularly septic peritonitis. Rarely, extremely low blood glucose may occur as a
result of sepsis but more typically the blood glucose is usually in the 40-60 mg/dl range.
Dipstick BUN (Azostik, Miles Inc., Elkhart, IN) provides an estimate of azotemia in an animal with an acute abdomen. We have found this a useful screening method but it
does have some limitations. The dipstick gives only major
categories of BUN concentration. Overall, these dipsticks
are a reliable estimate of BUN, especially when BUN is low.
When performed properly, if the dipstick reading is low it is
accurate. At times, the dipstick has read very high and the
BUN is only mildly elevated. In the middle range or mildly
elevated categories the BUN can sometimes be very high but
the reading only records mild elevations. In summary, dip-
130
stick BUN is relatively accurate but should only be considered a screening test and actual measurements should be determined in questionable cases. Most animals with an acute
abdomen have a normal to increased BUN. Increased BUN
may be due to pre-renal, renal, or post-renal causes, which
should be investigated when increased BUN is detected.
Disproportional increases of BUN compared to creatinine
suggest possible gastrointestinal hemorrhage (as a source of
protein for the increased production of urea) or due to prerenal causes.
Reliable assessment of a blood smear depends upon the
production of a good quality blood smear. All cell lines
should be systematically evaluated including the red cell
line, white blood cells, and platelets.
The average number of platelets per monolayer field
under oil immersion should be obtained. In normal dogs
and cats, there are 11-25 platelets per field; each platelet in
a monolayer field under oil immersion is equivalent to approximately 15,000 platelets per microliter. The smear
should be screened at low power to search for platelet
clumps that may result in a falsely low platelet estimate
prior to evaluating the counting area. If there are more than
four to five platelets per field then it is unlikely that the
bleeding is strictly due to thrombocytopenia. Most patients
with spontaneous bleeding due to thrombocytopenia have
less than two platelets per oil immersion field. A decreased
number of platelets is one of the most consistent findings
in animals with DIC.
Animals with an acute abdomen may have DIC secondary to the systemic inflammation or massive peritoneal
inflammation.
A blood smear should be examined for evidence of regeneration (anisocytosis, polychromasia, etc) as well as for
the presence of neutrophils and platelets. Decrease in all parameters suggests a pancytopenia and possible bone marrow
problem. The morphology of the red blood cells should be
examined. Schistocytes and fragments of red blood cells are
suggestive in DIC. Heinz bodies are often seen in systemically ill cats. The smear should be scanned at lower power to
get an estimate of the number of white blood cells and then
at higher power to assess the character of the white blood
cells. A leukocytosis with a mature neutrophilia suggests an
inflammatory or infectious process. Severe inflammatory or
infectious processes may cause the release of less mature
neutrophils such as band cells. The absence of a leukocytosis or a left shift does not rule an inflammatory or infectious
process. A leukopenia can be due to decreased production or
sequestration of white blood cells. Viral infections such as
parvovirus can result in leukopenia as well as can administration of immunosuppressive drugs.
A venous blood gas provides an evaluation of metabolic
acid/base status. Animals that have severe vomiting due to a
high gastrointestinal obstruction can have a hypochloremic
metabolic alkalosis. In addition, these animals are often hypokalemic and hyponatremic. The combination of
hypochloremia, hypokalemia, hyponatremia and metabolic
alkalosis should prompt investigation into a high gastrointestinal or pyloric outflow obstruction. It should be kept in
mind that furosemide can cause similar acid/base and electrolyte changes. More often, metabolic acidosis is seen with
animals with an acute abdomen. This is most often due to severe diarrhea or lactic acidosis due to hypoperfusion.
Abdominal Radiographs
For detailed discussion, please see the notes on the radiography lecture elsewhere in these proceedings.
Abdominal Fluid Analysis:
Some of this information has been covered in the manuscript entitled “Acute Abdomen: Initial Assessment and Stabilization”.
If abdominal fluid is present in an animal with a
painful abdomen, it is important to obtain some for
analysis.
Abdominal fluid analysis can help rule out septic peritonitis and also possibly provide a diagnosis or direct further diagnostic investigation.
A pure transudate is grossly clear and is characterized by a total protein <2.5 g/dl and low cell count
(<500 cells/ul). There are few cells present and most are
either nondegenerate neutrophils or reactive mesothelial
cells. The most common causes of a pure transudate in
the abdomen include hypoalbuminemia and a portal venous obstruction.
A modified transudate is usually serous to serosanguineous
with a total protein between 2.5 - 5.0 g/dl and a moderate total
cell count (300-5500 cells/ul). Depending upon the cause there
may be variable numbers of red blood cells, nondegenerate
neutrophils, mesothelial cells, macrophages, and lymphocytes.
This type of effusion is often due to passive congestion of the
liver and viscera and impaired drainage of the lymphatics.
The most common causes are right-sided heart failure, dirofilariasis, and liver disease.
An exudate is often cloudy, has a total protein concentration greater than 3.0 grams/dl and a cell count greater
than 5000 to 7000/ul. The predominant cell type is the
neutrophil although numerous other cells may be present
as well. This is the most common type of free abdominal
fluid associated an acute abdomen. Exudates can be septic
or non-septic and making this classification can be challenging in these patients.
Septic exudates are characterized by the presence of intra and extracellular bacteria. In most animals with septic
peritonitis, cytological evidence of bacteria can be found,
particularly if one has patience and explores numerous microscopic fields and also examines the cytology of the sediment of the abdominal fluid. Rarely, septic peritonitis can be
present despite the absence of cytological evidence of bacteria in the fluid. In these instances, the clinician must use all
available information that can be obtained quickly to determine if exploratory surgery is warranted including signalment, history, physical examination, clinicopathology, imaging modalities, response to medical therapy, informed discussion with the owner and clinical intuition. Utilizing all
this information, the correct decision to perform exploratory surgery or not is usually made.
131
A List of Possible Causes of Acute Abdomen:
Gastrointestinal obstruction/rupture/perforation
Gastric dilatation/volvulus
Gastrointestinal surgical wound dehiscence
Mesenteric Volvulus
Infarction of the blood supply to the intestines
Pancreatitis
Pancreatitis abscess
Pyometra (not usually painful)/ rupture of pyometra
Prostatitis
Prostatic abscess
Ruptured urinary bladder/urinary tract
Pyelonephritis/renal abscess
Ruptured bile duct/bile peritonitis
Cholecystitis
Liver lobe torsion
Splenic torsion
Splenitis
Neoplasia
Sterile foreign body (e.g. surgical sponge)
Testicular torsion
Canine Parvoviral Enteritis
Intussusception
Salmonella infection
Campylobacter infection
Hemorrhagic gastroenteritis
Penetrating foreign body
Post-operative peritonitis
Uterine torsion
Torsion of the colon
Feline Infectious Peritonitis
Stump pyometra
Hepatitis
Steatitis
Retroperitonitis
Migrating foreign body (e.g. grass awn, tooth pick)
Blunt trauma to the abdomen
Urethral or ureteral obstruction
Ruptured gravid uterus
Post whelping metritis
Massive intestinal parasitism
Feline Panleukopenia
ALGORHYTHM FOR A SUMMARY APPROACH TO THE ACUTE ABDOMEN:
As with any algorhythm, this will not work with all patients. This algorhythm only provides an overview of the approach and
should only be used as a guideline.
Acute Abdominal Pain
Assess respiration, tissue perfusion
EDB
Stable
Unstable
Stable
EDB
Abdominal
Radiographs
ree air
Normal
Obstruction
Foreign Body
GDV
etc.
Loss of detail
Abdominocentesis
Bloodwork
Abd US
Contrast
Studies
Fluid
Analysis
Surgery
Septic
inflammation
???
Aseptic
133
Therapeutic approach to the acute abdomen
Kenneth J. Drobatz
INTRODUCTION
Animals with acute abdomen are primarily characterized
as having abdominal pain. Vomiting and/or diarrhea often
accompany this abdominal pain as well. In addition, the
spectrum of physiologic compromise that an animal with an
acute abdomen can have is very wide. Depending upon the
cause of the problem, the progression of the physiologic
changes that occur can be relatively slow to precipitous or a
combination thereof. As with any emergent patient, the basic principles of stabilization of the four major organ systems: respiratory, cardiovascular, neurologic and renal systems should be adhered to. The two systems more commonly compromised in these patients are the cardiovascular and
respiratory systems.
INITIAL RAPID ASSESSMENT
Respiratory rate, respiratory effort, mucous membrane
color, and thoracic and cervical auscultation provide a rapid
assessment of the respiratory system. Abnormalities in any
one of these physical parameters warrants consideration for
oxygen supplementation and further diagnostics to investigate why these abnormalities are occurring.
Mucous membrane color, capillary refill time, pulse
quality, pulse rate, and cardiac auscultation provide the basis
for the physical assessment of the cardiovascular system.
Abnormalities of tissue perfusion in animals with acute abdomen are often due to hypovolemia from fluid loss, hemorrhage or systemic inflammatory response syndrome. Fluid
loss usually occurs as a result of vomiting, diarrhea or third
space accumulation of fluid within the peritoneal space because of severe peritoneal inflammation. The fluid loss from
vomiting and diarrhea is usually isotonic with low protein
concentration, while fluid loss into the peritoneal space is
isotonic but relatively high in protein concentration. These
differences can affect one’s choice of the type of fluid for
volume resuscitation if it is necessary. In addition, fluid can
be lost from the vasculature due to systemic inflammation
and generalized vasculitis secondary to the systemic inflammatory process that might occur from peritonitis. Abnormalities of heart rate or rhythm should be evaluated by a lead II
ECG. Animals with ventricular tachycardia that is exces-
sively rapid or is affecting tissue perfusion should be treated. Other modalities can be used to assess the cardiovascular status including measurement of blood pressure, central
venous pressure measurement and serum lactate.
Further rapid assessment of physiologic derangements in
the acute abdomen patient includes an emergency database.
Our database includes PCV, TS, Dipstick BUN, Dipstick
glucose, electrolytes, blood gas analysis, and a blood smear.
This database is rapidly available and provides a relatively
well-rounded assessment of the patient. Any patient presenting with vomiting, abdominal distention, and/ or abdominal
pain should at least have a minimum database performed
(Packed cell volume, total solids, dipstick glucose, dipstick
BUN). Packed cell volume (PCV) and total solids (TS) give
the clinician an assessment of hydration or presence of anemia. The PCV and TS will usually be increased in a nonanemic patient that is dehydrated. Animals that have acutely
hemorrhaged may have a completely normal PCV and TS
but as intravenous fluid replacement ensues, these parameters may dramatically drop into low ranges. The absolute
value is important, as is the relative change of these parameters with treatment.
Reagent strips can be used for rapid assessment of the
BUN and Glucose. Increased BUN may be due to pre-renal,
renal, or post-renal causes. Response to fluid therapy as
well as urine specific gravity should help to rule-out pre-renal azotemia. Glucose concentration may be increased in
diabetes mellitus or stress (particularly cats). Hyperglycemia in a nondiabetic dog that presents in extremis signifies severe physiologic compromise and will die soon if
aggressive therapy to relieve the cause is not instituted. Hypoglycemia can occur due to a variety of causes, but in the
emergent or critical patient, sepsis should be high on the
differential list. Animals with blood glucose less than
60mg/dl should be considered for IV supplementation of
glucose (1/4 - 1/2 g/kg IV bolus and/or supplementation in
intravenous fluids to a concentration of 2.5%-5.0%). Glucose concentration should be evaluated after therapy to assure normalization of the blood glucose.
Na+, K+, Chloride and blood gases should be evaluated
(if possible) since severe electrolyte and acid/base disturbances may occur with vomiting and diarrhea. Any constellation of electrolyte disturbances may occur with vomiting
or the underlying causes of vomiting. Pure gastric vomiting
134
can result in hyponatremia, hypokalemia, hypochloremia,
and metabolic alkalosis. Life-threatening hyperkalemia
may occur with hypoadrenocorticism or urethral obstruction. The combination of hyponatremia and hyperkalemia
should alert the clinician to the possibility of hypoadrenocorticism or pseudohypoadrenocorticism (whipworm or other GI parasite infection). Evaluation of electrolytes will also
help guide fluid selection and therapy. Dehydrated patients
with hyponatremia, hypochloremia, hypokalemia, and metabolic alkalosis will benefit the most from 0.9% saline with
potassium supplementation. The higher chloride concentration in this solution combined with restoration of volume
and blood pressure will help correct the hypochloremic
metabolic alkalosis.
Once initial emergency assessment of the respiratory and
cardiovascular systems has been completed. Abnormalities
in these systems should be treated and stabilized. In animals
that are stable, definitive diagnostics can proceed. Animals
that are unstable will require initial stabilization prior to further diagnostics. Prior to further emergency therapy, bloodwork for a complete blood count, chemistry screen, urinalysis, and coagulation evaluation should be drawn if possible.
Basic principles of emergency and critical care should be
adhered to at all times in the approach to these patients. The
animal’s ability to oxygenate should be assessed and treated
appropriately. Signs of respiratory abnormalities include increased respiratory rate and effort, changes in lung sounds
on auscultation (increased or decreased sounds), loud upper
airway sounds, and cyanotic mucous membranes. If there is
any suspicion of respiratory compromise, then oxygen supplementation should be provided. Some of the more common causes of respiratory distress in animals that have an
acute abdomen include aspiration pneumonia, pulmonary
thromboembolism, hemorrhage, neoplasia, adult respiratory
distress syndrome, and pleural effusion.
Physical signs of abnormal tissue perfusion include pale,
gray, or hyperemic mucous membranes, weak or hyper dynamic pulse quality, prolonged or shortened capillary refill
time, and changes in heart rate. The most common perfusion
abnormalities in animals with acute abdominal disease are
usually a result of hypovolemia or systemic inflammatory
response. If poor tissue perfusion is evident on physical examination, then careful auscultation of the heart and lungs
should be performed. If auscultation is normal then aggressive fluid therapy is warranted to correct the hypovolemia or
tissue perfusion. Balanced electrolyte solutions can be administered at 90 ml/kg/hr in the dog or 40-60ml/kg/hr in the
cat. We usually bolus 1/2 of this volume and reassess perfusion. If physical parameters or other assessments of perfusion indicate improvement or normalization, then the fluid
therapy is decreased and adjusted as needed to maintain perfusion, replace fluid deficits, and correct electrolyte abnormalities. If perfusion is not improved or corrected after the
initial bolus then fluid therapy at the “shock rate” should
continue but other methods of improving blood pressure and
perfusion should be considered. Colloid therapy (such as
Dextran 70 or Hetastarch) may improve blood pressure in
hypoproteinemic patients or patients not responding to crystalloid resuscitation. In animals that require aggressive and
continued fluid therapy, central venous pressure should be
measured to avoid fluid overload. If fluid and colloid therapy do not provide adequate blood pressure or perfusion, then
positive inotropes (Dobutamine) or pressor agents (phenylephrine, epinephrine, or dopamine) should be considered.
Any animal that requires prolonged support of pressor
agents despite adequate fluid and colloid resuscitation warrants a guarded to poor prognosis.
DIAGNOSTIC CONSIDERATIONS
Once the animal is more stable, evaluation for the underlying cause of the acute abdomen should be begun so
that definitive therapy can ensue. The list of specific causes
of abdominal pain is endless. It should be remembered that
any portion of the abdomen could be a source of pain when
examining an animal. Intervertebral disc disease may also
simulate a painful abdomen and should be considered in the
differential, although this is rarely associated with vomiting
and only occasionally associated with loss of appetite. The
general causes of abdominal pain include distention of a
hollow viscus, stretching of a capsule, ischemia, and inflammation secondary to variety of causes. The clinician
may utilize knowledge of the anatomy of the abdominal
cavity to assess the source of pain. The source of pain may
be the skin over the abdomen, the subcutaneous tissues, abdominal musculature, peritoneum, retroperitoneum, liver,
pancreas, biliary system, intestines, urogenital system,
spleen, and mesentery. One may occasionally locate the
specific area of pain, for example, a loop of intestine, the
prostate, or the kidneys, and this may help in the diagnostic
approach. Many times, a specific area cannot be identified.
Diagnosing the cause of abdominal pain requires assimilation of information from a variety of sources including signalment, history, physical examination, bloodwork, radiographs, abdominal ultrasound, radiographic contrast studies, abdominocentesis, peritoneal lavage, response to treatment, and/or exploratory laparotomy.
Signalment can be a clue to the cause of abdominal pain
or vomiting. Young animals commonly swallow foreign bodies, or develop infectious diseases, whereas older animals
tend to be a little more selective in their eating habits and are
less prone to contract infectious diseases such as parvovirus.
The sex of the patient and whether it is sexually intact may
also indicate the source of pain. An older, intact male dog
may have a painful prostate. An intact male dog that has
acute onset of pain and only one scrotal testicle may have a
testicular torsion. Female dogs with pyometra generally are
not painful on abdominal palpation. Abdominal pain in a patient with a pyometra should create concern for a possible
uterine rupture and septic peritonitis. Young adult German
Shepherd dogs are predisposed to intestinal volvulus. String
foreign bodies are common in cats. Acute pancreatitis commonly occurs in middle-aged, obese female dogs. Attention
to the signalment of the patient may be quite helpful in the
eventual diagnosis.
An accurate history may be the most important diagnostic clue in the assessment of the vomiting patient. The clinician’s first task is to assess whether the animal is actually
vomiting or regurgitating. Accurate determination of this
point will affect the diagnostic approach. Vomiting is characterized by hypersalivation, retching, and repeated contraction of the abdominal muscles and diaphragm. Regurgitation
is a more passive process. Once it is established that the patient is vomiting, important questions should include the potential for exposure to toxins or dietary indiscretion. Is ingestion of a foreign body a possibility? Are any other animals affected? Has the animal had any major medical problems in the past? Is the patient currently receiving any medications including over the counter drugs such as aspirin or
other nonsteroidal anti-inflammatory medications? Is there a
possibility of trauma? The clinician should determine when
the animal was last normal, what was the first abnormal sign
noted and the progression of abnormal signs since then.
Could the patient have been exposed to any other animals?
Is the patient current on all vaccinations?
The progression of the clinical signs can also help determine the urgency to obtain the diagnosis of the underlying
cause. Chronic abdominal pain that has remained relatively
static in its progression is not usually an emergency, although at some point, the problem could progress to become
an emergency. An animal that has had a chronic problem that
has now rapidly deteriorated or an animal with an acute problem that is or is not rapidly deteriorating warrants a more aggressive and expedient approach to define the underlying
cause of the painful abdomen.
Abdominal radiographs should be obtained in a patient
that is persistently vomiting or has abdominal pain. The radiographs should be carefully evaluated. Evidence of free gas
without prior abdominocentesis or recent abdominal surgery
suggests intestinal perforation or the presence of gas-forming
organisms within the abdominal cavity. The volume of free
abdominal gas can sometimes help in differentiating the
cause although this is not 100% specific. A large volume of
fee gas in the peritoneal space tends to be more associated
with pneumocystography of a ruptured urinary bladder, a
ruptured vagina, post abdominal surgery, ruptured gastric dilatation/volvulus, pneumoperitoneography, or extension of a
pneumomediastinum. Pneumomediastinum is most often associated with pneumoretroperitoneum although on rare occasions, pneumoperitoneum can occur. A small volume of free
gas in the peritoneal space is most often associated with rupture of the gastrointestinal tract or infection with a gas-forming organism. Rarely, we have seen small amounts of gas in
the spleen associated with a Clostridia infection in the
spleen. Free gas is most commonly detected between the
stomach or liver and the diaphragm on the lateral radiograph.
A horizontal beam radiograph with the animal in left lateral
recumbency and focused at the least dependent area can increase the sensitivity of radiographically identifying free gas
in the peritoneal space.
Gaseous or fluid distention of the small bowel proximal
to an obstruction should prompt the clinician to consider upper gastrointestinal contrast study or exploratory laparotomy. Another option to help determine complete bowel obstruction is to repeat radiographs 3 hours later and see if the
localized bowel dilation has changed or not. If the bowel remains distended in the same area, this suggests a bowel obstruction. Generalized small bowel distention suggests generalized small bowel ileus or a very low gi obstruction.
135
Loss of abdominal detail may be due to lack of fat in the
abdomen (puppies or very thin animals) or due to free abdominal fluid. Loss of abdominal detail that is possibly due
to free fluid within the peritoneal cavity is an indication for
further diagnostic procedures to characterize the abdominal
fluid.
All organs in the abdominal cavity should be evaluated
for density, shape, size and location. Abnormalities in any
organ may help localize the cause of the acute abdomen. Extra-abdominal structures should be evaluated as well for
completeness of evaluation and further diagnostic clues. The
retroperitoneal space should be assessed as well. Loss of detail of the kidneys, a “streaky” appearance, or distention of
the retroperitoneal space suggests fluid accumulation, a
space occupying mass or sublumbar lymphadenopathy. The
structures that make up the abdominal compartment “walls”
should be carefully assessed for integrity to rule out herniation or rupture.
Abdominocentesis can be very helpful diagnostically, and
in distinguishing the “medical” abdomen from the “surgical
abdomen”. Other indications for abdominocentesis include
blunt trauma, penetrating injuries with possible abdominal
perforation, and shock with no obvious cause, or suspicion
of a septic abdomen from intestinal leakage or previous abdominal surgery. It must be remembered that a substantial
amount of fluid may be present but not retrievable by abdominocentesis. When this occurs or is suspected, then diagnostic peritoneal lavage or ultrasound-guided abdominocentesis is indicated. Diagnostic peritoneal lavage
involves infusion of saline into the abdomen (approximately 20 ml/kg of sterile saline) and retrieval of the fluid followed by cytological analysis.
Submitting abdominal fluid to the clinical laboratory
for determination of cell counts, protein concentration, and
cytological analysis is warranted, although the delay in obtaining these results can be detrimental to the patient with
a septic abdomen. This warrants that immediate evaluation
by the clinician in charge is necessary. Gross appearance of
the fluid should be noted, total solids should be determined, a direct smear and a smear of the sediment should
be cytologically evaluated. A direct smear gives an impression of the relative cellularity of the fluid and a cytological
evaluation of the sediment increases the number of cells
that can be evaluated and enhances the chances of seeing
bacteria.
Toxic or degenerate neutrophils with intra or extracellular bacteria are an indication for exploratory laparotomy.
The appearance of toxic or degenerate neutrophils without
bacteria should be interpreted in light of all other findings
and the clinical appearance and progress of the patient. Vegetable fibers in the retrieved fluid indicate bowel perforation
and exploratory laparotomy is indicated.
Free fluid may also be analyzed for creatinine or K+ if
urinary tract leakage is suspected and compared to peripheral blood concentrations. Some clinicians suggest that amylase or lipase determinations should be performed on abdominal fluid for the diagnosis of pancreatitis but this is of
questionable value. Measurement of fluid pH, pCO2, glucose concentration, and lactate concentration may be helpful
in diagnosing a bacterial peritonitis. These measurements
136
can be compared to simultaneously collected peripheral
blood pH, pC02, glucose and lactate concentrations. Decreasing gradient of glucose from peripheral blood to abdominal fluid and increasing gradient of peripheral blood
lactate to abdominal fluid lactate suggests septic peritonitis
as the cause of the abdominal fluid. In addition, a pH of
<7.2, pCO2 > 55mHg, glucose < 50 mg/dl, or a lactate concentration >5.5 mmol/L is strongly suggestive of bacterial
peritonitis.
Abdominal ultrasound may be utilized to evaluate the abdominal organs. A thorough ultrasound examination should
evaluate all organs within the abdominal cavity. Particular
attention should be paid to the pancreas when vomiting and
abdominal pain are present concurrently. Ultrasound may be
helpful in detecting a gastric or intestinal foreign body but
should not be a substitute for abdominal radiographs and
barium contrast study in ruling out an intestinal obstruction
or foreign body. In addition, abdominal ultrasound can be
challenging to interpret and the results can be quite user dependent. Relying on the information obtained from this type
of study should be evaluated in the light of the expertise of
the person performing it.
The dilemma of “surgical” versus “medical” abdomen
will always challenge emergency and critical care clinicians.
It is important to gather as much information as possible when
the decision is not clear. Many times, the diagnostic clues are
not definitive and the decision depends on clinical experience
and the response of the patient to medical therapy.
In general, any perforations into the abdomen are an indication for immediate abdominal exploratory. Abdominal
hemorrhage (not due to a coagulation defect) that is not responsive to medical and transfusion therapy should prompt
the clinician to pursue the surgical option. Witnessed foreign body ingestion with clinical signs is an indication for
surgery before intestinal damage occurs. String foreign bodies in cats can cause substantial damage and perforation of
the small intestine due to persistent peristalsis and should be
removed as soon as possible. Any animal that does not respond to symptomatic medical therapy should be a considered for exploratory laparotomy.
TREATMENT CONSIDERATIONS
Antibiotics are not used to specifically treat causes of
vomiting or abdominal pain. Indications for antibiotic therapy include loss of the intestinal mucosal barrier due Canine
Parvovirus, Panleukopenia virus, or intestinal invasive bacteria. Therapy should be broad spectrum with antibiotics that
are particularly effective against gram-negative bacteria and
anaerobes. Ampicillin/gentamicin is bactericidal, inexpensive, broad spectrum and effective. One should use aminoglycosides with caution due to their nephrotoxicity, particularly in renal compromised patients (dehydrated and poorly
perfused patients). Other antibiotics with gram-negative
spectrum include fluoroquinolones, other aminoglycosides
(amikacin), Trimethoprim-sulfa, and cephalosporins. Drugs
with anaerobic spectrum include penicillins, clindamycin,
and metronidazole. A parenteral route should be utilized in
the vomiting or critically ill patient.
Anti-emetics should be avoided in undiagnosed conditions because they may mask clinical signs of disease progression. If the vomiting is causing compromise of the patient, then anti-emetics are indicated. Critical patients are
particularly sensitive to the vagal effects of vomiting and can
collapse, develop respiratory arrest, have severe bradyarrhythmias, and even suffer cardiac arrest. Vomiting in a
critical patient should not be taken lightly.
Patients with an acute abdomen should not be taken
lightly. After stabilization of the respiratory and cardiovascular systems, aggressive attempts should be made to diagnose the cause of the abdominal pain. Rapid evaluation to
determine whether the patient requires immediate surgery or
not will optimize the chances for a successful outcome.
137
Approach to the patient in urinary emergency
Kenneth J. Drobatz
Critically ill patients often have multiple life-threatening problems and present a confusing challenge to even the
most experienced clinician. Prioritization of treatment of
the most immediate life-threatening problems is key to the
successful outcome of these patients. This lecture will present an overview of the medical assessment and management of the critically ill emergency patient. Important
points in the assessment and stabilization of the emergency
patient include:
1. Cellular and organ function depend upon adequate
cellular nutrient and oxygen delivery and waste removal.
2. Assessment and stabilization of the 4 major organ
systems: respiratory, cardiovasclar, central nervous, and
renal are the primary goals in the approach to the emergency patient.
3. The primary survey of the emergency patient is to
assess the patient’s ability to oxygenate the blood and deliver that oxygen to the tissues.
4. The major components of the assessment of the
emergency patient include medical history, thorough physical examination, ancillary assessment of the 4 major organ
systems, and the emergency database.
OVERVIEW
Treatment and monitoring of the four major organ systems - respiratory, cardiovascular, central nervous system
(CNS), and renal system are important in the successful
management of the critically ill patient. The initial goal of
the critical care clinician is to maintain adequate oxygen
delivery to the tissues through treatment of the respiratory and cardiovascular systems.
Failure of this goal results in the demise of the patient
despite successful management of other major problems.
Management of central nervous and renal systems follows.
OXYGENATION OF BLOOD
Adequate oxygenation of blood must be assured. Oxygen
supplementation should be provided to any critically ill pa-
tient until proven that it is not necessary. Complications of
oxygen toxicity don’t develop until 12 hours or more of inspired oxygen concentrations of greater than 40-50%.
Modes of oxygen supplementation include mask oxygen,
nasal insufflation, tracheal catheter, oxygen cage, “oxygen
tent”, and positive pressure ventilation.
In the acute situation, we have found mask oxygen
supplementation is inexpensive, effective, and convenient because it allows simultaneous examination and
treatment of the patient. Nasal oxygen is also effective
and has similar advantages although some patients do not
tolerate the nasal catheter well and continually dislodge
it. We have not had much requirement or experience with
the tracheal catheter. The major advantages of the oxygen cage are that humidity, temperature, and inspired
oxygen concentration may be controlled, as well as there
is minimal stress to the patient. The major disadvantages
are expense, oxygen wastage, and most importantly-inability to monitor the patient. The oxygen cage tends to
give the clinician a false sense of security, but if used judiciously, it is quite efficacious. Positive pressure ventilation allows for absolute control of a patients respiration, control of inspired oxygen concentration, airway
pressures, tidal volume, etc.. In many critically ill patients with respiratory problems we can often breath and
ventilate them much more effectively than they can
alone. Positive pressure ventilation carries with it many
disadvantages including need for sedation, intubation
and bypassing of upper airway defense mechanisms, intensive monitoring, and barotrauma. The decision to ventilate a patient should not be taken lightly but should not
be avoided when it is necessary.
Indications for positive pressure ventilation include respiratory distress resistant to high inspired oxygen concentration, inadequate ventilation (increased PaC02), required
high inspired oxygen concentrations for a prolonged period
of time, and respiratory muscle fatigue.
Assessment of oxygenation of hemoglobin include simple evaluation of mucus membrane color, pulse oximetry,
and arterial blood gas measurement.
Pale mucous membranes may indicate anemia, poor tissue perfusion, or peripheral vasoconstriction secondary to
pain, catecholamines, or hypothermia.
138
saturation and can detect serious desaturation of hemoglobin
saturation that is not detectable from physical examination.
We often use this instrument as a constant monitor in our
critically ill patients as well as in routine anesthetic procedures. It’s major disadvantages are that the probe is most
consistently effective when placed on the tongue or lip
(therefore precluding its continuous use in fully alert or fractious patients) and it is difficult to obtain accurate readings
in patients with poor tissue perfusion.
Arterial blood gas measurements are considered the gold
standard in assessment of respiratory function in the clinical
patient. It is important to remember that arterial blood gases
measure the partial pressure of oxygen within the plasma
which is a minor component of total oxygen content of the
blood (see below).
TISSUE OXYGEN DELIVERY
Cyanosis isn’t detected in tissue until there is greater than
5 grams/deciliter of unoxygenated hemoglobin. This value
implies two major points - anemic patients may be severely
hypoxemic yet have no detectable cyanosis and cyanosis is an
insensitive and late indicator of respiratory dysfunction. The
former point is illustrated by a patient with a packed cell volume of 15% or less. This packed cell volume corresponds to
a hemoglobin concentration of 5 grams/dl. In order for this
patient to manifest cyanosis the hemoglobin must be 100%
unsaturated, an extremely unlikely situation. The latter point
is illustrated by a patient with a normal packed cell volume
(45%). This PCV corresponds to 15 grams/dl of hemoglobin.
Five grams/dl of hemoglobin in this patient would be a loss
of 33% of hemoglobin saturation. In other words, this patient
would have a hemoglobin saturation of 66%. This corresponds to a Pa02 of approximately 40 mmHg on an unaltered
hemoglobin/oxygen dissociation curve. This is profound hypoxemia (normal Pa02 on room air is approximately 100
mmHg). Therefore, cyanosis represents severe hypoxemia.
The hemoglobin/oxygen dissociation curve also illustrates another important point. Many of our patients with
respiratory difficulty have a Pa02 of 60mmHg to 80 mmHg
or lower. These patients may be maintaining enough oxygenation and delivery to appear stable. Looking at the sigmoidal shape of the curve, the Pa02 of these patients rests at
the junction of the steep portion of the curve. Any minor
change in Pa02 from simple procedures such as venipuncture, restraint, radiographic positioning, or change in posture
may cause a profound decrease in hemoglobin saturation
and demise of the patient. Patients with respiratory distress
are fragile and may decompensate at anytime. All efforts to
improve oxygenation should be attempted before stressful
procedures are employed.
Oxygen saturation of hemoglobin may be non-invasively
evaluated with the pulse oximeter. This monitor is becoming
more frequently used in critical as well a routine veterinary
care. It gives moment by moment changes in hemoglobin
Adequate tissue oxygen delivery requires oxygenation of
the blood and delivery of that blood to the tissues. The latter
requires adequate cardiovascular function.
The major parameters that contribute to whole blood
oxygen content include blood hemoglobin concentration,
oxygen saturation of hemoglobin, and the plasma concentration of hemoglobin. The contribution of hemoglobin and the
oxygen it carries far outweigh the amount of oxygen carried
in plasma. Therefore maintenance of adequate hemoglobin
concentration and its saturation are extremely important in
maintaining oxygen delivery. A packed cell volume of 30%
has been recommended by some clinicians to maintain adequate blood oxygen content and optimal rheological blood
characteristics for tissue perfusion.
The three major causes of inadequate tissue perfusion are
hypovolemia, sepsis, and inadequate cardiac function. The
most common cause of hypoperfusion in critically ill patients is hypovolemia.
Physical examination parameters such as pale mucus
membranes, prolonged capillary refill time, and rapid, weak
pulses suggest inadequate tissue perfusion. Septic patients
often have hyperemic mucus membranes, rapid capillary refill time, and bounding pulses. Immediate auscultation of the
heart and lungs is indicated to determine cardiovascular dysfunction as the cause of the poor perfusion. A heart murmur,
gallop rhythm, and/or persistent arrhythmia is usually present in most dogs and cats with cardiac disease . Cardiac disease is unlikely if cardiovascular abnormalities are not present on auscultation.
The initial therapy for patients with hypovolemia or sepsis is intravenous fluids, colloids, and/or blood products as
indicated. The initial choice is a balanced electrolyte fluid
challenge. Initial fluid volumes and rates of administration
are 90 ml/kg/hr in the dog and 40 - 60 ml/kg/hr in the cat, although the volumes and rates should be tailored to the individual patient by monitoring physical perfusion parameters.
Most cases of uncomplicated hypovolemia respond to half
this amount of fluid. A positive response is indicated by improvement in mucous membrane color, normalization of
capillary refill time, decreased heart rate, and improved
pulse quality. Frequent auscultation of the lungs is indicated
to detect vascular volume overload and pulmonary edema.
Arterial blood pressure measurement may be used to
guide fluid therapy and perfusion status in the critically ill
patient. The draw back is that patients may have poor tissue
perfusion despite normal or even high blood pressure measurements. Blood pressure may be indirectly measured by
doppler ultrasound and oscillometric methods.
Doppler ultrasound gives a measurement of systolic
blood pressure. In clinical human studies, a systolic blood
pressure of 90 mmHg or less is used as a indicator of shock
in trauma patients.
Oscillometric measurements utilize blood vessel wall vibrations and give systolic, diastolic, and mean arterial blood
pressures as well as heart rate. The machine is easy to use
but somewhat expensive. The other major disadvantage is
that is sometimes difficult to get accurate measurements in
patients that have move around a lot, have poor perfusion or
irregular heart rhythms (Unfortunately, the very patients we
prefer to use it on). One criteria for belief in the measurement obtained is if the actual heart rate and the machine
measured heart rate are similar.
Direct measurement of arterial blood pressure is the gold
standard. We place a catheter percutaneously in the dorsal
metatarsal artery as our first choice. If it is too difficult to
palpate the artery, then we cutdown to the artery to place the
catheter or catheterize the femoral artery percutaneously.
Another arterial access is the ear in long, floppy ear dogs
such as the Basset Hound. Direct arterial measurements require a transducer and oscilloscope that has arterial measurement capabilities. Direct arterial pressure measurement
allows visualization of the arterial waveform and accurate
measurement of systolic, diastolic, and mean arterial pressures.
Central venous pressure may be used to guide fluid therapy. Central venous pressure measures the pressure within
the jugular vein and gives an indirect assessment of the
heart’s ability to pump the blood it is receiving. It is inexpensive and relatively easily performed. Measurements from
0 - 5 cm H20 are considered normal though it is the trend
that is more important. Rapid increases of 3 to 5 cm of H20
during fluid therapy suggests possible fluid overload and decreased fluid administration is indicated. Using central venous pressure as a guide for fluid administration may prevent fluid overload and pulmonary edema.
A relatively new technique in veterinary critical care is
the use of the pulmonary artery catheter. This inflatable balloon tipped catheter is placed via a percutaneous introducer
into the jugular vein. The balloon is then inflated and the
139
blood flow guides the catheter into the right atrium, right
ventricle and finally into the pulmonary artery. The catheter
is connected via a pressure transducer to an oscilloscope so
that pressure waveforms transmitted from the end of the
catheter may be visualized. The location of the catheter can
be determined by characteristic pressure waveforms that are
produced by the various blood vessels as well as the right
atrium and ventricle. The location may also be confirmed by
fluoroscopy or radiography. Valuable information may be
obtained from the catheter including thermodilution cardiac
output measurements, pulmonary capillary wedge pressure,
pulmonary artery pressures, central venous pressure, right
atrial and ventricular pressures, pulmonary vascular resistance, peripheral vascular resistance, oxygen delivery, oxygen consumption, and central venous oxygen concentration
and saturation. The pulmonary artery catheter allows a more
accurate assessment of tissue oxygen delivery and cardiovascular dynamics.
CENTRAL NERVOUS SYSTEM
We are limited in our ability to assess and monitor the
central nervous system. Serial neurologic examination is the
mainstay of monitoring of this organ system. Although computed tomography scans, magnetic resonance imaging, and
direct measurement of intracranial pressure are routine
modalities in human medicine, expense and limited access
make these techniques impractical in veterinary critical care.
Every critical patient should have a baseline complete
neurologic examination performed. This should include assessment of mentation, cranial nerve function, spinal reflexes and peripheral nerve function. The frequency of monitoring should reflect the degree of central nervous system function and the potential for CNS insult. Critically ill patients
with CNS dysfunction should be monitored as constantly as
possible, at least every one to two hours.
Maintenance of adequate oxygen delivery and ventilation optimize CNS function. In patients with increased intracranial pressure administration mannitol, mild elevation
of the head (avoiding jugular vein obstruction), and mild hyperventilation (PaC02 = 25 - 30 mmHg) will help decrease
intracranial pressure.
In patients with CNS dysfunction, good nursing care
such as turning the patient every four hours, corneal lubrication in patients without a blink reflex, maintenance of oral
mucus membrane hydration, urinary bladder expression, and
keeping the patient clean, dry, and well padded go a long
way in decreasing morbidity in these critically ill patients.
RENAL SYSTEM
Inadequate urine production and renal dysfunction is a
common problem in emergency and critically ill patients.
Prompt recognition and aggressive treatment of the oliguric
patient may prevent serious complications related to inadequate urine production. Oliguria may result from poor renal
perfusion, renal parenchymal disease or obstruction to urine
flow. Successful diagnosis and therapy requires the clinician
140
to be aware of factors which predispose to oliguria and to
monitor the renal function and urine production in those patients at risk.
In the canine, oliguria has been defined as urine production less than 6.5 ml/kg/day (0.27ml/kg/hr). Inadequate
urine production may be related to diminished glomerular
filtration or obstruction of urine flow as it travels through the
tubules, collecting ducts, renal pelvis, ureters, bladder and
urethra.
Changes in renal blood flow, glomerular capillary hydrostatic pressure, hydrostatic pressure within the tubular lumen, concentration of plasma proteins, and the glomerular
ultrafiltration coefficient all affect GFR. The most common
cause of oliguria in critically ill patients is diminished hydrostatic pressure gradient across the glomerular capillary
membrane secondary to hypovolemia, sepsis and/or poor
cardiac function. The glomerular hydrostatic pressure is determined by systemic blood pressure and the balance between the pre and post glomerular capillary sphincters. GFR
and renal blood flow remain constant through a range of
mean arterial blood pressures form 80 -100 mmHg. This occurs as result of renal autoregulation through a balance of
pre and post glomerular capillary vasoconstriction. When
mean systemic arterial blood pressure decreases to less than
80 mmHg this autoregulation is lost and glomerular hydrostatic pressure diminishes in parallel with systemic blood
pressure.
In critically ill patients, an indwelling, closed urine collection system allows for precise measurement of urine
output. Urine output should be measured every 2 - 4 hours.
Normal urine output in the dog is 1 -2 ml/kg/hr but should
be evaluated in light of the amount of fluid that is being
given and other areas of loss such as the gastrointestinal
tract. Aggressive fluid therapy for oliguria should be initiated if urine output is less than 1 ml/kg/hr and there are no
fluid losses that could account for a discrepancy in urine
production.
In addition to urine output measurement, monitoring of
patients at risk for renal dysfunction or oliguria should involve daily assessment of renal function by measurement of
serum creatinine, serum urea nitrogen, and serum electrolytes as well as serial urinalysis.
The goal in the management of the oliguric patient is to
minimize detrimental changes in water, solute, and electrolyte balance while optimizing renal perfusion and urine
output until renal function and urine production returns. In
many instances, the underlying cause may not be known and
therapy to improve urine output should be directed at correcting perfusion abnormalities, renal parenchymal, and obstructive causes of oliguria.
Obstructive causes of oliguria are reversible and should
be treated as soon as possible. Urinary obstruction may result in the death of the patient within 65 to 72 hours of onset. In our critically ill patients, one of the most common
causes of oliguria in a patient with an indwelling urinary
catheter is catheter obstruction secondary to kinking. In any
patient, catheter patency should be assured.
Therapy for inadequate perfusion and renal parenchymal
causes of oliguria are similar. Both involve optimization of
renal perfusion and judicious use of diuretics and vasopres-
sor agents. Hypovolemia is the most common cause of hypoperfusion in our critically ill patients. In a patient with
oliguria, measurement of arterial blood pressure is indicated
as an indirect assessment of renal perfusion (see above).
Judicious use of intravenous fluids, colloids, and vasopressor agents may be necessary to treat the oliguria and
provide adequate renal perfusion when poor perfusion is the
suspected cause of the oliguria and primary cardiac disease
has been ruled out. Frequently, aggressive fluid therapy is all
that is necessary. An intravenous fluid challenge of 90
ml/kg/hr may be required in the hypovolemic, hypotensive
canine patient (40-60ml/kg/hr in the feline patient). Mean
arterial pressure should be maintained at 80 mmHg or higher. Fluid therapy should be used with great care in the oliguric patient because of the potential for vascular fluid overload. Measurement of central venous pressure in these patients is a useful guide. Auscultation of the heart and lungs
and measurement of packed cell volume and total solid will
also help guide fluid volume and rate of administration.
If fluid therapy alone is not adequate to improve or maintain sufficient arterial blood pressure then a positive inotrope
such as dobutamine (5 - 10 ug/kg/min) or a vasopressor such
as dopamine (5 - 10 ug/kg/min) should be utilized. If oliguria persists despite improvement in arterial blood pressure,
other pharmacologic agents will be required.
Mannitol (0.1 g/kg - 0.5 g/kg), an osmotic diuretic may
be given intravenously. Mannitol improves GFR, renal blood
flow, osmolar clearance, and preserves renal tubular blood
flow and prevents tubular obstruction resulting in increased
urine output. Mannitol is most effective in the early stages of
oliguric renal failure. Diuresis should be expected within
one hour of mannitol infusion. If diuresis does not occur
then mannitol will probably not be ineffective. Mannitol
should not be used in the patient that has a high CVP and is
near vascular volume overload.
Loop diuretics should be used to promote diuresis only
when proper fluid therapy has been applied and blood pressure is adequate. We combine furosemide (2 mg/kg IV bolus
followed by a constant rate infusion of 1 mg/kg/hr) and
dopamine (2 - 5 ug/kg/min) to promote diuresis. Diuresis
should occur within 30 minutes of therapy.
If urine output is still inadequate, any further medical
therapy to induce diuresis is pointless. Elimination of uremic
toxins can only be achieved by hemo or peritoneal dialysis.
If diuresis is achieved, monitoring of urine output, serum
electrolytes, blood gases, and serum creatinine should be
continued.
THE EMERGENCY DATABASE
Physical examination and history provide the most
amount of information in assessing the emergency patient. Rapid clinicopathologic assessment can augment
the information obtained from the history and physical
examination and can sometimes even confirm a diagnosis within minutes of presentation. The basic emergency
database in our emergency room includes packed cell
volume, total solids by refractometry, dipstick BUN, and
dipstick glucose.
BLOOD COLLECTION
We collect three heparinized capillary tubes full of
blood at presentation. This amount of blood is enough to
measure PCV, TS, blood glucose, diptick BUN, and a
blood smear. If an intravenous catheter is being placed,
the easiest way to fill the capillary tubes is by placing the
end of the capillary tube into the hub of the catheter after
the catheter has been placed and before the injection cap
or fluid line is placed. If a catheter is not being placed
then a 25 gauge needle placed into a peripheral vein will
suffice. The needle is placed into the blood vessel and 3
capillary tubes are filled from the hub of the needle as it
fills with blood. Two capillary tubes are plugged on one
end, placed into a microhematocrit centrifuge and centrifuged. While those tubes are spinning, a blood smear is
performed and set to dry and dipstick blood glucose and
BUN are determined. Once the blood smear has dried, it
is stained and examined under the microscope. By this
time, the centrifuged samples are completed ,PCV and TS
are determined and the database is complete. The whole
process takes approximately 3-4 minutes to complete.
PACKED CELL VOLUME AND TOTAL
SOLIDS
PCV and TS should be interpreted in conjunction with
each other. The changes in these two parameters often
parallel each other with free water loss or hemorrhage.
Decreases in both suggest hemorrhage as the cause for the
changes. A rare exception may be the individual patient
that has two separate reasons for the lowering of each parameter. For example, the patient with a protein losing
nephropathy and anemia secondary to chronic kidney disease. Fortunately, these circumstances are rare and when
an emergency patient has decreased PCV and TS the most
likely cause is blood loss or hemodilution secondary to
aggressive fluid therapy.
Acute blood loss does not immediately affect PCV
and TS because it takes time for interstitial fluid to move
into the vascular space and dilute out the remaining red
blood cells and proteins. In dogs, splenic contraction secondary to catecholamine release may actually cause an increase in PCV despite severe hemorrhage. With intravenous fluid replacement during resuscitation, the
changes in packed cell volume will become immediately
apparent. We feel that total solids is a more sensitive indicator of blood loss compared to PCV. We have seen several patients present with acute hemorrhage with normal
PCV but mildly decreased TS (<6.0g/dl). When faced
with a trauma patient with normal PCV but decreased total solids there is a strong possibility that severe hemorrhage has occurred.
A decreased PCV with a normal total solids suggests
red blood cell destruction or decreased red cell production. Decreased PCV with hemolyzed serum suggests hemolytic anemia. A slide agglutination test should be performed but can sometimes be difficult to assess accurately. Icteric serum with decreased PCV suggests the possi-
141
bility of hemolytic anemia as well, although hepatic and
post hepatic causes of icterus cannot necessarily be ruled
out. Likewise, the absence of icteric or hemolyzed serum
does not rule out hemolytic anemia as the cause of the
anemia. Anemia of chronic disease is characterized by a
decreased PCV with a normal total solids.
The major clinical significance to a decreased PCV is
decreased oxygen carrying capacity of the blood. The major carrier of oxygen within the blood is hemoglobin. Dissolved oxygen with in the plasma is a minor contributor
to the total oxygen content of the blood. Physical signs of
a clinically significant decrease in PCV include tachycardia, bounding pulses, pale mucous membranes, tachypnea
and weakness. Blood transfusion is recommended when
clinical signs of anemia are present. Some patients may
have very low PCV but no signs of being affected by the
anemia. These patients probably have a chronic anemia.
Though these patients may appear stable, stressful procedures such as radiography or restraint for blood collection
may precipitate rapid decompensation and transfusion
should be considered based on the clinician’s anticipation
of potential physiologic stresses.
Decreased total solids may occur due to loss from hemorrhage, protein loss into third spaces such as the pleural or peritoneal space or external loss (or malabsorption )
through the intestines or kidneys. Protein loss through the
gut usually results in a panhypoproteinemia (decreased
globulins and albumin) while loss in the urine causes a
hypoalbuminemia.
Decreased total solids may also occur due to decreased
production from liver dysfunction. Generally, when liver
failure is the cause of hypoalbuminemia other liver functional abnormalities are often present including decreased
blood urea nitrogen, hypoglycemia, hyperbilirubinemia,
hypocholesterolemia, hyperammonemia, and/or coagulation abnormalities.
The major clinical significance to hypoproteinemia
(particularly hypoalbuminemia )is decreased intravascular oncotic pressure. Decreased intravascular oncotic
pressure may result in loss of fluid from the intravascular
space and decreased ability to maintain vascular volume
and blood pressure. The level at which this occurs depends upon the absolute oncotic pressure as well as the
vascular permeability. In critically ill patients the vascular permeability is often increased. Once synthetic colloid
support is administered, the use of refractometry to assess
total solids and use them as an indirect estimate of intravascular colloid osmotic pressure becomes inaccurate.
This is when the colloid osmometer becomes particularly
useful because of the ability to measure colloid osmotic
pressure directly.
Increased PCV is most often due dehydration. This is
paralleled by an increase in total solids. Absolute polycythemia rarely occurs. Increased PCV can increase the
viscosity of blood and interfere with blood flow. This can
result in inadequate tissue oxygen delivery or sluggish
blood flow that may predispose the patient to intravascular
coagulation. (One of the more common presenting complaints due to a absolute polycythemia is CNS dysfunction,
particularly seizures.)
142
BLOOD GLUCOSE
Blood glucose is easily and rapidly obtained by dipstick methods and a glucometer. It is important to recognize that the accuracy of these methods may be affected
by the packed cell volume. High packed cell volumes give
falsely low glucose measurements and low packed cell
volumes may give falsely increased glucose measurements.
This variation is not consistent from manufacturer to
manufacturer therefore it is best to consult the manufacturer of your dipstick and glucometer regarding these and
other affects. If in doubt, a more accurate reading may obtained by separating the plasma from the red blood cells
and measuring the glucose on the plasma sample.
Causes of increased blood glucose may be due to insulin resistance and/or lack of insulin (diabetes mellitus)
or stress. The later is most common among cats but we
have seen it in dogs with head trauma , other CNS insults,
and massive acute hypovolemia. This may be a result of
massive sympathetic discharge from the CNS during
episodes of CNS trauma, seizures, hypoxia. or severe hypovolemia.
The hyperglycemia in this situation is transient and often resolves within the first hours of presentation. With
diabetes mellitus the hyperglycemia persists without insulin therapy.
The clinical consequences of hyperglycemia include
an osmotic diuresis (free water loss) and potential CNS
changes due severe hyperosomolality from extreme hyperglycemia. Hyperglycemia may cause free water to
shift from the intracellular space into the extracellular
space resulting in hemodilution and hyponatremia. In
general, every 62 mg/dL increase in the plasma glucose
concentration will reduce the plasma sodium concentration by 1 meq/L. As the hyperglycemia is corrected the
plasma sodium concentration will rise. Metabolic acidosis (ketoacidosis) may be severe in patients with uncontrolled diabetes mellitus and blood gas evaluation should
be performed if available.
Hypoglycemia is a common presenting complaint in
the emergency patient. Hypoglycemia may be due to a variety of causes including liver dysfunction (usually other
signs of liver failure are present), increased insulin concentration secondary to neoplasia or insulin overdose,
stress in the neonate or toy breeds, laboratory artifact, hypoadrenocorticism, and sepsis. CNS dysfunction such as
depression, stupor, coma, or seizures is the primary clinical manifestation of hypoglycemia.
DIPSTICK BUN
We include a dipstick BUN (Azostik, Miles Inc.,
Elkhart, IN)to give us an estimate of azotemia in our
emergency patients. We have found this a useful screening method but does have some limitations. The dipstick
gives only major categories of BUN concentration Overall, these dipsticks are a reliable estimate of BUN especially when BUN is low. When performed properly, if the
dipstick reading is low it is accurate. At times, the dipstick has read very high and the BUN is only mildly elevated. In the middle range or mildly elevated categories
the BUN can sometimes be very high but the reading only records mild elevations. In summary, dipstick BUN is
relatively accurate but should only be considered a
screening test and actual measurements be determined in
questionable cases.
Very low BUN concentrations may be normal or due
to fluid diuresis. Polydipsia/polyuria due to non-renal
diseases may result in decreased BUN. Decreased production of BUN due to liver disease or a portal-caval vascular shunt may cause a decrease in BUN.
Increased BUN may be due to pre-renal, renal, or
post-renal causes which should be investigated when increased BUN is detected. Disproportional increases of
BUN compared to creatinine suggest possible gastrointestinal hemorrhage (as a source of protein for the increased production of urea) or due to pre-renal causes.
BLOOD SMEAR
Reliable assessment of a blood smear depends upon
the production of a good quality blood smear. All cell
lines should be systematically evaluated including the red
cell line, white blood cells, and platelets.
Bleeding patients should be evaluated for platelet
numbers. The average number of platelets per monolayer
field under oil immersion should be obtained. In normal
dogs and cats, there are 11-25 platelets per field; each
platelet in a monolayer field under oil immersion is
equivalent to approximately 15,000 platelets per microliter. The smear should be screened at low power to
search for platelet clumps that may result in a falsely low
platelet estimate prior to evaluating the counting area. If
there is more than four to five platelets per field then it is
unlikely that the bleeding is strictly due to thrombocytopenia. Most patients with spontaneous bleeding due to
thrombocytopenia have less than two platelets per oil immersion field.
Anemic patient blood smears should be examined for
evidence of regeneration (anisocytosis, polychromasia,
etc.) as well as for the presence of neutrophils and
platelets. Decrease in all parameters suggests a pancytopenia and possible bone marrow problem. The morphology of the red blood cells may suggest a cause for the
anemia such a spherocytes in patients with immune mediated hemolytic anemia or heinz bodies in onion toxicity
or zinc intoxication.
The smear should be scanned at lower power to get an
estimate of the number of white blood cells and then at
higher power to assess the character of the white blood
cells.
A leukocytosis with a mature neutrophilia suggests an
inflammatory or infectious process. Severe inflammatory
or infectious processes may cause the release of less mature neutrophils such as band cells. The absence of a
leukocytosis or a left shift does not rule the an inflammatory or infectious process. A leukopenia can be due to de-
143
The emergency database provides important diagnostic information for the initial assessment of the emergency patient. Serial emergency databases and physical
examinations provide important information that will improve medical care and detect subtle changes before a patient’s condition deteriorates and becomes irreversible.
Summary
creased production or sequestration of white blood cells.
Viral infections such as parvovirus can result in leukopenia as well as can administration of immunosuppressive
drugs.
Animals are presented to an emergency service for a
variety of reasons that can make the initial assessment of
these dynamic patients seem confusing. Firstly and most
importantly, the emergency clinician needs to focus on
the 4 major organs systems - respiratory, cardiovascular,
neurologic and renal. Compromise in one of these systems can be the most devastating and life-threatening,
therefore, stabilization of these systems first allows the
clinician to keep the patient alive while the underlying
problem is diagnosed and definitively treated.
145
Therapeutic management of the patient
in urinary emergency
Kenneth J. Drobatz
Urinary tract emergencies may be due to dysfunction in
any portion of the urinary tract although the physiologic and
metabolic disturbances manifested are similar. The first portion of this lecture will focus on the immediate life-threatening metabolic abnormalities that occur with urinary tract
emergencies and how to treat them. The latter portion will
deal with more specific areas of the urinary tract.
FLUID BALANCE, TISSUE PERFUSION
AND METABOLIC DISTURBANCES
Critically ill dogs and cats with urinary tract dysfunction
may have severe fluid deficits resulting in hypovolemia and
decreased tissue perfusion. Dramatic electrolyte changes
that occur with urinary tract dysfunction can also affect tissue perfusion by their effects on cardiovascular function (see
below).
When an animal is presented with urinary tract dysfunction, we obtain intravenous access and perform an emergency database that includes packed cell volume, total
solids, blood glucose, dipstick BUN, sodium, potassium,
ionized calcium, and a venous blood gas. Initial physical
evaluation should be focused on cardiovascular function and
tissue perfusion. If there are weak pulses, prolonged capillary refill time and severe dehydration, intravenous administration of balanced electrolyte solutions is extremely important. Although, potassium free solutions such as 0.9% saline
are recommended, any balanced electrolyte solution will
provide vascular volume support and not contribute substantially to the serum potassium concentration on an acute basis. There are arguments that 0.9% saline will contribute to
the metabolic acidosis, although studies evaluating the efficacy of 0.9% saline and other balanced electrolyte solutions
have not been performed in acidemic dogs and cats to resolve this question. The dilution provided by 0.9% saline or
a balanced electrolyte solution will help lower the potassium
concentration but will not lower it rapidly enough in patients
that are affected by hyperkalemia. We generally administer
one half of the estimated vascular volume of the patient (2030 ml/kg body weight in the cat, 40 – 50 ml/kg body in the
dog) as an intravenous bolus and re-evaluate perfusion status
as fluid is being administered. We adjust the dose depending
upon the response to this fluid challenge as well as the response to treatment of the electrolyte abnormalities.
The rapid assessment of the emergency database provides a basis for further therapeutics based on the electrolyte
derangements and their physiologic effects on the patient. If
the electrolyte changes are severe, yet the patient seems relatively unaffected by these changes, definitive treatment of
the electrolyte abnormalities is not attempted. In other
words, we treat the patient and not just “the numbers”.
Metabolic acidosis can be severe in critically ill uremic
patients. Blood pH can drop below 7.0. Metabolic acidosis
can result in deterioration of cardiovascular, and neurologic
function. Of primary importance is that severe acidosis
(<7.0) can predispose the heart to ventricular arrhythmias,
decrease cardiac contractility, and decrease the cardiac inotropic response to catecholamines. The irregular rhythm
and decreased contractility may contribute to poor tissue
perfusion in the severely affected uremic animals. The main
treatments for metabolic acidosis associated with urinary
tract dysfunction is definitive treatment of the urinary tract
disorder, fluid diuresis, and bicarbonate therapy. In the majority of patients, the first two are usually all that is required.
In the unstable dog or cat with a pH <7.0 due to metabolic
acidosis, sodium bicarbonate administration should be considered. The formula often recommended is 0.3 X body
weight (kilograms) X the base deficit. This gives an approximation for the total bicarbonate deficit. Administration of
one third of this dose slowly intravenously and the rest
placed in the intravenous fluids will correct the metabolic
acidosis over several hours. Rapid intravenous boluses of
sodium bicarbonate should be avoided because of the production of C02 and its diffusion into the central nervous system making cerebral spinal fluid acidosis even worse. Other
disadvantages of sodium bicarbonate administration include
shifting of the oxygen/hemoglobin dissociation curve to the
left and increasing osmolality. When monitoring the response to bicarbonate administration through the measurement of blood gases, it is important to remember that bicarbonate will increase initially in the intravascular space but
then it will be buffered by intracellular buffers. Immediate
measurement of blood gases after bicarbonate administration may over estimate the effect of the therapy. Diffusion
and buffering of administered bicarbonate by intracellular
buffers takes approximately 2 to 4 hours and a blood gas
analysis should be performed after this time period as well.
Serum phosphorus increases when urinary excretion of it
is compromised. In some cats with urethral obstruction, we
146
have observed serum phosphorus concentrations > 20 mg/dl.
The most serious consequences of hyperphosphatemia are
hypocalcemia (tetany or seizures as a result), and tissue deposition of calcium phosphate salts potentially causing dysfunction of the kidney, heart, and other organs. Therapy for
hyperphosphatemia includes definitive therapy for the urinary tract disorder, intravenous fluid therapy and fluid diuresis.
Potassium concentration can be normal to extremely
high (>10 meq/L) in patients with urinary dysfunction.
Potassium plays a major role in cell function and neuromuscular transmission. The major tissue of concern affected by
hyperkalemia is the conducting fibers of the heart. The characteristic ECG changes seen with hyperkalemia include
peaking and narrowing of the T wave with a shortened QT
interval, widening of the QRS complex, decreased amplitude or loss of the P wave, and as the QRS and T waves
merge - a sine wave can be recognized. The relationship between specific ECG changes and potassium concentrations
is quite variable. This lack of correlation is largely due to
other changes that affect cardiac conduction fibers including
serum calcium concentration, sodium concentration, and
acid base changes. Since the severity of signs does not correlate with the magnitude of change in the plasma potassium
concentration, treatment of hyperkalemia should be guided
not only by the degree of potassium increase but also by the
functional consequences (by monitoring the electrocardiogram). A patient with high potassium concentration but no
functional consequences, does not require specific therapy
for hyperkalemia. Patients with poor perfusion as a result of
cardiac conduction disturbances may require more specific
therapy directed at the hyperkalemia or its functional effects.
Reversing the effects of hyperkalemia can be achieved by direct antagonism of the high potassium’s membrane actions
and by lowering the plasma potassium concentration. Administration of 50 to 100 mg/kg of calcium gluconate intravenously will antagonize the membrane effects of hyperkalemia but it will not change the potassium concentration.
The effects of calcium gluconate administration are immediate. It is for this reason that this is our first drug of choice in
patients that have significant cardiac rhythm disturbances
due to hyperkalemia. The effects last approximately 20 to 30
minutes. We generally infuse the dose over 2-3 minutes with
continuous ECG evaluation.
Administration of regular insulin at 0.1 U/kg to 0.25
U/kg IV will stimulate cell membrane sodium /potassium
ATPase and cause potassium to move intracellularly. The insulin administration should be followed by a glucose bolus
of 1-2 grams per unit of insulin given to prevent hypoglycemia. This regimen will begin lowering plasma potassium concentration within several minutes to one hour. Blood
glucose monitoring should be maintained for several hours
after the administration of insulin and intravenous fluids
should be supplemented with glucose to maintain normoglycemia.
Sodium bicarbonate administration can lower plasma
potassium concentration by raising the pH and driving
potassium into the cells. Administration of sodium bicarbonate will also help correct the metabolic acidosis that is
often present in these patients. The recommended dose of
sodium bicarbonate administration is 0.3 X base deficit X
body weight (kg). One half of this dose can be given slowly
IV over 15 to 30 minutes and then acid/base status can be reassessed. The effect on the plasma potassium concentration
begins within 30 to 60 minutes and may persist for hours.
The effects of calcium, insulin and dextrose, and sodium
bicarbonate are transient. The administration of these drugs
buys the clinician time to treat the underlying cause of the
urinary tract disorder.
KIDNEY
Acute renal failure is the most common urinary tract
emergency associated with the kidney. The causes of acute
renal failure (ARF) are numerous and include infectious
(leptospirosis, bacterial pyelonephritis), ischemia (hypovolemia, cardiogenic, thrombosis), toxins (aminoglycosides,
ethylene glycol, nonsteroidal antiinflammatories etc.), and
metabolic such as hypercalcemia. The diagnosis of ARF is
made when an animal is severely azotemic and pre-renal and
post-renal causes have been ruled out. Initial diagnostics
should include a complete blood count, chemistry screen,
urinalysis, +/- urine culture. Further diagnostics should be
focused on defining the underlying cause of the renal failure.
In severely azotemic patients, evaluation for the previous
mentioned electrolyte and acid/base changes is warranted. A
urinary catheter should be placed to monitor urinary output.
The patient should be volume replaced. If urine output is inadequate (<1-2 ml/kg/hr) after normalization of blood pressure and blood volume, diuretic therapy should be considered. Mannitol is an osmotic diuretic and can be administered as a slow bolus (0.5 - 1.0 g/kg, 10%-20% solution, over
15-20 minutes). Diuresis should be noted within one hour. A
second dose may be repeated but volume overload should be
avoided. Furosemide (a loop diuretic) can be given at
2mg/kg intravenously as a bolus and followed by a constant
rate infusion of 1mg/kg/hr. Diuresis should be noted within
one hour of giving the bolus. Dopamine at a constant rate infusion of 1 to 3ug/kg/min can promote renal vasodilation
and increased renal perfusion. A continuous lead II ECG
should be utilized to monitor for cardiac arrhythmias or
tachycardia which are potential side effects when administering dopamine. Should all attempts to increase urine output fail, peritoneal or hemodialysis should be considered.
URETER
The common emergencies associated with the ureters include rupture and obstruction. Ureter rupture may occur secondary to blunt trauma, neoplasia, or obstruction. Obstruction may occur secondary to ureteral calculi, neoplasia, or
strictures. Clinical signs of ureter dysfunction may be nonspecific but commonly reported signs include lethargy, sublumbar pain, vomiting, and anorexia. Abdominal distention
may occur if urine leakage communicates with the abdominal cavity (the ureters are located in the retroperitoneal
space). The clinical signs may occur suddenly but often are
gradual over a few to several days. The diagnosis of ureter
abnormalities is usually provided by excretory urography although abdominal ultrasound can provide valuable information as well. Therapy of ureteral abnormalities should be directed at cardiovascular stabilization and correction of lifethreatening metabolic abnormalities followed by surgical
correction of the ureteral abnormality.
URINARY BLADDER
Rupture of the urinary bladder occurs with blunt abdominal trauma, aggressive palpation of a damaged urinary bladder, overdistention from urethral obstruction, or poor urethral catheterization technique. Clinical signs of urinary
bladder rupture will vary depending upon the cause. Animals
with ruptures secondary to urethral obstruction will often already be uremic and extremely ill. Patients with traumatic
rupture after blunt abdominal trauma may not manifest signs
of uremia until 12 – 24 hours later. Ability to pass urine does
not rule out urinary bladder rupture. Positive contrast cystography with leakage of contrast material out of the bladder
provides a diagnosis. Injecting contrast and observing with
fluoroscopy will optimize localization of the leak.
Treatment of urinary bladder rupture includes stabilization of the cardiovascular system, treatment of the lifethreatening metabolic effects of the uremia, and definitive
surgical repair of the bladder. In unstable, severely uremic
patients, benefit may be gained from stabilization with peritoneal dialysis prior to attempting general anesthesia and
performing surgery. Urine can be irritating to the peritoneal
space so copious lavage of the abdominal cavity with sterile
saline is recommended at surgery. Septic peritonitis may be
present if there was a urinary tract infection at the time of the
rupture and this possible complication should be kept in
mind.
147
in urine leakage into the abdominal cavity causing signs
similar to rupture of the urinary bladder. Diagnosis of urethral rupture is provided by positive contrast urethrography.
It is advantageous to perform the study using fluoroscopy so
that the location of the leak can be more easily identified.
Definitive repair of the urethra may require surgical re-anastomosis although passage of a urinary catheter and healing
by second attention is sometimes effective for more distal incomplete tears.
Urethral obstruction is one of the more common urinary
tract emergencies. Clinical signs are straining to urinate
without any passage of urine. These conditions constitute an
immediate emergency to prevent the development of the severe metabolic derangements noted above as well as prevention of urinary bladder rupture. A urinary catheter should be
passed to the level of the urethral obstruction and the urethra
should be flushed to try to flush the urethral calculus/calculi
back into the urinary bladder or to try to pass the urinary
catheter around the the urethral stone. Urethral hydropulsion
can facilitate passage of the catheter. This can be achieved
by placing the urinary catheter up to the obstruction, sealing
around that catheter so no fluid escapes from the tip of the
penis during flushing. Simultaneously while flushing, a finger is placed in the rectum and pressure is applied over the
pelvic urethra to occlude it. The sealing around the tip of the
penis and the occlusion of the pelvic urethra creates a closed
system of the urethra around the urethral calculus. Flushing
into this closed area will cause distention of the urethra. The
distention will hopefully free the urethral caculus or caculi
and it will be flushed back into the urinary bladder when the
occlusion of the pelvic urethra is released. In animals where
patency of the urethra cannot be achieved via a catheter, then
emergency perineal urethrostomy may be necessary.
Once the urethral obstruction is relieved, the patient
should be closely monitored. Post-obstructive diuresis, in
rare instances, can be profound leading to severe dehydration, hypovolemia and hypokalemia if left untreated.
URETHRA
Rupture of the urethra may occur due to trauma, pelvic
fractures, urethral obstruction, and poor urethral catheterization technique. Clinical signs will vary depending upon the
location of the rupture. Rupture of the urethra distal to the
neck of the bladder will result in urine leakage into the surrounding soft tissues and into the hindlegs. This is often
manifested as swelling, pain, and cellulitis in those areas.
Rupture of the urethra near the neck of the bladder can result
Summary
Initial approach to the patient with a urinary tract emergency should focus on evaluating and stabilizing tissue perfusion and the severe metabolic disturbances associated with
severe uremia. Once these critical issues are addressed, more
definitive evaluation and treatment of the specific urinary
tract defect should be performed.
149
How to cover major skin losses with flaps
Gilles P. Dupré
Dipl. ECVS, DIU pneumology and thoracoscopic surgery, Clinique Frégis Arcueil/Paris
The surgeon’s choice for skin closure depends on many
factors:
• Size and localization of the wound
• Potential contamination
• Age of the wound
From these factors the practicionner will have to make
his decision on how to close the skin defect:
• Primary, delayed primary, secondary closure. or second intention healing.
• Direct apposition, local flaps, distant flaps, graft
Finally, given the ability of small animals to potentially
heal by second intention, many veterinarians spend a lot of
time and money in bandaging techniques to cover a wound
that has been improperly closed and finally dehisced. The final cosmetic result is often poor and the psychological impact over the client may be disastrous whereas a correct timing in closure and correct technique would have been possible and would have save time and money.
GENERAL PRINCIPLES FOR TREATMENT
OF MASSIVE SKIN LOSSES
Basic skin vascular supply
Vessels of the sub-dermal plexus run parallel to the skin
in the sub-cutaneous tissue and provide most of the vascular supply of the skin. Direct cutaneous arteries vascularize
large territories of skin which can be used as axial patern
flaps.
Timing for reconstruction
On fresh wound or after tumor removal, reconstruction
can be done readily. In all other cases, the surgeon must wait
for a nice uncontaminated wound, and, in some cases, for a
granulated bed.
Aseptic surgery
Major skin surgery must be conducted with the same
type of principles than an orthopedic surgery
Granulation bed
The granulation bed can be left in place partially or totally excised at the time of final closure. We usually trim the
edges of the granulation bed to obtain a nice skin apposition.
Dead space
Dead space must be closed by several means: Active or
passive drains, tacking sutures (dangerous since they can
damage the direct cutaneous arteries), and bandages.
Local flaps
Local flaps are useful to cover small defects and prevent
dehiscence over wounds that would otherwise be closed under tension.
Basic principles
The donor site must be rich in loose skin
The flap must be mobilised parallel to the tension lines
Two small flaps are better than one big
A bipedicular flap is richer in blood supply than a monopedicular flap
Never incise the base of the flap : it may include a direct
cutaneous artery
A ratio base/length of 1/1 to 1/2 is generally used but depends on the vascular supply of the base of the flap
FLAP TYPES
Monopedicular and double monopedicular
flaps
These are the “basics” of skin reconstruction and must be
used in any occasion of mass removal, specially over the
flank and trunk area. They also permit the coverage of the
donor site of massive axial pattern flap.
Bipedicular flap
By essence a bipedicular flap is a relaxing incision. It is
specially usefull to cover distal limb injuries.
Suture material
Transposition, rotation and interposition
flap
Small suture material is preferred (Braided or monofilament absorbable dec. 1,5 to 3 for sub-cutaneous and dec. 1,5
to 2 nylon for the skin)
Most of these flaps rotate around a point or an axis. Among
those, the inguinal and axillary flaps are specially usefull to
cover local deficits over the inguinal or sternal areas.
150
In many cases several types of flaps can be used simultaneously. For example, the excision of a huge fibrosarcoma
over the shoulder area will be covered by combination of
two monopedicular flaps harvested over the neck and trunk
areas combined with rotational flaps from the axillary region
to cover the most ventral aspect of the wound.
Distant flaps (pouch flaps)
By definition a pouch flap is a direct distant bipedicular
flap.
vascular supply of an axial pattern flap is well-known.
The design of the flap is governed by the arborization of
a known direct cutaneous artery. Thanks to M. Pavletic
and co-workers many axial pattern flaps have been described. The flap is usually named by the name of its direct cutaneous artery : Omocervical, thoracodorsal, superficial brachial, cranial and caudal epigastric, ventral
and dorsal circumflex iliac, genicular, caudal auricular,
superficial temporal…
Indications and limits
General principles
A pouch flap is indicated to cover major deficits distal to
the elbow or the knee joints. We have used it in many different formats from 1,5 kg Yorkshire to 60 kgs Bull mastiff.
Insular or peninsular
Surgical technique
The vascular supply of a pouch flap comes from the
pedicles of the donor area and progressively from the recipient bed. The surgical treatment always follow the same
steps:
• Preparation of the recipient bed. It can be a fresh or a
granulated wound.
• Flap design. The flap is designed over the chest or
flank area and two incisions are made perpendicular
to the long axis of the body to create the tunnel in
which the limb will be slided.
• Position of the limb. Once the limb is positionned in
the tunnel, the cranial and caudal incisions are partially closed. No tacking sutures are placed to avoid damage to the underlying blood vessels.
• Flap section. After 2 weeks, the dorsal and ventral pedicles are cut and the limb is freed from its attachments.
In some occasions the pedicles are cut stepwise.
• Closure. Once the flap has taken over the initial
wound, it can be completely closed over the limb.
• Pain control, drainage and bandages are mandatory to
allow a good healing.
A peninsular flap remains attached to the skin surrounding the direct cutaneous artery, whereas the insular design
remains attached only to the vascular pedicle. We regularly
use the insular design of caudal epigastric and thoracodorsal
flaps.
Anatomical landmarks
These landmarks have been described for many axial
pattern flaps. However, in many instances the flap design
can be extended to the controlateral side or in an L fashion.
Dead space
The dead space needs to be drained and compressed in a
bandage. Tacking sutures are avoided over the flap.
Surgical technique
Flap size
The surgeon should overestimate the size of the flap
since it has a tendency to shrink a little bit.
Dissection
It needs to be conducted very safely around the vascular
pedicle, anatomy of which should be well known.
Cutaneous trunci and sub-cutaneous nedd to be incorporated in the flap.
Pros and cons
The main advantage of this technique is an almost 100 %
“graft intake”. The main disadvantage is a staged procedure
with 2 major surgeries and the incomfort for the patient having “one leg in the chest”.
Closure of the donor area
The donor area is closed using monopedicular and rotationnal flaps.
CONCLUSION
AXIAL PATTERN FLAPS
The main particularity of this type of flap is its vascular supply. In cases of pedicular flaps or pouch flaps,
the vascular supply of the pedicle is random whereas the
Given the peculiar vascular supply of the skin of dogs
and cats, the veterinary surgeons can use a great variety of
flaps to cover major deficits. In these conditions needs for
grafts become very rare.
151
Surgical treatment of prostatic diseases
Gilles P. Dupré
PREOPERATIVE
A candidate to surgical treatment of prostatic disease always suffer of specific or non specific alterations of its physical status. Therefore a thorough physical examination is
mandatory. When a big cavitation is suspected and when it
is accessible to a needle puncture we recommend to aspirate
and decompress it as soon as possible. Surgery can then be
delayed. Because renal disease and urinary tract infection
are two major complications of prostatic disease and surgery
specific attention must be carried to appropriate selection of
antibiotics and to adequate monitoring of renal function.
Preoperatively, an urethral catheter must be set in whenever
stranguria, dysuria or pollakiuria exist. Urinary excretion
must be monitored with the indwelling catheter in place in a
closed collection system.
ities of the omentum to do internally what drains do externally. The omentum (need not to be divided for this use) is
brought through natural or artificially created cavities in
the prostatic or paraprostatic tissue. Results on prostatic
epiploïsation are encouraging!
Prostatectomies
Theoretically, indications for prostatectomies are numerous: Non metastatic tumors, chronic recurrent prostatitis,
prostatic trauma. But it carries majort pitfalls as surgical
complications (Bladder necrosis, stenosis or leak at the anastomosis) and urinary incontinence. 85 to 100% of animals
having prostatectomy will suffer from detrusor instability or
urethral incompetence. However, a local prostatectomy with
a specific ultra-sound device seems to have good results.
POSTOPERATIVE CARE
SURGICAL TREATMENT
Surgical approaches
A xypho-pubic celiotomy is necessary to provide a good
surgical field. Plastic drapes and laparotomy sponges are
useful for lavaging the surgical site and for protecting the
rest of the abdominal cavity.
Surgical techniques
Culture and biopsy
Omentalisation
Because of its richness in vascular and lymphatic supply, the omentum has many capacities which led to its
nickname: the surgeon’s best friend!. The basis for omentalisation of the prostate gland is the use of natural capac-
It includes:
- Fluid therapy and enteral feeding if the patient is not
eating spontaneously
- Blood work repeated according to progress
- Control of pain
- Antibiotics
The most serious complication is sepsis or septic shock. It
can occur secondary to spontaneous rupture of prostatic or
paraprostatic abcesses but also secondary to surgery of an infected prostate. Early signs of multiorgan failure must be recognized to be aggressively treated. Congestive mucous membranes characterise the hyperdynamic state of septic failure .
Urinary incontinence seems to be rare with omentalisation,
however it can appear secondary to detrusor instability or urethral sphincter incompetence. Most of them resolve after medical treatment or temporary cystostomy tube.
153
Use of laparotomy or laparoscopy
in the treatment of perineal hernia
Gilles P. Dupré
Current proposals for treatment of perineal hernia rely on
closure of the pelvic diaphragm. Pros and cons as well as results and complications rates have been published fort most
of them. Muscle apposition techniques resulted in excessive
tension on the external anal sphincter and could not be used
in face of severe muscle atrophy. Complications ranged from
28,6% to 61% (Burrows and Harvey, JSAP, 1973- Bellenger,
Aust Vet Journ, 1980) and recurrence rate from 10 to 46%
(Pettit Cornell Vet Journal 1962, Burrows and Harvey, JSAP,
1973). To overcome this problem muscle transpositions
were proposed. The superficial gluteal muscle transposition
involved a large approach and filling of the ventral part of
the defect was not easy. Complications ranged from 15 to
58% (Spreull and Frankland JSAP 1980- Weaver and
Omamegbe JSAP 1981) and recurence was rated 36%
(Weaver and Omamegbe JSAP 1981).The internal obturator
flap had been first been described in 1963 but the technique
gained popularity since 1978 and was published in 1983 by
Hardie and others VS, 1983. Complications ranged from 19
to 45% (Hardie and others Vet. Surg 1983- Sjollema and Van
Sluijs, Vet Quaterly, 1989) and recurrence from 2,38 to
18,75% (Hardie and others Vet. Surg 1983, Orsher Vet Surg,
1986). Also, because of muscle atrophy, combined techniques have been proposed as internal obturator and superficial gluteal transposition (PJ Raffan, JSAP, 1993) or the use
of remote flaps as the semitendinosus flap (JM Chambers
and CA Rawlings, JSAP, 1991). Closure with stainless steel
(Viant, Meynard and J Drouault) or polypropylene mesh
have also been proposed (Larsen JAVMA, 1966, REE
Clarke, Aust Vet Pract, 1989) but results and complications
have not been published.
Besides rupture of the pelvic diaphragm other lesions as
rectal diseases, bladder retroflexion and prostatic diseases
are encountered during perineal herniation and have been
specifically studied (Dupré and Prat PMCAC 1992). They
contribute to the severity of the hernia and may even discourage further treatment. In a previous retrospective study
on 60 cases of perineal hernias the authors specifically
screened the incidence of associated lesions and defined a
new protocol of treatment in which a laparotomy was used
as a first step of treatment in specific indications. Since then
a new prospective study was engaged on 142 new cases with
specific criteria for inclusion in the laparotomy group. More
recently laparoscopy has been introduced in veterinary
surgery. In our practice it has been used in place of laparotomy and allowed a proper evaluation of the abdominal cavity as well as colopexy and vas deferens pexy. Many practicionners, frightened by the technicity of perineal hernia repair recommend a medical treatment when surgery is the
sole possibility for definitive cure. The consequence is an
aggravation of the process leading to bilateral hernias, severe
rectal diseases and bladder retroflexion .
Given the severity of the cases presented to our hospital
we defined the following protocol for treatment of perineal
hernia in the canine. We believe this protocol to be useful in
any case of perineal hernia
1- Upon admission: Is the bladder in place?
Retroflexion of the bladder is the most life threatening
problem of perineal hernia and its early recognition is necessary. If catheterization is impossible a perineal cystocentesis must be done, then the bladder can be manually reduced
and catheterization becomes possible. Diuresis is monitored
through a closed-circuit.
2- Complete physical exam and lab work
Given the age of the patients concurrent diseases are not
rare, particularly renal or cardiac diseases. Also some patients can be debilitated by tenesmus and anorexia. Preoperative enteral feeding becomes necessary.
3- Diagnosis of associated lesions
Gentle enemas allow rectal emptying and diagnosis of
lateralization and rectal deformations. Preoperatively, ultrasound of the prostate is mandatory for diagnosing prostatic
diseases.
154
4- Classification of surgical candidates for
a laparotomy. or a laparoscopy
In our experience the presence of one or more of the followings are an indication for an exploratory laparotomy or scopy
- retroflexion of the bladder,
- surgical prostatic disease,
- bilateral hernia with bilateral or ventral rectal deviation
- recurrence
- patient debilitation.
During laparotomy only patients suffering from vesical
retroflexion undergo a vas deferens or a cysto-pexy but
colonopexy, prostatic biopsies and castration are done on all
laparotomized patients. All these procedures can be conducted with a laparoscopy or a regular laparotomy. We have
shown more recently that a standard vas deferens pexy does
not prevent bladder retroflexion and that a cystopexy should
be done whenever a bladder retroflexion is present.
5- Medical care
When a laparotomy has been the first step, herniorraphy is delayed for about 48 hours during which rectal
emptying and enteral feeding (no residue) can be accomplished.
In some debilitated patients the herniorraphy can be
delayed even further. Amazingly most patients in which
a pexy of herniated organs has been done do very well
for a period of time. However perineal herniorraphy must
not be delayed too long.
6- Perineal herniorraphy
Herniorraphy is the last step of this protocol. When a laparotomy has first been done, closure becomes real easy.
155
Open and close safely the digestive tract
Gilles P. Dupré
Dehiscence used to be a major complication in intestinal surgery. In one study in the dog, Allen, Smeak and
Schertel observed 15,7% of wound dehiscence; the mortality in this group was 73,3% against 6,9% in the non dehiscent group. Another study by Wylie and Hosgood
showed a 7% dehiscence with a group mortality of 80%
against 7,2% in the non dehiscent. Given these numbers
we completed a retrospective study on 116 cases of intestinal tract surgery (entero or enterectomies) in cats and
dogs treated in our hospital during a 6 year period of time.
Among those, 85 cases could be followed up through
recheck and an owner questionnaire. Our dehiscence rate
was 1%. It is similar to a recent study from Ohio State university comparing simple continuous and simple interrupted sutures.
BASIC SURGICAL TECHNIQUES
ic and mucosal bridging is effective only after 2 weeks. Finally, at least in man, the mucosal inversion seems to be
painful and tends to modify intestinal motility.
Effects of everting sutures
Although used in the past to overcome the disadvantages
of inverting pattern they are stenotic and create a huge local
inflammation. During the lag phase their tensile strength is
low which may render this type of anastomosis more prone
to dehiscence.
Effects of appositional sutures
This pattern allows direct apposition of the arterio-venous plexuses, early epithelialization and collagen formation. However mucosal inversion is still a concern.
What suture material, what needle, what
diameter?
What factors influence our choice
The intestinal wall structure
The sub mucossa is rich in elastin and collagen fibers; also the majority of vessels run into the submucosa. Then it is
the most solid layer of the intestine and any suture of the intestinal tract must penetrate the sub-mucosa.
Healing of the digestive tract
During the lag phase (from day 1 to 3) most of the holding power of the anastomosis is due to the sutures. During
the proliferation phase (day 3 to 14) the fibroblasts product
collagen and the sutures must not interfere with collagen
production. During the maturation phase (day 15 to 180) the
collagen reorganizes; during this period the sutures have no
role.
Effect of suture patterns
Effects of inverting sutures
They look proof as soon as they are done. Also, their tensile strength is greater than other patterns up to the fifth day,
but they carry a major cons. This suture pattern is very stenot-
Everything has been used in the past : from Gut to stainless steel. Today two main types of suture material meet the
criteria -Holding during the lag phase and avoiding a violent
inflammatory reaction- the synthetic braided absorbable as
Polyglactin 910 and polyglycolic acid or the absorbable
monofilament as Polydioxanone and polyglyconate. We prefer these latter because of their longer half life, their very
small tissue drag and local reaction. Decimal 1 to 1,5 (4/0 or
5/0) on a round needle is preferred in the cat. In the dog we
can use decimal 1,5 to 2 (4/0 or 3/0)
Simple interrupted, simple continuous,
crushing?
A fluorescein study has been conducted to compare histologically the suture line of simple interrupted, simple continuous or crushing sutures. It reveals that crushing techniques generate many tissular trauma, necrosis, hemorrage
and mucocœle formation. They should be avoided. A simple
continuous suture promotes a better vascularisation of the
wound up to day 20. Adhesions and mucosal eversion are
less frequent.
156
SURGICAL APPLICATIONS
ADJUVANT TECHNIQUES TO PROTECT
THE SURGICAL SITE
Enterotomy
Omentalisation
1. Incision in healthy tissue on the antimesenteric border
2. Excision of protruded mucosa
3. Closure with simple continuous or simple interrupted
The omentum, rich in blood vessels helps in nutrition,
drainage and protection of the anastomosis. Suture is unnecessary.
Serosal patch
Enterectomy
1. Pressing back the intestinal content
2. Placement of atraumatic intestinal clmaps and of the
assistant fingers.
3. Ligation of the mesenteric vessels
4. Resection
5. Excision of the everted mucosa
6. Adjustement of diameters
7. Anastomosis
8. First suture on the mesenteric border
9. Second one on the antimesenteric
10. Completion of the anastomosis
11. Closure of the mesentery
A serosal patch is indicated in case of mulitple injuries or
for non resequble site as the descending duodenum. Also it
is a very convenient technique to cover a dehiscent wound.
Pedicle graft
In some cases a vascularised segment of jejunum can be
used to cover a defect.
CONCLUSION
Many veterinarians continue to believe that the digestive
tract needs to be hermetically closed after its opening. This
leads to an exagerated use of sutures, tension and trauma to
the tissue. On contrary a tensionless appositionnal suture
will not impair healing and will promote an early fibrin formation and seal. The early use of the digestive tract by the
body will also promote contraction and vascularisation that
will diminish the risk of dehiscence. Therefore an early feeding (24 hours post-operatively) is recommended.
157
Video-surgery (laparoscopy, thoracoscopy),
friend or foe?
Gilles P. Dupré
INDICATIONS OF MINI-INVASIVE
SURGERY
Indications for laparoscopy are numerous and depend on
the technicity of the surgeon. It include the obtention of
specimen, ovariectomy and ovario-hysterectomy, orchyectomy, cholecystectomy, prophylactic gastropexy, colposuspension etc…In thoracoscopy the indications are growing. The
camera and instruments can be used as a diagnostic tool to
get cultures and biopsies.
But we recognize more and more therapeutic indications
and have successfully performed many pericardectomies,
lobectomies, omentalisation of chylothorax, emphysematous bullae and foreign body removal. Also, in some instances thoracoscopy can be used as an aid to reduce the surgical approach (video-assisted thoracic surgery) and this
technique has gained a lot of popularity among the human
surgical community.
SPECIFIC REQUIREMENTS
OF MINI-INVASIVE SURGERY
Specific material
Mini or noninvasive surgery requires specific material: A
tiltable surgical table, a complete video setting with 0° thoracoscope and laparoscope, a three CCD camera and recording facility. In the abdominal cavity and in some instances in
the thoracic one, an insufflator will also be used. An electrosurgical unit with uni and bipolar cautery for endoscopic instruments as well as irrigation and vacuum system are necessary. All types of endoscopic instruments must also be
available: laparoscopic and thoracoscopic trocarts, endograspers, endodissectors, endoretractors. Endosutures and
endoligatures as well as endoclips and surgical staples are
necessary for many procedures.
damaging intracavitary organs. In laparoscopic surgery, this
space is obtained by insufflating carbon dioxide into the abdominal cavity, creating a pneumoperitoneum. In thoracoscopic surgery, the space can be created in several ways. An
infusion of carbon dioxide unilaterally at a maximum pressure pressure of 3 cm of water may be sufficient to collapse
the lung and work efficiently and may compromise the gaz
exchange. Unilateral ventilation with pulmonary exclusion
using specific endobronchic devices can also be used but require more monitoring and anesthetic equipment. Therefore
as with human neonates and infants we developped thoracoscopic techniques without pulmonary exclusion by placing
the patient in dorsal recumbency or by using adequately intrathoracic retractors.
Monitoring
Monitoring the patient during the procedure is mandatory and requires an anesthetist (nurse or vet) and instrumental equipment: Spirometer, EKG, Pulse oxymetry and moreover capnography. We believe that miniinvasive surgery,
with or without carbon dioxide insufflation, does require
capnography.
Specific training
Finally, beside the list of instruments and setting necessary starting with miniinvasive surgery, requires learning
and experience. A new philosophy of surgery where the minimum morbidity is the rule must be gained and for this,,
hours, days and weeks of specific trainings are necessary.
Throughout the learning process of miniinvasive surgery, I
usually recommend to start with arthroscopy, then laparoscopy and finally with thoracoscopy.
Obtention of a space to work
MINI-INVASIVE SURGERY:
FRIEND OR FOE?
Miniinvasive surgery requires the obtention of an “empty space” to be abble to manipulate the instruments without
Less pain, shorter hospital stay, small incisions are the
usual benefits of miniinvasive surgery. In veterinary mini-in-
158
vasive surgery, the owner’ satisfaction is another source of
benefit for the practicionner. However these benefits should
not make us forget the number one rule in mini-invasive
surgery: do not put the patient at risk.
To achieve this, several points should be kept in mind:
- At the beginning of the experience in mini-invasive
surgery, procedures are usually longer than open-surgery.
- An emergency conversion to open-surgery must always
have been planned and discussed with the owner previously .
- One must respect his own learning curve and go step by
step in this process
Laparoscopy and thoracoscopy are new, and really exciting tool that allow to see, diagnose and treat many intraabdominal and thoracic diseases. It just reached a certain level of expertise in human surgery and is practiced
by few veterinary teams throughout the world. Given the
low morbidity of open abdominal approaches in veterinary medicine, the advantages of laparoscopic surgery
can be argued. However, the advantages of thoracoscopy
on thoracotomy are obvious and we are confident that the
technique is promised to a great future in veterinary medicine.
159
Uso delle diete idrolizzate nella diagnosi
e nel trattamento dell’ipersensibilità alimentare
Fabrizio Fabbrini
Clinica Veterinaria Papiniano, Milano
L’allergia alimentare, secondo vari Autori, ha un’incidenza del 1-5% nei cani e del 6% dei gatti con problemi
dermatologici. Inoltre, rappresenta circa il 10-15% delle malattie allergiche, ed è spesso segnalata (75% dei casi) in associazione ad altre malattie come la DAP o la Dermatite atopica, da cui talvolta è difficile da distinguere per la presenza
dello stesso quadro clinico.
A tutt’oggi l’unico metodo per la diagnosi, riconosciuto
attendibile internazionalmente, si basa sull’uso di una dieta
ad eliminazione (che contenga una sola fonte di carboidrati
e una sola fonte proteica mai ingerite prima, scelte in base
all’anamnesi alimentare del paziente) per almeno 6-8 settimane, di una risposta positiva (scomparsa o diminuzione importante della sintomatologia), seguita dall’induzione di una
recidiva della malattia dopo somministrazione del cibo abituale (dieta di provocazione).
Idealmente solo le diete di tipo “casalingo”, sono in grado di ottemperare a quanto sopra esposto, inoltre, hanno il
vantaggio di non contenere aditivi “a rischio” di una intolleranza alimentare; per contro, sono diete “frustranti” per alcuni proprietari privi di tempo da dedicare alla loro preparazione, sono carenti da un punto di vista nutrizionale e non indicate per somministrazioni prolungate nel tempo.
Negli ultimi anni sono state immesse in commercio diete bilanciate specifiche per cani e gatti a base di proteine
idrolizzate. Il concetto su cui si basano è che l’idrolisi porti
alla formazione di peptidi con peso molecolare insufficiente
ad indurre una reazione immunitaria, in quanto è stato ipotizzato che gli allergeni chiamati in causa nell’allergia alimentare, siano composti da glicoproteine idrosolubili dal peso molecolare compreso tra 10 000 e 60 000 dalton.
In base a questi dati sono stati rivalutati 7 cani con sintomatologia pruriginosa non stagionale compatibile con una
allergia alimentare, precedentemente vagliati tramite dieta
casalinga o diete “ipoallergeniche” non idrolizzate. Tutti e
sette, non avevano in precedenza risposto a svariate diete
“ipoallergeniche” mentre, tre che avevano utilizzato anche
diete “casalinghe”, erano risultati allergici alimentari.
Tutti gli animali sono stati sottoposti a test dermatologici e trial terapeutici per eliminare le infezioni batteriche, da
lieviti ed ecto/endoparassitosi presenti, ed identificare la
concomitanza di altre malattie allergiche.
È stata utilizzata una dieta ad eliminazione a base di amido di mais, proteine di soia idrolizzate ed olio di cocco, sino
ad ottenere risposta clinica, per un periodo massimo di 8 settimane. Ad ogni risposta clinica, seguiva l’esposizione alla
dieta a provocazione di base del paziente per un periodo
massimo di due settimane per confermare od escludere la
presenza dell’allergia alimentare.
I tre cani precedentemente vagliati con dieta “casalinga”,
hanno risposto positivamente alla dieta idrolizzata, riconfermando la diagnosi d’allergia alimentare.
Anche i restanti quattro cani, nonostante non avessero in
precedenza risposto a diverse diete “ipoallergeniche”, hanno
risposto positivamente alla dieta idrolizzata e successiva dieta a provocazione, permettendo così di emettere diagnosi di
allergia alimentare.
I tempi necessari per ottenere la scomparsa o diminuzione significativa della sintomatologia, sono stati: entro la prima settimana per un cane, entro la seconda per tre, entro la
terza per due ed entro quattro settimane per un solo cane.
La dieta idrolizzata è stata utilizzata come dieta di mantenimento e sino ad oggi non sono stati segnalati problemi
da parte dei proprietari.
Questi dati, seppur statisticamente non significativi, stanno ad indicare che nella diagnosi dell’allergia alimentare, la
risposta alla dieta idrolizzata sembra essere molto rapida, ed
avere una buona correlazione con i risultati delle diete “casalinghe”, suggerendo inoltre, un valore diagnostico superiore delle diete idrolizzate rispetto a quelle “ipoallergeniche” non idrolizzate.
Bibliografia
1.
Groh M, Moser E, Diagnosis of food allergy in the non-seasonally
symptomatic dog using a novel antigen, low molecular weight diet:
a prospective study of 29 cases. Vet Aller Clinic Immunology,
1998, 6: 5-6.
2. Roudebush P, Hypoallergenic diets for Dogs and Cats. In: Bonagura
JD, ed: Current Veterinari Therapy XIII. Philadelphia: WB Saunders,
2000, 530-535.
3.Scott DW, Miller WH, Griffin CE: Skin Immune System and Allergic
Skin Diseases. In: Muller and Kirk’s Small Animal Dermatology, 6th
ed. Philadelphia: WB Saunders, 2001, 615-627.
161
Ossimetria pulsatile e capnometria: pro e contro
Emilio Feltri
Med. Vet. Tortona (AL)
CAPNOMETRIA E CAPNOGRAFIA
Cenni Storici
Anche il capnografo come il pulsossimetro viene ideato
e costruito durante la seconda guerra mondiale.
Il motivo per cui viene inventato è la ricerca di uno
strumento che permettesse un controllo della anidride carbonica negli spazi angusti e non aerati dei sottomarini, e
per consentire all’equipaggio di sapere quando risalire per
depurare le vasche di soda deputate al trattenimento dell’anidride stessa.
Tecnologia e Funzionamento
Il capnografo rileva la quantità di anidride carbonica
(CO2) contenuta nella fase finale dell’espirazione.
Questo valore è paragonabile con un errore di 5 mmhg in
eccesso (come tutti i monitoraggi non invasivi) alla pressione parziale arteriosa della CO2.
Quest ultima può essere ricavata con precisione dall’emogasanalisi che però oltre ad essere invasivo come metodo,
è limitatao al momento del prelievo.
Le tecniche di campionamento dei capnografi sono essenzialmente due:
1) Tecnica Mainstream: Prevede una sonda di medio
grandi dimensioni molto delicata che viene posizionata tra
tracheotubo e circuito repiratorio.
Al passare del flusso, la sonda che null’altro è che una
cella galvanico ottica, legge un impedenza luminosa di ritorno ed elabora il dato.
Ha il vantaggio di fornire un valore in tempo reale, ma
come detto prima, in pazienti molto piccoli costituisce uno
spazio morto strutturale troppo imponente. Inoltre le lenti di
lettura spesso per via dell’umidità durante le fasi respiratorie si appannano e non leggono più.
2) Tecnica Sidestream: Questa metodica prevede un
campionamento di aria tra tracheotubo e circuito a mezzo di
aspirazione (da 100 a 250 ml/min) e sucessiva analisi del
campione in una camera detta Cuvetta posta sul pannello
frontale della macchina.
Logicamente i valori poi espressi saranno di pochissimo
in differita.
Ha il vantaggio di costituire uno spazio morto ridottissimo, infatti per i pazienti più piccoli, esistono dei campionatori da inserire all’attacco del tracheotubo sfilando l’originale.
Molto meno delicato del precedente, richiede la pulizia della cuvetta se molto umida a fine intervento e la sostituzione della linea di campionamento allorche troppo usurata (ricordo che in realtà la linea sarebbe monouso).
Esiste infine una tecnica che riconduce comunque ad un
sidestream si tratta della:
3) Tecnica Microstream: Prevede sempre la linea di campionamento collegata come per la sidestream ad un campionatore tra tracheotubo e circuito, solo che il campione non va ad
una cuvetta ma direttamente attraverso un filtro per il trattenimento dell’umidità alla macchina che elabora il valore finale.
Quindi ha i vantaggi del sidestream e del Mainstream
(lettura in tempo reale) allo stesso tempo.
Infine il campionatire in microstream è l’unico che ci
può fornire il dato in pazienti non intubati.
Interpretazione del dato campionato:
EtCO2 (End Tidal dell’anidride carbonica)
Come per tutti i monitoraggi suggerisco sempre non fossilizzarsi su una singola variazione del valore monitorato ma
di studiare un trend dello stesso durante un certo arco di tempo (3-5 minuti).
Comunque, vediamo ora di focalizzare innanzitutto quali sono i valori fisiologici della anidride a fine espirato.
I valori fisiologici, prendendo in considerazione che la
situazione arteriosa prevede un massimo di 50 ed un minimo di 30 mmhg di CO2 e sapendo da prima che la sottostima del capnografo rispetto un analisi gasematica è di circa 5mmhg, i valori che posso considerare limiti (dove anche posizionerò i miei allarmi) saranno di 5 mmhg in più e
cioè: 35-55 mmhg.
Dunque la condizione di valori più bassi di 35mmhg di
EtCO2 rispecchieranno una situazione di troppa anidride rimossa con conseguente calo arterioso della pressione parziale della stessa.
A quale motivi può far capo tale condizione?
Considerando l’unità funzionale del polmone, cioè, alveolo e componenete circolatoria annessa, potremo identificare la causa relativa ad una o l’altra parte.
162
Se si tratta di un problema relativo all’alveolo le cause
possono essere: Iperventilazione conseguente a superficialità del piano anestesiologico, percezione del dolore profondo, ipertermia o ipertensione. Quindi cercheremo tra queste
indagando il nostro miglior monitor: Il Paziente.
Se invece il problema è relativo alla componente vascolare la causa può essere: mancato scambio di Co2 per ipotensione, conseguente a eccessiva somministrazione di alogenati, scarsa infusione di fluidi, emorragie, dolore, eccessivo approfondimento del piano anestesiologico…etc.
Per contro in condizioni di EtCO2 superiore ai valori
massimi, analizzando ancora la componente respiratoria e
quella vascolare si potrà dedurre:
Ipoventilazione da eccessivo approfondimento dell’anestesia, o da depressione centrale respiratoria di natura farmacologica.
Iperperfusione da ipertensione arteriosa, o da eccesso di
fluidi somministrati, o da farmaci (Dopamina).
Una volta capito il problema inteso come sintomo e ricercata la causa bisogna ovviamente porre il rimedio corretto.
Come si può dedurre da quello affermato prima il numero di informazioni che ci da questo strumento non ha eguali:
Ci informa sullo stato di ventilazione e perfusione del paziente, ci avverte di condizioni preambolo di arresto cardiaco, ci informa infine sullo stato di efficienza del circuito respiratorio e della calce sodata deputata alla depurazione della CO2 .In ultimo ma non meno importante ci avvisa se l’intubazione è stata eseguita in modo corretto.
Vediamo infine di intepretare la grafica che ci viene proposta dal capnografo.
Possiamo analizzare la singola curva inerente un atto respiratorio e le sue variazioni rispetto la norma, tuttavia ricaviamo più informazioni da una serie di curve cioè un trend
registrato a velocità maggiore.
Schematizzando possiamo così dividere le possibili variazioni di trend:
Trend in costante aumento: ipoventilazione, iperperfusione, calce sodata esausta, passaggio di CO2 dal comparto
addominale
Trend in costante diminuzione: iperventilazione, ipoperfusione, perdita nel circuito.
Trend a zero: intubazione esofagea, disconnessione del
paziente al circuito.
Trend con valore basale che non torna a zero: rirespirazione di CO2.
Modelli
Il mio consiglio è quello di scegliere comunque un capnografo piuttosto che un capnometro, in quanto ritengo la
grafica molto più esaustiva rispetto al dato numerico.
Esistono modelli, integrati ad altri monitoraggi di solito
con il saturimetro od anche singoli.
Non avrei dubbi sul scegliere un sidestream od un microstream, portatile o no dipende poi dall’utilizzo finale.
Se si decide per un capnografo, opterei per un buon display, con luminosità e contrasto modificabili,con un buon
numero di pixel cioè alta risoluzione video.
Cercherei uno strumento con tutti gli allarmi settabili e
silenziabili.
Inoltre ambirei ad avere sul display due curve una dei
singoli atti ed una registrata a velocità maggiore per l’analisi di un trend.
OSSIMETRIA PULSATILE
Cenni Storici
Come purtroppo spesso accade nella storia dell’umanità
anche l’invenzione di questo apparecchio elettromedicale avviene durante una guerra, per motivi tutt’altro che nobili, infatti, il suo impiego si rese necessario al fine di economizzare la
somministrazione di ossigeno ai piloti dei caccia così da ridurre il carico dell’ossigeno stesso a favore dell’armamento.
Tecnica e Funzionamento
È oggettivamente molto difficile ricavare lo stato di ossigenazione arteriosa di un paziente.
L’abilità di rilevare un decremento della saturazione
emoglobinica, dipende da molti fattori quali lo stato del circolatorio, la pigmentazione della cute, la concentrazione dell’emoglobina e la luce ambientale (intensità).
Il pulsossimetro riesce a ricavare tramite la sua elettronica un dato che poco si discosta dalla reale situazione di saturazione in un dato momento ed in un continuo periodo.
Si tratta di un monitoraggio non invasivo, poco pericoloso per il paziente e tutto sommato economico.
Solo comprendendo bene il suo modo di campionare si
potrà anche capirne i limiti intrinsechi.
Si tratta di un apparato molto diffuso in medicina umana
ma che oramai è presente anche in molte realtà veterinarie.
Il principio su cui fonda il suo funzionamento è l’assorbimento di una luce infrarossa che trasmessa attraverso un arteria, produrrà un DELTA diverso all’incontrare emoglobina
piuttosto che carbossiemoglobina piuttosto che metaemoglobina.
Questo Delta luce è associato ad un software spesso studiato e tarato per l’essere umano (ecco il primo limite) che
interpreta il dato e lo correla ad una percentuale di saturazione arteriosa preimpostata.
Tecnicamente la sorgente luminosa, (sonda) proietta gli
infrarossi con due lunghezze d’onda (660nm; 950nm) attraverso tessuti periferici: dito, lingua, padiglione auricolare e
setto nasale.
L’energia che riemerge dopo il passaggio attraverso tutti
i tessuti (cute, connettivo, osso e vascolare) viene letta da un
trasduttore o semiconduttore. Per far si che il delta venga
percepito completamente la corrente viene alternata tra sorgente ed emittente.
Ora abbiamo visto che la luce attraversa tutti i tessuti ma
la lettura del delta avviene solo sull’assorbimento che si ha
a livello arterioso perché?
Semplicemente perché gli altri tessuti primo non pulsano
e secondo e conseguentemente assorbono sempre in modo
costante.
Questo ci fa capire la genialità di questa invenzione e tuttavia un altro limite: in taluni casi vi è pulsatilità venosa.
Una volta letto il delta luce, il dato verrà trasmesso ad un
microprocessore che assegnerà come già detto prima, la corrispondente e preimpostata percentuale di saturazione.
SONDE
Esistono diverse sonde di campionamento non tanto nella loro tecnologia quanto nella loro architettura.
DIGITALI: da applicare al dito umano ma altrettanto utili in veterinaria se posizionate sulle estremità anteriori o posteriori in toto di un gatto o di un piccolo cane se queste non
sono molto pigmentate (polpastrelli neri, pelo scuro).
AURICOLARI: si tratta di pinzette che vengono applicate al lobo auricolare umano, ma molto utili in veterinaria posizionate sulla lingua o sul padiglione auricolare (stesse precauzioni d’impiego viste per le Digitali) od ancora sul margine del labbro superiore; consiglio di cercare quelle pinzette
più piccole che chiudano bene (molla rigida) di solito queste
caratteristiche si trovano in quelle neonatali (Fig. 1).
A FORMA di “C”: vengono applicate nel setto nasale.Hanno l’inconveniente di essere molto aperte e dunque
difficile trovare nei nostri pazienti superfici così spesse dove
poterle applicare.
RETTALI: sono a stilo piatte e di diverse dimensioni
.Superfluo dire dove vengono applicate, ed inoltre essendovi residui di feci non si avrà lettura; consiglio il loro acquisto pensando per esempio ad una chirurgia odontostomatologica dove tutta la cavità orale va lasciata al chirurgo per la
sua opera .
A FASCETTA: non hanno parte rigida di applicazione e
non sono utili in veterinaria.
INTERPRETAZIONE DEI DATI:SPO2
Veniamo ora alla cosa più importante, cosa ci dice il Saturimetro e che significato assume il dato durante l’anestesia.
Normalmente l’apparecchio ci informa sulla frequenza
cardiaca in continuo e sulla parziale saturazione dell’ossigeno nell’arterioso.
163
La frequenza cardiaca ci viene fornita in battiti per minuto mentre la saturimetria in percentuale.
I valori fisiologici in un paziente veterinario ( cane, gatto) di saturazione sono tra l’80% ed il 100 e più percento;
(questo dato lo si può ricavare con un emogasanalisi e si
chiama PaO2 o pressione arteriosa dell’ossigeno).
Questi valori sono l’espressione di come deve essere la
tensione dell’ossigeno emoglobinico, ma allora il valore che
ci deriva dalla sonda non invasiva del polsossimetro di quanto si discosta ?
Di norma e per i migliori strumenti si può semplificare e
schematizzare che:
PaO2: >80……SpO2: >95%………condizioni normali
PaO2: <60……SpO2: <90%………Ipossiemia
PaO2: <40……SpO2: <75%………Grave ipossiemia
Quindi come poi vedremo spesso per questi apparati elettromedicali non invasivi anche il polsossimetro tende a sottostimare ma facendolo con una certa costanza di errore si
può benissimo ragionare ed agire sul valore espresso.
Come per tutti i monitoraggi, non è un singolo numero
anomalo a doverci preoccupare ma un trend un andamento
del valore monitorato nell’arco di un tempo determinato.
Ecco perché l’emogasanillazzatore, strumento eccezionale, ha un limite enorme seppur più preciso nel fatto che i
dati che ci fornisce sono solo relativi al momento del prelievo non un minuto prima ne uno dopo ed in corso di anestesia le cose cambiano anche velocemente.
Il mio consiglio comunque è di settare gli allarmi dello
strumento ponendo come valore minimo accettato l’85-90%
ricordando però la corrispondenza di questo valore con la situazione reale.
Il limite superiore non lo attiverei ammesso che ci sia
poiché in realtà la saturazione va ben oltre il 100% (massimo dato espresso da tutti gli strumenti) durante un anestesia
dove il paziente riceve una miscela con ossigeno al 90%.
Nella frase precedente si vela il terzo limite della macchina, infatti, in un paziente che respira aria ambiente
(21% di ossigeno), al minimo problema riguardante la saturazione vi sarà un immediato calo della PaO2 e della
SpO2; ma in un paziente che respira quasi il 100% di ossigeno si viene a creare una certa riserva per cui se vi fosse
un problema inerente la tensione di ossigeno nel sangue arterioso prima che il nostro apparecchio lo rilevi poterbbero
passare minuti preziosi.
Dunque a mio parere il saturimetro è lo strumento per eccellenza che ci dice quando a fine anestesia dovremo sospendere l’erogazione dell’ossigeno al paziente aspettando il
tempo dell’estubazione.
Infatti se il nostro paziente scollegato dall’ossigeno manterrà con la sua ventilazione spontanea una saturazione accettabile in aria ambiente sicuramente sarà superfluo somministrare altro ossigeno.
Chiaramente è utilissimo anche durante l’anestesia, dove ci informa su possibili situazioni di ipossiemia che possono far capo a problemi circolatori o pressori o di scambi
gassosi.
Quindi se ci aiuteremo con il monitoraggio dei parametri clinici (refill time, colore mucose) e di altri monitoraggi
potremo far diagnosi eziologica della condizione ipossiemica che si è venuta creando.
164
Esiste infine un ultima informazione che ci deriva da alcuni strumenti che naturalmente lo incorporano: Il Pletismogramma.
Si tratta di un grafico che tecnicamente deriva dalla sensibilità dello strumento alla pulsatilità arteriolare.
Da questo il software elabora un grafico ad onde che
esprime il polso del paziente o meglio esprime in modo
grossolano l’ampiezza dello stesso.
MODELLI
Esistono vari tipi di macchinari, portatili, fissi, solo
numerici od anche grafici, associati al monitoraggio di altri parametri (il più comune è con quello dell’anidride
carbonica ma anche con la temperatura corporea o con i
parametri respiratori) o singoli, a batterie, corrente, od
ambedue.
Sorge spontanea la domanda ma quale è il migliore?
Dipende dalle vostre necessità se desiderate per esempio
spostarvi da un reparto ad un altro monitorando la saturazione allora un portatile a batteria è sicuramente ciò che fa
per voi.
La cosa più importante che terrei in considerazione è
possibilmente un software studiato per la veterinaria, una
sonda poco influenzabile dalla luce ambientale (scialitica). Escluderei invece un apparecchio che funzioni solo
sotto corrente elettrica perché limiterebbe l’impiego ad
un solo luogo della struttura o meglio a luoghi muniti di
presa.
165
Impiego del leflunomide
Alessandra Fondati
Med Vet, Dipl ECVD
Universitat Autònoma de Barcelona, Barcellona, Spagna
Il leflunomide è un nuovo farmaco immunomodulatore
che, somministrato per via orale, viene rapidamente convertito, nella parete intestinale e nel plasma, nel suo metabolita
attivo, A77 1726. L’effetto immunomodulatore si attribuisce
all’inibizione della proliferazione dei linfociti attivati, attraverso l’inibizione dell’enzima di-idro-orotato deidrogenasi
(necessario per la sintesi de novo delle pirimidine) e delle tirosin-chinasi. Il leflunomide inibisce inoltre la produzione di
immunoglobuline, la glicosilazione delle molecole di adesione, il fattore nucleare κB, l’attività della ciclo-ossigenasi
e la produzione di radicali liberi; aumenta l’espressione di
IL-1Rα sui monociti e di IL-10R sui cheratinociti e ha un’attività antiproliferativa sull’epidermide.
Il leflunomide entra nel circolo entero-epatico e forse
questo contribuisce ad allungare la sua emivita (circa 2 settimane). Viene metabolizzato nel fegato ed eliminato sia
con le feci che con le urine. È un inibitore del citocromo
P450 2C9 per cui è possibile osservare interazione con farmaci metabolizzati da questo stesso enzima. È un prodotto
teratogeno.
Gli effetti avversi del luflenomide osservati nell’uomo
(in ≥ 5% dei casi trattati) sono diarrea, infezioni respiratorie,
nausea, cefalea, rash cutanei, aumento delle amminotransferasi epatiche e alopecia. Nello 0.02% di casi è stata osservata pancitopenia. Non si consiglia di somministrare leflunomide a pazienti con alterata funzionalità epatica, con displa-
sia midollare e con infezioni concomitanti, si consiglia di
utilizzarlo con cautela in pazienti con alterata funzionalità
renale e si raccomanda il controllo periodico degli enzimi
epatici durante la terapia.
Il leflunomide viene utilizzato nell’uomo principalmente
per la terapia dell’artrite reumatoide. È stato inoltre riportato il suo uso in alcuni problemi dermatologici infiammatori
autoimmuni e/o caratterizzati da iperproliferazione epidermica. quali, tra gli altri, pemfigoide bolloso, lupus eritematoso sistemico e psoriasi.
In dermatologia veterinaria è stato riportato l’uso empirico del leflunomide per la terapia del pemfigo foliaceo e
della istiocitosi cutanea e sistemica nel cane. La dose consigliata è di 2-4 mg/Kg per via orale ogni 24 ore, fino a raggiungere la concentrazione plasmatica di 20 mcg/mL. Effetti avversi descritti nel cane sono leucopenia, piastrinopenia, anemia ed ulcera gastrica. Non si consiglia somministrarlo in cani con insufficienza epatica e si raccomanda
l’esecuzione di controlli ematologici ed emato-chimici
ogni 2-4 settimane.
Letture consigliate
Prakash A and Jarvis B. Leflunomide. A review of its use in active rheumatoid arthritis. Drugs 1999; 58(6): 1137-1164.
167
Criteri di immunocompetenza specifica
nella leishmaniosi canina
Alessandra Fondati
Med Vet, Dipl ECVD
Universitat Autònoma de Barcelona, Barcellona, Spagna
La risposta immunitaria del cane nei confronti di Leishmania infantum è estremamente variabile e si relaziona in
gran parte a fattori genetici individuali. Dal tipo di risposta
immunitaria dipende sia la “resistenza” del soggetto nei
confronti del parassita, per cui non tutti i cani infettati sviluppano la malattia, sia, almeno in parte, la risposta alla terapia. Alcuni soggetti sviluppano solo una risposta immunitaria umorale, altri solo una risposta cellulo-mediata ed
altri entrambe.
Per definire quindi la risposta immunitaria specifica di
un determinato paziente nei confronti di Leishmania è necessario utilizzare tecniche che siano in grado di valutare i
due tipi di risposta immunitaria.
La risposta umorale si può valutare attraverso prove sierologiche misurando il livello di immunoglobuline (IgG) circolanti Leishmania-specifiche. Cani infettati non malati hanno titoli anticorpali bassi mentre cani infettati e malati hanno titoli elevati che tendono a diminuire con la risposta alla
terapia.
La risposta immunitaria specifica cellulo-mediata si può
valutare in vivo con l’iniezione intradermica (nella regione
inguinale) di sospensioni di L. infantum inattivata (test di
Montenegro). La risposta positiva dopo 72 ore indica la presenza di una risposta immunitaria cellulo-mediata. Altre tecniche utili per valutare in vitro la risposta immunitaria specifica sono la proliferazione linfocitaria e la produzione di
citochine (INFγ, TNFα) da parte dei linfociti circolanti in
presenza dell’antigene solubile di Leishmania e la determinazione mediante RT-PCR della presenza di citochine (IL-4,
IL-10, IL-13, IL-18, IFNγ) nei tessuti infettati.
Anche l’uso della citometria di flusso, utile per determinare il numero di linfociti circolanti CD4+ e CD8+, potrebbe aiutare a valutare la risposta immunitaria, non specifica,
del paziente.
Letture consigliate
Solano Gallego L. Leishmania infantum and dog: immunological and epidemiological studies about infection and disease. PhD Thesis, Facultat de Veterinària, Universitat Autònoma de Barcelona (Spain)
May 2001.
Quinnell RJ, Courtenay O, Shaw MA et al. Tissue cytokine responses in canine visceral leishmaniasis. The Journal of Infectious Diseases 2001;
183: 1421-1424.
169
Protocolli per il trattamento delle rickettsiosi
croniche: opzioni terapeutiche,
monitoraggio e prognosi
Tommaso Furlanello
Laboratorio d’Analisi Veterinarie San Marco, Clinica Veterinaria Privata “San Marco”, Padova
Marco Caldin
Clinica Veterinaria Privata “San Marco”, Padova
George Lubas
Dip. Clinica Veterinaria, Facoltà di Medicina Veterinaria, Università di Pisa, Pisa
INTRODUZIONE
Nella letteratura veterinaria l’unica rickettsiosi per la
quale è descritta una forma cronica è l’ehrlichiosi indotta da
Ehrlichia canis (Canine Monocytic Ehrlichiosis, CME). I
dati disponibili sono comunque molto scarsi, soprattutto per
quanto riguarda il management del paziente. Nella nostra
esperienza abbiamo frequentemente riscontrato altre due infezioni trasmesse da zecche (Tick Borne Diseases, TBDs),
quali l’ehrlichiosi granulocitaria (Canine Granulocytic Ehrlichiosis, CGE) ed un’infezione da Rickettsia spp., sierologicamente e antigenicamente correlata con Rickettsia rickettsii
(Febbre Maculosa delle Montagne Rocciose, Rocky Mountain Spotted Fever, RMSF).
Pur ammettendo l’esiguità dei dati pubblicati a sostegno
di molte delle nostre considerazioni, vogliamo condividere
con i medici veterinari italiani i concetti che abbiamo elaborato a partire dal 19981, riguardo ad eziopatogenesi, sintomatologia clinica e protocolli terapeutici ad alcune TBDs
che noi riteniamo di primaria importanza. Ogni clinico potrà
così valutare il nostro approccio a tali patologie rispetto alle
proprie esperienze per ottimizzare la gestione dei pazienti,
considerando eventualmente problematiche che non sono
presenti nella letteratura.
EPIDEMIOLOGIA
La TBD batterica meglio conosciuta è senz’altro la CME,
indotta da E. canis (famiglia delle Rickettsiaceae, genere Ehrlichiae). I dati presenti in letteratura riguardo alle manifestazioni cliniche di questa patologia non erano però per noi (e per
altri2) sufficienti a motivare la grande varietà di manifestazioni
cliniche e patologiche osservate nella pratica clinica, come pure le a volte imprevedibili risposte alle terapie farmacologiche
antimicrobiche. Non mancavano inoltre presentazioni simili a
quelle attese nella CME, ma in cani sierologicamente negativi
ad Ehrlichia canis. Abbiamo così intrapreso una ricerca per altre TBDs che potessero essere presenti separatamente o contemporaneamente alla CME. Dal punto di vista sierologico
abbiamo segnalato l’eccezionale diffusione di sieropositività
all’agente dell’ehrlichiosi granulocitaria canina (antigenicamente omologo all’agente dell’ehrlichiosi granulocitaria
umana). Analizzando 448 sieri raccolti in cani provenienti da
tutto il territorio nazionale ed inviati al Laboratorio d’Analisi
Veterinarie San Marco, come approfondimento diagnostico
perché sospettati di CME, abbiamo riscontrato una sieropositività relativa a tale infezione solamente nell’8% dei casi, sia per
CME che per CGE nel 28% e a CGE singolarmente nel 30%.
Di contro erano sieronegativi il 34% dei pazienti3. L’osservazione delle caratteristiche morule nei granulociti neutrofili ed
una chiara sieroconversione hanno anche permesso di descrivere un caso clinico di CGE4. Analogamente ad altri pazienti,
il cane descritto ha presentato, alcuni mesi dopo la forma acuta, gravi manifestazioni derivanti da patologie midollari.
Un’altra infezione di primaria importanza è, a nostro giudizio, quella provocata da un agente eziologico analogo a
Rickettsia rickettsii, che genera sieropositività nel 69,9% dei
cani affetti da una sintomatologia genericamente ascrivibile
ad una TBDs5. In cani sieropositivi a tale agente abbiamo
descritto sia una forma acuta1 che una cronica6.
Ampiamente diffuse sono anche sieropositività concomitanti di CME, CGE e RMSF5, 7, 8. Ad esempio, su 1.091 campioni sieropositivi per R. rickettsii, 928 sono stati testati anche per CME con positività in 389 (41,9%); inoltre 205 sono stati valutati per CGE con positività in 138 casi (67,3%)8.
170
È indubbio che la sieropositività riporti solo una risposta
immunologica evocata da un agente infettivo e che esistono,
specialmente per R. rickettsii, ampie cross-reattività con altre “Spotted Fever”. Una quota rilevante dei sieropositivi è
comunque affetto da condizioni patologiche compatibili, come ad esempio una febbre d’origine sconosciuta, in assenza
di altre cause. Inoltre è da valutare l’impatto addizionale di
tali infezioni quando siano presenti simultaneamente nello
stesso paziente.
FORME CRONICHE: PATOGENESI
E MANIFESTAZIONI CLINICHE
Se per le forme acute di CME9, CGE10 e RMSF11 sono
disponibili in letteratura dati sia sperimentali che originati da infezioni spontanee, per le forme croniche esistono
informazioni solo per CME9, con comparsa di pancitopenia. Nella nostra esperienza le TBDs in esame sono in grado di provocare condizioni riferibili alla sindrome di mielodisplasia (myelodysplastic syndrome, MDS)12, ovvero
una serie di turbe delle cellule staminali del midollo emopoietico, a patogenesi complessa, che portano ad alterata
proliferazione e maturazione (emopoiesi inefficace). La
MDS non è a nostro parere un’evenienza rara e nella nostra
esperienza si manifesta nel 61,6% dei casi di valutazione
midollare13. In un precedente studio, considerando l’eziologia di tali forme di displasia , erano sieropositivi per
TBDs 5 cani su 1314.
Abbiamo elaborato un’ipotesi patogenetica per la MDS
(Fig. 1), utilizzando anche le informazioni disponibili dalla
medicina umana relative alla mielosoppressione indotta dall’agente della ehrlichiosi granulocitaria umana (Human Granulocytic Ehrlichiosis, HGE)15: l’agente infettivo si localizza nel midollo emopoietico e determina la liberazione di citochine, tra le quali TNF-α e IL-1. Queste ed altre citochine
modificano il microambiente midollare e inducono apoptosi
delle cellule staminali ed alcune perturbazioni evolutive che
sono tipicamente alla base della MDS16.
Infezione sistemica
Induzione di emopatia
immunomediata
Localizzazione
intramidollare
Iperplasia mieloide/
megacariocitaria
Liberazione di citokine
apoptotiche
Induzione di emopatia
immunomediata
Localizzazione
intramidollare
Mielofibrosi
Figura 1
Le alterazioni midollari morfologiche da noi riscontrate
nei cani affetti da TBDs soddisfano pienamente quelle necessarie per la definizione di MDS13, 14 ed è di grande interesse il reperimento tramite nested-PCR di Rickettsia spp. in
strisci midollari di cani sieropositivi per R. rickettsii ed affetti da MDS16. Nel sangue periferico i rilievi più comuni per
la linea eritroide sono: anemia non rigenerativa variamente
associata ad anisocitosi, macrocitosi, microcitosi, dacriocitosi, schistocitosi, presenza di corpi di Howell-Jolly, punteggiature basofile e codocitosi. Tali reperti sono spesso associati a neutropenie e piastrinopenie. La cronicizzazione della patologia comporta un’evoluzione da uno stato di mielodisplasia a quello di mielofibrosi, presumibilmente conseguente all’iperplasia megacariocitaria presente nella fase
mielodisplastica. Secondo la nostra esperienza solo pochi
cani raggiungono una condizione di mielofibrosi.
Alla flogosi cronica midollare indotta da citochine si associano spesso altre manifestazioni sistemiche ad analoga
patogenesi, quali febbre persistente, artriti, neuropatie infiammatorie, vasculiti e cachessia. L’elettroforesi sierica è
frequentemente alterata, con presenza di iperglobulinemia,
talora anche monoclonale.
In conclusione la nostra opinione è che la componente
immunomediata di tutte le manifestazioni fino ad ora elencate è di grande importanza e l’apporto patogenetico indotto
dall’agente infettivo nelle forme cronicizzate appare di minore interesse. Anche altri Autori hanno recentemente sottolineato l’importanza della componente immunologica nelle
discrasie ematiche associate a malattie infettive, in particolare nelle TBDs18.
MANAGEMENT CLINICO
La gestione del paziente affetto da TBDs in forma cronica è estremamente complessa sia per la molteplicità delle
manifestazioni cliniche che per l’empiricità su cui si basano
i protocolli da noi utilizzati, che derivano principalmente
dall’esperienza clinica accumulata negli ultimi 4 anni. Il presente approccio medico è in realtà dinamico e si è modificato e affinato più volte, in base alle nostre valutazioni e ai dati provenienti per lo più dalla medicina umana. Il lettore è invitato a utilizzarli con lo stesso spirito, mantenendo una costante attenzione verso le nuove conoscenze.
Il primo passo per il trattamento del paziente affetto da
TBDs comprende un’attenta valutazione clinico-patologica,
al fine di stadiare la patologia e di riconoscere le complicazioni multiorganiche della risposta infiammatoria all’infezione. I titoli sierologici per CME, CGE e RMSF fanno parte dello studio di base, ma sono solo una componente di una
valutazione globale che comprende quasi costantemente la
valutazione citopatologica del midollo emopoietico. E’ già
realtà la sistematica ricerca delle TBDs in esame tramite metodica PCR, da sangue intero o strisci midollari, e ciò porterà a definire con maggiore precisione la storia naturale di
queste TBDs. L’aspirato midollare permette anche di escludere altre patologie, quali ad esempio quelle mieloproliferative, che possono mimare (o causare) molte manifestazioni
“tipiche” di TBDs, quali MDS, splenomegalia o febbre d’origine sconosciuta.
La terapia antimicrobica rappresenta il primo approccio
terapeutico e il farmaco di prima scelta è tipicamente la
doxiciclina, che noi somministriamo alla posologia di 10
mg/kg q12h PO per 3-6 settimane, a seconda della cronicità
dell’infezione. Se è sospettata una CME viene utilizzato anche l’imidocarb diproprionato (5 mg/kg IM, da ripetere dopo 2 settimane)19.
Qualora non vi sia risposta alla doxiciclina si utilizza, in
caso di CGE e/o RMSF, l’enrofloxacina (10 mg/kg q24h
PO) o un altro chinolonico di III generazione. L’enrofloxacina non viene utilizzata in caso di CME data la sua dimostrata inefficacia nei confronti di E. canis20.
In caso di persistenza di uno stato infiammatorio presumibilmente legato ad una TBDs, utilizziamo empiricamente
anche la claritromicina (5 mg/kg q12h PO), in virtù della sua
efficacia nei confronti di Rickettsia spp., mentre è ignota la
sua attività nei confronti di CME e CGE. Nella nostra esperienza, cani che erano stati trattati ripetutamente con antimicrobici quali doxiciclina, enrofloxacina ed altri, senza presentare miglioramenti clinici, hanno risposto brillantemente
a terapie con claritromicina (di durata non inferiore a 3-4
settimane). Ignoriamo se tale antimicrobico sia efficace nei
casi “intrattabili” per le sue capacità di concentrarsi a livello
intracellulare, o perché esistono dei ceppi di TBDs ”resistenti” ai più comuni antibiotici, o piuttosto perché è attivo
anche contro batteri quali Bartonella spp.21, che nel cane è
da considerare un agente di TBDs, probabilmente di rilevante importanza clinica6.
Ricordando l’ipotesi patogenetica che abbiamo proposto
per le importanti alterazioni ematologiche in corso di TBDs,
risulta indispensabile, preferibilmente dopo aver compiuto
dei tentativi terapeutici con gli antimicrobici prima elencati,
l’utilizzo di farmaci immunosoppressivi. Ovviamente la prima opzione comprende sempre i corticosteroidi (esclusivamente prednisone/prenisolone 1-2 mg/kg q24h PO). L’evidente efficacia di tale terapia in alcuni soggetti può essere legata, oltre che alle note attività anti-infiammatorie ed immunosoppressive, all’inibizione nella traslazione del mRNA
per la sintesi del TNF-α22, una citochina di grande importanza patogenetica nello sviluppo della mielodisplasia. In
caso di mancata risposta ai corticosteroidi ed in presenza di
gravi alterazioni ematologiche si propone una terapia immunosoppressiva con ciclosporina, utilizzando la recente formulazione ad assorbimento migliorato, ad una posologia iniziale di 5 mg/kg q12h PO, per ottenere una ciclosporinemia
di circa 400-500 ng/mL. Questa molecola è ampiamente
usata in medicina umana per il trattamento delle mielodisplasie e delle mielofibrosi. Tra i suoi effetti si segnalano una
stimolazione in vitro e in vivo della formazione di colonie
ematopoietiche, forse per diminuzione del numero dei linfociti CD823. Eventuali risposte si presentano a medio termine
e la terapia viene di solito protratta per mesi, monitorando i
livelli ematici della molecola e la funzione renale.
In medicina umana, in caso di mielodisplasia con citopenia periferica, vengono comunemente utilizzate eritropoietina e filgrastim (Granulocyte-colony stimulating factor, GCSF)24. Esiste un singolo caso pubblicato in medicina veterinaria riguardante un cane pancitopenico affetto da CME,
che ha risposto favorevolmente alla somministrazione giornaliera di G-CSF per 41 gg. e di eritropoietina ogni 3 gg.
171
prima e poi ogni due settimane per un totale di 142 gg. Il cane veniva anche trattato con corticosteroidi e vincristina25.
Anche nella nostra esperienza i fattori di crescita hanno risolto gravi condizioni di pancitopenia, ma esistono importanti limitazioni a questa terapia, quali il costo e soprattutto
l’antigenicità di queste citochine di derivazione umana. Le
posologie da noi utilizzate sono: filgrastim 5 µg/kg q24h SC
e EPO 50-100 UI/kg 2-3 volte a settimana. La terapia viene
utilizzata “ad effetto” e viene preferibilmente interrotta entro un mese per evitare la comparsa di anticorpi anticitochine esogene che possono cross-reagire con le citochine endogene.
Per il monitoraggio sono indispensabili esami di laboratorio quali l’esame emocromocitometrico, l’elettroforesi e
più in generale gli esami ematobiochimici di base. Di grande interesse è la ripetizione seriale della citopatologia midollare, che permette di valutare l’evoluzione del quadro
mielodisplastico. La valutazione dei titoli anticorpali non
viene utilizzata routinariamente perché essi non sono correlati con l’evoluzione clinica del paziente e possono permanere, ad esempio in caso della CME, anche per anni dopo la
risoluzione dell’infezione26.
L’elaborazione di una prognosi in un paziente affetto da
TBDs risulta oltremodo complessa, considerate le molteplici complicazioni e presentazioni cliniche e la risposta alle
manovre terapeutiche prima descritte risulta solitamente imprevedibile. Nella nostra esperienza un fattore nettamente
sfavorevole, per quanto raro, è rappresentato dalla presenza
di mielofibrosi, in quanto stadio terminale di uno stato di
MDS o d’iperplasia megacariocitaria cronica e persistente.
Bibliografia
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Caldin M, Furlanello T, Lubas G, (1998), Case report of Rocky
Mountain Spotted Fever in a dog from north-eastern Italy, Proc 4th
European FECAVA-SCIVAC Congress, Bologna, 510
Breitschwerdt EB (1996), Ehrlichiosis: One or Many Diseases ?, Proc
14th ACVIM Forum, San Antonio, 608-609
dati non pubblicati, 2000
Caldin M, Furlanello T, Campagna C et al., (2000), Segnalazione di
un caso clinico di Ehrlichiosi Granulocitaria acuta in un cane, Atti del
2° Congr Int Merial, Riccione, 123-124.
Furlanello T, Caldin M, Lubas G et al. (2000), Occurrence of Rickettsia rickettsii in dogs living in Italy – a serological survey, Proc 10th
ESVIM Congr, Neuchatel, 115-116
Caldin M, Furlanello T, Bertoldi A et al. (2000), Displasia eritroide in
corso di infezione cronica da Rickettsia rickettsii in un cane proveniente dal Veneto orientale, Atti del 2° Congr Int Merial, Riccione,
121-122
Furlanello T, Caldin M, Lubas G et al., (2001), Infezioni concomitanti in cani sieropositivi per Rickettsia rickettsii: studio sierologico
su 802 casi, Atti del 42° Congr Naz SCIVAC, Milano, 259
Furlanello T , Caldin M, Lubas G et al., (2000), Concurrent coinfections in dogs detected by serology during a survey for Rickettsia
rickettsii: results from 1093 serum samples collected in Italy, J of Vet
Int Med, 15, 3, 276
Harrus S, Bark H, Waner T, (1997), Canine Monocytic Ehrlichiosis:
an update, Comp of Cont Ed, 19, 4, 431-444
Lilliehöök I, Egenvall A, Tvedten HW, (1998), “Hematopathology in
dogs experimentally infected with a swedish Granulocytic Ehrlichia
species, Vet Clin Path, 27, 4, 116-122
Gasser AM, Birkenheuer AJ, Breitschwerdt EB, (2001), Canine
Rocky Mountain Spotted Fever: a retrospective study of 30 cases,
JAAHA, 37, 1, 41-48
172
12.
13.
14.
15.
16.
17.
18.
19.
20.
Lubas G, Caldin M e Furlanello T (2001), Non Regenerative Anemias: A Diagnostic Challenge, 7th FECAVA & 47th Ann Cong FKDVG, Berlin, 157-167
Loewer S, Caldin M e Furlanello T, (2002), Incidenza della sindrome
mielodisplastica nel cane, rilevata dall’esame di 151 aspirati midollari, Atti del 44° Congr Naz SCIVAC di Milano (presente volume)
Caldin M, Furlanello T, Loewer S, (2001), Mielodisplasia nel cane:
descrizione di 13 casi clinici, Atti del 42° Congr Naz SCIVAC, Milano, 259
Klein MB, Xu S, Chao CC et al., (2000), The Agent of HGE Induces
the production of Myelosuppressing Chemokine without Induction of
Proinflammatoriy Cytokines, J of Infect Dis, 182, 200-205
Raza A (2000): Myelodysplastic syndromes may have an infectious
etiology, J of Toxicol and Envirom Health, Part A, 6a, 387-390
Tognin F. (2001): Approccio molecolare per il riconoscimento ed
identificazione di Rickettsia spp., Tesi di laurea, Facoltà di Medicina
Veterinaria, Università di Padova, pp. 199
Day MJ (2001), Insight into the immunological basis of blood disorders, Proc 7th FECAVA & 47 th Ann Cong FK-DVG, 89-94
Harrus S (1998), Recent advances in Canine Monocytic Ehrlichiosis,
ESVIM Proceedings, 87-94
Neer TM, Eddlestone SM, Gaunt SD et al., (1999), Efficacy of enro-
21.
22.
23.
24.
25.
26.
floxacin for the treatment of experimentally induced Ehrlichia canis
infection, J Vet Intern Med, 13, 5, 501-504
Ives TJ, Marston EL, Regnery RL et al., (2000), In vitro susceptibilities of Bartonella and Rickettsia spp. to fluoroquinolone antibiotics as
determined by immunofluorescent antibody analysis of infected Vero
cell monolayers, Int J Antimicrob Agents, 18, 3, 217-22
Raza A Qawi A, Lisak L et al., (2000), Patients with myelodysplasia
benefit from palliative therapy with amifosfine, pentoxifylline, and
ciprofloxacin with or without dexamethasone, Blood, 95, 1580-1587
Pietrasanta D, Clavio M Vallebella E et al., (1997), Long-lasting effect of cyclosporin-A on anemia associated with idiopathic myelofibrosis, Haematologica, 82, 458-459
Hellstrom-Lindberg E, Willman C, Barrett JA et al., (2000), Achievement in understanding and treatment of myelodysplastic syndromes,
Haematology 2000, 1, 110-132
Aroch I & Harrus S, (2001), The use of recombinant human granulocyte colony stimulating factor and recombinant human erythropoietin in the treatment of severe pancytopenia due to canine monocytic ehrlichiosis, Israel J Vet Med, 56, 2, 65-69
Harrus S, Waner T, Aizenberg I et al., (1998), Amplification of Ehrlichial DNA from dogs 34 months after infection with Ehrlichia canis,
J Clin Microbiol, 36, 1, 73-76
173
Impiego della ciclosporina A e del tacrolimo
Giovanni Ghibaudo
Med. Vet.
Clinica Veterinaria Malpensa, Samarate (Varese)
La terapia farmacologia della dermatite atopica nel cane
e nel gatto è costituita dall’utilizzo principalmente di glucocorticoidi e/o anti-istaminici (Scott 2001). Recentemente altre molecole sono state studiate per verificarne l’efficacia in
corso d’allergia cutanea. Tra queste la Ciclosporina A (CsA)
e il Tacrolimo. La CsA è un composto isolato all’inizio degli
anni ’70 da estratti del fungo Tolypocladium inflatum gams
(Stähelin 1986). È un peptide lipofilico ciclico. Il suo meccanismo d’azione è diretto nei confronti dei linfociti T. La CsA,
infatti, induce un’immunosoppressione reversibile inibendo
la fase d’attivazione iniziale dei linfociti CD4+ verso l’antigene. In particolare induce un blocco della trascrizione di geni per la formazione di molte citochine (soprattutto l’interleuchina 2) (Hess 1993, Ho et al 1996). In dermatologia canina, la CsA si è dimostrata promettente non solo nel trattamento delle fistole perianali (Mathews 1997) e nella dermatite atopica (Fontaine 2001) ma anche per altre dermatosi immunomediate (pannicolite nodulare sterile, cellulite piogranulomatosa giovanile, adenite sebacea granulomatosa).
Nei gatti, studi preliminari recenti mostrano che la CsA
è utile per il trattamento delle placche e granulomi eosinofi-
lici, prurito cervico-facciale allergico, dermatite atopica e altre dermatosi immunomediate come l’urticaria pigmentosa
nei gatti Sphinx (Guaguère 2000).
Il Tacrolimo (FK-506) è un lattone macrolide prodotto
dal fungo Streptomyces tsukubaensis. Ha un’azione simile
alla CsA pur avendo una diversa struttura chimica (Kino
1987). FK-506 inibisce la risposta dei linfociti T all’antigene e la produzione di citochine responsabili della proliferazione delle cellule T (Schreiber e Crabtree 1992). Recentemente è stato utilizzato nella dermatite atopica come lozione topica nel cane. Tale lavoro ha dimostrato una diminuzione dell’eritema ma non del prurito (Marsella 2001). In un altro studio è stato utilizzato, sempre come terapia locale, nelle fistole perianali del cane; dimostrando di potere essere utilizzato come alternativa terapeutica alla somministrazione di
CsA per via sistemica nelle forme lievi o moderate di fistole o come continuazione nella fase di mantenimento dopo il
trattamento con la CsA (Misseghers 2001).
Bibliografia disponibile su richiesta.
175
Diagnosis and treatment
of portosystemic shunts
Elizabeth M. Hardie
DVM, PhD, Professor of Surgery, North Carolina State University, Raleigh, NC, US.
The spectrum of clinical signs associated with portosystemic shunt is broad: seizures, behavioral changes, transient
blindness, transient disorientation, vomiting, diarrhea,
anorexia, stranguria, hematuria, poor growth and preference
for vegetarian diets are among the more common. With such
a wide spectrum of signs, the veterinarian must test for suspected portosystemic shunt in many patients. A CBC and
serum chemistry panel often hold clues that shunt might be
present: microcytosis, decreased serum albumin, decreased
BUN, increased aspartate aminotransferase, increased alkaline phosphatase. Pre and post prandial serum bile acid values will be increased. An experienced ultrasonographer
made be able to image the shunt, but failure to find a shunt
on ultrasound examination does not rule out its presence. If
nuclear medicine is available, transcolonic sodium pertechnetate Tc 99m scintigraphy is a non-invasive method of
demonstrating whether or not shunting is present. The gold
standard for demonstrating the presence of portosystemic
shunt remains portal venography, an invasive procedure.
With the advent of contrast enhanced three dimensional CT
scan reconstructions, invasive imaging may no longer be
necessary.
Once shunting of blood around or through the liver has
been demonstrated, a decision must be made whether or not
the patient is a candidate for surgical therapy. The presence
of ascites, even in a young dog, indicates that surgery is likely not a treatment option. Ascites develops secondary to portal hypertension. The shunts are multiple and extra-hepatic,
a physiologic response to the hypertension. Surgical and
medical methods of treating these cases have been shown to
have equivalent results. If ascites is not present, microscopic shunting must be distinguished from macroscopic shunting. Dogs with microscopic shunting have normal or slightly increased shunt fraction on technetium scan and no
macroscopic shunt can be found with other imaging techniques. Surgery may be needed for definitive diagnosis in
these dogs, but is not therapeutic. Dogs with macroscopic
shunting are best treated with surgical therapy, regardless of
their age. The prognosis and difficulty of surgery differs de-
pending on whether the shunt is extrahepatic or intrahepatic.
Extrahepatic shunts are most common in small breed
dogs. Complete or partial ligation with silk, occlusion with
an ameroid constrictor or occlusion with a cellophane band
are commonly used for treatment. A recent study comparing
ligation with the ameroid constrictor found fewer operative
and post-operative complications with the constrictor. The
most serious post-operative complication is post-surgical
neurological syndrome, occurring in 10-12% of patients.
Prophylactic administration of anticonvulsants reduces the
severity of signs, but does not prevent the complication.
Overall, the peri-operative mortality rate is 2%. The long
term success rate of surgical treatment is that 75-80% of patients become normal. Long term success appears related to
the ability to fully occlude the shunt and the experience of
the surgeon.
Intrahepatic shunts are most common in large breed
dogs. Left-sided shunts are most common, are often accessible with minimal dissection and can be often treated using
ligation or an ameroid constrictor. Central and right-sided
shunts usually require intravascular techniques. The peri-operative mortality rate for dogs with intraoperative shunts is
18%. The long term success rate is that 62% of dogs become
normal.. Long term success is related to the ability to fully
occlude the shunt and the presence of adequate hepatic vascular in the unaffected liver lobes.
References
Murphy ST, Ellison GW, Long M. Gilder JV. A comparison of the ameroid
constrictor versus ligation in the surgical management of single extrahepatic portosystemic shunts. J Am Anim Hosp Assoc 2001; 37:
390-396.
Hunt GB, Hughes J. Outcomes after extrahepatic portosytemic shunt ligation in 49 dogs. Aus Vet J 1999; 77:303-307.
White RN, Burton CA, McEvoy FJ. Surgical treatment of intrahepatic portosystemic shunts in 45 dogs. Vet Rec 1998; 142: 358-365.
Center SA, Schermerhorn T, Lyman R, Phillips L. Hepatoportal Microvascular Dysplasia. In Bonagura JD (ed) CVT XIII, W. B. Saunders,
Philadelphia, 2000, p682.
177
Management of urinary calculi in dogs and cats
Elizabeth M. Hardie
The management of urinary calculi in dogs and cats involves nutritional, medical and surgical treatment. The veterinarian must assess the ability of the client to comply with
the suggested treatment and then design an appropriate
regime. For example, if a cat lives outdoors and is only seen
by the owner at mealtime, performing a perineal urethrostomy on the first episode of urethral blockage may be the best
method to prevent death during an unobserved episode of
obstruction. On the other hand, if a female dog with probable struvite calculi and urinary tract infection is well observed and the owner can provide frequent visits to the veterinarian for monitoring, medical and dietary dissolution are
appropriate.
The first step in the treatment of urinary calculi is to provide relief of obstruction, if present. This may involve urethral catheterization, urethrostomy or cystostomy in the lower urinary tract. For stones in the ureter, diuresis is attempted for 24 hrs. If the animal is moribund, or diuresis fails,
nephrostomy tubes are placed to stabilize the animal. Once
the animal is metabolically stable, definitive removal of the
calculi can be performed.
After relief of obstruction, the next task is assessing the
location of all calculi. This can be performed using radiographs if the stones are radiodense, but in many cases ultrasound provides superior imaging of calculi. Sterile urine
samples are obtained for culture and urinalysis. The breed,
sex, radiodenisity of the calculi, size of the calculus, the
presence or absence of infection, and the compliance of the
owner are used to recommend treatment. If struvite calculi
are likely, medical dissolution is attempted. Once the stones
are a small size, they are removed using voiding hydropropulsion. If calcium oxalate calculi are likely, they are
removed using surgery (if large) and voiding hydropropulsion (if small). If other calculi types are likely, they are usually removed using surgery.
The most important aspect of removing calculi from the
lower urinary tract is making sure that all the stones are removed. Counting the calculi, and re-radiographing or re-ultrasounding after surgery are wise ideas. If re-obstruction is
likely, a permanent urethrostomy is created to prevent re-obstruction.
Decisions regarding calculi removal in the upper urinary
tract can be difficult. If ureteral calculi are present in one
ureter, they should be removed to preserve renal function. If
ureteral calculi are present in both ureters, the animal may
already have severely compromised renal function due to
prior obstruction. The stones should be removed, but the
owner should be warned that relief of obstruction may not
improve the animal’s renal status. If stones are present in the
kidneys, the type and size matters. Struvite nephroliths are
often large and maintain chronic urinary tract infection.
They should be removed. Small oxalate nephroliths often
lodge in the calices and are extremely difficult to remove.
They are best left in place.
Once calculi have been removed and identified, a plan
for prevention is initiated. The primary goal in the prevention of urinary calculi is to increase water intake. Placing
water on dry food, switching to canned food, and administering KCl are all methods of increasing water consumption.
Utilizing the correct diet for the stone type is also important.
Give the owner acceptable treats for the animal. The urine
pH needs to be monitored on a regular basis to assess
whether further medical treatment is needed. Routine urine
cultures are performed if infection has played a role in calculi formation. Keep the owner engaged and interested, because prevention is usually a life-long program.
References
Osborne CA, Lulich JP, Polzin, JP, et al. Analysis of 77,000 canine uroliths:
perspectives from the Minnesota urolith center. Vet Clin N Am Small
Anim Prac 1999; 29:17-38.
Ling GV, Ruby AL, Johnson DL, Thurmond M, Franti CE. Renal calculi in
dogs and cats: prevalence, mineral typr, breed, age, and gender interrelationships (1981-93). J Vet Int Med 1998; 12: 11-21.
Stone EA, Kyles AE. Diagnosis and management of ureteral obstruction.
Bonagura JD, CVT XII. WB Saunders Philadelphia, 2000, pp. 868870.
179
Surgical management of urinary tract infections
Elizabeth M. Hardie
Recurrent and persistent urine tract infections (RPUTI)
are frustrating for both owners and veterinarians. Many factors have been associated with the development of these infections. First, recent focus has centered on the role of bacteria with adaptations for attaching to uroepithelium and inherited differences in uroepithelial susceptibility to bacterial
attachment. Escherichia coli has been shown to be present in
the majority of RPUTI and uropathogenic strains are identical in dogs and humans. Familial tendencies towards RPUTI
exist in humans and certain dog breeds. Second, hyperadrenocorticism or diabetes mellitus increase susceptibility to
RPUTI and occult infection is common. Third, anatomical
abnormalities leading to urine stasis or chronic vaginitis/prostatitis increase susceptibility. Fourth, the presence of urinary calculi can injure the uroepithelium and can serve as a
nidus for infection. Fifth, urinary incontinence increases the
risk of RPUTI. Surgical therapy can help in the treatment of
the latter three factors.
Young animals presenting for recurrent infection
should be carefully examined for the presence of congenital abnormalities. Diverticuli can occur in any segment of
the urinary tract. In humans, the gold standard for diagnosis of diverticuli is MRI, but contrast urography and cystoscopic examination can be used to demonstrate the presence of these lesions. In the male, ectopic ureter can be
demonstrated with an excretory urogram. In the female,
vaginal stricture, vaginal septum, ectopic ureter and abnormalities at the junction of the urethra to the vagina can be
demonstrated with a retrograde vagino-urethrogram or
vaginoscopic examination. Intersex clitoral lesions and
hooded vulva can be found with careful physical examination. If calculi are present in young dogs, portosystemic
shunt must be considered as a cause.
In older intact male dogs, the prostate must be considered a potential nidus of infection. Ultrasonic examination
and aspiration/biopsy can aid in the diagnosis of prostatic
disease. In older female dogs, low level urinary incontinence
can predispose to RPUTI. In older dogs of both sexes, can-
cer and urinary calculi must be ruled out as underlying causes of RPUTI. Ultrasound examination is useful for demonstrating calculi and large mass lesions, but screening bladder
tumor antigen dipsticks and cystoscopic examination aid in
determination of cancer at a early stage.
If a predisposing cause for RPUTI that can be surgically
corrected is found, a plan is made for both surgical correction and treatment of the infection. For example, if ectopic
ureter is found to be the underlying cause, an assessment is
made whether to reimplant the ureter or to remove the affected kidney and ureter. This assessment is based on the
condition of the kidney and whether or not the defect is unilateral or bilateral. A unilateral severely dilated ureter and
kidney with pyelonephritis will be removed, while bilaterally affected ureters with less evidence of pyelonephritis will
be re-implanted. As a second example, if vaginal stricture is
resulting in urine pooling within the vagina and chronic
vaginitis, resection of the stricture will be performed to aid
in the management of vaginitis. In some cases, dilation of
the cranial vagina may be severe enough to warrant removal.
The infecting organism is cultured prior to or at the time of
surgical correction. Long term antibiotic therapy is initiated
and careful followup, with repeated cultures of the urine, is
used to assure resolution of infection.
References
Johnson JR, Stell AL, Delvari P, Murray AC, Kuskowski M, Gaastra W.
Phylogenetic and pathotypic similarities between Escherichia coli
isolates from urinary tract infections in dogs and exraintestinal infections in humans. J InfecDis 2001; 183: 897-906.
Mulvey MA, Schilling JD, Hultgren SJ.Establishment of a persistent Escherichia coli reservoir during the acute phase of a bladder infection. Infect Immun 2001 Jul;69(7):4572-4579
Norris CR, Williams BJ, Ling GV, Franti CE, Johnson DL, Ruby AL. Recurrent and persistent urinary tract infections in dogs: 383 cases
(1969-1995) J Am Anim Hosp Assoc 200; 36:484-492.
Rawlings CA. Correction of congenital defects of the urogenital system. Vet
Clinics N Am 1984; 14:49-59.
181
Surgery for incontinence
Elizabeth M. Hardie
Urinary incontinence is a problem that can result in the
demise of the animal, mainly because the owner cannot cope
with the house-soiling. Incontinence also increases the risk
of urinary tract infections. The diagnosis is usually simple:
the animal leaves puddles of urine in the sleeping areas, actively dribbles urine, and/or has a wet, urine soaked haircoat
around the urethral opening. This is a mainly a disease of female dogs, particularly spayed female dogs. Holt has shown
that the risk of incontinence in intact bitchs is 0.0022/animal/year, while the risk in spayed bitches is 0.0174/animal/year. This means that spayed females are 8 times more
likely to become incontinent than intact bitches. Factors that
do not affect the risk of incontinence include spaying before
or after the first heat, ovariectomy vs. ovariohysterectomy,
or removal of the cervix. Certain breeds are at high risk:
Dobermans, Old English Sheepdogs, Irish setters, Springer
Spaniels, and miniature/toy poodles. Age and polyuria increase the risk of incontinence: 60% of patients are over 5
years of age.
Ectopic ureter and sphincter mechanism incompetence
(SMI) are the major causes of urinary incontinence, with approximately 2/3 of dogs experiencing sphincter mechanism
incompetence. A small percentage (4-5%) have both ectopic
ureter and SMI. Thus, in a female dog with incontinence, ectopic ureter must first be ruled out using a retrograde contrast vaginogram, excretory urogram or cystoscopy. If present, the ectopic ureters are corrected. If ectopic ureters are
not present or incontinence persists after correction, then the
animal is treated for SMI. The diagnosis of SMI is made after ruling out other causes of incontinence. A cystogram often demonstrates the presence of a large “square” bladder,
caudal displacement of the bladder into the pelvis and a
short wide urethra. The condition is confirmed using urodynamic studies.
Medical treatment of treatment of SMI involves the use
of estrogens (67% response) or α-adrenoceptor agonists
(75% response). Surgical treatment may involve coloposus-
pension, cystourethropexy, injection of Teflon ® or collagen
into the urethra or creation of a sling around the urethra at
the bladder neck. Colposuspension is well studied: short
term results with this technique are good (50% of patients
continent), but as time goes on, many patients require medical therapy. At one year, 75% of patients are well controlled
with either surgery alone or a combination of surgical and
medical treatment. Similar results are achieved with cystourethropexy or injection techniques: up to 75% of patients
respond well to surgery/injection alone or surgery/injection
and medical therapy. Multiple injections may be needed to
maintain continence, particularly if collagen is used. Sling
techniques are used as salvage procedures for animals that
are still incontinent after using the previous techniques.
Slings can improve continence, but carry a risk of urethral
obstruction or erosion of the synthetic sling material into the
urethra. Slings made of natural materials are currently being
investigated to determine if erosion can be avoided.
In male dogs, ectopic ureter and prostatic disease must be
excluded before treatment of SMI. Male dogs with SMI are
less likely to respond to medical therapy than female dogs.
Surgical treatment of SMI involves fixation of the deferent
ducts to the abdominal wall. Results in a small series were
similar to results of bladder neck fixation in female dogs.
References
Rawlings C, Barsanti JA, Mahaffey MB, Bement S. Evaluation of colposuspension for treatment of incontinence in spayed female dogs. JAVMA 2001; 219:770-775.
Weber UT, Arnold S, Hubler M, Kupper JR. Surgical treament of male dogs
with urinary incontinence due to urethral sphincter mechanism incompetence. Vet Surg 1997; 26:51-56.
Aaron A, Eggleton K, Power C, Holt PE. Urethral mechanism incompetence in male dogs: a retrospective analysis of 54 cases. Vet Rec 1996;
136:542-546.
Holt PE, Hotston Moore A, Canine ureteral ectopia-analysis of 175 cases
and comparison of surgical treatments. Vet Rec 1995; 136:345-349.
183
Perineal hernia repair
Elizabeth M. Hardie
Perineal hernia is a disease found largely in older, intact
male dogs. Common presenting signs include perineal
swelling, tenesmus, and constipation. Less commonly, diarrhea, vomiting, depression, anorexia, dysuria, anuria,
dyschezia, hematechezia, perineal pain, ribbon-like stool,
weight loss and fecal incontinence occur. The hernia may
be unilateral (right side more common) or bilateral. Diagnosis is made by rectal palpation of a defect in the muscular diaphragm of the perineum.
Retroflexion of the bladder into the hernia, present in
approximately 20% of dogs, is a surgical emergency. Death
due to bladder necrosis had been reported to occur in up to
30% of these cases. Even if the animal lives, there is risk of
long term urinary incontinence. Diagnosis is made by aspiration of urine from the perineal swelling, inability to pass
a urinary catheter, or a contrast cysto-urethrogram. The
urine is drained from the bladder via cystotocentesis, an attempt is made to place an indwelling urinary catheter, and
the bladder is repositioned into the abdomen, if possible.
The hernia is then repaired. The abdomen is entered using a
conventional midline approach or laproscopy and a
cystopexy is performed. If the bladder is visibily discolored
(blue-black), the owner should be warned about the possibility of necrosis.
In addition to retroflexion of the bladder, many dogs
with perineal hernia have other associated diseases that
must be corrected at the same time the hernia is repaired.
Rectal deviation into the hernia is present in most dogs with
perineal hernia, but more severe rectal pathology (dilation,
diverticulum) may be present in 40-60%. Diagnosis is by
barium enema and treatment is pleating or amputation of
the dilation or diverticulum. Testicular tumor has been
found in approximately 25% of dogs castrated at the time of
hernia repair. Prostatic disease, found in 11-17% of dogs
with perineal hernia, is identified with rectal palpation, ultrasound, aspiration and biopsy. Treatment depends on the
nature of the disease. Hypertrophy is treated with castration
alone, cysts and abscesss are treated with partial prostatectomy/omentalization techniques and cancer is treated with
radiation and chemotherapy. Inquinal hernia is present in
approximately 3% of dogs with perineal hernia. Treatment
is surgical repair.
Prompt correction of the hernia is imperative, because the
presence of more severe clinical signs prior to correction has
been associated with poor results after surgical correction.
Neutering at the time of surgical correction has been shown
to reduce the recurrence rate. Correction of rectal pathology
has been shown to reduce the incidence of recurrence and to
lengthen the time to recurrence. Experienced surgeons have a
lower recurrence rate than unexperienced surgeons. The internal obturator flap technique has a lower failure rate than
the conventional technique. Despite improvements in technique, recurrence rates as high as 20% continue to be reported. Recurrence of the hernia is not synonymous with poor
functionality, but overall owner reports also indicate a 2025% poor functionality rate. Causes of long term failure other than recurrence include urinary incontinence, fecal incontinence and chronic fistula development.
The challenge in the management of perineal hernia is to
identify which patients need more aggressive management.
Utilization of techniques such as colopexy, cystopexy, pleating or amputation of the enlarged rectal wall appear to be
beneficial in more severely affected patients. Reinforcement
of the repair using mesh or additional muscle flaps (semitendinosus, superficial guteal) also appears to be beneficial
in severe cases.
References
Szabo P, Bilkei G. Rectum diverticulum/perineal hernia surgery through
longitudinal contracting of the wall of the rectum. Berliner und Munchener Tierrarztliche Wochschririft. 2001; 114:3-3, 139-141.
Hosgood G. Hedlund CS, Pechman RD, Dean pw. Pernineal herniorrhaphy:
perioperative data from 100 dogs. J Am Anim Hosp Assoc 1995; 31:
4,331-342.
Dupre G, Bouvy B, Prat N. Nature et traitement des lesions associees aux
hernies perineales. Etude rerospective a partir de 60 cas et definition
d’un protocole de traitement. Pratique Medicale et Chirurgicale de
l’Animal de Compangnie 1993; 28: 333-344.
185
Rear limb lameness: how to differentiate
between hip dysplasia and stifle joint disease
Don Hulse
DVM, Texas A&M University
Rear limb lameness in the dog is one of the most common
reasons clients seek veterinary consultation. The lameness
may be acute or long standing; if acute, the problem may have
been present for some period of time and only recently been
exacerbated by a minor injury or overuse. If a chronic lameness has been present, generally the dog is presented because
the problem has worsened to the stage that the dog’s quality
of life has been effected. The key to optimal outcome is a correct diagnosis and treatment. Often more than one problem is
present and in these cases, optimal outcome is dependent upon identifying which problem is more clinically significant.
This lecture will address avenues to assist the veterinarian in
differentiating between conditions of the hip joint and stifle
joint responsible for clinical dysfunction.
Signalment and history: Important considerations are
Breed, age, and sex of the dog. Of these, Breed and age are most
useful in assisting the veterinarian with the process of differentiating between problems arising from the hip joint and those
arising from the stifle joint. For example, lameness in large
Breeds (Rottweiler) and sporting Breeds (Retriever) in younger
dogs is more often attributed to Hip Dysplasia than to stifle joint
problems. However, one should not discount that Stifle joint
problems (OCD, Patella Luxation, Ligament injury) do occur in
these Breeds at a young age. Conversely, in these same breeds
of dogs at an older age (2 years or more), lameness is more frequently attributed to the stifle joint. However, as before do not
discount the fact the lameness may be attributed entirely or partially to the hip joint. In the young, smaller breeds of dogs (Poodle, Terrier) lameness may be attributed to the hip (LeggPerthes) or stifle joint (patella luxation). In mature, smaller
breeds more problems are more commonly attributed to the stifle joint (patella luxation, ACL injury).
More often, a unilateral lameness is attributed to the stifle joint whereas a bilateral problem (difficulty rising, shifting weight to the front limbs) can be attributed either to the
hip joints, stifle joints, or low back. Also, be aware that the
owner may describe the lameness as being in the opposite
normal limb since they are often looking at the dog from the
front. When doing so, the owner’s right side is the dog’s left
side and the owners left side is the dog’s right side. I believe
a good “rule” of thumb is that all rear limb lameness in
young dogs is attributed to the hip joints until proven otherwise. Conversely, all rear limb lameness in mature dogs is
attributed to the stifle joint until proven otherwise.
Young dog…think hip
Mature dog...think stifle
Physical Examination: The physical examination begins
with observation of the dog standing, walking, and trotting.
Dogs with bilateral joint pain will shift their weight to the
front limbs giving a “bowed” appearance to the low back
(often owners will think the problem is in the low back). In
younger animals, this appearance is commonly associated
with the hip joints (Hip Dysplasia) while in mature animals
this appearance is more commonly associated with the stifle
joints (bilateral partial ACL injury).Unilateral lameness is
often associated with the stifle joint in the mature dog (a
“clicking” while walking is characteristic of a meniscal
tear). In the young dog unilateral lameness might indicate
rupture of the round ligament and subluxation of the hip
joint or less commonly a problem in the stifle joint (OCD,
patella luxation). Bilateral lameness may be present but often one limb exhibits more clinical dysfunction than the other. Bilateral lameness in the young dog is more often related
to hip dysplasia while in the mature animal related to stifle
joint problems (bilateral ACL injury). Physical exam findings characteristic of hip dysplasia include passive (Otolani)
and dynamic subluxation of the hip joints (young dog) loss
of full motion (extension) in mature and pain upon manipulation. To detect passive subluxation of the hip joint, the dog
is positioned in lateral recumbency with the limb in neutral
position. An upward, dorsal force is transmitted through the
hip joint via the knee. If laxity is present, the femoral head
will subluxate. The limb is then slowly abducted until one
feels the femoral head reduce into the acetabular cup. The
rapid reduction is easily detectable. To examine for the presence of dynamic subluxation, follow behind the dog as he is
walking. Place your hands over the greater trochanters; if the
hips are subluxating under weight bearing load, you will
detect this as an upward movement of the trochanter. In
186
younger animals, pain is detected on external rotation of the
hip whereas in mature dogs extension is uncomfortable.
Physical exam findings characteristic of dogs with stifle
joint injury include proliferation of medial restraints, loss of
full flexion upon sitting, and abnormal translation. Examine
the stifle joints for effusion and thickening of the surrounding soft tissue as the dog is still standing. Standing behind
the dog, cup your hands over the front of both stifles and
check for side to side symmetry of the medial aspect of the
joints (be careful, some dogs have bilateral injury). Dogs
with stifle joint injury (primarily cases with ACL injury) will
exhibit proliferation and thickening of the medial joint restraints (medial buttress). Ask the dog to sit from a standing
position. As the dog sits, watch to see if he can flex the stifle completely (sit test). Dogs having joint effusion and/or
proliferation of the surrounding joint capsule lose the ability
to completely flex the stifle joint. As they sit, they will turn
the stifle laterally.
Abnormal sit test
Normal sit test
Once the dog is lying on his side, position yourself behind
the dog to evaluate stability of the stifle joint. As you stabilize
the femur with one hand, gentle apply an anterior force to the
tibia. Assess the degree of joint movement and compare side to
side difference (be careful…bilateral injury may be present). If
the dog is apprehensive or very muscular, sedate the dog to
evaluate stability. The joint may appear very stable even under
sedation. Do not rely solely on palpation to diagnosis stifle
joint pathology. A partial ACL tear can be very stable upon palpation but unstable under physiologic load. The instability under load leads to inflammation and clinical dysfunction.
Note: the joint may be stable at the human level but unstable
at the cell level
Couple information gained on palpation with other
physical exam findings and radiographic evaluation. Also,
note that young dogs will have 4-5mm of normal translation.
In the mature dog with bilateral symptoms, neurologic
disease must be a consideration. To help differentiate between orthopedic disease and neurologic disease, perform a
thorough neurologic/orthopedic exam before and after exercise. Dogs with a neurologic condition often will worsen after exercise whereas dogs with an orthopedic problem will
improve with exercise (Hip Dysplasia) or remain the same
(ACL injury).
Diagnostics: Radiographs remain the standard to assess the hip joint and stifle joint. However, information
derived from radiographs must be interpreted with the
knowledge gained from the signalment and physical examination. Assimilating information acquired from the
signalment and physical exam is necessary because the
presence of radiographic changes does not always correlate with clinical dysfunction. Often an attending veterinarian will focus on the radiograph appearance of the stifle or hip joint leading to misinterpretation and an erroneous diagnosis. Frequently this occurs with the large
breeds of dogs presented with rear limb lameness. Many
of these dogs will have moderate to severe radiographic
evidence of DJD as seen in Fig. 1. In a significant number of cases such as this, the problem is located in the stifle joint(s). Many large Breed, young dogs with rear limb
lameness will have radiographic Hip Dysplasia (hyperlaxity). Clinical lameness may be erroneously attributed
to the hips when the problem is located in the stifle joint.
As such, all dogs with rear limb lameness should have the
hips and stifles radiographed. The hip joint can be assessed using the standard OFA position, Penn Hip, DLS
(dorsolateral) position. The majority of young dogs presented for clinical signs associated with hip dysplasia exhibit a degree of hyperlaxity that can seen with a standard
OFA position Fig. 2.
The Penn Hip and DLS assessment are valuable in the
young animal with marginal hyperlaxity. Standard OFA
position is sufficient to evaluate hip joints in the mature
dog (Fig. 1). Both lateral and AP views of the stifles must
be taken. The earliest indication of stifle joint pathology
is joint effusion. Later, one will recognize osteophytes
and periarticular buttress. Joint effusion is recognized by
examining the posterior compartment on the lateral projection. Normally the soft tissue line between the muscles
and joint capsule lies adjacent to the fibular head. Early
effusion and capsular proliferation displaces this line posteriorly. (Fig. 3 “a” denotes tissue line) Often dogs with
unilateral or bilateral rear limb lameness will have radiographic evidence of DJD (Fig. 1) and stifle joint pathology (Fig. 3).
The difficulty facing the veterinarian is determining
which anatomic area is responsible for the clinical dysfunction. Experience dictates that the stifle joint pathology is always a major factor and is generally responsible
for the clinical lameness. The attending veterinarian
should recommend appropriate treatment for the stifle
joint pathology. This is usually a partial tear of the ACL
187
with or without a meniscal tear. (Fig. 4..”a” denotes ACL
on left and bucket handle tear of medial meniscus on
right) Following recovery, one can re-evaluate the hip
joints and recommend surgical intervention or conservative treatment.
189
Juvenile orthopaedic problems
Don Hulse
Juvenile orthopedic problems are one of the most common reasons for consultation with a veterinarian. They can
be classified as traumatic, congenital, or inflammatory. This
lecture will address congenital conditions which cause forelimb and hindlimb dysfunction. Of the myriad of conditions,
the most commonly encountered conditions of the forelimb
(OCD, elbow dysplasia) and hindlimb (hip dysplasia, patella luxation) will be addressed. Mention will be made of
panosteitis and hypertrophic osteopathy since these may occur concurrently with other problems.
Osteochondritis dissecans (OCD) is a manifestation of
osteochondrosis. Osteochondrosis is a disturbence in endochondral ossification which affects the humeral epiphysis.
Although the abnormal endochondral ossification is seen
throughout the epiphysis on CT (see figures below), the
most apparent gross clinical finding is a section of cartilage
lifted from the articular surface. Areas of abnormal endochondral ossification of the articular surface become thickened and are susceptible to fissure and loosening (OCD). In
the shoulder it is usually evidenced as a cartilage flap found
on the midline or lateral aspect of the dorsocaudal humeral
head. The abnormal cartilage may fissure and cause protrusion of a loose flap of cartilage into the joint, or the cartilage
may completely detach from the underlying bone and become lodged in the caudomedial joint pouch. Despite unilateral lameness, this condition is often bilateral.
CT of OCD
CT of OCD
CT of OCD
Large and giant-breed dogs are commonly affected and
males are more often affected than females. Clinical signs
often develop between 4 and 8 months of age; however,
some dogs may not be presented for veterinary evaluation
until they are mature or middle-aged. Affected animals are
usually presented for examination because of unilateral
forelimb lameness.
Owners usually report a gradual onset of lameness that
improves after rest and worsens after exercise. On physical
examination, the shoulder should be palpated and moved
through a complete range of motion. Crepitation or palpable swelling of the joint is seldom evident, but affected animals usually exhibit pain when the shoulder is moved into hyper-extension or extreme flexion. Often the examiner
can detect muscle atrophy of the forelimb by loss of muscle mass adjacent to the spine of the scapula. Differential
diagnoses include osteochondrosis, bicipital tenosynovitis,
shoulder instability.
Despite apparent lameness in only one limb, both shoulders should be radiographed because this condition is often
bilateral. Sedation may be required for quality radiographs
particularly in large hyper-active dogs. The earliest radiographic sign of OCD is flattening of the caudal humeral
head. This is due to thickening of the articular cartilage and
deviation of the subchondral bone line. As the disease progresses, a saucer-shaped radiolucent area in the caudal
humeral head may be visualized. Calcification of the flap
may allow visualization of the flap either in situ or within
the joint if it has detached from the underlying bone. In
chronic cases, large calcified joint mice are often observed
in the caudoventral joint pouch or cranially within the bicipital groove.
OCD
OCD
A complete orthopedic examination is essential in that
other juvenile orthopedic conditions can occur concurrently
with shoulder OCD. Elbow dysplasia (FCP, UAP), panosteitis, hypertrophic osteodystrophy, bicipital tenosynovitis,
and shoulder instability are some conditions that may occur
with shoulder OCD. Diagnosis of OCD is based upon signalment and history, physical findings, and confirmed with
radiographic appearance typical of OCD. Medical treatment
of OCD consists of anti-inflammatory medication and moderate exercise.
190
Surgery is the treatment of choice in cases of OCD.
Surgery can be accomplished via open arthrotomy or arthroscopically. We prefer to manage OCD arthroscopically; mobidity is decreased such that both shoulders can be operated
(if bilateral). Details of the technique for open arthrotomy or
arthroscopy can be reviewed in detail within textbooks related to canine surgery.
Biceps groove
Fragments around
biceps tendon
Free fragments
Elbow dysplasia is used to denote an abnormal development of the elbow joint. It is used to describe developmental
diseases which include ununited anconeal process, fragmentation of the medial coronoid process and osteoarthritis secondary to joint incongruity. Some surgeons include OCD as
part of the syndrome of elbow dysplasia. I prefer to classify
OCD separate from elbow dysplasia. In my opinion, OCD is
more closely associated with an underlying abnormality of
cartilage development. The pathophysiologic mechanism
leading to elbow dysplasia is thought to be a lack of elbow
congruity secondary to improper growth of the radius/ulna
during maturation. For example, the axial length of the ulna
is shorter in cases with ununited anconeal process as compared to breed matched cases without UAP. The hypothesis
is that as growth proceeds the anconeal process of affected
dogs presses against the humeral trochlea. This creates a
shear force separating the anconeal process from the ulnar
metaphysis. (Fig. 1–lateral radiograph showing UAP)
In cases with abnormal medial coronoid process of the
ulna, CT has shown the articular surface of the radial head to
be positioned below (distal) the joint line of the coronoid
process. This finding leads one to speculate that the growth
Figure 1
of the radius was retarded at some point during development
(alternatively, ulnar growth could have been accelerated
leading to a longer ulna). In either circumsatnce, with the
coronoid positioned higher than the radial articular surface,
increased weight bearing forces are directed onto the lateral
region of the medial coronoid. Increased force could give
rise to abnormal stresses which initiate fragmentation of the
medial coronoid (Fig. 2) or result in an osteomalacia coronoid (similar to legg perthes of the femoral head) (Fig. 3).
The degree of elbow incongruity will vary in severity
(similar to hip dysplasia!!). Some dogs have severe incongruity which causes abrasion of the articular cartilage overlying the medial coronoid and under surface of the humerus.
In these cases, the only structure with a cartilage surface is
the often the fragmented portion of the medial coronoid because the free fragment can move in response to pressure.
(Fig. 4..free FCP; note cartilage surface on FCP and erosion
on humeral condyle).
Clinical signs are variable and dependent upon the degree of incongruity. The worse the incongruity the more severe the clinical findings and the earlier the clinical signs are
expressed. Moderate to severe joint effusion, pain on manipulation of the elbow, and loss of full range of motion are
signs indicative of significant incongruity. A dog presenting
with these clinical findings at an early age will have large
fragments and erosion of the cartilage surface in the medial
compartment of the elbow joint. (Fig. 5-arthroscopic view of
large FCP and cartilage erosion of the medial coronoid and
humeral condyle. Fig. 6 CT of same case showing mishappen coronoid and FCP)
Dogs presenting later in life with severe incongruity have
significant osteoarthritis. (Fig. 7, 8....radiograph showing
moderate OA; arthroscopic view showing severe erosion of
the medial compartment of the elbow.)
191
Figure 6
Figure 7
Although the above clinical presentation is indicative of
significant incongruity, clinical signs in the majority of dogs
with FCP/incongruity are not as severe. In most dogs the
presenting complaint is a periodic lameness associated activity are present. Gait observation may or may not show a
lameness; similarly effusion and pain are variable. The most
consistent clinical finding is loss of normal flexion. Normally, the forearm will be no more than 2 finger widths from the
shoulder upon full flexion. In cases with loss of flexion, the
forearm stops short of this mark. This is caused by effusion
and thickening of the joint capsule. Incongruity and cartilage
damage will vary but are generally mild to moderate.
Some dogs present with lameness later in life (2-5 years
of age); The only notable clinical sign in these cases is often
a discernable limp. No joint effusion, pain or loss of motion
in elbow is seen. Radiographs often show no obvious signs
of DJD. These cases are commonly misdiagnosed as having
“soft tissue” injury or shoulder “instability”. A nuclear bone
scan will localize the problem to the elbow; a subsequent CT
will be diagnostic of a fragmented coronoid or osteomalacic
coronoid. (Fig 9, 10,11, - AP radiograph showing no discernible OA; bone scan showing increased uptake in the elbow; CT showing osteomalacic coronoid.
These cases have traumatically dislodged an FCP or experienced micro-fractures of a osteochondromalacic coronoid .
Congruity in these joints is excellent leading on to hypothesize
that at some point in development incongruity existed. At the
time incongruity was present, a fissure line or multiple fissures
were created in the medial coronoid. The incongruity self-corrected as the dog grew but the underlying coronoid abnormality was established. Later in life, a traumatic incident separated the fissure line(s) leading to clinical signs.
Treatment and prognosis are controversial. Some studies
have not shown a difference in outcome between non-operative or operative treatment. However, these studies did not
classify the severity of incongruency making it difficult to
judge accuracy. Our clinical experience suggests outcome is
dependent upon the degree of incongruency and associated
cartilage erosion. Surgical intervention is warranted in all
cases and will improve clinical function. Dogs with minimal to no incongruency, no cartilage erosion, and a fragmented of osteomalacic coronoid a have a good long term
prognosis with arthroscopic intervention. Fragments or osteomalacic bone can be removed (arthroscopically) from
both elbows at the same time without causing significant
discomfort. Dogs presenting with severe incongruency and
cartilage erosion will improve with surgical intervention.
Removal of fragments and osteomalacic bone will improve
limb function. Proximal ulnar ostectomy will improve function and may slow progressive OA. However OA is likely to
progress and the long term prognosis is questionable. (1215...CT frames showing incongruity and severe sclerosis of
the medial humeral condyle. Arthroscopic view showing
wearing and erosion of articular cartilage in the medial
compartment. Radiograph of proximal ulnar ostectomy;
note the caudoventral displacement of the coronoid following ulnar ostectomy).
192
Hip dysplasia is an abnormal development of the coxofemoral joint. The syndrome is characterized by subluxation or complete luxation of the femoral head in the younger
patient while in the older patient mild to severe degenerative
joint disease is present. The cause is multifactorial in nature
with both hereditary traits and environmental factors playing
a part in the disease process. Rapid weight gain and growth
through excessive nutritional intake can lead to hip dysplasia by causing a disparity in development of the supporting
soft tissues and bony skeleton. Factors that cause synovial
inflammation, such as mild repeated trauma and viral or bacterial synovitis, may be important in the pathogenesis of hip
dysplasia. Synovitis leads to increased joint fluid volume,
which abolishes the joint stability associated with the negative suction-like action produced between the articular surfaces by a thin layer of normal synovial fluid. Although
many factors may contribute to the development of hip joint
laxity, it is the resulting laxity that is responsible for the early clinical signs and joint changes. Subluxation stretches the
fibrous joint capsule, producing pain and lameness. Also the
surface area of articulation is decreased, which concentrates
the stress of weight bearing over a small area through the hip
joint. Subsequently fractures of the trabecular cancellous
bone of the acetabulum can occur, causing pain and lameness. The cancellous bone of the acetabulum is easily deformed by the continual dorsal subluxation of the femoral
head. This piston-like action causes a tilting of the acetabular articular surface from a horizontal plane to a more vertical plane. As the plane of the articular surface becomes more
vertical, subluxation worsens. The physiologic response to
joint laxity is proliferative fibroplasia of the joint capsule
and increased thickness of the trabecular bone. This relieves
the pain associated with capsular sprain and trabecular fractures. However, the surface area of articulation is still decreased which causes premature wear of articular cartilage,
exposure of subchondral pain fibers and lameness. This may
occur early in the pathologic process or later in life. The incidence of hip dysplasia is greatest in the Saint Bernard and
German Shepherd but most sporting breeds are affected.
History and clinical signs vary with the age of the patient.
There are two general recognizable clinical syndromes associated with hip dysplasia: (1) patients 5 to 16 months of age,
(2) patients with chronic degenerative joint disease. Patients
in group 1 present with lameness between 5 to 8 months of
age. Symptoms include difficulty when rising after periods
of rest, exercise intolerance and intermittent or continual
lameness. Some patients will present with an acute nonweight bearing lameness of one rear leg. This latter group of
patients have torn the round ligament of the affected hip
joint and severely sprained the fibrous joint capsule. The majority of patients will spontaneously improve clinically when
15 to 18 months of age. This clinical improvement is due to
pain relief as proliferative fibrous tissue prevents further
capsular sprain, and increased thickness of the subchondral
bone prevents trabecular fractures. Of these patients which
improve, a significant percentage (may be as high as 50% to
70%) will not exhibit clinical difficulty at any point later in
life. However, these patients are still afflicted with hip dysplasia and have a decreased surface area of hip joint articulation. Depending on the degree of articular cartilage wear
and progression of degenerative joint disease, 50% to 30%
within this group of patients may develop clinical signs later in life. Symptoms may include difficulty in rising, exercise intolerance, lameness following exercise, atrophy of the
pelvic muscle mass, and a waddling gait with the rear quarters.
Physical findings in the younger group of patients include pain during external rotation and abduction of the hip
joint, poorly developed pelvic muscle mass, and exercise intolerance. Hip exam performed under general anesthesia
will reveal abnormal angles of reduction and subluxation reflecting excessive joint laxity. Physical findings in the older
group of patients include pain during extension of the hip
joint, reduced range of motion, atrophy of the pelvic musculature, and exercise intolerance. There is generally no joint
laxity but crepitus may be detected on joint manipulation.
Differential diagnoses include panosteitis, osteochondrosis, physeal separation, and ligament injury in the younger
patient. In the older group of patients it is extremely important to rule out neurologic problems as a cause of the clinical symptoms. Orthopedic conditions such as ruptured cranial cruciate ligament, polyarthritis, and bone neoplasia
must also be considered before attributing clinical signs to
hip dysplasia. Radiographically, there are seven grades of
variation in the congruity between the femoral head and acetabulum established by the Orthopedic Foundation for Animals. Excellent, good, fair, and near normal are considered
within a range of normal. (Fig. 1) Dysplastic animals fall into the categories of mild, moderate, and severe. (Fig. 2) It is
important to note that clinical signs do not always correlate
with radiographic findings. More recently, patients may be
evaluated using a distraction index. With this technique, the
degree of hyperlaxity is measured and correlated with standards for each breed. A correct diagnosis of hip dysplasia as
the cause of clinical problems is based on age, breed, history, physical findings, and radiographs.
Treatment is dependent upon the age of the patient, the
degree of patient discomfort, physical and radiographic findings, client expectations of patient performance, and financial capability of the client. Conservative treatment is beneficial to a large number of patients in both the young and
older patient groups. Conservative management is divided
into acute management and long term management. When a
dog exhibiting signs of hip dysplasia enters the clinic, it is
generally because they have sprained the hip joint. The dysplastic joint is either hyperlax (young dog) has a limited
range of motion (mature dog). In either case, the joint is easily sprained and the dog that is presented with symptoms has
generally overused (sprained) the hip joint. The management
Figure 1
Figure 2
of the case at this time period is the same as treating any other acute sprain. Rest, physical therapy, and non-steroidal
analgesics will relieve signs in the majority of patients. Rest
is just that!!!, controlled activity with slow walking on a
leash only. There should be NO free activity for 2 weeks.
Physical therapy includes cold therapy for the initial 24
hours followed by heat therapy for 1-4 days. Commercial
cold packs are the most convenient and precise way to apply
cold therapy. The application of cold should only be 5-10
minutes. Heat therapy is again best applied with commecial
heat packs. Be careful not to burn the skin!! NSAIDs recommended by the author are: 1. Aspirin (Ascriptin), carprofen (Rimadyl), etodolac (Etogesic). I would not recommend
any other “over the counter NSAIDs). The advantage of aspirin (25mg/kg TID) is the low cost. The disadvantage of aspirin is the low efficacy and incidence of GI upset. Aspirin is
a COX 1 inhibitor; inhibition of COX 1 de-regulates the balance of normal homeostasis giving rise to a higher incidence
of side effects. Aspirin should always be given with a small
amount of food. Preferably, give a dose late in the evening
so higher blood levels are present early in the morning.
Carprofen (1mg/lb BID) is FDA approved for use as an anti-arthritic medication in the dog. It too should be administerd with a small amount of food. Carprofen is a COX 2 inhibitor accounting for a low incidence of side effects.
Carprofen is very effective in controlling discomfort associated with hip dysplasia. The attending veterinarian must always consult with owners relative to side effects of any
NSAID. NSAIDs can cause serious side effects and even
death in some humans and animals. There is a reported incidence of liver failure in dogs having been given carprofen.
The common age of dogs afflicted is most commonly mature
adults (8yrs) but liver failure can occur in any age. Although
the incidence of liver failure is very low, the clients must be
advised of this possibility. Etodolac (Etogesic) is also an
NSAID aproved by the FDA for use in the dog. It too is very
effective in controlling pain associated with arthritis in dogs
and is administered 1/day (4-7mg/lb). The attending veterinarian must emphasize that REST and PT are the most important considerations when treating an acute sprains.
Following the acute phase of treatment, the attending
veterinarian must consult with the owner regarding long
term management of the dysplastic dog. The foundation for
long term management of any arthritic joint is weight control, exercise therapy, and anti-inflammatory drugs or supplements. The majority of mature dogs with hip discomfort
are over weight. Studies have shown a significant improvement in function if an ideal target weight is achieved. The
foundation for weight control is exercise therapy, diet, and
owner behavior modification. There are a number of excellent commercial diets on the market. The owner in conjunction with the dog undergo behavior modification. This is a
weight reduction program; their dog will be hungry. The
owner must not feel guilty but must understand the long term
benefits of weight reduction. Convincing evidence might be
pictures showing the outcome of previously treated dogs.
The attending veterinarian should become familiar with
them and chose one or two for use in their clinic. Exercise
programs aimed at developing pelvic muscles should begin
gradually. Swimming (if available) develops endurance and
193
flexibility. Repetitions of sit-stand exercises also increase
endurance and flexibility. Standing, forced flexion-extension
exercises (squats) develop strength as does walking uphill
with leg weights. Following exercise therapy, the owner
should passively extend the hip joint. This will increase the
range of motion and help prevent pathologic stretching of
the surrounding soft tissue.
Administration of drugs (NSAIDs, steroids, PSGAGs,
Hyaluronate) or supplements (glucosamine, chondroitin sulfate, manganese) are useful to control discomfort. This is
particularly true in the early stages of treatment before the
benefits of weight reduction and exercise therapy are realized. The administration of drugs should be at a minimum
level (dose and frequency)to achieve comfort. My preference is to begin with carprofen or etodolac. Steroids are useful as pulse therapy: 1mg/lb, BID for 3 days, .5mgs/lb BID
3 days, .5migs/lb SID 3 days. Steroids are used if NSAIDs
are ineffective. Supplements of glucosamine, chondroitin
sulfate and manganese alone or in combination have been
shown in vitro as well as in clinical studies to ameliorate discomfort or reduce the dose of drugs needed to control discomfort. The combination of glucosamine, chondriotin sulfate, and manganese ascorbate (Cosequin) has been shown
to be significantly more effective in retarding the progression of OA in a rabbit model than was either supplement
used alone. This combination has also recently been shown
to increase proteoglycan formation in bovine explants and
inhibit IL-1 induced collagenase activity. There are a number of supplements (alone and in combination) on the market. There is a great varience in the purity and quality of
products. The attending veterinarian must become familiar
with the manufacturing process and efficacy data of a supplement he/she intends to use.
Surgical intervention also is divided into techniques useful in the younger population and those useful in mature
dogs. Techniques useful in the younger population include
Triple Pelvic Osteotomy (TPO), femoral head ostectomy,
and possibly total hip replacement. My preference in this
aged dog is either a TPO or conservative mangement. In the
older dogs, my prefernce is total hip replacement or conservative management. Femoral head ostectomy is a good option also in cases where financial contraints limit the possibility of a total hip replacement.
Patella luxation is a problem in all Breeds and sizes of
dogs. Medial patella luxation is the most common direction
of luxation in both small Breeds and large Breeds of dogs.
Treatment of medial patella luxation may be conservative
(small Breeds only) or surgical. The decision as to which
method is applicable for a patient is dependent upon the clinical history, physical findings and the age of the patient. An
older patient in which patella luxation is noted as an incidental finding on physical examination and in which the
client reports no clinical lameness does not warrant surgical
intervention. Rather, the client should be informed as to the
clinical signs associated with patella luxation. Surgery is advised in the young adult patient even though no clinical
problem is apparent since intermittent luxation may prematurely wear the articular cartilage of the patella. Surgery is
indicated in any aged patient exhibiting lameness and is
194
strongly advised in a patient with active growth plates since
skeletal deformity may worsen rapidly. However surgical
techniques used in actively growing animals should be those
that will not adversly affect skeletal growth.
There are numerous surgical techniques aimed at restraining the patella within the trochlear groove. Tibial
tuberosity transposition, collateral restraint release, collateral restraint reinforcement, trochlear groove deepening,
femoral osteotomy and tibial osteotomy have all been advocated for correction of patella luxation. Generally, a
combination of techniques are required. The techniques
used are dependent upon the severity of luxation, skeletal
deformity, and surgeon preference. The techniques used for
patella luxations are dependent upon the pathology present.
Not every patient with a luxating patella will need all of the
techniques listed below for surgery to be successful. The
surgeon must recognize which abnormalities are present ia
a given stifle and then use the technique(s) that addresses
each problem.
Tibial tuberosity transposition: Tibial crest transposition is an effective method of treatment for Grades II, III, and
IV patella luxations. Make a craniolateral skin incision 4cm
proximal to the patella and extend the incision 2cm below the
tibial tuberosity. Incise the subcutaneous tissue along the same
line. Make a lateral parapatellar incision through the fascia lata and carry the incision distally onto the tibial tuberosity below the joint line. Reflect the cranialis tibialis muscle from the
lateral tibial tuberosity and tibial plateau to the level of the
long digital extensor tendon. Use sharp dissection to gain access to the deep surface of the patellar tendon for placement
of the osteotome. Beginning at the level of the patella, make a
medial parapatellar incision through the fascia and distally
through the periosteum of the tibial tuberosity. Position an osteotome beneath the patellar tendon 3-5mm caudal to the cranial point of the tibial tuberosity. Use a mallet to complete the
osteotomy in a proximal to distal direction. The distal periosteal attachment should not be transected. The degree of
lateral movement of the tibial tuberosity is subjective but is
based on the longitudinal realignment of the tuberosity relative to the trochlear groove.
Once the site of relocation
is chosen, remove a thin
layer of cortical bone with
a rasp or the osteotome.
Lever the tibial tuberosity
into position and stabilize
it with one or two small
kirschner wires directed
caudally and slightly proximally. It is important to
gage the depth and direction of pin placement. The
pin should not exit the tibia
caudally but should only
engage the caudal cortex.
If the pin protrudes too far
from the caudal cortex of
the tibia, persistent lameness will result.
Lateral reinforcement: Reinforcement of the lateral
retinaculum is accomplished with suture placement and
imbrication of the fibrous joint capsule, by placement of a
fascia lata graft from the fabella to the parapatellar fibrocartilage, or excision of redudant retinaculum. For suture
reinforcement, place a polyester suture through the
femoral-fabellar ligament and lateral parapatellar fibrocartilage. Next, place a series of imbrication sutures through
the fibrous joint capsule and lateral edge of the patella tendon. With the leg in slight flexion, tie the femoral-fabellar
suture and imbrication sutures. Alternatively, the lateral
retinaculum may also be reinforced through transposition
of fascia lata. A section of fascial lata equal in width to the
patella and in length twice the distance from the patella to
the fabella is isolated. Free the graft proximally and leave
it attached to the proximal pole of the patella distally. Pass
the free end of the graft deep to the femoral-fabellar ligament and back to the lateral parapatellar fibrocartilage. Suture the graft to itself and the femoral-fabellar ligament
with the leg in slight flexion.
If the patella is out of position most of the time, the retinaculum opposite the side of the luxation will be stretched;
with medial luxations, there is redundant lateral retinaculum.
Once the patella is reduced, excise the excess retinaculum
and joint capsule allowing tight closure of the arthrotomy.
None of the reinforcement techniques alone are adequate to
permantly prevent reluxations. If the mechanical forces
pulling the patella out of the trochlear groove have not been
neutralized, the reinforced retinaculum will stretch again
with time.
Medial release: The medial joint capsule is thicker than
normal and contracted in patients with grade III or Grade IV
patella luxations. In this group of patients, the medial joint
capsule and retinaculum must be released to allow lateral
placement of the patella. and vastus medialis muscle directs
the patella medially, the insertions of these muscles at the
proximal patella are released. Redirect the insertions and suture them to the vastus intermedius. Make a medial parapatellar incision through the medial fascia and joint capsule
with a scalpel. Begin the incision is begun at the level of the
proximal pole of the patella and extend it distally to
the tibial crest. Allow the
incision to separate and do
not suture the cut edges
when surgery is completed.
Rather, suture medial subcutaneous tissue to the cranial cut edge of the incision. If dynamic contraction of the cranial sartorius
muscle and vastus medialis
muscle directs the patella
medially, the insertions of
these muscles at the proximal patella are released.
Redirect the insertions and
suture them to the vastus
intermedius.
Deepening of the
trochlear groove: If the
medial and lateral trochlear
ridges do not constrain the
patella, the trochlear groove
must be deepened. This
technique is generally necessary in patient swith a
grade III or grade IV luxation. Deepening the groove
may be achieved with a
trochlear wedge recession
or a trochlear resection. A
trochlear wedge recession
is technically more demanding but preserves the articular cartilage while a simple
trochlear resection is less demanding but destroys the articular cartilage.
Trochlear wedge recession deepens the trochlear groove
to restrain the patella and maintains the integrity of the
patellofemoral articulation. Make a diamond shaped outline
cut into the articular cartilage of the trochlea with a scalpel.
The width of the cut must be sufficient at its’ midpoint to
accommodate the width of the patella. An osteochondral
wedge of bone and cartilage is removed by following the
outline previously made. Make the osteotomy so that the
two oblique planes which form the free wedge intersect distally at the intercondylar notch and proximally at the dorsal
edge of the trochlear articular cartilage. In larger patients,
use an oscillating saw but in smaller breeds and toy breeds
of dogs use a fine-tooth hand held saw or the cutting edge
of a number 20 scalpel blade and mallet. Remove the osteochondral wedge and deepen the recession in the trochlea
by removing additional bone from one or both sides of the
newly created femoral groove. With medial luxations, it is
often best to take more bone from the lateral side of the
groove, thus preserving as much of the medial ridge as possible. Remodeling the free osteochondral wedge with
rongeurs may also be necessary to allow the wedge to seat
deeply into the new femoral groove. The wedge can also be
rotated 180 degrees when it is returned to the femoral
groove if doing so will aid in heightening the medial ridge.
Replace the free osteochondral wedge when the depth is
195
sufficient to house 50% the height of the patella. The osteochondral wedge remains in place due to the net compressive
force of the patella and the friction between the cancellous
surfaces of the two cut edges.
Trochlear resection is a method of deepening the
trochlear groove through removal of articular cartilage and
subchondral cancellous bone. Measure the width of the articular surface of the patella and use this measurement to determine the proper width of the trochlear resection. Remove
articular cartilage and bone with a bone rasp, power burr, or
rongeurs. The length of the trochlear resection should extend
to the proximal margin of articular cartilage and distally to
the cartilage margin just above the intercondylar notch. The
depth of the groove should be such as to accommodate 50%
of the height of the patella and allow the parapatellar fibrocartilage to articulate with the newly formed medial and lateral trochlear ridges. Make the medial and lateral trochlear
ridges parallel to each other and the base of the groove perpendicular to each trochlear ridge. The advantage of this
technique is its’ simplicity. The disadvantage is that this
technique removes the articular cartilage of the trochlea and
articulation of the patella on the rough cancellous surface results in wearing of patellar articular cartilage. Nevertheless,
the trochlear groove eventually fills with a combination of fibrous tissue and fibrocartilage and the patients appear to
have acceptable limb function.
Osteotomy of the femur: This procedure is only used in
patients with severe skeletal deformity in which it is determined that the success of maintaining patellar reduction is
not possible with the techniques described previously. The
deformities usually seen are a varus bowing of the distal femur and medial torsional deformity of the proximal tibia.
The goal of surgery is to realign the stifle joint in the frontal
plane where the transverse axis of the femoral condyles is
perpendicular to the longitudinal axis of the femoral diaphysis. This requires accurate preoperative measurement and
wedge osteotomy of the femur. Transposition of the tibial
crest, lateral retinacular reinforcement, medial restraint release, and deepening of the trochlear groove are also required for success. These techniques require special equipment and training; as such, these techniques should be performed by a trained specialist.
197
New and advanced concepts in fracture management
Don Hulse
A treatment method which is gaining popularity in fracture management is that of “Biologic” osteosynthesis. Actually this is probably not a good term since all fracture healing is
“biologic” but it seems to be the term coined in the human and
veterinary literature. A term which I prefer and one which
more accurately describes the concept is “bridging” osteosynthesis. Bridging osteosynthesis is an idea based upon two concepts: first, minimal surgical manipulation of the fracture site,
and second, an implant’s ability to buttress the fracture site.
The concept of minimal surgical manipulation of the fracture
site is not a new idea! Our surgical instructors during our years
in veterinary school and instructors we hear at continuing education courses have always preached the importance of
atraumatic surgery. What then is the difference between atraumatic surgical intervention and “bridging” osteosynthesis?
The difference is that although we were always instructed to
perform atraumatic surgery, we were also instructed to
anatomically reduce and rigidly stabilize all fracture lines.
This works well with injuries having single fracture lines
(transverse or oblique fractures) or with comminuted fractures
having 1 or 2 large fragments which can be atraumatically reduced and stabilized with cerclage wire or lag screws (in todays language we call this a reducible comminuted fracture).
In both situations, minimal soft tissue manipulation is required to anatomically reduce and stabilize the fracture.
Reducible fx
8 weeks PO
However, if the same concept of anatomic reduction and
rigid fixation is used with highly comminuted fractures (in
todays language a non-reducible comminuted fracture), significant soft tissue manipulation is needed to bring all the
fragments into their proper alignment. Indeed, the surgeon is
often left with a section of diaphysis having all the fragments
nicely reduced with cerclage wire but with little or no soft
tissue attachments. Excessive soft tissue manipulation for
the purpose of fragment alignment, extends our operative
time, escalates our chance of infection, and significantly
lengthens our time to bone union. Additionally, we are commonly left with small fracture gaps which are notorious for
concentrating strain (micromotion) since strain is a function
of gap size. In short, single fracture lines concentrate strain
(transverse fractures, small fracture gaps!). High levels of
strain preclude bone deposition and when coupled with slow
union due to loss of blood supply lead to extended healing
and an increased chance of implant failure. All of these factors lead to a greatly increased amount of time the implant
must carry the physiologic loads and remain functional. The
more loads the implant must carry and the longer period of
time it must do so, the greater the risk of postoperative complications and implant failure.
198
The concept of “bridging” osteosynthesis primarily relates to highly fragmented injuries where the above conditions are likely to result but can also be applied to the more
simple fracture configurations. The idea is to perform either
closed reduction and stabilization, or open reduction and stabilization without attempting to reduce and stabilize each of
the small fracture fragments. We may “lasso” fragments
which are located to far from the diaphyseal bone column
but we do so without interrupting the soft tissue envelope. To
do so, use a wire passer to gentle encircle the fragment(s)
and pass heavy absorbable suture (do not use wire) around
each fragment. Tie the suture to bring the pieces closer into
alignment. We realized the benefit of this method of fracture
management with the renewed popularity in external fixators. We saw case after case of comminuted tibial and radial
fractures treated through closed reduction with external fixators heal in what was seemingly record speed (even in older patients). We soon applied the concept of no manipulation
of the comminuted section of diaphysis to femoral and
humeral fractures requiring open reduction. Here too, we
saw the value of allowing our implant to serve as a buttress
and simply “bridge” the fracture without attempting to reduce and stabilize small fracture fragments. Although our
implant must serve as a buttress and is at a mechanical disadvantage, this is quickly overcome by the formation of callus if we do not disturb the fracture environment. The second
factor which has allowed us to manage fractures using the
concept of “bridging” osteosynthesis is an increased awareness of factors which permit an implant to effectively serve
in a buttress mode. Increased knowledge of mechanical parameters which enable an implant and its’ connection to the
bone to withstand high physiologic loads has given us the
flexibility of adding “bridging” osteosynthesis to our arma-
mentarium of fracture treatment methods. For example positive profile threaded transfixation pins for use with external
fixators, combinations of external fixators with intramedullary
pins to construct “tie in” configurations, and improved performance of frame configurations have improved our ability
to apply buttress implants. Additionally, interlocking nails
and plate/rod combinations have been researched and tested
clinically are ideal systems for bridging comminuted sections of a diaphyseal fracture. Following the principles of
application of the chosen implant system and preserving the
“biology” of the fracture environment will greatly improve
the surgeon’s chances of optimal outcome.
Non-reducible fx
4 weeks PO
199
Treatment of trigger points
Luc A. Janssens
DMV, Ph.D., Dipl ECVS, CVA, Oudestraat 37, 2610 Antwerp, Belgium
INTRODUCTION
Trigger points (TP) have been described in human medicine (4, 8, 9) since the early fifties. TP can be palpated in
most cases as small, nodular, hard structures within a muscle or fascia. Rarely TP are localised subcutaneously, in connective tissue or in periosteum. TP can be active or passive
(6, 9). Chronic TP cause muscle weakness, shortening and
stiffness however without atrophy. Active TP cause referred
pain plus the symptoms of passive TP. Passive TP may become active under certain influences such as stress, trauma,
fatigue, fever, etc (6, 9).
Referred pain caused by a TP may be in the same body
segment but it can also be localised a far distance away (4,
6, 9). Although well known to some specialists, TP seem to
be unknown to almost all the veterinarians and to the vast
majority of human practitioners. TP are always extremely
painful when squeezed, when squeezed they trigger the
painful myofascial pain that was the original complaint. This
pain may last for hours or days even if the squeezing lasted
only seconds. TP treatment consists of TP stimulation. This
may be achieved by dry needling, injection of saline or local
anaesthetics and transcutaneous electrical stimulation. Some
stimulation techniques such as ultrasound and faradism are
not effective (6, 9). One short stimulation may abolish all
pain symptoms for hours, days, weeks or even permanently
(6, 9). There is a remarkable high degree of correspondence
(71%) between human TPs and acupuncture point (6, 7); this
both for their localisation and for their clinical use. This is
even more remarkable if one considers the total independence in which both systems were discovered (6, 7). Although acupuncture points have been described extensively
in veterinary medicine, TP have, up till now, not been described in animals, this article describes 47 dogs with myofascial pain syndromes in which TP were discovered. Five
different points are described, compared with human TP and
with canine acupuncture points. Their treatment results are
analysed.
tion, were studied. Most were chronically limping and had
been examined routinely by veterinarians. A diagnoses had
not been made in most of them and all treatments had been
without result. Careful palpation of the muscles revealed localised and extremely painful spots. even very timid, nice
dogs would bite immediately when these spots were
squeezed. The age distribution pattern is presented in Fig. 1.
The limping leg distribution pattern is presented in Table 1.
The total number of treated legs was 65. Almost half of these
were the left frontleg. The breed distribution is presented in
Table 2. Radiographs were taken in 32 dogs* (68%).
But radiological pathology was found in only 7 dogs
(15%); three having hip dysplasia, one having rheumatoid
arthritis in knees and elbows, two having arthritis of the elbow and one having osteochrondritis dissecans of the shoulder. In two other dogs there was a history of previous trauma. The pre-TP treatment period varied between 1 day and
± 150 weeks, with a median of 24 weeks. Thirty-one dogs
(66%) had already been treated before. In most cases the
treatment consisted of corticoid administration and administration of antiphlogistics (such as phenylbutazone and
acetylsalicylate). Acupuncture had been used in six cases.
All these treatments had been without success. The patients
were examined by careful palpation of the musculoskeletal
system. TPs were found. These were always extremely
painful on palpation. Once the TP had been localised it was
treated at weekly intervals by dry needling or injection of 1.3
to 2 cc of 1% xylocaine, with a 25 gauge disposable needle.
Dry needling was performed with a 28 gauge stainless steel
acupuncture needle. Care was taken to “hit” the TP into its
centre. The dry needle was left in situ for about 5 minutes.
In some cases the treatment consisted of dry needling one
week and injection the other week, depending on the results
obtained by the former treatment. As a rule dry needling was
only performed in calm dogs. Dogs that moved during the
treatment were injected as this method was tolerated easier.
No other form of therapy was administered. The follow-up
ranged from 2 months to 6 years.
MATERIAL AND METHODS
Forty-seven dogs, 29 males and 18 females, brought for
treatment on account of limping and troubles with locomo-
*
Radiographs were interpreted at the State University of Gent - Belgium by
Dr. P. VAN BREE - Radiologist.
200
RESULTS
TPs were found in the following muscles: the Triceps,
the Peroneus Longus, the Gluteus Medius, the iliocostalis
lumborum, the Adductor-Pectineus complex and the quadriceps. Their relative prevalence is shown in Table 4. The triceps TP tends to be unilateral and left side while hindleg TPs
are mostly bilateral, except for the Adductor and Pectineus
TP, which are mostly unilateral. Frontleg TPs are responsible for about 2/3 of the cases. There is a definite breed
predilection. Boxers are affected many times. Poodles are affected as much but they are much more represented in the
Belgian practices. This makes the relative prevalence of TP
in this breed lower. Sixteen dogs relapsed (33%), 14 dogs
several times. Most of these relapses were on the same
points and were retreated with the same method. The mean
age was 5 years. Two thirds of the patients were male dogs.
Eleven dogs were treated with dry needle stimulation only.
Thirty-one dogs were treated by local anaesthetic injection
and five dogs were treated with injection and dry needles.
The mean number of treatments was 2.8. The success rate is
shown in Table 5. On a total of 82 TPs, 28 recovered completely, twenty became very good, 7 better, 19 had a slight
amelioration and 8 showed no improvement at all. The best
treatment results were obtained in the treatment of the Triceps TP, where a total of 34 dogs had a very good result or a
complete recovery (79%). The results of the treatment of the
other points are less favourable (see Table 5).
DISCUSSION
According to Melzack, Still well and Fox (6), TPs are
spots with abnormal physiological activity. They show local
vasoconstriction and muscular hypertonia and in some cases
they are associated with fibrous nodules. Areas which are especially susceptible to produce TPs are those where large
nerves and blood vessels lie close to the surface. The Triceps
TP, the Pectineus - Adductor TP and the Peroneus Longus
TP are typical examples of this observation as they lie close
to the n. radialis, n. femoralis and n. peroneus. In humans
seventy per cent of the TPs are acupuncture points. We see a
correlation in three points: the Peroneus Longus point is Gall
Bladder 34; The Adductor Pectineus point is Liver 10 or 11
and the Gluteus Medius point correlates with Gall Bladder
29. If we compare canine and human TPs, we find the Gluteus, the Adductor Pectineus and Peroneus points, Iliocostalis points anatomically comparable in dog and man (6, 10).
The Triceps TP is definitely not an acupuncture point; it
lies between the human TP of the subscapularis and infraspinatus. The quadriceps TP is variable in localisation and
not an acupuncture point. Although veterinary acupuncture
is used frequently for varying conditions (ref. 1, 2, 3, 5) it
should be differentiated from TP therapy. Acupuncture uses
painful points (A-shi points) sometimes as a “part” of the total treatment. TP therapy focuses on this TP point(s) only.
Some TP were treated by injections and some by dry needle
stimulation. The main reason for the choice was the dogs
temperament. Only lethargic dogs support a needle in a TP
for several minutes. On the other hand the injection is a fast
method that “hits” a larger area and thus needs less anatomic accuracy, thus making it more appropriate for nonacupuncture trained veterinarians. Most probably, much
more TPs exist in the dog. Probably these will be described
and labelled in next years. This will enable veterinarians to
treat some “problem” patients in a more efficient way.
SUMMARY
Forty-seven limping dogs had one or more Trigger points
in six different muscle areas; squeezing these points was extremely painful. Treatment consisted of stimulation of the
point by needling or injection of a local anaesthetic. The
treatment gave very good results to complete recovery in
about 60 per cent of the cases in about 2.8 weeks (treatment
once a week).
ACKNOWLEDGEMENTS
I am grateful to D. Janet Travell, as her work introduced
me to the subject of Trigger Points.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Janssens L.A. Acupuncture treatment for canine thoracolumbar disc
protrusions: A review of 78 cases. J.M.S.A.C. 1983, 78, 1580.
Janssens L.A. General acupuncture with special reference to therapeutic and analgetic aspects in animals. Vlaams diergeneeskundig
Tijdschrift. Part 1: 1977, 46, 244. Part 2: 1978, 47, 399. Part 3: 1980,
49, 31.
Janssens L.A. Acupuncture points and Meridians in the Dog.
I.V.A.S., Rd 1, Chester Springs, Pennsylvania 1984.
Kennard M.A., Haugen F.P. The relation of subcutaneous focal sensivity to referred pain of cardiac origin. Anesthesiology 1955, 16, 297.
Klide, A., Kung S. Veterinary Acupuncture. University of Pennsylvania Press, Philadelphia, 1977.
Melzack R., Stillwell D., Fox E. Trigger points and acupuncture
points for pain: correlations and implications. PAIN, 1977, 3, p. 3.
Melzack R. Acupuncture and musculoskeletal pain. J. Rheumathology 1978, 5, 119.
Sola A., Williams R. Myofascial pain syndromes. Neurology 1956, 6,
91.
Travell j., Rinzler S. The myofascial genesis of pain. Post graduate
Med. J. 1952, 11, 425.
Travell, J., Simons D. Myofascial pain and dysfunction. The Trigger
point Manual 1983. Williams and Wilkins, Baltimore, London.
201
Treatment of Thoracolumbar Disk Disease in Dogs
by Means of Acupuncture:
A comparison of Two Techniques
Luc A. Janssens
Erik M. De Prins
One hundred ninety-one dogs with thoracolumbar disk
disease were treated over an 11-year period with acupuncture treatments. Two different types of acupuncture techniques were used. In technique A (57%), six distal and several local needles were used, and an injectable anabolic was
administered. In technique B (43%), only two distant needles and two local needles were used. Additional aftercare
consisted of rest and urinary and gastrointestinal monitoring.
One hundred sixty-two (85%), were cured completely. The
mean treatment period was 3.6 weeks (one treatment per
week). Treatment B gave slightly better results than treatment A. Results compare favourably to more classically
used surgical and chemical treatments.
INTRODUCTION
Thoracolumbar disk disease in dogs is a relatively frequently encountered disease in small animal practice. It is
treated in several possible ways. surgical treatments include
fenestration, hemilaminectomy, and dorsal laminectomy
with or without durotomy.1-12 Chemical treatments consists
of analgesics, anti-inflammatory agents, or both and may be
used alone or in combination with surgery.8-9 Conservative
treatments consist of rest, physiotherapy, swimming, ultrasound, and massage.9,13 The purpose of this article was to
record 19 cases of thoracolumbar disk disease, to describe
results of acupuncture treatment, and to compare these with
results of other treatments described in literature.
MATERIALS AND METHODS
Over the last 11 years, 191 dogs with thoracolumbar disk
disease (TLDD) were treated with acupuncture (case details
can be obtained on demand). The total number of cases
(191) consisted of 137 different animals: 71 males (51%)
and 66 females (49%). Thirty-four of these animals relapsed
(25%); 20 relapsed once, 10 relapsed twice, two relapsed
three times, and two relapsed four times. Thus, a total of 54
relapses occurred (28%).
Mean age was 6.2 years (± 0.1 year) with a minimum of
one and a maximum of 14 years. Age distribution is presented in Figure 1 and is comparable to literature results.15 Breed
distribution is presented in Table 1. Thirteen breeds were affected, the dachshund being the one in which the condition
was encountered most often (58%).
All animals were examined neurologically, and radiographs were taken in 101 cases (53%) for additional information. According to the neurological examination, the dogs
were classified into four different neurological groups:
group I = only back pain present, no neurological deficit;
group II = back pain plus negative proprioception in hind
legs and paresis; group III = paralysed, unable to stand or
walk or bear weight, pain sensitivity intact; group IV = as in
III but pain sensitivity absent.
One hundred and twenty animals (63%) had been pretreated with rest, corticosteroids, vitamin B, antiphlogistics,
and analgesics. Mean pre-acupuncture treatment period was
two weeks. Patients were examined for gastrointestinal complications such as diarrhoea, constipation, and loss of central
control over defecation and for urinary complications such
as bladder paralysis, urinary infections, uraemia, and loss of
central control over urination.
Acupuncture treatment consisted of weekly treatments.
In animals of groups I and II, a minimum of two treatments
was performed, while in groups III and IV a minimum of
three treatments was performed. Treatment persisted until
recovery was complete or sufficient to allow the animal to
walk for long periods and to be without pain. Two different
techniques were used. In technique A, six distant needles
(three symmetrical) were inserted in acupuncture points
bladder 60 (BL 60), gallbladder 30 (GB 30), and gallbladder
34 (GB 34) bilaterally, and up to eight symmetrical paravertebral local needles were inserted into local bladder points.
Gallbladder 30 is located between the trochanter major and
202
tuber ischium. Gallbladder 34 is just beneath the lateral fibular head. Bladder 60 is between the distal caudal tibial edge,
proximal calcaneal border, and Achilles tendon. The local
bladder points are located segmentally about 1 cm laterally
from the dorsal spinal process in anatomical dimples of the
dorsolumbar musculature. Local points used here are those
where maximal discomfort or pain could be elicited by manual pressure. The needles were 28-gauge 6 cm-long sterile
acupuncture needles (Figure 2). They were left in situ for 15
minutes without manipulation. One intramuscular injection
of a long-acting anabolic was administered (Laurabolin 1
mg/kg body weight, maximum 25 mg). Gastrointestinal and
urinary complications were treated when necessary (for example, urinary infection was treated with an appropriate antibiotic, constipation with an enema and laxative diet, bladder paralysis by manual emptying or catheterization bid).
The owner was told to keep the dog restricted and quiet (in
a playpen) for four weeks to avoid skin ulcerations caused
by dragging the paralysed hind legs over floors and carpets
and to avoid aggravation of the neurological status in milder
or recovering cases.
Technique B consisted of the use of one distant needle
symmetrically (GB 34) and a maximum of two local needles. No anabolic was administered. All other aftercare was
identical to technique A.
In some rare cases when violent back pain was present,
an analgesic was administered (pentozacin 5 mg.kg body
weight tid PO) for the first one to five days. When extreme
restlessness was present and the animal could not be restricted in a playpen, a tranquilliser was administered (acepromazine 0.5 mg/kg body weight bid PO). Follow-up period ranged from six months to 10 years. For statistical analysis, a two-tailed Student t test was used; p = 0.05 was considered significant statistically.
RESULTS
Group I
Eighty-five cases were treated (45%). Seven had constipation, and two had urinary retention. Mean pre-treatment
period was two weeks. Total number of acupuncture treatments for this group was 211. This brings the mean number
of treatments per patient to 2.5. Forty-nine animals were
treated with treatment A. Mean number of treatments of this
group was 2.6. Thirty-six were treated with treatment B.
Mean number of treatments for this group was 2.3. Five
(6%) in group I were not cured, persisted in having violent
pain, and were euthanized. The difference of results between
treatment A and B is not significant (p = 0.27).
Group II
Thirty-seven dogs were treated (19%). Twelve showed
gastrointestinal complications (mainly constipation), and
seven had urinary complications (mainly urinary retention).
Mean pre-treatment period was 2.7 weeks. Total number of
acupuncture treatments was 126. Mean number per patient
thus was 3.4. Twenty-two animals were treated with treatment schedule A. Mean number of treatments for this group
was 3.9. Fifteen were treated with treatment schedule B.
Mean number of treatments was 2.7. Three animals showed
only partial recovery, and one did not recover (total four
dogs, 11%). The difference of results between treatment A
and B is significant (p = 0.03).
Group III
Fifty-nine dogs were treated (31%). Thirty showed gastrointestinal complications (21 had constipation, two diarrhoea, five no central control over defecation, two multiple
gastrointestinal problems), and 39 had urinary problems (31
bladder paralysis, two infection, three retention, and three
multiple problems). Mean pre-treatment period was 1.6
weeks. Total number of acupuncture treatments was 286.
Mean number of treatments per patient was 4.8. Thirty-two
were treated with schedule A. Mean number of treatments
for this group was 5.0. Twenty-seven were treated with treatment schedule B. Mean number of treatments for this group
was 4.7. Five animals did not recover, while seven showed
only partial recovery (total 12 dogs, 18%). The difference of
results between treatment A and B is not significant (p =
0.25).
Group IV
Ten dogs were treated (5%). All showed gastrointestinal
and urinary complications (constipation, loss of central control, diarrhoea, bladder paralysis). Mean pre-treatment period was 1.2 weeks. Total number of acupuncture treatments
was 68. Mean number per patient was 6.8. Five were treated
with schedule A and five with schedule B. Mean number of
treatments for schedule A was 9.4, while for schedule B it
was 4.2. Eight showed no recovery. The difference of results
between treatment A and B is not significant (p = 0.07).
Overall Results
A total of 191 dogs were treated. Fifty-nine had gastrointestinal complications, and 58 had urinary complications (31% each). Complication rates for gastrointestinal as
well as urinary complications were higher for each consecutive group (p < 0.001). Mean pre-treatment period was two
weeks. Total number of acupuncture treatments was 691.
Mean number per patient was 3.6. As the treatment schedule
consisted of one treatment per week, mean treatment period
was 3.6 weeks. One hundred and eight dogs (57%) were
treated with schedule A. Mean number of treatments for this
schedule was 3.9. Eighty-three were treated with schedule B
(43%). Mean number of treatments for this group was 3.3.
The difference of results between treatment A and B is at the
borderline of significance (p = 0.0505). Ten dogs (5%)
showed only partial recovery (for example, good walking
ability but incapable of mounting stairs or chairs, perfect
mobility but incomplete control over urination or defeca-
tion). Nineteen (10%) did not recover; some developed ascending hematomyelia, some persisted in having pain, and
some were in group IV and showed no recovery at all. Follow-up ranged between 0 and 36 months. Most of these were
euthanized after a variable period of time depending upon
the case (for example, when ascending hematomyelia present, non-responsive group IV patient after only several
weeks), while others were operated upon.
In order to investigate the importance of pre-treatment
with corticosteroids, groups I, II and III with and without
corticosteroids were compared. The difference of outcome
was very significant (p < 0.0005) and in favour of the noncorticoid pre-treated animals.
DISCUSSION
To evaluate the results that have been obtained by
acupuncture, it is necessary to compare them with results of
surgical treatments and chemical or conservative treatments
(Table 3). Up to now, acupuncturists have treated dogs with
TLDD in non-standardised ways, and few statistical results
have been published. In this series, 85% of the dogs made
complete recoveries. An average of 3.6 treatments were necessary to obtain this result. Results compare favourably with
those obtained by Denny, Funquist, Gambardella, Hoerlein,
Jadeson, Olson, and Prata.2,5,9,10,12,14,15 It should also be stated
that 63% already had been treated for about two weeks with
classic chemical therapy without any success.
Acupuncture has been said to cure certain diseases and to
prevent or alleviate pain in humans and animals.16-19 This
study showed that puncturing the described points can stop
thoracolumbar pain effectively, even when it had been present a long time. Therapeutic effects of acupuncture are as
good in groups I, II, and III as the success claimed by
surgery or by chemotherapeutical methods. Group IV patients can be helped better by immediate surgery. But if the
patient is presented more than 36 hours5 after onset of symptoms, acupuncture still could be tried.
Some authors mention high percentages of relapses in
non-surgically treated patients.15,20 In this trial, 54 our of 191
cases relapsed (28%): 34 out of 137 dogs (25%), which compares with cervical disk relapses in conservatively treated
dogs.
An anabolic was administered at the start of this study. It
was believed that it would ameliorate recovery by attenuating muscle atrophy and by activating muscle strength. The
original (schedule A) choice of points was made by using a
human textbook.16 Once results of this treatment had been
described,21 a new and simpler technique was started (schedule B). It seemed to be as good as the original, more complicated treatment schedule. Every veterinarian with proper
anatomical knowledge can use it without special training
techniques.
Acupuncture alone will not cure such a high percentage
of patients if at the same time no attention is given to urinary
and gastrointestinal problems, prevention of skin trauma,
and prevention of neurological aggravation. Group IV patients presented early after onset of symptoms should be operated upon as soon as possible. surgery is the method of
203
choice in these cases, and no time should be wasted trying
acupuncture.
The negative effect of pre-treatment with corticosteroids
in groups I, II, and III is astonishing; corticosteroids are
widely used as the treatment of choice for these animals (at
least in Europe). The negative effects of corticosteroid treatment in neurological trauma have been described recently by
several authors.22-24 Because of their and the author’s present
findings, it is suggested that corticosteroids not be used more
than 24 hours after onset of herniation or more than once;
their use may cause additional complications25;26 and a slower cure rate.
The results of acupuncture treatment of TLDD in the dog
certainly will be sceptically interpreted by certain colleagues. If, however, it is true that acupuncture is a placebo,
the authors can only conclude that this “placebo treatment”
gives as good results in groups I, II, and III as the (expensive) surgical and drug treatments. If it is true that acupuncture treatment of TLDD in the dog is only a placebo, the results of this study should make us think critically about the
use of the treatments we now employ.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Dammrich K. Zur Pathologie der degeneratieven Erkrankungen der
Wirbelsaule bei Hunden. Kleintierpraxis 1981;26:467-90.
Denny HR. The lateral fenestration of canine thoracolumbar disc protrusions: a review of 30 cases. J Small Anim Pract 1978;19:259-66.
Egger EL, Bojrab MJ. Ventral decompression of the canine spinal
cord using the 3-M perforator. Vet Surg 1978;7:12-7.
Flo GL, Brinker WO. Lateral fenestration of thoracolumbar discs. J
Am Anim Hosp Assoc 1975;11:619-26.
Gambardella PC. Dorsal decompressive laminectomy for treatment
of thoracolumbar disc disease in dogs: a retrospective study of 98 cases. Am Coll Vet Surg 1980;9:24-6.
Hegge GFS. Acute traumatische spinaal leasies bij de hond. Etiologie, pathogenese, diagnostiek, therapie. Vakgroep kleine huisdieren,
1975 Aug.:1-34.
Henry WB Jr. Dorsal decompressive laminectomy in the treatment of
thoraco-lumbar disc disease. J Am Anim Hosp Assoc 1975;11:62735.
Janssens LAA. Investigation and treatment of canine thoracolumbar
disk disease: one practitioner’s perspective. VM/SAC 1983;77:123540.
Jadeson WJ. Intervertebral disk lesions. J Am Vet Med Assoc
1961;138:411-23.
Olsson SE. Observations concerning disc fenestration in dogs. Acta
Orthop Scand 1951;20:349-56.
Prata RG, Stoll SG. Ventral decompression and fusion for the treatment of cervical disc disease in the dog. J Am Anim Hosp Assoc
1973;9:462-72.
Prata RG. Neurosurgical treatment of thoracolumbar disks: the rationale and value of laminectomy with concomitant disk removal. J Am
Anim Hosp Assoc 1981;17:17-25.
Hoerlein BF. Comparative disk disease: man and dog. J Am Anim
Hosp Assoc 1979;15:535-45.
Funquist B. Thoraco-lumbar disk protrusion with severe cord compression in the dog. Acta Vet Scand 1962;3:344-66.
Hoerlein BF. Canine neurology, 2nd ed. Philadelphia: WB Saunders,
1971;307-91.
Academy of Traditional Chinese Medicine; an outline of Chinese
acupuncture. Peking: Foreign Languages Press, 1975.
Janssens LA, De Moor A. General acupuncture with special reference to analgesic and therapeutic aspects in domestic animals. Vlaams
Diergen Tijdschr 1976;45:262-70.
Klide A, Kung S. Veterinary acupuncture. Univ. of Pennsylvania
Press, 1977.
204
19.
20.
21.
22.
23.
Rogers PA. Success claimed for acupuncture in domestic animals: a
veterinary news item. Irish Vet J 1974;28:182-92.
Bojrab M. Discushernica in the dog. Proceedings of the Belgian Annual Small Animal Congress. Brussels, Belgium: 1981.
Janssens LA. Acupuncture treatments for canine thoracolumbar disc
protrusions, a review of 78 cases. VM/SAC 1983;78:1580-4.
Deutschman CS, Konstantinides FN, Raup S, Cerra FB. Physiological and metabolic response to isolated closed-head injury. Part 2: Effects of steroids on metabolism. Potentiation of protein wasting and
abnormalities of substrate utilisation. J Neurosurg 1987;66:388-95.
Koide T, Wieloch TW, Siesjo BK. Chronic dexamethasone pretreat-
24.
25.
26.
ment aggravates ischemic brain damage by inducing hyperglycemia.
J Cereb Blood Flow Metab 1986;6:395-404.
Sapolsky RM, Pulsinelli WA. Glucocorticoids potentiate ischemic
injury to neurons: therapeutic implications. Science 1985;229:13971400.
Moore RW, Withrow SJ. Gastrointestinal hemorrhage and pancreatitis associated with intervertebral disk disease in the dog. J Am Vet
Med Assoc 1982;180;1443-7.
Bellah Jr. Colonic perforation after corticosteroid and surgical treatment of intervertebral disk disease in a dog. J Am Vet Med Assoc
1983;193:1002-3.
205
The treatment of canine cervical disc disease
by acupuncture: a review of thirty-two cases
Luc A. Janssens
Abstract
The results of acupuncture treatment in 32 cases of canine cervical disc disease are reported with special reference
to the outcome, follow up and recurrence. Acupuncture was
an effective therapeutic method of treatment in about 70 per
cent of the cervical intervertebral disc protrusions. It had no
prophylactic effect on the recurrence of the symptoms.
INTRODUCTION
Cervical dics disease (C.D.D.) in dogs (consisting of a
prolapse and/or hernia of a cervical dics into the spinal
canal) can be treated by chemotherapy (Brasmer, 1974;
Parker, 1974; Delatorre, 1975; Mendenhall et al., 1976;
Parker & Smith, 1976; Parker, 1978); by surgical techniques such as fenestration (Russel & Griffiths, 1968; Hoerlein, 1971; Parker, 1974; Delahunta, 1977; Denny, 1978;
Creed & Yturaspe, 1983) or decompression (Allen, 1911;
Hoerlein, 1971, Swaim, 1982) which is achieved by hemilaminectomy, dorsal laminectomy or ventral decompression. Physical therapy, rest and vitamin B administration
are also used especially when pain is the only symptom
(Olsson, 1951; Jadeson, 1961). Some authors use combinations of surgery, chemotherapy and other physical therapy
(Parker, 1974; Mendenhall et al., 1976; Rucker, Lumb &
Scott, 1982).
Acupuncture has been used for the treatment of thoracolumbar disc disease (Janssens, 1983). It also has been reported for cervical disc disease (Buchli, 1975) and has been
described as a valuable therapy for analogous problems in
man (The Academy of Traditional Chinese Medicine, 1975).
The purpose of this article is to describe 32 cases with cervical disc protrusion and their treatment with acupuncture.
The follow up period ranged from 4 months to 8 years.
MATERIAL AND METHODS
Material
Thirty-two dogs had cervical disc protrusions. The clinical details such as age, distribution, breeds affected, sex ratio and neurologic ratings are represented in Tables 1, 2, 3
and 4. Seven breeds of dogs were affected (Table 1). The
condition was frequently encountered in Poodles and Dachshunds, French Bulldogs and Pekes. The age of the dogs
when presented; ranged from four to thirteen years, with a
peak incidence between 5 and 8 years. The sex ratio was 17
males to 15 females. The average duration of clinical signs
before the first treatment was 6 weeks with a range of from
1 to 52 weeks.
Most dogs had been previously treated with drugs, 63
per cent had been treated with corticoids; 31 per cent had
been treated with anti-inflammatory agents (acetylsalicilate, phenylbutazone, etc.); 1 per cent had been treated
with analgesics; 76 per cent had been treated with vitamin
B preparations and 10 per cent had been treated with anabolic steroids. The clinical signs were recorded, and graded
according to the neurologic examination (Parker, 1974;
Janssen, 1984) (Table 2). The details are summarized in Tables 4, 5 and 6. Radiographs were taken in 53 per cent of the
cases, to assess the site of the disc protrusion. Ten dogs (30
per cent) that had recovered relapsed; the total number of
relapses was thirteen.
Method
The treatment consisted of acupuncture treatment at
weekly intervals. The needles used were stainless steel, 28
gauge, 5 cm long acupuncture needles. They were placed at
six standard anatomical spots known as acupuncture points
(Fig. 1).
Puncturing was bilateral symmetrical. Thus twelve needles were used. The needles were left in situ for 15-20 minutes without any form of manipulation. During this period
the dogs were left on the table, but they were allowed to sit
or lie down if they intended to. Occasionally, in cases with
severe pain, the treatments were given twice a week. Adjuvant treatment consisted of restricted movement for one
month, high bulk diet, analbolics* and only if necessary analgesics** and/or tranquillizers***
The number of treatments varied between one and six.
Treatment was discontinued if the owner stated the symptoms had ceased and if on examination no neck pain could
be elicited. However, the oldest cases (before 1980) were always treated three times as a minimum. The follow up period ranged from 4 months to 8 years.
206
RESULTS
DISCUSSION
Twenty-five dogs had pain with or without radiation in
one or both fore legs (78 per cent). The other seven dogs had
pain and neurological deficits; six (19 per cent) had uni- or
bilateral paresis with negative proprioception in hindlegs
and eventually in the fore legs and one (3 per cent) had quadriplegia of one week duration.
The first group consisted of 25 dogs. Twenty recovered
after the first series of treatments (80 per cent). The average number of treatments for the first group was 2.8 and
the average recovery time was 1.5 weeks. Five dogs out of
this first group (20 per cent) did not improve sufficiently
with this treatment and two were subsequently fenestrated.
One recovered 4 weeks after surgery (NR 20). The other
did not and was treated again 4 weeks after surgery (NR
3). The dog then recovered very rapidly (2 days). Two
other dogs (NR 21 and 14) did not recover and the owners refused surgery. The animals were kept on analgesics.
Both recovered after a total period of about 17 weeks. The
fifth animal (NR 22) that did not recover after 4 weeks
was destroyed. Six dogs (19 per cent) subsequently relapsed in this first group, but the total number of relapses
in this group was eight. Only one dog relapsed with more
severe neurologic signs (NR 16). The relapsed dogs were
treated again in the same way. Of the eight relapses, four
recovered completely, and one partially with continued
proprioceptive abnormalities. The two other relapses
were not cured after two weeks. One (NR 8) was treated
with corticoids and recovered after 3 weeks. The other
(NR 24) was given analgesics and recovered after 8 weeks
(the total duration of clinical signs being 13 weeks). The
final number of completely cured dogs in this group was
18 out of 25 (72 per cent).
The second group consists of six dogs. Four recovered
after treatment (67 per cent). The average number of treatments for this group was 3.5 and the average time of recovery was 3 weeks. Two dogs did not recover; one (NR 7) was
fenestrated and recovered after 6 weeks but had a permanent
proprioceptive deficit in the fore and hind legs. Three out of
the four non-operated dogs relapsed (71 per cent) and the total number of relapses was four. Two cases had similar neurologic signs while two others were less severe and classed
as group I.
The relapses were retreated in the same way. Three out
of the four relapses recovered completely. The fourth dog
(NR 30) was destroyed as the owner refused further treatment. The final number of dogs cured after all treatment was
three out of six (50 per cent).
The one dog in the third group was cured after four
treatments in three weeks. He relapsed after three years
with the neurologic signs of group I and recovered completely after the same treatment (two treatments, 5 days recovery time).
The total number of completely recovered dogs in
group I, II and III after the first and following treatments is
22 out of 32 (69 per cent). The total number of dogs that
relapsed is 10 (37 per cent). The average number of treatments for all dogs was 2.5 and the average recovery time
was about 2 weeks.
The breeds mostly affected in this series were Poodles,
Dachshunds, French Bulldogs and Pekingese. French Bulldogs seem relatively more susceptible to the disease as they
are rare in Belgium. Jack Russell Terriers and Beagles are almost non-existent in Belgium, this may explain the breed
differences with other authors (Hoerlein, 1971; Denny,
1978; Funkquist & Svalastogae, 1979). The sex ratio M 51
per cent - F 47 per cent was very close to the population ratio in the practice (M 56 per cent - F44 per cent). The mean
age was 7 years which is similar to other reports (Hoerlein,
1972; Denny, 1978; Funkquist & Svalastogae, 1979).
The total recovery rate was 69 per cent. This compares
favourably with the results of fenestration. Denny (1978) reports out of a follow-up of 38 dogs a recovery of 28 (74 per
cent). In this series there was a relapse rate of 37 per cent.
This is conform with the statements published by Russell
and Griffiths (1968). They found after a three year follow-up
period a recurrence of 36.3 per cent of the conservatively
treated patients, while after this period only 5.6 per cent of
the surgically treated patients relapsed.
The average recovery time of two weeks is favourable
when compared with other authors (Hoerlein, 1971; Denny,
1978; Swaim, 1982). Nine per cent of the dogs recovered
within 2 days, and twenty-eight per cent within 1 week. Occasionally a very rapid recovery was seen (cases NR 6, 11,
15, etc.) even when the symptoms had been present for long
periods. Of special interest was case NR 3 which suggests
that acupuncture may be of value in the already fenestrated
dog that still suffers pain. Although the average duration of
clinical signs before the first acupuncture treatment was 6
weeks and most animals had already been treated medically
without success the acupuncture treatment still resulted in a
cure. It could be suspected that the anabolic steroids may be
responsible for the recovery instead of acupuncture itself.
However, nine dogs recovered within 1 week, thus before
the maximal analbolic effects and seven dogs recovered
without anay anabolic administration.
In conclusion it can be said that acupuncture appears to
be an effective therapeutic method of treatment in about 70
per cent of the cervical intervertebral disc protrusions. However, it has no prophylactic effects on the recurrence. Therefore the owner should be advised to consider surgery later
on. Treatment by acupuncture should not be continued beyond 2 weeks if there is no improvement; surgery is then advisable. Acupuncture could still be of use after surgery if
pain persists.
ACKNOWLEDGEMENTS
I am grateful to Dr. Dierckxens and Dr. Devries for referring the cases. Special thanks go to Dr. P. Rogers and Dr.
I. Griffiths for their remarks.
References
Academy of Traditional Chinese Medicine (1975). An Outline of Chinese
Acupuncture. Foreign Languages Press, Peking.
Allen, A.R. (1911) Surgery of experimental lesion of spinal cord equivalent
to crush injury of fracture dislocation of spinal column. J. Am. med.
Ass. 57, 878.
Brasmer, T. (1974) Evaluation and therapy of spinal cord trauma. In: Current Veterinary Therapy (ed. R. Kirk). W.B. Saunders, Philadelphia.
Buchli, R. (1975) Successful acupuncture treatment of cervical disc syndrome in a dog. Vet. Med./Small Anim. Clin. 70, 1302.
Creed, J.E. & Yturaspe, D.J. (1983) Intervertebral disc fenestration. In: Current Techniques in Small Animal surgery (ed. M.J. Bojrab), 2nd Edn.
Lee and Febiger, Philadelphia.
Delahunte, A. (1977) Veterinary Neuranatomy and Clinical Neurology.
W.B. Saunders, Philadelphia.
Delatorre, J. et al. (1975) Pharmacological treatment and evaluation of permanent experimental cord trauma. Neurology 25, 508
Denny, H. (1978) The surgical treatment of cervical disc protrusions in the
dog. J. small Anim. Pract. 19, 25.
Funkquist, B. & Svalastogae, E. (1979) A simplified approach to the last
two cervical discs of the dog. J. small Anim. Pract. 20, 593.
Hoerlein, B. (1971) Canine Neurology, 2nd edn. W.B. Saunders, Philadelphia.
Jadeson, W. (1961) Rehabilitation of dogs with intervertebral disc lesions
by physical therapy methods. J. Am. vet. med. Ass. 138, 411.
Janssens, L.A. (1983) Acupuncture treatments for canine thoracolumbar disc
protrusions. A review of 78 cases; Vet. Med. Small An. Clin. 78, 1580.
207
Janssens, L.A. (1984) The investigation and treatment of canine cervical disc disease: an overview. (In publication).
Mendenhall, A. et al. (1976) Aggressive pharmacologic and surgical treatment of spinal cord injuries in dogs and cats. J. Am. vet. med. Ass.
168, 1026.
Olsson, S. (1951) Canine Neurology (ed. B. Hoerlein), 2nd edn, p. 372.
W.B. Saunders, Philadelphia.
Parker, A. (1974) Diagnosis and treatment of canine spinal cord disease.
Vet. Scope 18, 1.
Parker, A. (1978) Practical treatment of neurological disease and signs in
cats and dogs. Proceedings of the Netherland Small Animal Vet. Ass.
Voorjaarsdagen.
Parker, A. & Smith, C. (1976) Functional recovery from spinal cord trauma
following dexamethasone and chlorpromazine therapy in dogs. Res.
vet. Sci. 21, 246.
Rucker, N.C., Lumb, W.V. & Scott, R.J. (1982) Combined pharmacologic
and surgical treatments for acute spinal cord trauma. Am. J. vet. Res.
42, 1138.
Russell, R.W. & Griffiths, R.C. (1968) Recurrence of cervical disc syndrome in surgically and conservatively treated dog. J. Am. vet. med. Ass.
153, 1412.
Swaim, S.F. & Hyams, D. (1982) Clinical observations and client evaluation of ventral decompression for cervical intervertebral disc protrusion. J. Am. vet. med. Ass. 181, 259.
209
Acupuncture for thoracolumbar
and cervical disk disease
Luc A. Janssens
Thoracolumbar and cervical disk disease is commonly
seen in small animal practice. According to certain authors,
0.5-1% of all dogs show signs of neck or back problems
caused by disk disease.1 About 14% of all disk protrusions
or extrusions occur in the neck, while 85% occur between
T9 and L7. The approximate distribution pattern in the neck
is 55% at C2-C3, 29% at C3-C4, and 12% at C4-C5, with
about 1% each at C5-C6 and C6-C7.2
The strong longitudinal ligament at the floor of the
vertrebral canal and the fortified dorsal anulus of the intervertebral disk spaces between T1 and T10 make protrusions
or extrusions extremely rare in this region. In the region between T10 and L7, the approximate distribution of disk protrusions or extrusions is 1% at T10-T11, 12% at T11-T12,
25% at T12-T13, 25% at T13-L1, 12% at L1-L2, 7% at L2L3, 7% at L3-L4, 1% at L5-L6, and 1% at L6-L7.
The breeds most commonly affected are Dachshunds,
Pekingese, Jack Russell Terriers, Cocker Spaniels, Beagles,
Miniature Poodles, French Bulldogs and other chondrodystrophic breeds. There is no sex predilection. The mean age is
5-6 years of age.6
The intervertebral disk consists of a central spongy mass
called the anulus fibrosis and a peripheral mass of concentric collagen fibers. The anulus is smallest at the dorsal side.
The nucleus pulposus may degenerate because of aging and
genetic factors (chondroid metaplasia). The latter occurs in
chondrodystrophic breeds. This degeneration alters the mechanical properties of the disk, causing microruptures of the
anulus, which may lead to bulging of the anulus into the vertebral canal. This is called a Hansen Type-2 protrusion. Disk
protrusion impinges on the spinal cord or nerve roots and incites a local inflammatory reaction.4
Eventually the anulus may rupture, and nuclear material
may enter the spinal canal. This is called a Hansen Type-1
protrusion or an extrusion. When the extrusion occurs rapidly, the extrusion is called a disk explosion. Extrusins that occur slowly may be minimal or massive. When massive, compression of the spinal cord and nerve roots is more significant than the resultant inflammatory reaction. When minimal, the inflammatory reaction is of more importance. When
a disk herniates or protrudes into the spinal canal, the resultant clinical signs depend on location of the extrusion, kinet-
ic energy involved, and the mass of the herniated material
versus the space available in the vertebral canal (the cervical
canal is much wider than the thoracolumbar canal). Extrusions can occur only once or may recur.3
CLINICAL SIGNS OF THORACOLUMBAR
DISK DISEASE
In the first category (grade I), only back pain is present.
About 45% of all patients with thoracolumbar disk disease
are in this category. These animals walk slowly, are reluctant
to jump or to climb stairs, and are sometimes constipated.
Some of them cry when moving or when picked up. Back
palpation is painful and back musculature (eventually also
abdominal musculature) are spastic.12
Patients in the second category (grade II), show signs
similar to those of grade-1 dogs and also show rear leg paresis and ataxia. About 20% of patients are in this category.
These dogs have no proprioception in the rear limbs (knuckling of the hind leg toes is not corrected).10,12
Dogs in the third category (grade III) have caudal paralysis and are unable to stand or bear weight with the hind
legs. About 25% of affected dogs are in this category. Some
dogs in this category have control over bladder function and
defecation, while others do not. Reflexes in the hind legs
usually are normal because the lesion most commonly occurs cranial to L3. pain sensitivity is normal.10,12
The fourth type of patient (grade IV) is paralyzed, with
no conscious perception of pain in the rear toes. About 10%
of patients are in this category. Pain sensitivity should be
tested by pinching the rear toes with mosquito forceps. Care
should be taken to distinguish pain perception from the withdrawal reflex. Perception of pain is manifested as biting,
looking, micking, moaning or crying.10,12
The last category (grade IV) includes patients with ascending-descending hematomyelia, with spread of myelomalacia in the spinal cord. These animals are in extreme
pain, and their reflexes are progressively diminished over
several hours (patellar reflex → tibial reflex → gastrocnemius reflex → anal reflex). Eventually the dog dies from
paralysis of the intercostal and diaphragmatic muscles.10,12
210
CLINICAL SIGNS OF CERVICAL
DISK DISEASE
In the first category (grade I), only neck pain is present.
About two-thirds of patients with cervical disk disease are in
this group.13,14 In the second category (grade II), neck pain
and proprioception deficits are observed. About 25% of patients are in this category.13,14
Dogs in the third group (grade III) have neck pain and
paralysis (tetraparesis or hemiparesis when unilateral). Less
than 5% of patients are in this category. Some patients show
a “root sign”, lifting one foreleg as though painful. This is
caused by irritation of a nerve root innervating the leg. Lesions caudal to C4 typically show this signature.13,14
Definitive diagnosis is based on the history, clinical examination, radiography, myelography, and CSF and blood
analysis. Conservative therapy consists of rest, analgesics,
corticosteroids and muscle relaxants (Table 1).1,15,16
Surgical therapy consists of fenestration, hemilaminectomy, dorsal laminectomy with or without durotomy or myeolotomy for thoracolumbar disk disease, and ventral decompression with or without fenestration in cervical disk disease. Surgery at a later stage is useless here.10,17
Approximately 30-50% of dogs treated nonsurgically
recover, vs 85% of dogs treated surgically. However, not
all authors agree on this difference, and many claim equal
results for all treatments used. Few dogs with grade-IV
thoracolumbar disk disease recover, regardless of treatment.3,10,18-23
ACUPUNCTURE TREATMENT FOR DISK
DISEASE IN DOGS
The mechanism of action by acupuncture for disk disease is not yet fully understood. The following mechanisms
may be involved. Acupuncture can destroy trigger points
and thus abolish muscle pain, muscle shortening, stiffness
and referred pain.24 Acupuncture can activate regrowth of
destroyed axons in the spinal cord.25,26 Acupuncture may
decrease local spinal inflammation, edema, vasodilation or
constriction, and histamine or kinin release.27,29 This decreases scar tissue formation, spinal cord compression and
pain.
It is not likely that acupuncture works in these conditions
by augmenting endogenous release of corticosteroids, as
some authors believe that administration of corticosteroids
delays recovery from thoracolumbar disk disease.30 Also,
acupuncture probably does not work by vasodilation because the pathophysiologic reaction after spinal cord truama
is vasodilation.31,32 Whether endorphins are involved after
therapeutic acupuncture treatments without stimulation is
uncertain. If they are involved, they might be partially responsible for the analgesic effect.
Apart from several case reports of successful acupuncture treatments in dogs with disk disease, only 2 authors
have reported detailed studies on large groups of dogs with
thoracolumbar disease and only one on dogs with cervical
disease.34*37 Thoracolumbar disk disease is treated by
acupuncture with variability as to number and type of points
used, stimulation method, duration of treatments, interval
between treatments, and adjunctive treatments. However,
most veterinary acupuncturists agree their success rates are
comparable.37 If this is so, the simplest method might be the
best.
ACUPUNCTURE FOR THORACOLUMBAR
DISK DISEASE
Acupuncture points used can be divided into local and
distant points.39 Local points are segmental Bladder points.
Mostly points BL-14 to BL-28, vertebrae T10-L7 are used.
Some authors also use points of the outer (lateral) branch in
the same spinal segments (BL-47 to BL-53, T10-L7). Local
points on the Governing Vessel in these segments are also
used. The logic of using local points is that they may have
segmental effects at the site of the lesion (spinal). They also
treat local trigger points.
The distant points used vary enormously. Mostly points
on the Urinary Bladder (BL), Galbladder (GB) and Stomach
(ST) meridians are used. BL-40 and BL-60, GB-30 and GB34, and ST-36 are the most popular point selections here.
The logic of using distant points is that they stimulate nerve
fibers with afferent input on higher centers and on the inured
spinal segment. These impulses may combat inflammation
and pain, and activate regeneration.
A treatment may use very few points (eg, 4) or many (eg,
20). A treatment protocol using only 4 needles proved to be
as effective as a slightly more extensive treatment (GB-34
and one local BL point bilaterally, vs GB-30, GB-34, BL-60
and 3 local BL points bilaterally).30,39 The choice of these
points has been based on human literature and on a computerized program of commonly used acupoints.40-42
Other points used vary considerably and include Liver
meridian points (LIV-1 to LIV-3), Kidney meridian points
(KI-3 to KI-6), Spleen meridian points (SP-4, SP-6). Many
others are also used (LIV-4, LIV-10, LIV-11, BL-11, BL-13,
BL-67).
Stimulation methods include simple puncturing, electrostimulation of needles, laser therapy and injections at
acupuncture points. The needles used are sterile 32-to 38gauge acupuncture needles. They are left in place without
stimulation for 10-20 minutes. Sometimes, however, they
are manually stimulated by rotation and/or by lifting and
thrusting. If the needles are stimulated, the stimulation
period may last 10-20 minutes or only a few seconds.
Short-term activation of a point may be done with a heated needle.
Electrostimulation is applied with machines, using a
wide variety of wave forms, wave patterns, treatment intervals, frequencies and amplitudes. Usually, the amplitude is
augmented until muscle twitching and pain are observed. In
one report, electrostimulation worsened the condition of the
patient.43 No better results have been reported by those using
electrostimulation than by those using plain puncturing.
Electrostimulation is used more frequently in the United
States than in Europe and China.
Laser therapy is used by few practitioners. Dr. Demontoy
from Paris was certainly one of the first.44 A variety of ex-
pensive instrumentation is available. Different wave
lengths, power outputs and frequencies are used. Lasers
are used both locally and on the ponts, in intervals ranging from 3 seconds to several minutes per area. This extreme variability in methodology makes it difficult to
compare results of treatment groups with standard treatment protocols. Therefore, we do not know how the results of laser therapy for disk disease compare with those
of other treatment methods.
Injections are commonly used. I prefer injections of
0.25% lidocaine solution at the local points. The results
of pain abatement seem to be more rapid and more profound than with simpling needling. This impression, however, has not yet been documented statistically. Other solutions that can be injected include vitamins B1, B32, B6,
B12, C, D and E, dimethyl sulfoxide (DMSO), sodium
chloride (NaCl), water, NaOH, procaine and caffeine,
nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids and homeopathic solutions. This wide variety
makes it very difficult to prove that injections are superior to standard puncturing.
Treatment intervals vary from once daily to once
every 2 weeks. Once-daily treatments seem to be superior regarding analgesia over treatments at longer intervals,
but only in acute cases in grades I and II.45,46 Most dogs
are treated once a week. Acutely affected dogs, especially in extreme pain, should be treated more frequently (eg,
twice a week). In chronic cases, treatment every 2 weeks
may be sufficient.
Supportive treatment includes rest, laxative diets, bladder emptying and antibiotics. Rest is needed in all grades to
prevent deterioration caused by further disk extrusion and, in
grades III and IV, to prevent abrasions from dragging. The
animal should be placed in a playpen or a cage for 4 weeks.1
If the animal is too nervous in confinement, sedatives or
tranquilizers can be administered during the confinement period. I give acepromazine 1-4 times a day. laxative diets facilitate defecation and minimize straining.
The bladder must be manually expressed in some gradeIII and all grade-IV dogs. This should be done carefully and
at least every 8-12 hours. The bladder should continue to be
emptied until the dog can urinate voluntarily. Antibiotics are
administered if the dog has a bladder infection or skin ulcers.
Though analgesics can alleviate severe pain, they can aggravate the problem by encouraging more activity. Therefore, analgesic use should be combined with strict rest.
Anabolic steroids appear to be of no benefit.30 Corticosteroids should be used with caution and only on the first day
of onset of signs. Reports indicate that corticosteroids delay
recovery of central nervous tissue after trauma.30,47-54
The results of acupuncture treatment for thoracolumbar
disk disease vary according to the severity of disease. Approximately 90% of dogs with grade-I disease recover after
2 or 3 treatments over 1- to 2-week period. Approximately
90% of dogs with grade-II disease recover after 3 or 4 treatments over a 3-week period.30 Approximately 80% of dogs
with grade-III disease recover after 5-6 treatments over a 6week period. Only 10% of these animals do not recover,
while the remaining 10% recover partially (eg, no conscious
bladder control).30 Less than 25% of dogs with grade-IV dis-
211
ease recover after 10 or more treatments over a 3- to 6month period. Overall, in grades I-III, 90% recover over a
mean period of 4-5 weeks after a mean of 4 treatments (1
treatment a week). In dogs with grade-IV disease, acupuncture treatment is only half as effective as prompt decompressive surgery. Acupuncture can be tried in grade-IV dogs
in which surgery has not been performed within the first 36
hours of onset of signs.30
Acupuncture results in grade-I and grade-II thoracolumbar disk disease are comparable to those of surgery
and/or drug therapy. However, surgical fenestration of the
affected and adjacent disks has the advantage of reducing
or totally preventing recurrence. Of my acupuncture patients, approximately 10-25% had relapses over a period
of up to 8 years.
ACUPUNCTURE FOR CERVICAL
DISK DISEASE
A wide variety of points, methods of stimulation and
treatment intervals have been used in acupuncture treatment
of cervical disk disease. Only one study described results
from a standard treatment protocol.13
Local and distant points are used to treat cervical disk
disease. The local points are GV-13, GV-16, GB-20, GB-21,
TH-16, SI-15, SI-16, LI-15, LI-16, BL-8, BL-9, BL-10, BL11, BL-20, BL-21, BL-23, BL-25, BL-28 and local trigger
(or painful or oh shi) points. Distant points used to treat cervical disk disease are LI-4, LI-11, SI-3 and TH-5. Intervals
between treatments, methods and duration of stimulation,
and adjunctive therapies are the same for treatment of thoracolumbar disease.
The results of acupuncture treatment for cervical disk
disease are as follows: approximately 80% of dogs with
grade-I disease recover after 3 or 4 treatments over a 1- to 2week period. Approximately 67% of dogs with grade-II disease (neck pain, paresis) recover after 5 or 6 treatments over
a 3- to 4-week period. Too few grade-III cases have been described to report adequate results.
Dogs that do not respond to acupuncture may benefit
from cervical disk fenestration and ventral decompression.
Approximately 33% of dogs successfully treated for cervical
disk disease by acupuncture relapsed within 3 years.39 This
percentage is higher than for thoracolumbar disk disease and
is the same as for other conservative treatments.55
Acupuncture can be useful in treatment of intervertebral
disk disease in dogs, provided the dog is strictly confined,
closely monitored and given good nursing care. Results of
acupuncture are as good as those for surgical therapy. However, surgical intervention is indicated for dogs with gradeIV thoracolumbar disease if they are presented within 24
hours after the onset of signs. Acupuncture should only be
performed on dogs with grade-IV disease if they are presented at a later stage. Results of surgical decompression for
cervical disk disease are probably better than those of
acupuncture. Surgical treatment, however, is expensive and
sometimes risky. Therefore, acupuncture might be tried initially and surgery considered as the second choice if
acupuncture or medical treatment is ineffective.
212
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
Oliver J et al: Veterinary Neurology. Saunders, Philadelphia, 1987.
Hoerlein BF: Comparative disk disease: man and dog. Vet Med
15:535-545,1979.
Hoerlein BF: Canine Neurology, Diagnosis and Treatment. 3rd ed.
Saunders, Philadelphia, 1987.
Hoerlein BF: Intervertebral disc protrusions in the dog. 1. Incidence
and pathological lesions. Am J Vet Res 14:260-269, 1953.
Funquist B and Svalasoga E: A simplified approach to the last two
cervical discs of the dog. J Small Anim Pract 20:593-599, 1979.
Gage E: Incidence of clinical disc disease in the dog JAAHA 11:135138, 1975.
Tarlov IM et al: Spinal cord compression studies. 1. Experimental techniques to produce acute and gradual compression. Arch Neurol
Psychiat 70:813-819, 1953.
Tarlov IM and Klinger H: spinal cord compression studies. II. Time
limits for recovery and acute compression in dogs. Arch Neurol Psychiat 71: 271-290, 1954.
Tarlov IM: Spinal cord compression studies. III Time limits for recovery after gradual compression in dogs. Arch Neurol Psychiat
52:588-597, 1955.
Gambardella PC: Dorsal compressive laminectomy for treatment of
thoracolumbar disc disease in dogs: a retrospective study of 98 cases.
Vet Surgery 9:24-26, 1980.
Olson SE: The dynamic factor in spinal cord compression. J Neurosurg 15:308-321, 1958.
Janssens LAA: Cervicale discus herniation in the dog: an overview.
Ned Tijdschur Geneskd 115:199-206, 1990.
Janssens LAA: The treatment of canine cervical disc disease by
means of acupuncture: A review of 32 cases. J Small Anim Pract
26:203-210, 1985.
Seim H and Prata R: Ventral decompression for the treatment of cervical disc disease in the dog: a review of 54 cases. JAAHA 18:233240, 1982.
Bojrab MJ: Disc disease. Vet Record 89:37-41, 1971.
Van Nes J: Some neurological pathology. Proc First Conf Werkgroep
Kleine Huisdieren, Antwerp, Belgium, 1980.
Chrisman C: Problems in Small Animal Neurology. Lea & Febiger,
Philadelphia, 1982.
Jadeson D: Rehabilitation of dogs with intervertebral disc lesions by
physical therapy methods. JAVMA 138:411-425, 1961.
Funkquist B: Decompressive laminectomy in thoracolumbar disc
protrusion with paraplegia in the dog. J Small Anim. Pract 11:445451, 1970.
Black AP: Lateral spinal decompressive laminectomy in thoracolumbar disc protrusion with paraplegia in the dog. J Small Anim Pract
29:581-588, 1988.
Bojrab M: Disc disease in the dog. Proc Belgian Ann Small Anim
Cong, 1981.
Braund KG, in Bojrab MJ: Pathophysiology in Small Animal Surgery. Lea & Febiger, Philadelphia, 1981.
Denny HR: The lateral fenestration of canine thoracolumbar disc protrusions: A review of 30 cases. J Small Anim Pract 19:259-266, 1978.
Travell JG and Simons DG: Myofascial Pain Syndromes and Dysfunction: The Trigger Point Manual. Williams & Wilkins, Baltimore, 1983.
Dekker AJAM: Enhancemente of Peripheral Nerve Regeneration in
the Rat By a Previous Nerve Injury and By Treatment With Neuropeptides. Graad van Doctore in de Geneeskunde aan de Rijksuniversiteit te Utrecht, Proefschrift, The Netherlands, 1987.
Kajdos V: Peripheral paresis of facial nerve treated with acupuncture.
Am J Acupuncture 3:233-236,1975.
Academy of Traditional Chinese Medicine: An Outline of Chinese
Acupuncture. Foreign Languages Press, Beijing, China, 1975.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
Klide A and Kung S: Veterinary Acupuncture. Univ Pennsylvania
Press, Philadelphia, 1975.
Martin BB and Klide AM: Use of acupuncture for the treatment of
chronic back pain in horses: Stimulation of acupuncture points with
saline solution injections. JAVMA 190:1177-1180, 1987.
Janssens LAA and De Prins EM: Treatment of thoracolumbar disk disease in dogs by means of acupuncture: A comparison of two techniques. JAAHA 25:169-174, 1989.
Griffiths RC: Spinal cord blood flow after acute experimental cord
injury in dogs. J Neurol Sci 27:247-259, 1976.
Kobrine AI et al: Local spinal cord blood flow in experimental traumatic myelopathy. J Neurosurg 42:144-149, 1975.
Bunchli R: Successful acupuncture treatment of cervical disc syndrome in a dog. VM/SAC 70:1302, 1985.
Still J: Analgesic effects of acupuncture in thoracolumbar disc disease in dogs. J Small Anim Pract 30:298-301, 1989.
Janssens LAA: Investigation and treatment of canine thoracolumbar
disk disease and practitioner’s perspective. VM/SAC 78:1235-1240,
1983.
Janssens LAA: Thoracolumbar disc disease in the dog: An overview.
Vlaams Dierg Tijdsch 59:128-136, 1990.
Janssens LAA et al, in Janssens LAA: Some Aspects of Small Animal Acupuncture. Belgium Vet Acupuncture Soc, 1987.
Janssens LAA: Atlas of Acupuncture Points and Meridians in the
Dog. Blondiau Print, Belgium, 1984 (Available in the United States
from IVAS, RD 1, Chester Springs, PA 19425).
Janssens LAA: Acupuncture treatment for canine thoracolumbar disc
protrusions: a review of 78 cases. VM/SAC 78:1580-1584, 1983.
Mann F: Acupuncture, The Ancient Chinese Art of Healing. Heinemann Medical Books, London, 1971;
Mann F: Scientific Aspects of Acupuncture. Heinemann Medical
Books, London, 1977.
Rogers PAM: A computerised point choice list for acupuncture treatment. Proc 1st Belgium Conf Vet Acupuncture, 1984.
Janssens LAA: Prolapse of thoracolumbar disc: A contraindication
for electroacupuncture in dogs. Am J Acupuncture 14:61-64, 1986.
Demontoy A: Manuel d’acupuncture canine. Ed du Point Vétérinaire
43, 1986.
Still J: Acupuncture treatment of type-III and type-IV thoracolumbar
disc disease. Mod Vet Pract 7:35-39, 1987.
Still J: Acupuncture treatment of thoracolumbar disc disease: a study
of 35 cases. Compan Anim Pract 2:19-25, 1988.
Bracken MB et al: Efficacy of methylprednisolone in acute spinal
cord injury. JAMA 251:45-52, 1984.
De la Torre JC et al: Pharmacological treatment and evaluation of
permanent experiment spinal cord trauma. Neurology 25:508-514,
1975.
Deutschman CS et al: Physiological and metabolic to isolated closedhead injury. Part 2: effects of steroids on metabolism. Potentiation of
protein wasting and abnormalties of substrate utilization. J Neurosurg
66:388-395, 1987.
Koide T et al: Chronic dexamethasone pretreatment aggravates ischemic neuronal necrosis. J Cereb Blood Flow Metab 6:395-404, 1986.
Rucker NC et al: Current techniques for evaluation of spinal cord
injury. Vet Surgery 10:30-34, 1981.
Sapolsky RM and Pulsinelli WA: Glucocorticoids potentiate ischemic
injury to neurons: Therapeutic implications. Science 229:1397-1400,
1985.
Saul TG et al: Steroids in severe head injury. A prospective randomized clinical trial. J Neurosurg 54:596-600, 1981.
Janssens LAA et al: An experimental spinal cord trauma model in the
rat to test pharmacotherapeutics. Res Neurol & Neurosci (In press).
Russel RW and Griffiths RC: Recurrence of cervical disc syndrome
in surgically and conservatively treated dogs. JAVMA 153:1412,
1968.
213
Acupuncture in small animal practice
Luc A. Janssens
A CRITICAL VIEW ON MEDICAL
TREATMENTS
Today, the word acupuncture (Ac) is probably familiar to
every veterinarian and veterinary student in Europe and the
Americas. That was quite different 25 years ago when Ac
was a mystical term for most non-Asian people apart from a
small group of “alternative” Western individuals.
If we look at the Western population today, there are two
groups of people who unconditionally believe in the efficacy of acupuncture: (a) academics, neuroscientists and researchers involved in neurophysiology and pain research
and (b) credulous people; those who believe in the superiority of alternative healing methods (homeopathy, herbal
medicine, acupuncture, etc.). A large scale inquiry by consumers organizations in some West- European countries revealed that more than 50% of the population believes in the
efficiency of alternative medical treatments. It must also be
said that important organizations such as the World Health
Organisation (WHO) and the National Institute of Health
(NIH) have officially recognised Ac as an effective treatment for several diseases. Still, the group of non-believers,
who believe that Ac is a placebo based on suggestion or a
form of hypnosis is in many Western countries much larger
than the one of believers.
It is as incorrect to believe uncritically in a type of medicine with no scientific foundation (e.g. precious stone therapy), as it is to disbelieve in the efficacy of alternative therapies (such as Ac), with overwhelming - but unprecedented
- scientific data which construct its foundation.
TRADITIONAL CHINESE ACUPUNCTURE A CRITICAL REVIEW.
Ac is an ancient Chinese art of healing which consists
of diagnosing and treating disease. (1,2) The diagnostic aspects consist basically of pressure point diagnosis and
pulse diagnosis. The treatment aspects consist of “activation” of acupuncture points (AP) which are thought to be
localized on one of 12 meridians (Mer). Each Mer contains
a certain number of AP. The minimum number is 9, the
maximum is 67. Traditionally the total number of AP is
365 (one for each day).
Pressure point diagnosis is performed by minute palpation of the body surface with emphasis on exploring the AP
areas, the anatomical location of which should be memorized. Sensitive or painful points under palpation pressure
suggest an ‘energy’ disturbance. Reckognized focal painful
points or areas in Western medicine (3) include right
trapezes muscle pain in gall bladder disease, McBurney’s
point in appendicitis, left arm pain in myocardial hypoxia,
the experimental pain zones of Head (in humans) as well as
the Clavier of Roger in the (3,4). These sensitive areas are
anatomically standardized, are often localized far away from
the locus of disease and become sensitive when internal organs are inflamed or experimentally irritated. There are viscero-cutaneous reflexes on the basis of this phenomenon
(4). This reflex starts with intestinal irritation. The neurogenic pathway runs from here through the afferent visceral
sympathetic to the dorsal root ganglion and dorsal horn and
communicates with the efferent sympathetic neurone in the
lateral horn. From there an efferent signal runs through the
ventral root into the sympathetic ganglion and to the segmental periphery (skin, muscle, blood vessels). This causes
referred skin sensitivity, vasoconstriction, contraction of the
erector pili muscles, muscle hypertonicity and sweating in
the referred area (4). Kothbauer (5) searched experimentally
for these reflexes in the cow by injecting iodine solutions at
different points of the urogenital tract while he searched for
sensitive areas or points on the animal’s back with the help
of an electric measuring device. Before the iodine injections
no painful areas or points were detectable on the skin. Injection however, produced reproducible sensitive areas in
which very focal points were identified that were extremely
painful under pressure and electrical current and that developed a decreased local skin resistance. These points are considered to be AP. They can than be used diagnostically since
a specific sensitive point under palpation refers to a specific
internal origin. This reflex has also been examined experimentally in different animal species. In these, destruction of
the sympathetic chain, but not the spinal cord or vagus, destroyed the reflex (6).
A cutaneo-visceral reflex exists. Stimulation of the skin
in rats, rabbits, amphibians and fish (4) induced gastro-intestinal changes in vascularity and motility which were
again abolished only when the sympathetic trunk was destroyed. These two reflexes reflect the basics explaining the
working mechanism of Ac therapy (AT).
Ac pulse diagnosis is the second diagnostic tool. It is not
comparable with our Western method of pulse palpation. It
is a much more elaborate and sophisticated method. It has
214
been explained in much detail for human use in old and recent Chinese texts, but only in one ancient equine text. The
method consists of sensing the arterial pulse with three different fingers on the left and right wrist (Figure 1). The pulse
is felt with minor finger pressure (superficial pulse) and deep
pressure (deep pulse). As thus 12 different pulses are perceived. Each of these correlates with a different Mer and
gives information about its condition or “energy” status. It
seems to take several years of practice to study the sublety
of pulse diagnostics and no apparatus exists yet to record the
many variables in each pulse described by experts. This
makes the system subjective, non-reproducible and nonrecordable. Although it might be a valuable and subtle diagnostic method for humans, if applied by well trained experts,
it is impractical for veterinary use. Yet pulse diagnosis is the
core of classical Ac since it determines the “energy” disturbances in each Mer. Only after that exam, one will logically
determine, by the use of certain reasoning patterns, which
AP on which Mer to stimulate.
There are 12 different symmetrical meridians (also called
channels or vessels) in the body, each with a different name
(Figure 2). Each name relates to a hypothetical “organ system” (e.g. lung, heart, kidney). Some of these systems have,
however, no meaning to us (e.g. triple heater). Some names
have questionable translations (e.g. large intestine might also mean long intestine and thus small intestine). The fact
that most Mer have anatomical names does however not
mean that they “represent” this organ or that all AP on this
Mer have an influence on that organ.
The Chinese were aware of the blood flow and intestinal
motility (food flow) a few thousands year ago. Since their
nature philosophy was one of consistent change and thus
flow from one state into another (such as the seasons e.g.),
they saw the body as a system with many channels (tendons,
blood vessels, nerves, etc.) through which the bodies energy
and fluids were circulating. The Mer were thought to be one
among the many types of channel systems in which this “energy” flows, from one channel into the next, order???? and
directed and at a certain speed with a maximal energy state
of an organ/Mer system at a certain hour of the day. The total energy flow circle takes 24 hours. There is no scientific
evidence of any such circle but this “flow description” is
probably the first mention of biorhythms.
It is unclear how the Chinese detected AP, but probably
most were defined by palpation of sensitive spots and recognition of spontaneous painful spots. AP can now be searched
for with modern methods. Indeed the skin impedance (resistance) of an AP is much lower (7-70 kOhm) than of surrounding skin ((300-2000 k Ohm) in humans and in the dog
(7). The surface of this low resistance spot is about 1 mm2.
A lower skin resistance means better electric conductivity
which explains why many AP are motor points. A motor
point is the skin point where the lowest electrical current still
causes muscle contraction of the underlying muscle. Still (7)
examined the canine skin over reported Mer for low resistance points and found that these are stable in location if
searched for over time. About 80% of the points correspond
with known anatomical AP (8). There is no difference in localization depending on sex, breed, weight, body condition,
temperament, time of day or year. The number of low resis-
tance points found on Mer tracts was always higher (115% 226%) than the defined number on accepted anatomical
charts. Measurements outside of Mer also revealed the existence of low resistance points. Discovering so many low resistace points nowadays correlates with the historical evolution of acupuncture. Indeed the number of AP gradually increased from 365 to about 1000 in recent times. It is puzzling
to see that so many low resistance points exist on and next to
Mer. Can all these be used as effective treatment points too?
And why was the course of the Mer designed to run through
certain AP and not through other nearby (nowadays nonmeridian) points? These questions will be resolved later.
Some work was done on the anatomical variability of AP
in different dogs using impedance meters (9). There was
variability at some points while other were very stable. The
fact that some anatomical variability exists and that treatments are based on stimulation of chart-based anatomical
AP, signifies that often vicinity points and not the “real” AP
is stimulated.This seems not to affect clinical results.
Another phenomenon of AP is that in internal disease
specific AP will display a decrease in electrical resistance
(10) which reverses increase after recovery from disease.
This is not only the case for AP on the body, but even more
so for AP on the ear lobes. The latter represent and connect
to internal organs. They were discovered in the sixties and
can be used for diagnostic as well as therapeutic reasons.
Skin resistance is determined by extracellular ion concentrations and thus by sweat production and local blood flow. The
latter is defined by the local cutano-sympathetic tone. Histological research of AP has identified many local neuro-vascular (aterio-venous) bundles under the point. These bundles
have a high incidence of arterio-venous shunts which are always richly innervated by the sympathetic nervous system.
This finding helps to explain lower local skin resistance of
AP than that of surrounding skin and also that it is variable
and under the influence of the viscero- cutaneous sympathetic reflex.
Although there is convincing evidence of the existence of
AP, there is no scientific evidence that Mer are physiologically measurable entities (11). We assume that they are
imaginary lines connecting AP. Their origin is probably
based on the sometimes radiating sensation humans experience when an AP is stimulated (called T’ chi of Qi sensation). The sensation is however anatomically vague. The fact
that they are imaginary allows for arbitrariness when decisions have been made on which of 3 anatomically close and
sensitive points have to be incorporated into one Mer; which
to make a non-meridian point and which to assign to another Mer. These decisions have been made historically and a
general consensus of acceptance of the system exists now.
This explains why consecutive points may have totally different clinical indications (2).
In traditional (Taoist) Chinese Medical philosophy
(TCM) there are three fundamental statements (axioms)
which are at its origin. The first axiom is that all living creatures possess life energy, called Qi, which flows through the
body in Mer in a 24 hr circle. If the circulation is disturbed,
disease originates. This disturbance can be observed by
pulse diagnosis. The second axiom is that all phenomena can
be divided in two opposite categories: yin or yang. Six of the
12 Mer are yin the other six yang, the six hollow organs are
yang, the six solid yin. In a healthy body there is an equilibrium between yin and yang. If the balance is disturbed (e.g.
too much yang in one organ) disease originates. The third
axiom is that all phenomena can be classified in one out of
five element categories: earth-metal-water-wood and fire
(Figure 3). These elements have an influence on each other.
This influence can be constructive (X forms Y, e.g. wood
creates fire) or destructive (e.g. metal destroys wood). A
pentagon schematically represents these interactions.
Treatment of disease consists of a specific sort of activation (stimulation or sedation by difference in use of needling
technique)of a specific Ap on a specific Mer. To decide on
which AP to use, one has to understand the previous interactions. One of the most important is that stimulation of one
Mer will automatically stimulate the next one, draw energy
from the former one and sedate the second next one. This allows one to stimulate a Mer by using AP not on the Mer itself but e.g. on the former one. To find out which AP to activate on that Mer , the system had to be made more complex
because not any arbitrary AP on that Mer will do the job.
One AP on each Mer (localised distal from knee or elbow)
represents one of the five elements. There is however no
consistency in the follow-up of these “element points and
some AP are just skipped without explanation. This is a first
inconsistency. A second inconsistency exists in the followup of the energy and five element cycles. The 24 hr energy
cycle runs in the reverse direction from the constructive pentagon cycle and thus they might be considered mirror flows,
but in the latter there are some unexplainable jumps. Two
meridians are e.g. skipped (liver and gall bladder) and the
flow goes than back from where it came from. A third inconsistency originates when trying to fit 12 meridian/organs
into a pentagonal system. Indeed, two organs are left over.
As an exception these are attributed to the element fire
which thus contains 4 Mer).
Once one has defined which AP on which Mer to activate, there are still two methods to activate each point. Activation also called tonification is produced by manipulating
(rotating, twirling, lifting and thrusting) the needle, while sedation is caused by inserting a needle without further manipulation. For a long time, and sometimes even now, two
different types of needles were used for each purpose: tonification was performed with golden, sedation with silver
needles (again the yin yang idea) and golden needles were
often heated. There is no scientific proof however that the
material of the needle has any influence on treatment efficiency. Important seems to be that the correct is stimulated
with a stimulus strong enough to effectively activate the afferent nerve endings of importance for acupuncture. This
can be done by needles, massage, electricity, laser, etc..
TCM theories have been elaborately expanded over the
centuries and many more interactions, many more meridians
and many more AP have been added to the original system.
The reasoning and theories were relatively clear and simple
in the beginning but grew to an elaborate, overcomplex, system which tried spasmodically to fit exceptions or new observations into the framework of the existing theories. It did
so by introduction of new connections and new laws or by
accepting exceptions and keeping them out of the theory
215
framework. Clearly this system uses post-factum reasoning.
For a new phenomenon a new theory was constructed and
integrated more or less in the existing system. This way of
theorising does not allow to distract new knowledge or predict facts except by coincidence. TCM lacks globalisation
and unity even in its early form.
TCM is phenomenally complex and can be admired for
its inventiveness. The reasoning can be used in practice to
perform AT but in the absence of pulse diagnosis, the treatment will lack fine tuning and accuracy. Pulse diagnosis,
however is hardly ever used by Western doctors and veterinarians who apply acupuncture as a therapy. Instead traditionally oriented practitioners will use symptom classifications that attribute disease to an element and an energy state
(e.g. tachycardia is excess of heart energy, is thus fire element yin excess). They will start the classical reasoning
based from there and not from palpation of the pulse.
There is another way to decide which AP to use for a certain disease. This is consulting human formula books (cookbook Ac). In these, a certain formula (a prescription of certain AP) is mentioned for a certain disease. These formula’s
are the result of many centuries of clinical Ac experience.
One author (34) computerised these formula from a massive
amount of books which were valued on importance. The result is a disease oriented appreciation list of AP. We recommend the use of this list for small animal applications and restrict ourselves to the top 3-5 AP for those conditions on
which no specific veterinary publications exist. Up to now
there is no clinical or statistical proof that the use of TCM
theories is superior to cookbook Ac. It is temptative to expect a complex system to be better but there is no proof for
it. As Dr. Felix Mann described in his last book on acupuncture (4) after studying TCM for 20 years, after learning Chinese language and reading all texts in their original writing:
“After... I mastered the subject... I seriously examined the
validity of all I had learned, only to discover that most of it
was fantasy... and that most of the laws of acupuncture are
laws about non-existent entities” (p. 1).
A SHORT FLIGHT OVER THE WORKING
MECHANISM OF ACUPUNCTURE
Classical theories are incapable of explaining the working mechanism of Ac in a physiological way. So how must
we think about Ac? Is it a form of hypnosis; a complex
placebo therapy; a method of stress analgesia; or other?
Ac is not hypnosis since it does not use suggestion and
repetitive stimulation and since no immobility is obtained
(12). Hypnosis can cause analgesia in ± 10% of its patients,
while acupuncture analgesia (AA) has proved to be successful in 70-90% in treated patients
Ac is not a placebo, since double blind studies including
placebo treatments have proved Ac to be far more successful
than placebo treatments which generally obtain a 20-30%
success ratio (13).
Ac is not stress analgesia. Stress analgesia can be induced by a very short stimulus period, while a 15-20 min induction-stimulation period is needed to produce AA and
stress analgesia is not naloxone reversible while AA is.
216
Is Ac a stimulation method which works by means of humoral and neurological pathways? Humoral pathways of Ac
certainly exist since cross-over tests with dogs and rats both
with linked blood circulation or transfer of cerebrospinal fluid produced analgesia in the recipient animals that did not
receive Ac treatment while the donor animals did. The substances involved here are mainly endorphins since naloxone
treatment of the recipient animals abolished analgesia (14).
Humoral factors are, however, not involved in Ac stimulus
propagation since avascularization of a limb in which Ac
stimulation is applied still results in normal Ac effects.
Neurogenic pathways are without a doubt the most important factors in the working mechanism of Ac. Local
anaesthesia of the skin around the AP did not abolish Ac induced oral analgesia in monkeys, while deep local anaesthesia did (15). Local anaesthesia or section of the inervating
nerve of the periostal and musculoskeletal structures beneath
the AP did abolish Ac effects. When AP are used in the lower limbs (legs) no Ac effects occur after epidural anaesthesia
or somatic and sympathetic denervation.
Ac stimuli are captured by somatic and sympathetic free
nerve endings in deep tissues.From here afferent impulses
run mostly through A delta fibres, to arrive in an interactive
“gate -like” system in the dorsal horn of the spinal cord grey
matter. There connections run to segmental and intersegmental sympathetic neurons or segmental interneurons, ascending and descending spinal segments and the brain.
AA mechanisms have been studied most in detail. Most
of these pathways were unravelled by focal transection or
administration of chemical agonists or antagonists of different neuropeptides in experimental animals. We know now
that Ac is effective through interactions with segmental
(mostly ipsolateral) spinal cord pain pathways and with activation of the enkephalin-endorphin and serotinin production and release.
The endorphins produced under AA are multiple, but
dynorphin seems to be important in the spinal cord and beta- endorphin in the brain. (14,16) This type of analgesia is
naloxone reversible and produced by low frequency (2-8 Hz)
stimulation of the needles (manual twirling, mechanical
twirling or low frequency electric stimulation). 20-30% of
patients do not respond to AA. Many can turn into responders by preloading them with D-phenylalanine or L-tryptophan. Both block carboxypeptidase a catabolic enzyme for
endorphins. Serotonin on the other hand is produced in the
brains nucleus raphe magnus, preferentially by high frequency stimulation (about 200 Hz) of the AP. This centrally
produced serotonin flows through a spinal descending pathway in the lateral white matter adjacent to the dorsal horn
and blocks or attenuates incoming pain signals at the spinal
level (17). There are several other important substances involved in AA (e.g. cholecystokinin(CCK), noradrenaline,
GABA)(18).
The therapeutic effects of Ac have have revealed that the
autonomic nervous system plays a pivotal role. Stimulation
of AP stomach 36 e.g. causes parasympathetic phenomena
which are counteracted by atropine administration. AP governing vessel 26 stimulation causes respiratory and cardiac
activation which is counteracted by propranolol (beta-blocker) and to a lesser extent by phentolamine (alpha- block-
er).Ac is capable of releasing endorphins, serotonin and
adrenaline. Endorphins have a negative influence on intestinal motility and serotonin and noradrenaline are important
modifiers of mood and appetite. The link between trigger
points (TP) and AP (± 70% of TP are AP) and the vast
amount of TP research and understanding (19,20) explain
the working mechanisms of Ac in muscle and joint disease.
APPLICATIONS OF ACUPUNCTURE
IN SMALL ANIMAL PRACTICE
Ac can be used during surgical procedures for analgesic
purposes or as a form of therapy.
AA can be used in practice as one part of the cocktail of
anaesthetic methods or as a sole procedure. We found it to be
time -elaborate, requires a lot of technical assistance, is impredictable and suffers from several inconveniences such as
muscle tension, patient movement, patient reaction, vagal reactions and incomplete analgesia in certain regions. As thus
it can not compete with modern anaesthetic techniques but it
may still be of value in animals with a high anesthetic risk if
sophisticated methods are not available.
Most frequently Ac will be used as a therapy and most
often for neurologic and musculoskeletal problems. Ac can
be of benefit for other conditions such as respiratory and cardiac arrest under anesthesia, after trauma or due to heart failure (22). If a 25-28 gauge hypodermic needle is placed in the
midline of the nasal plane (Figure 5) between the nostrils
about 1-5 cm deep and vigorous twirling and pecking is applied for 10-600 seconds, there is a strong activation of the
respiratory and cardiovascular system. Several methods of
stimulation of this point have been compared for effectiveness. Manual needle stimulation and heat (80°C) were most
effective. Still applied the method in pentobarbital overdosed dogs and cats and tried to revitalise them. The method
was highly successful in dogs and produced more favourable
results (88%) than I.V. adrenaline injection (75%) or
needling of a very nearby non- AP (40%). In cats stimulation
of the point yielded comparable results to doxapram injection (res. 76 and 69%) but better results than seen with stimulation of a nearby non- AP(23). Patients with respiratory arrest react more rapidly and favourably than those with cardiac arrest. Experimental work in cats with hemorrhagic
shock showed that the group that received stimulation of this
point had a much higher survival rate than the group of nontreated cats.
Ac isbe effective in a high percentage of chronic
arthropathies in man and in animals with arthritis. In general a 60-70% success rate can be expected in dogs. Some
joints, such as the shoulder, hip and knee seem to be better
Ac candidates than carpi, tarsi and elbows but this observation is preliminary and may change when more effective
treatment protocols are discovered. (24,25) In deciding on
when to use Ac as a treatment modality for chronic identify
whether the arthritic joint is stable or not. If not (hip dysplasia in young dogs with a positive ortolani sign and clinical
subluxation; recent rupture of an anterior cruciate ligament
with a positive drawer movement or a dog with vascular
necrosis of the femoral head and progressive “crumbling” of
the cartilage) Ac is of limited and short lasting benefit since
its analgesic and anti-inflammatory actions will automatically be deleted by new joint trauma induced by abnormal biochemical movement. These joints require surgical stabilisation. If a joint is stable, shows arthritis and causes symptoms,
two treatment options exist: surgery (e.g. total hip replacement) or conservative treatment. The latter may consist of
weight reduction, restricted and controlled movement and
drug therapy.If these treatment options are refused or if there
are drug side effects or unfavourable clinical results, Ac is an
alternative. The advantage of Ac is that it does not produce
side effects apart from a 1-2 day clinical aggravation in most
animals after the first treatments. Different treatment protocols have been used by different authors (24,25) but mostly
one or two treatments a week are administered for 3-10
weeks. Thereafter animals often function well for long periods of time (months-years) and most will need one or two periodic booster treatments. (This type of treatment schedule is
quite comparable with polysulfated glycosaminoglycan injection therapy). It is not fully understood why Ac is effective
in arthritis, but many pathophysiological processes that occur
in chronic osteoarthritis are also unknown. One aspect of Ac
in the treatment of musculoskeletal problems has been understood; namely that AT is largely TP therapy. Indeed more
then 70% of human TP correspond with acupuncture points
and many canine TP correspond with AP (19,20,26). TP are
hard, palpable nodular structures which occur in muscles and
fascia often after even minimal strain or trauma. They are
much more prevalent in older than younger individuals.Although most TP disappear spontaneously some tend to persist
for many years. When acute, TP cause active local pain (e.g.
sore back). When chronic (passive) they are silent causing
muscle shortening, stiffness, and weakness without atrophy.
Many TP cause referred pain, often at a distance from their
origin. When squeezed or compressed, they are painful
(healthy muscle is not painful under compression) and then
trigger the referred. These painful points have since long
been described in Ac texts as Ashi points and were always
added to the classic treatment protocol. Chronic TP can become active and thus spontaneously painful under certain
conditions such as exercise, stress, fever, viral infections and
fatigue.Although TP have become quite well known topractitioners, they are unknown to most small animal practitioners.
Research has revealed that the basic pathology of a TP is a
muscle endplate disease. Neuromuscular endplates of TP
show acetylcholine levels are 100 times as high as in normal
endplates. This hyperactivity allows us to see TP actively on
EMG recordings. In these, typical seashell noise, rapid low
voltage activity is recorded. This activity disappears once the
TP is abolished. Sympathetic activity seems to play a pivotal
role in TP since general and local sympathetic blockade abolished TP temporarily. The main treatment for TP however is
TP stimulation. This is achieved by dry needling or injection.
There is no advantage to injection of any fluid (water, physiologic, vit. B, local anaesthetics) and moreover injection
techniques, cause more afterpain. When needling TP it is pivotal to obtain (see and feel) the twitch response. This is a
rapid contraction of a small number of muscle fibres when
the TP is hit. Since one TP consists often of many small TP
in the same vicinity, dry needling must consist of hitting all
217
TP and thus several twitches will be evoked. Treatment is
considered finished when no new twitches can be produced.
Since these treatments are often painful it is often necessary
to sedate the animal especially when many TP have to be
treated. As in Ac treatments, once a week therapies are mostly performed and often 3-5 treatments are sufficient. TP therapy can improve the quality of functioning, the speed of recovery, the angles and range of motion of arthritic joints. TP
become objectively smaller or disappearafter therapy. TP
may also exist in muscles without concurrent joint disease.
We found the left triceps muscle to be quite susceptible to TP
development. Treatment of this TP yielded very favourable
results, with ± 80% of the chronically lame animals becoming free of lameness in mean 3 weeks (26) We encourage
practitioners to search for TP in lame dogs that show no
arthritic or neurologic abnormalities.
Ac assists in dogs with disc protrusions or herniations.
Cervical, thoracolumbar and lumbosacral disc disease
(CDD, TLDD) have all been treated successfully. A variety
of treatment protocols exists with veterinary acupuncturists.
Different choices of the type and number of AP, stimulation
methods (injections, dry needling, electrostimulation, etc.)
duration and interval are used. There is agreement however
that success rates are comparable. If this is true we think the
simplest method may be the best.
Two authors have reported detailed studies of large
groups of dogs with TLDD or CDD (27-31). In both cases
distant and local AP were used and clinical results were
comparable. Most protocols treat the animals once a week
but there is evidence that more frequent treatments (2or3 a
week) lead to faster recovery in acute non paralysed TLDD
cases (27). The simplest method for TLDD treatment consisted of dry needling of one AP on the hindleg between the
tibia plateau and the head of the fibula and several local paravertebral tense and painful (Ashi or TP) back AP. There
seems to be no benefit in stimulating the latter points with
injection therapy in regard to plain needling in back pain patients. In all acutely (less than 24 hrs) presented patients, and
independent from whether they will undergo surgery or not,
we now advocate to administer once a bolus of sodium prednisolone succinate at 30 mg per kg, IV as a free radical scavenger. About 90/95% of non-paralysed animals (pain only or
grade 1, pain plus paresis or grade 2) were cured with this
technique in 2 to 3 weeks. Approximately 80% of paralysed
dogs with intact pain sensation (grade 3) were cured in about
6 weeks and 25% of those paralysed with absence of pain
sensation (grade 4) recovered in 3 to 6 months. We have
proved that treating these animals with normal dose and long
term corticosteroids before or during the onset of AT prolongs recovery significantly (28). this findings in accordance
with recent experimental and clinical human observation
(32). The success of AT for non paralysed patients is greater
than for other treatments both surgical and conservative. Results for grade 3 patients are comparable with rapid decompression and better than conservative treatments and success
percentages in grade 4 patients are half that for rapid surgical decompression. We recommend Ac therefore as the first
treatment option in grade 1 and 2 (33). If dogs do not respond favourably to AT, if the condition aggravates neurologically, if there is excruciating pain, if there are frequent
218
relapses or if it is the owners wish, surgery should be performed (see Algorithm). In grade 3 dogs we leave the decision of surgery versus AT to the owner if the animal is presented within 24 hrs after the onset of symptoms. The advantage of surgery here is that recovery is faster and that
there is a smaller risk for aggravation to grade 4. decompression. If dogs are presented in grade 4 within 24 hrs we
advocate rapid decompression If the animal is presented
for therapy more than 24 hrs after the onset of paralysis,
surgery is of no use unless the lesion is in the low lumbar
region or of a very confirmed and very compressive nature. In that case the pathology is more of compressive
than kinetic origin and there is still some logic in retarded
ssion. If refused, non-available or of the patient is presented later we propose AT. AT is always accompanied by
good general care (GGC), which consists of cage or
playpen rest for 4 weeks (the healing -sealing period of the
dorsal anulus); sedatives (diazepam or acepromazine, 4
weeks) and stool softeners (4 weeks) to prevent straining
during defecation. These animals are indeed almost always constipated and augmented abdominal pressure
leads to elevated pressures in the disc and in the vertebral
canal. This creates extra pain and a higher risk for new extrusions. When the dog is paralyzed, the cage should be
padded and analgesics administered. When bladder paralysis is present (overflow bladder), the bladder should be
emptied twice a day. This can be done by catetherization
or the Crédé maneuver and urine should be checked weekly for infection. Physical exercises are started after the
four week period in all animals that were not operated upon. When permanent or long standing paralysis is present,
dogs are given a two wheel chart to walk in, a low bulk diet, rectal stimulation induced defecation after feeding and
perineal rubbing to induce urination.
In CDD patients Ac results are less favourable than in
TLDD (31). About 80% of neckpain patients and two thirds
of neck pain plus paresis patients cure within 2 to4 weeks.
Treatment schedules are mostly once a week but in severe
acute cases more regular treatments are beneficial. It is extremely important in CDD patients to treat all the TP in the
neck region efficiently. We do not recommend to treat tetraparetic animals with AT, and although we have treated dogs
in this group successfully, we find the recovery too longstanding, the complication rate too high and the pain too excessive. GGC consists in CDD animals of cage rest, sedatives, laxatives and strong analgesics or antiphlogistics or
low dosage corticosteroids. Since pain in CDD dogs may be
excruciating, long-lasting, exhausting and non-responsive to
medication, we strongly suggest an ethical solution and advocate ventral slot surgery if animals are not responding to
AT in 21 days, if pain is excessive, or if there are frequent relapses. Dogs that suffer pain after surgery are routinely treated with AT with emphasis on TP. In disc patients that were
treated successfully relapses occur as with all conservative
treatments. These were, in our series, about 25% in TLDD
over a 5 year period, and 33% over a 3 year period in CDD.
Ac has been used successfully in many other clinical
conditions in companion animals. Describing theseis beyond
the scope of this chapter.The interested reader may obtain
detailed information in the references ofthis chapter.
Acknowledgement
I am grateful to Roger Belderbosch from the Service of
Science philosophy of the University of Ghent, Belgium,
who was extremely helpful in critical analysis of the Taoist
medical reasoning.Suzy De Cauwer is thanked for the typing
of the manuscript and Lambert Leijssens is thanked for the
help with the preparation of the figures.
References
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
Mann F: Basic principles of acupuncture, IN Mann F (ed): The ancient Chinese art of Healing, London, W Heinemann Medical Books
LTD 1971, p.3.
Anon: Basics of Acupuncture, IN Academy of traditional Chinese
Medicine (ed): An outline of Chinese acupuncture. Peking, Foreign
Language Press,1975,p.12.
Kellner G: On the distribution of pain arising from deep somatic
structures with charts of segmental pain areas, Clinical Science 4:35,
1942
Mann F: Dermatomes, myotomes, sclerotomes, IN Mann F (ed):
Scientific aspects of acupuncture, London, W Heinemann Medical
Books LTD 1977, p.50.
Kothbauer O: Die provokation einer hyperalgetische Zone die Haut
und eines Schmertzpunkt durch die Reizung eines Uterushornes beim
Rind. Wiener Tierarztlicher Monatschau 56:803,1973
Wernoe TB Viscero-cutane Reflexe. Pflugers Archiv fur die gesamte
Physiologie: 210,1925
Still J: Relationships between electrically active skin points and o
points in the dog. Am. J. Acupuncture 16:55,1988.
Janssens LAA and Still J: Acupuncture points and meridians in the
dog. Sec Ed. Brussels, Van Wilderode print, IVAS distribution.
Janssens LAA, et al.: Anatomic variability of some major acupuncture points in the dog. Am.J. Acupuncture 16:263,1987.
Choh Luh Li: Survey of electrical resistance of the rabbit pinna during experimental peritonitis. Chinese medical J.7,1973(abstract)
Bensoussan A: The nature of meridians. IN Bensoussan A (ed): the
vital meridian, Melbourne, Churchill Livingstone, 1991, p.51.
Lecron LM: Analgesia under hypnosis IN Lecron LM (ed): Experimental hypnosis, The citadel Press, 1968, p..
Pomeranz B: Relation of stress induced analgesia to acupuncture
analgesia. New York academy of science 467:444,1986.
PeetsJM and Pomeranz B: Acupuncture-like transcutaneous electrical
nerve stimulation analgesia is influenced by spinal cord endorphines
but not by serotonin. IN Bonagura W (ed) Advances in pain research
and therapy, New York, Raven Press, 1985, p.519.
Vierck CJ et al:. Prolonged hypalgesia following acupuncture in
monkeys Life sciences 15: 1277, 1974.
He L: Involvement of endogenous opioid pepetides in acupuncture
anaesthesia. Pain 31:99,1987.
Cheng RS and Pomeranz B: Monoanergic Mechanisms of electroacupuncture analgesia. Brain Research 215:77,1981.
Han JS and Terenius L: Acupuncture Analgesia. Ann. Rev. Pharmacol. and Toxicology 22:193,1982.
Travell JG and Simons DG: General issues, IN Travell JG and Simons DG (eds): Myofascial pain and dysfunction: the trigger point
manual, Baltimore, Williams and Wilkins, 1992, p.1.
Melzack R et al: Trigger points and acupuncture points for pain: correlations and implications. Pain 3: 3, 1977.
Janssens L et al: Respiratory and cardiac arrest under general anaesthesia: treatment by acupuncture of the nasal Philtrum. Vet Rec
105:273,1977.
Lee DC et al: Some effects of acupuncture at jen soun on cardiovascular dynamics in dogs. Canadian J Comp.Med. 41:446,1977.
Still J: Comparision between stimulation of respiration through treatment by acupuncture or by noradrenalin in dogs suffering from respiratory arrest due to use of barbiturates. Ann. Med. Vet. 132:57,
1988.
Schoen A: Critical evaluation and documentation of acupuncture the-
25
26
27
28
29
rapy for the veterinary treatment of chronic arthropatics. Proceedings
9th International Veterinary Acupuncture Association 1983, Cincinnatti
Janssens LAA: Observations on acupuncture therapy in chronic
osteoarthritis in dogs: a review of sixty-one cases. J. Small Anim.
Pract. 27: 825, 1986.
Janssens LAA: Trigger points in 48 dogs with myofascial pain syndromes Vet. Surg. 20: 274, 1991.
Still J: Analgesic effects of acupuncture in thoracolumbar disc disease in dogs. J Small Anim Pract 30:298, 1989.
Janssens LAA and De Prins EM: Treatment of thoracolumbar disk disease in dogs by means of acupuncture: A comparison of two techniques. JAAHA 25:169-174, 1989.
Still J: Acupuncture treatment of type-III and type-IV thoracolumbar
219
30
31
32
33
34
disc disease. Mod Vet Pract 7:35, 1987.
Still J: Acupuncture treatment of thoracolumbar disc disease: a study
of 35 cases. Compan Anim Pract 2:19, 1988.
Janssens LAA: The treatment of canine cervical disc disease by
means of acupuncture: a review of 32 cases. J Small Anim Pract
26:203, 1985.
Sapolsky RM and Pulsinelli WA: Glucocorticoids potentiate ischemic
injury to neurons: therapeutic implications. Science 229:1397,1985.
Janssens LAA and Rogers PAM: Acupuncture versus surgery in canine thoracolumbar disc disease. Vet. Rec. 123: 257, 1989.
Rogers PAM: Choise of AP points for particular conditions, IN Post
graduate committe in veterinary science (ed): Acupuncture in animals, Sydney, Post graduate committe in veterinary science publications, 1991, p. 223.
221
Epidemiologia, diagnosi, terapia
e gestione delle neoplasie endocraniche
Donatella Lotti
Med Vet, Torino
Massimo Baroni
Med Vet, Genova
Sono stati presi in considerazione 88 casi riguardanti
soggetti affetti da Neoplasia Intracranica. I criteri per l’inclusione nello studio sono stati la presenza di un file clinico completo incluso il follow-up e l’accertamento diagnostico di Neoplasia intracranica effettuato con diagnostica
per immagini avanzata (Risonanza Magnetica, Tomografia
Computerizzata) e/o con esame autoptico. In particolare
84 animali sono stati sottoposti ad esame RM, 2 ad esame
CT, mentre l’accertamento post-mortem è stato effettuato
in 31 soggetti.
SEGNALAMENTO
I dati presentati riguardano 80 cani e 8 gatti. Tra i cani ben 18 razze sono rappresentate, sia di tipo dolicocefalo che brachicefalo, con una prevalenza significativa della razza Boxer e Pastore Tedesco. Il 31% dei cani sono infine di razza meticcio.
L’età al momento della presentazione oscilla nei cani
tra un minimo di 28 mesi ad un massimo di 14 anni. Nei
gatti si va da un minimo di 8,5 anni ad un massimo di 15
anni.
CLINICA
In tutti i soggetti, al momento della presentazione, è
stata effettuato un esame fisico completo ed una valutazione neurologica specialistica. I deficit neurologici riscontrati hanno consentito, nella maggioranza dei casi,
una localizzazione neuroanatomica della lesione in accordo con la sede della neoplasia.
Per quanto riguarda le neoplasie localizzate in fossa
anteriore, è interessante l’evidenza di soggetti presentati
per insorgenza improvvisa di crisi convulsive e considerati normali alla visita neurologica. Tale situazione si as-
socia a lesione emisferica, prevalentemente a sede prefrontale.
DIAGNOSTICA PER IMMAGINI
Sono disponibili dati significativi soprattutto per quanto
riguarda gli esami svolti in Risonanza Magnetica, in quanto
tale procedura ha riguardato la quasi totalità dei soggetti.
L’esame RM è stato considerato accurato nell’evidenziare lesioni situate sia in fossa anteriore che posteriore. Nella
maggioranza dei casi è stato possibile emettere una diagnosi RM riguardo al tipo di neoplasia. In alcuni casi è stato
possibile emettere solo una possibile diagnosi differenziale.
In particolare non è stato possibile differenziare gliomi di I
grado da lesioni ipointense di altro tipo, linfomi da lesioni
infiammatorie, un adenoma ipofisario da un meningioma
della base, un carcinoma del bulbo olfattorio da un meningioma.
TIPO DI NEOPLASIA IDENTIFICATO
I tumori endocranici più frequentemente identificati
sono stati quelli derivati dalla glia ( Gliomi), frequenti soprattutto nelle razze brachicefale ed in particolare nel
boxer e d i Meningiomi, più frequenti in razze dolicocefale ed in particolare nel pastore tedesco. Con incidenza minore sono state identificate altri tipi di Neoplasia: Neuroblastoma (1), papilloma dei plessi corioidei (3), ependimoma (1), Adenoma-adenocarcinoma ipofisario (6), tumore delle guaine dei nervi periferici (V nervo cranico)
(3), linfoma (2), metastasi (6).
La localizzazione più frequente è stata quella in fossa
anteriore. Tra le neoplasie localizzate in fossa posteriore,
significativa è risultata l’incidenza delle neoplasie dell’angolo cerebello-pontino.
222
TERAPIA
In 22 casi è stata effettuata terapia chirurgica In particolare sono stati trattati chirurgicamente 18 meningiomi, 2
gliomi, 1 adenoma pituitario, 1 carcinoma del bulbo olfattorio.
Le neoplasie localizzate in fossa anteriore hanno consentito un più facile accesso e nella maggioranza dei casi
è stata possibile una escissione macroscopicamente totale. In due casi l’escissione è stata parziale (meningioma
della falce in un gatto, meningioma della falce in un
boxer). Complicanze postoperatorie di rilievo si sono verificate in due soggetti: stato di male epilettico in un cane
affetto da meningioma parietale e ernia cerebellare in un
gatto con meningioma della falce di grandi dimensioni. In
un caso la rimozione non è stata possibile (macroadenoma ipofisario).
L’accesso chirurgico alle neoplasie situate in fossa posteriore è risultato più problematico e una rimozione totale è stata ottenuta esclusivamente in caso di meningioma
dell’angolo cerebello-pontino nel gatto.
In 4 casi alla terapia chirurgica è seguita terapia radiante
con megavoltaggio.
In due casi la terapia radiante è stata l’unica terapia d’elezione.
Tutti gli altri soggetti non sottoposti a terapia chirurgica
o radiante hanno ricevuto terapia palliativa o il proprietario
ha scelto l’eutanasia.
DECORSO
Quattro tra i gatti affetti da meningioma (6) e trattati chirurgicamente hanno avuto buona prognosi in assenza di recidiva a distanza di due anni. Un gatto è deceduto nell’immediato postoperatorio per ernia cerebellare. Un altro gatto
è deceduto per cause rimaste sconosciute a distanza di due
giorni dall’intervento.
I cani affetti da meningioma e trattati con chirurgia (+ terapia radiante) hanno avuto una sopravvivenza media di venti mesi con un soggetto sopravvissuto 5 anni e un altro soggetto senza segni di recidiva a distanza di 4 anni.
La sopravvivenza media dei soggetti affetti da meningioma e trattati con terapia palliativa è stata inferiore a quella dei soggetti trattati. La sopravvivenza dei soggetti affetti
da glioma è stata decisamente inferiore rispetto agli animali affetti da meningioma e la terapia chirurgica non è sembrata influenzarne il decorso. Un soggetto affetto da glioma
di I grado e trattato con radioterapia, è, al momento attuale
al terzo anno di vita post trattamento.
223
Come gestire il paziente addisoniano
Ugo Lotti
Medico Veterinario, “Clinica Veterinaria Valdinievole”, Monsummano Terme (PT)
CENNI DI ANATOMIA E FISIOLOGIA
Le ghiandole surrenali sono localizzate nello spazio retroperitoneale, in particolare la ghiandola di sinistra è più
grande e si trova in corrispondenza del margine craniomediale del rene sinistro e la destra a livello dell’ilo del rene destro.
Ciascuna ghiandola è composta da due parti distinte, sia
anatomicamente sia nella loro origine embriologica: la “medulla” che si trova nel centro della ghiandola, ne rappresenta
il 10-20% e secerne epinefrina e norepinefrina. e la “corteccia” che costituisce il rimanente 80-90% e a sua volta si divide istologicamente ed anche funzionalmente in tre parti: zona
glomerulosa o arcuata che è la più esterna, rappresenta il
25% di tutta la corteccia ed è formata da cellule disposte a
gruppi ovoidi subito sotto il tessuto connettivo capsulare, da
cui si dipartono linee radiali di cellule con attorno capillari sinusoidi che costituiscono la zona fascicolata, circa il 60% di
tutta la corticale. Infine la parte più interna della corteccia è
formata da reti di cellule circondate da vasi sinusoidi che rappresentano la zona reticularis. La zona glomerulosa secerne
principalmente mineralcorticoidi come aldosterone e desossi-
corticosterone. La zona fascicolata secerne principalmente
glucocorticoidi come il cortisolo, la zona reticularis secerne
gli androgeni ma in minor grado anche glucocorticoidi ed altri ormoni come progesterone ed estrogeni. La secrezione di
tutti questi composti parte dal colesterolo (v. Fig.1) assunto
con il cibo oppure sintetizzato dal fegato. La “zonazione” della secrezione di steroidi all’interno della corticale surrenale,
dipende dal fatto che gli enzimi steroidogenici che convertono il corticosterone ad aldosterone sono soprattutto nella zona
glomerulosa, mentre quelli che catalizzano la formazione del
cortisolo risiedono nelle zone più interne della ghiandola.
EZIOLOGIA
Ci sono due forme di ipoadrenocorticismo: l’insufficienza
corticosurrenale primaria che è una sindrome causata da una
malattia che abbia distrutto almeno il 90% di entrambe le corticali surrenali con conseguente insufficiente produzione di mineralcorticoidi e/o di glucocorticoidi e l’insufficienza corticosurrenale secondaria in cui la produzione di ACTH (ormone
COLESTEROLO
PREGNENOLONE
Progesterone
17α-OH-Pregnenolone
Deidroepiandrosterone
Desossicorticosterone
17α-OH-Progesterone
Androstenedione
Corticosterone
Desossicorticosterolo
TESTOSTERONE
Idrossicorticosterone
CORTISOLO
ALDOSTERONE
Via Mineralcorticoide
ZONA GLOMERULOSA
Via Glucocorticoide
Via Androgenica
ZONA FASCICOLATA E ZONA RETICULARIS
FIGURA 1 - Sintesi degli steroidi e “zonazione” all’interno della corteccia surrenale.
224
Insufficienza corticosurranale secondaria
(ICSS)
adrenocorticotropo) da parte dell’asse ipotalamo-ipofisi è danneggiata e questo influenza soprattutto la sintesi dei glucocorticoidi (zona fascicolata e reticularis), meno quella dei mineralcorticoidi, su cui l’ormone adrenocorticotropo ha un’influenza
minore. Questa forma secondaria si manifesta spesso in caso di
somministrazione cronica di steroidi (Cushing iatrogeno).
La forma secondaria di ipoadrenocorticismo, dovuta ad
una diminuita secrezione di ACTH da parte dell’ipofisi o di
CRH da parte dell’ipotalamo, si verifica raramente in forma
spontanea per lesioni dell’ipotalamo o dell’ipofisi stessa.
Mentre sono frequenti i casi di ICSS per causa iatrogena, dovuti cioè a somministrazione cronica di cortisonici o progestinici che bloccano l’asse ipofisi-surrene (v. Fig. 2) e quindi la secrezione di ACTH, in ogni modo questa forma influenza poco la secrezione mineralcorticoide e raramente dà
sintomi clinici importanti a parte la poliuria/polidipsia. Inoltre c’è una notevole variabilità individuale nella sensibilità ai
glucocorticoidi, nel senso che ci sono cani più o meno resistenti al cortisone ed ai suoi effetti collaterali. È bene rilevare che i cortisonici più facilmente causa di ICSS sono quelli
“depot” ed anche quelli a base di betametasone. Al fine di
avere un risultato attendibile, prima di eseguire un test da stimolazione con ACTH, sarebbe bene aspettare almeno 2 settimane e fino a due mesi dopo la somministrazione di cortisone esogeno per non confondere una ICSP da una ICSS, in
quanto in entrambi i casi avrei una risposta insufficiente alla somministrazione di ACTH.
Insufficienza corticosurranale primaria
(ICSP)
La forma più comune di ipoadrenocorticismo primario è la
forma idiopatica che si vede soprattutto nei cani di sesso femminile giovani o di mezza età dovuta, si pensa ma non si hanno le prove certe, ad una malattia immunomediata che distruggerebbe la ghiandola. Questa fase della malattia non è
mai stata dimostrata nel cane, ci sono articoli che descrivono
le fasi terminali di detto processo in cui la ghiandola appare
atrofica con infiltrazione di cellule mononucleate e con fibrosi della capsula, in ogni modo in questi casi l’ipofisi appare
normale. Nell’uomo si possono dosare gli anticorpi anti-surrenali circolanti, ma questo test è ancora in fase di studio nel
cane, sebbene ci siano articoli che ne dimostrano l’utilizzo.
Altre cause di ipoadrenocorticismo primario sono possibili ma molto rare, anche se sono stati descritti casi di istoplasmosi, tubercolosi, amiloidosi, emorragie dovute a tossicità da warfarin, traumi, metastasi tumorali ecc. che hanno
distrutto la corteccia surrenale. Mentre la forma iatrogena di
ICSP secondaria a terapia con Mitotane si verifica nel 2%
circa dei cani trattati per l’iperadrenocorticismo ipofisario.
In questo caso si deve tenere conto che le zone reticularis e
fascicolata, quelle cioè che producono cortisolo, sono più
danneggiate dal farmaco, perciò questi cani avranno sintomi
da ipocortisolemia. Più raramente e solo in caso di sovradosaggio si potranno avere anomalie elettrolitiche.
FISIOPATOLOGIA
Mineralcorticoidi (MC)
I MC (Aldosterone) sono secreti soprattutto dalla zona
glomerulosa della corteccia surrenale e controllano l’omeostasi del sodio, potassio, cloro e acqua. In particolare
promuovono l’assorbimento di sodio, acqua e cloro e l’escrezione di potassio da parte dei tessuti epiteliali come
STRESS
Fisico
Emozionale
Chimico
(ipoglicemia)
Altri
(malattie)
CRH
Feed-back
negativo lungo
Feed-back
negativo corto
IPOFISI
Cortisolo
Cortisone
esogeno
ACTH
SURRENE
FIGURA 2 - Asse ipotalamo (CRH)-ipofisi (ACTH)-surrene (Cortisolo).
l’epitelio tubulare renale, la mucosa intestinale, le ghiandole sudoripare e salivari. In ogni modo, il sito d’azione
principale dell’aldosterone è il tubulo renale dove aumenta l’assorbimento del sodio e del cloro e l’escrezione del
potassio. La secrezione dell’aldosterone è sotto il controllo del sistema renina-angiotensina (RA) e dell’apparato
iuxta-glomerulare renale. Questa struttura, situata a livello
del glomerulo renale, funziona come un trasduttore di
pressione per cui una caduta della volemia a causa di
emorragie, somministrazione di diuretici, disidratazione
ecc. provoca la sintesi e la secrezione di renina che a sua
volta reagisce con una alfa2-gobulina prodotta dal fegato
dando origine all’angiotensina I che, tramite un enzima di
conversione (ACE), nel polmone, diventa Angiotensina II,
potente vasocostrittore, che stimola la secrezione di aldosterone da parte delle cellule della zona glomerulosa surrenale. La secrezione di aldosterone provoca una ritenzione di sodio che, a sua volta, determina un aumento della
volemia con incremento della perfusione renale quindi,
con un meccanismo di feed-back, un blocco della secrezione di renina. Anche la potassiemia controlla la secrezione di aldosterone indipendentemente dal sistema renina-angiotensina, infatti, un aumento del potassio ematico,
provocato da una somministrazione endovenosa, stimola
direttamente la secrezione di aldosterone con uguale potenza rispetto al sistema RA ma, in vivo, l’aumento della
potassiemia ha un’importanza minore, rispetto al variare
della perfusione renale, sulla secrezione di mineralcorticoidi. Anche l’ACTH influenza la produzione di aldosterone ma in misura molto minore rispetto ai sistemi suddetti
(potassiemia e RA).
L’effetto della diminuita o assente secrezione di aldosterone è la perdita di sodio e di cloro mentre il potassio
viene trattenuto, per cui avremo una caduta della volemia,
infatti, la sodiemia è in rapporto direttamente proporzionale al volume plasmatico, perché assieme al Na e al Cl
viene eliminata anche l’acqua. Come conseguenza di tutto ciò avremo un’ipotensione con riduzione della gittata
cardiaca, ridotta perfusione tissutale e soprattutto diminuzione della filtrazione glomerulare renale (GFR), con
conseguente iperazotemia prerenale e leggera acidosi metabolica, microcardia, debolezza, depressione e perdita di
peso. Sebbene sia presente disidratazione, le urine sono
diluite perché la concentrazione urinaria è determinata
per il 50% dal sodio presente nella midollare renale che,
in questo caso, è insufficiente. Altro fenomeno è l’iperpotassiemia aggravata sia dalla ridotta perfusione renale che
dall’acidosi metabolica che porta, come conseguenza, al
passaggio del K da intra a extracellulare. Questa iperkalemia deprime la funzionalità del tessuto di conduzione
cardiaco con aumento del periodo refrattario e rallentamento della conduzione fino al blocco cardiaco. Inoltre
l’ipossia tissutale, secondaria alla diminuita perfusione,
provoca extrasistoli e fibrillazione ventricolare, questi effetti sono evidenti con valori di potassio intorno ai
10mEq/L.
L’acidosi metabolica è secondaria sia alla capacità ridotta di riassorbire bicarbonati e Cl a livello del tubulo renale,
che all’incapacità di eliminare prodotti di rifiuto e ioni H+
da parte del rene ipofunzionante.
225
Glucocorticoidi (GC)
I glucocorticoidi (Cortisolo) sono secreti principalmente
dalla zona fascicolata ma anche dalla zona reticularis che sono a loro volta stimolate dall’ipofisi anteriore mediante
l’ACTH che a sua volta è sotto l’influenza dell’ipotalamo
mediante il CRH (fattore di rilascio della corticotropina). Il
cortisolo è uno stimolatore della gluconeogenesi e glicogenesi da parte del fegato e del muscolo, aumenta il catabolismo proteico e lipidico, stimola l’eritrocitosi, sopprime lo
stimolo infiammatorio e la reazione del tessuto linfoide, aiuta il mantenimento della pressione sanguigna sistemica ed ha
un effetto protettivo sulla mucosa intestinale. I GC sono secreti mediante l’asse ipotalamo-ipofisi-surrene (v. fig. 2) che
risponde a vari stimoli stressanti per l’organismo.
Ormoni sessuali
Non sembra che in caso d’ipoadrenocorticismo, si manifestino sintomi clinici da ridotta secrezione di ormoni
sessuali.
SEGNALAMENTO, ANAMNESI,
ESAME FISICO
Malattia poco frequente nel cane e rara nel gatto. Colpisce soprattutto le femmine (68%), come sembra succeda per
tutte le malattie immunomediate e, nel 70% dei casi, cani con
meno di sette anni di età (media 4-5 anni), non sembra esserci una predilezione di razza (dati personali: 1 barboncino, 1
meticcio pastore maremmano, 1 chihuahua, 1 pincher ecc.).
Molto spesso i primi sintomi non sono capiti dal proprietario che magari si accorge del problema solo quando il
cane sta veramente male, quindi la valutazione dei segni clinici è molto soggettiva. Comunque i segni più comuni sono,
in ordine di frequenza: anoressia, debolezza, depressione,
magrezza, vomito, diarrea, collasso(tutti secondari a carenza
di cortisolo), poliuria da medullary wash-out (situazione in
cui il gradiente di concentrazione della midollare renale è
notevolmente diminuito per la carenza di sodio e quindi, per
i motivi suddetti, avremo una perdita di una grande quantità
di acqua), dolore addominale, tremori.
La malattia è spesso episodica, anche se il proprietario
non se ne accorge e spesso porta il cane dal veterinario solo
quando è in crisi addisoniana. Qualche volta il proprietario
descrive dei miglioramenti in caso di somministrazione parenterale di fluidi o di trattamenti cortisonici.
L’esame fisico è scarsamente significativo, infatti il sintomo più comune appare la depressione, la magrezza e la debolezza, quindi sintomi vaghi, solo occasionalmente si può
trovare bradicardia (30%) polso femorale debole o melena(20%), comunque imputabili anche ad altre malattie.
PATOLOGIA CLINICA
Nel 20 – 30% dei cani affetti da ipoadrenocorticismo è
presente una lieve anemia normocitica, normocromica e
226
scarsamente rigenerativa, magari mascherata dalla disidratazione. La presenza di melena e ulcere gastroenteriche, ovviamente, aggrava lo stato anemico.
I globuli bianchi, spesso, sono normali come numero totale ed inoltre l’eosinofilia e la linfocitosi che vengono citate come secondarie all’ipoadrenocorticismo, sono rare da
trovare in cani addisoniani non malati. Invece se ho un cane
in crisi addisoniana o molto malato e con eosinofili normali
o bassi e/o con linfociti normali o alti mi devo insospettire.
Eventualmente, per valutare grossolanamente la funzionalità
surrenalica senza dosare il cortisolo, si misurano i globuli
bianchi prima e dopo 4 ore dalla somministrazione (Test di
Thorn modificato) di ACTH. In cani normali ci dovrebbe essere un aumento post-ACTH del rapporto neutrofili:linfociti
di almeno il 30% e una diminuzione del 50% del rapporto
neutrofili:eosinofili. Come detto la perdita di sodio si accompagna a perdita di acqua e la disidratazione che ne consegue può mascherare un po’ l’iposodiemia. In ogni modo
più del 90% dei cani in insufficienza corticosurrenale primaria sono iponatriemici e iperpotassiemici e hanno il rapporto
Na/K inferiore a 27. Comunque, dato che la malattia ha un
andamento graduale e progressivo ma anche altalenante, non
bisogna affidarsi, in caso di sospetto, solo agli elettroliti ma
soprattutto al test da stimolazione con ACTH. Infatti, queste
alterazioni si possono presentare anche in corso di malattie
gastrointestinali oppure di problemi delle vie urinarie o di
insufficienza renale. Tuttavia la presenza delle suddette modificazioni elettrolitiche in un cane con debolezza, anoressia,
vomito e/o diarrea anche saltuarie, sono suggestive di morbo di Addison.
In caso di iperpotassiemia sono varie le diagnosi differenziali da fare, anche se tale problema va curato indipendentemente dalle cause che la determinano, le più comuni sono patologie delle vie urinarie in particolare l’insufficienza
renale acuta, un danno traumatico con rottura di vescica e/o
uretere od anche problemi ostruttivi. Altri possibili motivi di
disturbi elettrolitici tipo Addison sono alcune gravi patologie
gastroenteriche come massiccie infestazioni parassitarie, parvovirosi, torsione gastrica, ulcera duodenale perforata ecc. Si
può avere iperkalemia anche per un rapido rilascio di potassio secondario ad un grave stato acidosico di qualsiasi origine oppure ad un esteso danno tissutale (trauma, chirurgia
molto traumatica ecc.) ma anche ad una grave infezione, una
trombosi aortica o un episodio di rabdomiolisi.
Anche in caso di effusione chilosa pleurica si possono
avere tali anomalie elettrolitiche. La somministrazione di
farmaci a base di K oppure anche ACE inibitori e NSAID
possono provocare una lieve iperkalemia. Comunque quando si trova una iperpotassiemia, bisogna considerare la possibilità di artefatti dovuti all’emolisi, alla separazione siero/sangue ritardata ed ancora alla piastrinosi (>1.000.000) e
alla leucocitosi grave (>100.000). Inoltre la razza Akita ha
una quantità di K nelle sue emazie, molto più alta del normale per cui è sufficiente un contatto tra rossi e plasma in
frigo per alterare la potassiemia.
In caso di iponatriemia, le diagnosi differenziali possibili sono: malattie del tubulo renale, sindrome nefrotica e diuresi post-ostruttiva. Nel diabete mellito la diuresi osmotica
che ne consegue può provocare un’iponatriemia, aggravata,
in questo caso, dall’iperglicemia che provoca un richiamo di
acqua da intra a extracellulare e conseguente diluizione plasmatica. Il sodio si può perdere anche per gravi malattie gastrointestinali che provochino vomito e diarrea profuse. Anche possibili cause di edema (sindrome nefrotica, insufficienza cardiaca congestizia ecc.) portano a sequestro di Na
oltre a malattie che provocano grave polidipsia come il diabete insipido e la poliuria/polidipsia psicogena. Inoltre ci sono anche cause iatrogene d’iposodiemia come una diluizione del sangue con fluidi senza Na (soluz. glucosate) o numerosi svuotamenti pleurici. Come già detto, in corso di
ipoadrenocorticismo c’è un’iperazotemia prerenale a causa
di una diminuita filtrazione glomerulare e quindi con abbassamento del GFR secondari all’ipovolemia, alla riduzione
della gittata cardiaca e all’ipotensione. Questi problemi sono una diretta conseguenza di una perdita cronica di fluidi
attraverso il rene per la diuresi del Na, inoltre il vomito e la
diarrea oppure la gastroenterite emorragica possono aggravare l’iperazotemia.
A differenza dell’azotemia, la creatinina rimane normale
o si alza di poco forse a causa della gastroenterite emorragica
che fornisce un ottimo substrato di ammonio che viene convertito a urea dal fegato, ma il vero motivo non è conosciuto.
Riguardo al peso specifico, che nell’azotemia prerenale
dovrebbe essere maggiore di 1030, in questo caso rimane,
nel 96% dei casi, inferiore a 1030 e quindi non è possibile la
differenziazione con un’insufficienza renale classica. La ridotta concentrazione delle urine deriva dalla perdita cronica
di sodio che provoca una diminuzione del gradiente di concentrazione della midollare renale e quindi un’incapacità a
riassorbire l’acqua da parte del tubulo renale.
Una BUN e CREA elevate in un paziente addisoniano ritornano, di solito, nei range di normalità dopo 24-36 h di
fluidoterapia e questo deve farci insospettire. Le eccezioni
riguardano ovviamente pazienti non-addisoniani, oppure pazienti addisoniani in cui l’ipoperfusione cronica renale e l’ipossia hanno provocato un danno permanente al rene. Inoltre se i sintomi correlati con l’Addison, si presentano in pazienti nefropatici o cardiopatici, allora le cose si complicano
e sarebbe necessaria una valutazione della pressione venosa
centrale (PVC) tramite un catetere giugulare per evitare il rischio di somministrare un eccesso di fluidi. Infatti, se la
PVC è bassa si deve insistere con la fluidoterapia, ma se è alta allora significa che c’è un’insufficienza cardiaca o renale.
Comunque anche in caso d’ipoadrenocorticismo puro, può
succedere che i valori renali rientrino nella norma dopo più
giorni di fluidi.
Circa il 30% dei cani Addisoniani, hanno ipoglicemia
(<70mg/dl) che in qualche caso può dare anche sintomi clinici, la causa di quest’ipoglicemia è da ricercare nella carenza di cortisolo, anche se, in generale, i motivi più probabili di ipoglicemia sono altri come l’iperinsulinismo, una sepsi avanzata, una epatopatia grave.
Sempre nel 30% dei casi di ipoadrenocorticismo si può
trovare una ipercalcemia che sembra avere forte correlazione con l’iperkalemia. Comunque le cause potrebbero essere
la scarsa perfusione renale che determina una diminuita
escrezione renale di Ca e un maggiore riassorbimento dei tubuli. Inoltre, poiché un’iniezione di cortisone fa abbassare la
calcemia, si pensa che ci sia una stretta correlazione tra ipocortisolemia e ipercalcemia.
In conseguenza dell’insufficiente perfusione renale e della diminuzione della GFR in corso di Addison si verifica anche un aumento dei fosfati inorganici. In ogni modo le cause di ipercalcemia sono molteplici ma se mettiamo assieme
iperCa, iperK, iperazotemia, ipoNa, iperfosfatemia, le uniche possibili sono: insufficienza renale, Addison e intossicazione da vit.D. In corso di ipoadrenocorticismo con ipoaldosteronismo viene ridotta la escrezione renale di H+ ed in più,
a livello tissutale, la perfusione non è ottimale quindi una alta percentuale di questi cani è in acidosi metabolica, ma solo raramente è richiesta una terapia a base di bicarbonato.
Circa il 38% dei cani addisoniani, presentano un’ipoalbuminemia che si pensa sia dovuta alle perdite gastrointestinali ed ad una diminuita sintesi epatica.
Ci può essere una correlazione tra una malattia epatica e
il morbo di Addison, infatti in corso di epatopatia si può riscontrare: aumento di ALT e AST, ipoalbuminemia, ipocolesterolemia, ipoglicemia e microepatia. ma due o più di queste anomalie vengono spesso rilevate anche in corso di Addison in cui, a volte, si riscontrano anche alterazioni degli
acidi biliari e degli enzimi epatici. Per queste ragioni, oltre a
porsi il problema di una diagnosi differenziale, si potrebbe
anche verificare che una concomitante epatopatia sia presente in un cane addisoniano. Infatti l’ipoglicemia, l’ipoalbuminemia ed anche le alterazioni negli enzimi epatici le
posso spiegare con l’ipoadrenocorticismo, ma l’ipocolesterolemia, la microepatia e gli acidi biliari alterati possono essere spiegati solo da una contemporanea insufficienza epatica. In questi casi si tratta prima l’Addison e poi si rivaluta la
situazione, spesso migliorano entrambe le condizioni.
227
PROCEDURE DIAGNOSTICHE
DI CONFERMA
Cortisolemia basale e steroidi urinari
Sono test poco usati perché non valutano la riserva cortico-surrenale di cortisolo ed inoltre nel caso degli steroidi
urinari, richiedono un dosaggio nelle 24h.
Test da stimolazione con ACTH
È il test di scelta sia per il cane che per il gatto e deve essere sempre preceduto dagli esami detti prima (emogramma,
profilo biochimico, emogasanalisi, ECG, ecografia surrenalica), perché si deve considerare un test di approfondimento.
Si può usare sia l’ACTH naturale sia quello di sintesi. Si fa
un prelievo di sangue prima e dopo 1 ora dalla somministrazione di 0,25mg di ACTH sintetico IM o EV (disponibile in
Italia con il nome di Synacten®). L’intervallo di riferimento
della cortisolemia pre e post ACTH dipende dal laboratorio
in cui si esegue l’esame comunque i valori medi basali del
cortisolo sono circa 0,1 – 6 mcgr/dl mentre i valori post
ACTH variano da 6,5 a 15 mcgr/dl. I cani addisoniani, di solito, hanno il cortisolo sia pre che post-ACTH, inferiore a
1mcgr/dl. Uno dei limiti di questo esame è che non differenzia cani con ICSP da quelli con ICSS e neanche i cani cui è
stato somministrato il Mitomane da quelli con ICSP.
Dosaggio Aldosterone
Esame radiografico ed ecografico
Spesso si fanno radiografie a cani malati o che vomitano,
in caso di Addison si potrebbe vedere una microcardia, la vena cava caudale e l’aorta discendente più piccole, inoltre i
campi polmonari appaiono ipoperfusi e comunque questi reperti radiografici indicano la presenza di un’ipovolemia associata ad ipoperfusione ma non sono patognomonici di
morbo di Addison. Raramente si può riscontrare un megaesofago. Inoltre sembra, da uno studio ecografico di Reusch e
coll. (JAAHA 1998) fatto su sei cani addisoniani, che le surrenali possono diminuire diminuite in spessore e lunghezza
Elettrocardiogramma
Le alterazioni dell’ECG sono secondarie all’iperkalemia
ed in particolare, con valori di potassio superiori a 6-6,5
mEq/L c’è una depressione della conduzione per cui se auscultiamo una bradicardia oppure sospettiamo un Addison, si
dovrebbe sempre eseguire un ECG. Quando il valore di K+
sale a 5,5-6,5mEq/L, si vede un rallentamento del ritmo e le
onde T appaiono alte e a punta. In caso di potassiemia che arriva a 6,5 - 8,5 mEq/L diminuisce l’ampiezza delle onde R si
allarga il QRS, si prolunga lo spazio PR e l’onda P appare di
voltaggio minore e di durata aumentata. Come il valore di K
supera 8,5 mEq/L, scompare l’onda P (si può confondere con
una fibrillazione atriale) e il segmento ST si slivella.
Nei casi dubbi, in cui si sospetta la possibilità di un Addison secondario oppure una forma subclinica o quando la distruzione interessi solo la zona glomerulosa (cortisolo), si
può dosare l’aldosterone nel sangue. Tale dosaggio dovrebbe
essere eseguito prima e dopo la somministrazione di ACTH
che comunque ne stimola la sintesi. Tale esame in base alle
conoscenze odierne è di puro valore accademico in quanto ci
servirebbe solo in rarissimi casi di pazienti addisoniani.
ACTH endogeno
Il principio su cui si basa quest’accertamento è che, nei
casi di ipoadrenocorticismo primario l’ipofisi funziona quindi produce ACTH che però non riesce a stimolare le surrenali, mentre se c’è un problema ipofisario o ipotalamico come nell’Addison secondario, allora la quantità di ACTH nel
sangue è più bassa del normale. Il problema che si incontra
nel dosare l’ormone corticotropo endogeno, risiede nell’estrema deperibilità della molecola nel sangue, per cui l’esame andrebbe eseguito subito ed il campione spedito, dovrebbe essere mantenuto sempre congelato.
Nei cani normali il valore dell’ACTH endogeno varia da
45 a 110 pg/ml. In più del 90% dei casi di Addison primario,
il valore dell’ACTH è superiore a 400pg/ml che è stato preso come valore di riferimento in quanto nei casi di iperadrenocorticismo ipofisario (PDH), altra causa di aumento dell’ACTH endogeno, l’ACTH è comunque elevato ma di un
228
valore inferiore a 400pg/ml. Questo vuol dire che nei cani
con ipofisi normale ma in mancanza di feed-back negativo
(ICSP) i valori di ACTH sono maggiori rispetto a quelli con
tumori ipofisari (PDH).
Nell’ICSS, l’ACTH endogeno è normale o basso ed inoltre gli elettroliti sono nella norma. In questi casi di ipoadrenocorticismo secondario, l’aldosterone ha un valore molto
basso a dimostrare che l’ACTH stimola, come già detto, la
produzione di aldosterone anche se, in questo caso, i livelli
bassi di aldosterone non hanno effetti clinici.
Riassumendo, dando per scontato che il dosaggio di
ACTH nei pazienti addisoniani sia di puro interesse accademico, i cani con ipoadrenocorticismo ed ACTH endogeno
estremamente alto (>400) hanno un Addison primario mentre
quelli con elettroliti normali ed ACTH endogeno normale o
basso sono affetti da un Addison secondario. Se troviamo una
situazione descritta nella prima ipotesi (ICSP) ma gli elettroliti sono normali, allora si tratta di una forma latente di Addison primario, peraltro situazione molto rara, che svilupperà le
alterazioni elettrolitiche caratteristiche in tempi successivi.
TERAPIA DELLE CRISI ADDISONIANE
Una rapida scelta terapeutica è vitale e dovrebbe avere i
seguenti obbiettivi: correggere ipotensione e ipovolemia, migliorare l’integrità vascolare e fornire un’immediata fonte di
glucocorticoidi (comunque anche solo la fluidoterapia è
spesso sufficiente a risolvere il problema, perché a meno che
non tratti di una ricaduta di un paziente già sotto cura per
Addison, la somministrazione di cortisone esogeno mi complica la capacità diagnostica), correggere gli squilibri elettrolitici, correggere l’acidosi metabolica, confermare la diagnosi. In ogni modo, scendendo sul pratico, la situazione tipica che si presenta in questi casi è di un cane gravemente
prostrato, disidratato, con pochissime indicazioni sia anamnestiche che cliniche sulla possibile diagnosi. La chiave di
lettura di queste situazioni è il dosaggio degli elettroliti (magari con emogasanalizzatore che ci dà notizie anche dello
stato di acidosi e di ossigenazione del cane), che ci permette di iniziare la corretta fluidoterapia e ci potrebbe, soprattutto se troviamo una grave iponatriemia con contemporanea
iperpotassiemia ed acidosi metabolica, indirizzare verso una
diagnosi corretta, magari avvalorata da un miglioramento significativo del paziente dopo 24-36 ore di terapia fluidica. In
ogni caso, anche se non si tratta di Addison, trattare in forma sintomatica, l’iperpotassiemia, l’iposodiemia magari l’ipoglicemia non costituisce un errore terapeutico. Ovviamente, prima di formulare la diagnosi definitiva sono indispensabili tutti i test di approfondimento appropriati.
Ipovolemia
Spesso il decesso in caso di ICSP è causato, non tanto
dall’iperpotassiemia, ma dallo shock ipovolemico quindi il
trattamento chiave è la fluidoterapia intensiva. Il fluido di
scelta dovrebbe essere la soluzione salina NaCl allo 0,9%.
La dose dei fluidi è di 60 – 80ml/Kg/ora che dipende dalla
% di disidratazione, dalla quantità di urine emesse e dalle
perdite stimate con vomito e diarrea. Tenendo presente tutto
questo e valutando sia la pressione sanguigna sistemica che,
se possibile, la PVC questa dose si mantiene per le prime
ore. Dopo si passa ad una dose di 90 – 120ml/Kg/24 ore per
36–48 h. A questo punto la volemia dovrebbe essere stata recuperata, con una riduzione della potassiemia ed anche un
aumento della funzione renale e correzione dell’acidosi. Se
il cane è anurico si potrebbe anche iniziare una terapia con
pompa ad infusione a base di dopamina a basse dosi (2 – 5
µgr/Kg/min). Inoltre, se necessario va corretta anche l’ipoglicemia con soluzioni di glucosio al 33% data endovena alla dose di 2ml/Kg in bolo unico.
Glucocorticoidi
Una volta fatti i prelievi per il test ACTH, si somministra
Idrocortisone alla dose di 5mg/Kg in bolo unico e poi si
mantiene un dosaggio di 1mg/Kg ogni 6 ore. Preferisco l’idrocortisone a causa dei suoi effetti anche mineralcorticoidi.
In caso di grave shock si possono somministrare anche dosi
più alte fino a 50mg/Kg di idrocortisone. Si può ricorrere anche al Metilprednisolone Sodio Succinato (Solu-medrol®)
alla dose di 4-20mg/Kg in bolo unico e poi ripetuto ogni 46 ore. Una volta che il paziente è stabile, la dose di mantenimento di glucocorticoidi è 0,2mg/Kg al giorno di prednisone/prednisolone oppure 0,05 – 0,1 mg/Kg al giorno di Desametazone.
Squilibri elettrolitici
Come già detto è indispensabile, soprattutto nei casi molto gravi, misurare Na e K anche indirettamente con un ECG
che permette una valutazione grossolana della potassiemia.
Una volta diagnosticata l’iponatriemia e l’iperpotassiemia,
la sola fluidoterapia con NaCl 0,9% suddetta dovrebbe essere sufficiente a correggere i problemi elettrolitici. In caso di
grave iperpotassiemia per dare una protezione al miocardio,
peraltro raramente necessaria nei casi di Addison, si può
somministrare calcio-gluconato al 10% alla dose di 0,5 –
1ml/Kg in 10 – 20 minuti sotto controllo ECG continuo. A
questo punto, soprattutto se vogliamo mantenere costante la
stabilizzazione degli squilibri elettrolitici, si dovrebbero
somministrare dei mineralcorticoidi con il desossicorticosterone acetato (DOCA, ovvero il Cortico CE® - Teknofarma)
alla dose di 0,2 – 0,4mg/Kg IM una volta al dì oppure il desossicorticosterone pivalato (DOCP, ovvero il Percorten-V®
-Novartis). alla dose di 2,2mg/Kg IM o SC ogni 25 giorni.
Oppure dove la terapia iniziale ha funzionato bene si può
passare alla somministrazione orale di fludrocortisone (Florinef® - Squibb) alla dose di 0,015 – 0,02 mg/Kg al giorno.
Di questi farmaci l’unico disponibile in Italia per uso veterinario è il Cortico CE®, mentre esistono in Italia due farmaci
per uso umano che potrebbero essere usati, solo in condizioni di urgenza, a tale scopo. Uno di questi è il cortisone acetato (Cortone acetato®) che è un glucocorticoide ma che ha
anche attività mineralcorticoide simile all’idrocortisone.
L’altro è un mineralcorticoide iniettabile il desossicortone
(Cortiron® Shering) di cui, però, ci sono solo le dosi per uso
umano e cioè 10-20mg al giorno a persona. Di quest’ultimo
farmaco esiste, sempre per uso umano anche il prodotto “depot” sotto forma di desossicortone enantato che va somministrato alla dose di 1-3 fiale a persona ogni 21 giorni.
Acidosi metabolica
Normalmente le terapie suddette sono sufficienti per correggere anche lo stato acidosico, ma nel caso che il bicarbonato sia inferiore a 12mEq/L si dovrebbe trattare l’acidosi
somministrando bicarbonato alla dose, espressa in mEq, secondo la formula: peso corporeo x 0,4 x il deficit di base
calcolato sottraendo la CO2 totale normale (22mEq/L) da
quella misurata sul cane. A questo punto somministriamo
solo il 25% di questa dose nelle prime 6 – 8 ore e dovrebbe
essere sufficiente. La somministrazione di HCO3 favorisce
anche il passaggio del K da extra a intracellulare perciò diminuisce anche l’iperpotassiemia.
Nelle prime ore dall’inizio della terapia il cane dovrebbe
mostrare un deciso miglioramento a volte miracoloso, anche
dei parametri laboratoristici (Na, K, BUN, CREA,) e se questo avviene avremo un’ulteriore conferma diagnostica. In
ogni caso la terapia con fluidi dovrebbe essere mantenuta
per almeno 48 ore e dopo 24 ore di trattamento il cane si lascia bere e se non vomita, si dimezza la terapia con fluidi. A
questo punto si può introdurre il cibo facilmente digeribile,
come Jocc® e riso e se dopo l’introduzione di cibo e acqua il
cane non vomita si sospende la fluidoterapia.
A questo punto si riduce la dose dei glucocorticoidi fino
a quella minima efficace, che dovrebbe essere per il prednisone/prednisolone 0,22mg/Kg oppure per il desametazone
0,01 – 0,05mg/Kg, ma spesso sono sufficienti i mineralcorticoidi a risolvere il problema. Il cane dovrebbe rimanere
ospedalizzato per 1-2 giorni dopo la sospensione della fluidoterapia e quindi si dimette raccomandando un controllo
dopo 1-2 settimane quando dovranno essere controllati
ECG, BUN,CREA,Na e K e GLU, quindi,se tutto è a posto,
il controllo successivo dovrà essere fatto mensilmente per
sei mesi e quindi ogni 3 – 4 mesi.
POSSIBILI PROBLEMI TERAPEUTICI
Se il cane non recupera rapidamente con le terapie suddette, la causa più probabile è un errore diagnostico. In caso di
diagnosi sicuramente confermata, si deve pensare a lesioni ulcerative gastroenteriche ed anche agli effetti dell’insufficienza
renale che potrebbero essere permanenti, valutare anche la possibilità di una concomitante epatopatia. Raramente ci possono
essere dei pazienti addisoniani che pur avendo i parametri renali e gli elettroliti normali, non migliorano clinicamente nel
senso che continuano a manifestare depressione, letargia, inappetenza. In questo caso forse c’è una carenza anche di glucocorticoidi, perciò sarebbe bene aggiungere prednisone alla dose di 0,22mg/Kg BID per 2-4 settimane e se funziona mantenere detta terapia una volta al giorno. Le epatopatie si risolvono spesso con il trattamento dell’Addison. In teoria la grave
iponatriemia può portare anche ad edema cerebrale e quindi a
danno delle strutture nervose ma sono sempre casi rari.
229
TERAPIA DI LUNGO PERIODO
PER L’IPOADRENOCORTICISMO
PRIMARIO
Una volta che la situazione si è stabilizzata, si passa alla
terapia cronica che in genere richiede solo mineralcorticoidi,
ma qualche volta la corteccia surrenale è distrutta in modo
così esteso da rendere necessaria anche la terapia con glucocorticoidi.
MINERALCORTICOIDI
Fludrocortisone
Il farmaco di nome Florinef® (Squibb), non reperibile in
Italia, si trova sotto forma di compresse da 0,1mg ciascuna e
la dose proposta all’inizio è 0,015 – 0,02mg/Kg in dose unica giornaliera oppure suddivisa ogni 12 ore, quindi da 1,5 a
2 compresse al giorno ogni 10Kg di peso. I controlli su Na,
K, BUN, CREA e GLU dovrebbero essere eseguiti dopo 12 settimane dall’inizio della terapia e quindi ogni mese per 6
mesi. Successivamente è sufficiente un controllo due volte
l’anno. La terapia con fludrocortisone spesso deve essere
progressivamente aumentata per i primi 16-18 mesi di terapia, forse per la progressiva distruzione della corteccia surrenale residua, perciò da una dose iniziale di
0,013mg/Kg/die si deve passare ad un dosaggio di
0,022mg/Kg/die. I vantaggi dell’uso del Florinef sono legati alla sua breve emivita e quindi dalla possibilità di modulare il dosaggio in base agli elettroliti. Lo svantaggio è che il
fludrocortisone ha anche una spiccata attività glucocorticoide, paragonandolo all’idrocortisone, è 125 volte più potente
come mineralcorticoide ma anche 10 volte più potente come
glucocorticoide, quindi nel solito farmaco le due attività non
sono divisibili. La conseguenza di ciò è che se io devo somministrare una dose piuttosto alta di fludrocortisone per ottenere l’effetto mineralcorticoide, come conseguenza, potrei
avere i sintomi di Cushing iatrogeno, quindi poliuria/polidipsia, incontinenza urinaria, polifagia, perdita di pelo. Sotto
quest’aspetto potrebbe succedere che alla dose di Florinef®
idonea per non avere sintomi di Cushing, non si riesca a raggiungere una natriemia soddisfacente, in questo caso si potrebbe supplementare la dieta con sale da cucina. Nei casi
dove questi problemi non sono risolvibili, sarebbe necessario passare alla terapia con DOCP.
Desossicorticosterone pivalato (DOCP)
Si tratta di un estere del desossicorticosterone, a lunga
azione, in soluzione microcristallina. Il nome commerciale
del prodotto veterinario, peraltro non disponibile in Italia è
Percorten-V® (Novartis). Si può somministrare sia per via IM
che SC, l’efficacia non cambia. La dose raccomandata è di
2,2mg/Kg da somministrare ogni 25 giorni. Dato che il
DOCP ha quasi esclusivamente attività mineralcorticoide,
può essere necessario somministrare anche il prednisone alla
dose di 0,22mg/Kg ovviamente valutando gli effetti glucocorticoidi. Dopo 12 giorni dall’iniezione di DOCP si devono
230
dosare Na, K, BUN e CREA se ci sono ancora alterazioni da
Addison, la dose successiva si dovrebbe aumentare del 10%,
se invece il controllo al giorno 12 è normale ma non è quella
al giorno 25, la dose successiva si dovrebbe anticipare di 48
ore. Si proseguono questi controlli fino al raggiungimento
della dose e dell’intervallo ottimali e quindi si controlla mensilmente e semestralmente come detto per il Florinef®. Comunque questo sembra essere il trattamento più pratico da
usare poiché solo in una piccola percentuale (3 – 4%) dei casi trattati si è reso necessario un aggiustamento della terapia.
Glucocorticoidi
Spesso questi cani non necessitano di terapia con glucocorticoidi, comunque all’inizio del trattamento con mineralcorticoidi si dovrebbe aggiungere anche prednisone/prednisolone alla dose di 0,1 – 0,2mg/Kg/die che dovrebbe essere
raddoppiata o anche decuplicata in caso di condizioni stressanti: interventi chirurgici, anestesie, traumi, gare di lavoro,
viaggi ecc.
TERAPIA PER L’IPOADRENOCORTICISMO
SECONDARIO
Malattia spontanea
Condizione molto rara, ma che comunque richiede solo
una terapia con glucocorticoidi perché, sebbene l’aldosterone sia a livelli bassi, l’attività mineralcorticoide è sufficiente
a mantenere Na e K a livelli normali.
SOVRADOSAGGIO DI o,p’-DDD
(Lysodren®)
Una situazione che può capitare nei pazienti in cura per
PDH è il sovradosaggio di Mitotane, in questo caso si presentano sintomi da carenza di cortisolo e quindi anoressia,
vomito, diarrea e debolezza. Se gli elettroliti sono normali si
somministrano solo glucocorticoidi, se invece gli elettroliti
sono alterati, si devono dare anche i mineralcorticoidi
CUSHING IATROGENO
Questo è il caso di Addison secondario più frequente. La
somministrazione di cortisone va ripresa al più presto usando il prednisone/prednisolone alla dose di 0,25mg/Kg/die
per sette giorni, quindi si inizia la terapia a giorni alterni per
altre due settimane e poi si passa ad una dose ogni tre giorni e dopo 2-3 settimane possiamo sospendere il cortisone,
magari valutando la situazione con un test da stimolazione
con ACTH per vedere se l’asse ipofisi-surrene ha ripreso a
funzionare.
PROGNOSI
La prognosi del morbo di Addison primario è ottima anche sul lungo periodo, ma solo se il proprietario collabora e
somministra la terapia in modo preciso. È molto importante,
nei cani con Addison, prevenire le eventuali situazioni stressanti come traumi, interventi chirurgici, malattie, ecc. somministrando glucocorticoidi alle dosi suddette.
231
Antimicrobials in reptile patients
Douglas R. Mader
MS, DVM, Diplomate, ABVP, Marathon Veterinary Hospital, USA
Several new studies on the pharmacokinetics of various
antimicrobials have been published or reported over the past
few years. This new information adds to our armamentarium
in the fight against bacterial pathogens in herp patients. The
key is taking the laboratory data and applying it in a clinical
setting.
It has been well established that the majority of bacterial
pathogens affecting reptile patients are of the gram negative
type. However, proper isolation and evaluation of the resulting laboratory data can often times be somewhat confusing.
The practice of treating all gram negative isolates is no
longer acceptable as it is now realized that many reptiles harbor gram negatives as part of their normal flora, and are either commensals or opportunists.
There are a number of factors which must be considered
when choosing an antibiotic. The results of microbiological
culture and sensitivity testing, the species being treated,
physical condition of the patient, frequency of administration, cost of the therapy, owner compliance, and a host of
other factors are all important.
The veterinary clinician must have a thorough understanding of reptile physiology and biology prior to administering medications. Since all reptiles are ectotherms, and
their metabolism is temperature dependent, they will often
react unpredictably to the same drug in different settings. A
good working knowledge of the more common species of
reptiles, their life histories and their peculiarities will help
prevent potential disasters during therapy.
tant decrease in body clearance could potentially allow a
build up in concentration of the drug to a point where it
might reach toxic levels if dosing is not decreased accordingly.
When reptile pathogens are treated at higher temperatures the Mean Inhibitory Concentration (MIC) needed to
achieve effective treatment significantly decreases. This allows for a lower dose of antibiotic to be given, another positive factor when dealing with potentially nephrotoxic drugs.
Most researchers feel that it is best to treat sick reptiles
near the higher end of their preferred optimum temperature
zone. Not only is it beneficial for reasons already mentioned,
but elevated ambient temperatures have been shown to stimulate the host’s immune system and aid in fighting disease in
other ways already discussed.
When selecting the appropriate antibiotic it is important to
consider the status of the host’s immune system. In critically
ill or immuno-compromised reptiles, bactericidal, rather than
bacteriostatic antibiotics are preferable. In cases of gram negative sepsis, especially with Pseudomonas infections, the reptile patient is often severely immunocompromised.
In many cases the animals are infirmed because they
have been immunocompromised due to improper husbandry
conditions. The most common cause is from being maintained at suboptimal environmental temperatures.
METHODS OF ADMINISTRATION
GENERAL CONSIDERATIONS
ORAL ADMINISTRATION
OF MEDICATIONS
Before treatment is initiated the patient should be given
a thorough exam including a CBC and serum profile (including uric acid). Dehydrated or hyperuricemic patients
should be properly rehydrated prior to initiating therapy. It is
the rare case that cannot wait one to two days to assure appropriate hydration prior to treatment. However, if for some
reason treatment must be instigated immediately, it would
behoove the practitioner to choose a non-nephrotoxic drug.
Another important consideration is the ambient temperature of the reptile’s environment. Pharmacokinetic studies
have shown that an increase in ambient temperature tends to
increase both the volume of distribution and body clearance
of the drug. A decrease in ambient temperature with a resul-
In the past it was believed that eneteral medicaitons were
ineffective in herp patients. New studies have shown this not
to be true. When herps are maintained at their preferred optimum temperature zone they are capable of absorbing oral
medications in manners similar to their mammalian counterparts (assuming there are no complicating factors, such as
gastrointestinal pathology, to prevent oral absorption). Enteric infections may warrant oral administration of appropriate drugs.
If the patient is still feeding the antibiotic can be mixed
with the food or injected into the dead prey and fed to the animal. Gavaging, or stomach tubing, is a second technique
which can be used to administer oral medications.
232
TOPICAL THERAPY
It is not uncommon to treat the oral cavity itself. This is
done in cases of severe Infectious Stomatitis where the oral
cavity is abscessed. Since the vascularity to an abscessed
oral cavity is usually compromised, antibiotics given systemically may not be able to reach adequate therapeutic levels in the infected tissues. Aminoglycoside antibiotics have
decreased activity in anaerobic or acidic environments.
When treating with a drug like enrofloxacin systemically
you can also use topical flouroquinolone on the lesions in
the oral cavity. Daily application of Ciloxin® ophthalmic solution, one drop on each affected area, appears to be a clinically effective adjucnt to systemic flouroquinolone therapy.
Silvadene® is a soft, white, water-miscible cream containing the antimicrobial agent silver sulfadiazine. This
bactericidal cream is effective against a broad range of
both gram positive and gram negative bacteria, including
Pseudomonas aeruginosa, as well as some of the yeasts. Sil-
vadene® is easily applied with a cotton tipped swab or other
applicator. A dressing is not necessary unless the area being
treated is in a location where the cream may be rubbed off.
Otherwise, the cream will last for two to three days before a
new application is required.
INJECTABLE ANTIBIOTIC THERAPY
Injectable antibiotics are probably the best form for assuring proper delivery of the drug. The antibiotics are either
injected intramuscularly, or less commonly, subcutaneously.
The intravenous route is often limited by the availability of
venous access. The size and species being treated will determine whether intravenous infusion is possible.
Reptiles have an anatomical variation called the renal
portal system. In general, blood leaving the tail and pelvic
limbs passes through the kidneys before returning to the
heart. Recent papers suggest that avoidance of the renal por-
Table 1 - Common bacterial isolates, their pathogenicity and the antimicrobials recommended to be used for their treatment. (adapted with permission from Mader DR, Reptile Medicine and Surgery, WB Saunders, 1996)
ORGANISM
PATHOGENIC†
ANTIBIOTIC OF CHOICE*
Acinetobacter spp.
Actinobacillus spp.
Aeromonas spp.
Bacteroides
Citrobacter freundii
Clostridium
Corynebacterium spp.
E. coli
Edwardsiella spp.
Enterobacter ssp.
Klebsiella spp.
Micrococcus spp.
Morganella spp.
Mycobacteria
Pastuerella spp.
Proteus spp.
Providencia spp.
Pseudomonas spp.
Salmonella
Serratia spp.
Staphylococcus spp.
coagulase positive
Staphylococcus spp.
coagulase negative
Streptococcis spp.
alpha-hemolytic
Streptococcus spp.
beta-hemolytic
+++
+++
++++
+++
++++
+++
++++
++
+++
+++
++++
No
++++
++++
+++
++++
+++
++++
? to ++++
++++
A, F
A, F
A
P, C, M
A, F
P, C, M
P, C
A
A, F
A, F
A
F, C
A, F
Tx not recommended
F
F
A
A
treatment questionable
A
+++
F, C
NO
nn
NO
nn
+++
F, C
†(+)not pathogenic; (+) to (++) opportunist to varying degress of pathogenicity; (++++) pathogenic
*nn - none needed; A - Aminoglycoside; C - Cephalosporin; F - floroquinolone; M - Metronidazole; P - Penicillin
233
Table 2. 10 Steps for Rational Antimicrobial Use
1. Initial assessment - Always perform a proper, thorough physical examination, including evaluation of the animal’s state
of repletion (starvation plays a significant role in antibiotic choice due to catabolic effects and an increase in uric acid
production), and hydration.
2. Warm the animal up to its POTZ (it is the RARE case that cannot wait for the patient to be properly warmed prior to
initiating antibiotic therapy). Monitor the patient’s body (cloacal) temperature.
3. Fluids as needed.
4. Diagnostic sample collection - blood for (CBC/chem, culture), urine (microscopic analysis, culture), specific specimen
cultures (lung wash, cloacal or colon wash), aspirate of masses, etc. (if possible, obtain blood samples prior to fluids).
5. Determination of method of administration (oral, systemic, topical). Coordinate your choice with owner experience/compliance.
6. Choice of drug - general vs. specific, single drug vs. combination therapy - see later.
7. Adjustment of dosages (correction for dehydration, renal function, bacterial culture and sensitivity results, etc.).
8. Proper follow-up and patient monitoring (recheck and progress checks, serial uric acid measurements).
9. Author’s first drugs of choice: amikacin (caution renal patients), ceftazidime, enrofloxacin, trimethoprim-sulfa.
10. Drugs for combination therapy: metronidazole, piperacillin. Example, combine amikacin with metronidazole.
Table 3. Common Antimicrobials used in Reptilian Practice
DRUG
SPECIES
ROUTE
DOSE
INTERVAL
(mg/kg)
REF
(hrs)
Amikacin
alligator
tortoise
snake
IM
IM
IM
2.25
5.0
5.0
2.5
96
48
initial
72
13
14
10
Piperacillin
snake
IM
100
24
15
Ceftazidime
snake
sea turtle
IM
IM
20
20
72
72
9
16
Doxycycline
tortoise
IM
50
25
initial
72
17
Chloramphenicol
snake
SC
50
12-72
(species dependent)
1,2
Trimethoprimsulfadiazine
all
IM
30
q 24 1st 2 doses
48 thereafter
18
Enrofloxacin Hermann’s
tortoise
Gopher tortoise
Star tortoise
green iguana
all
alligator
IM
IM
IM
IM,PO
IM, PO
IV
10
5
5
5
5
5
24
24-48
12-24
not stated
24
36(for mycoplasma)
17
19
20
21
22
23
Metronidazole
snakes
PO
20
48
24
234
tal system, as previously practiced, may not be necessary.
However, until more extensive research, with all the common pharmaceuticals has been perfomed, caution should
still be advised.
Antibiotics excreted from he body via glomerular filtration bypass this renal portal system. Antibiotics that are secreted by the peritubular capillaries are affected and have the
potential of a decreased ciruclating concentration if the medications are injected into the rear legs or the tail. The renal
portal system can be avoided by making all injections in the
cranial half of the body.
An important consideration when selecting an antibiotic
is its ability to penetrate the target tissue site. In cases of severe Infectious Stomatitis, the vascular supply may be compromised to the oral cavity in the area of the lesions. This
may prevent good penetration of the antibiotic to the site of
infection.
Another method of assuring adequate antibiotic levels to
the affected tissue is to calculate the total systemic dose,
draw it into a syringe, and then add an equal volume of bacteriostatic water to dilute it out to half concentration. Inject
three-fourths of the dose intramuscularly, and the remaining
quarter dose directly into the region of the mouth where the
infection is present. If you need to inject in more than one
place in the mouth it is a good idea to switch needles to prevent seeding of bacteria from one site to another.
FLUID THERAPY
Since reptiles are uricotelic, that is, they excrete uric acid
as the end product of protein metabolism, they are readily
susceptible to visceral gout. If the patient is dehydrated or
develops renal pathology due to treatment with nephrotoxic
drugs, the insoluble uric acid forms microcrystals called
“tophi” on the serosal surfaces and within tissues such as the
heart, lungs, liver and kidneys.
Visceral gout can be prevented by utilizing proper drug
dosages, evaluating the patient’s hydration status and monitoring blood uric acid levels throughout therapy. A follow-up
blood uric acid should be checked one to two weeks after the
treatment is finished.
The patient should be supplemented with physiologic
fluids at 15-25 ml/kg on the days it receives antibiotic treatment. The fluids can be given orally, intracoelomically, or
subcutaneously in the lateral sinus.
235
Treating burns in reptiles (wound management)
Douglas R. Mader
Thermal burns in reptiles are one of the most common
injuries seen by herp veterinarians. The exact reason why
reptiles seem so prone to burns is not understood, but, something about their behavior makes them more susceptible to
this type of injury than any other captive animal.
Since reptiles do everything slowly, it is not uncommon
for an animal to get burned, but not actually show signs of
the injury for several days. This is especially true for minor,
or first degree burns. This is significant, since burns, even
apparently mild injuries, can have severe consequences if
not treated properly. In order to be able to treat burns properly, it is important to understand what causes burns, and
how to recognize them in their early stages.
THERMODYNAMICS
As herpetologists, we are all familiar with the importance of providing proper temperatures to the cage environment. Over the years we have seen the evolution of heating
devices from the original “hot rocks” to the more advanced,
thermostatically controlled environmental chambers.
We have learned that not only must captive reptiles have
supplemental heat, but, supplemental heat provided in the
proper fashion. For instance, a fifteen foot long python
would not fare well with a single, twelve inch hot rock. Likewise, a nocturnal lizard would suffer if its cage were heated
with a bright heat lamp.
A look at animals in their natural environment will help
us understand the principles of thermodynamics from a practical perspective. As an example, let’s evaluate the heating
strategies of the ever popular green iguana living in the rain
forest.
These animals live for the sun. On an initial glance, it appears that they derive their energy-providing heat from basking in the sunlight. But, on closer inspection, there is a lot
more involved than an animal merely perched atop a branch
soaking in the sun’s rays.
Before we analyze what is happening, let’s take a step
back and review some of the principles of heat and heat
transfer. The study of heat and its properties is called thermodynamics.
In order for an object to get warm, or “heat up,” there must
be a transfer of heat from some outside source to the object
that is being heated. Heat always moves from a warmer area
to a cooler area. As the heat leaves the first object and enters
the second object, the first object becomes cooler, and the
second object becomes warmer. Eventually, the temperatures of the two objects will become equal. In other words,
they will equilibrate. Heat will never continue to leave the
first object such that it becomes cooler, resulting in the new
object becoming the hotter of the two.
There are three ways that an object can gain heat, or become warmed. These are via conduction, convection and radiant heat.
Conduction is the transfer of heat within an object (such
as down a long metal pole) or between two objects that are
touching each other. A classic example of conduction is a
pan on a stove. The burner on the stove heats up. A cold pan
is then placed on the hot burner, and the heat then transfers
from the hot burner directly to the cooler pan, thereby heating up the pan and the contents inside.
A herpetological analogy here is the use of a “hot rock.”
Hot rocks, for those not familiar with these items, are a solid, block-like structure, usually made out of brick, concrete,
plaster or heavy molded plastic. Imbedded within the rock is
some sort of heating coil. When the heating coil is plugged
in it generates heat. This heat, in turn, heats up the rock.
If a lizard (or any reptile) crawls up on the rock, the heat
from the hot rock will then transfer, via conduction, to the
lizard. The path of the heat transfers from the surface of the
hot rock, through the feet and belly and tail of the lizard, or
whatever parts of the animal are in DIRECT contact with the
rock’s surface.
Convection, on the other hand, involves the motion of
large-scale quantities of matter. In plain words, convection
usually involves the movement of either gasses (such as air)
or liquids (such as water). Heat is transferred via movement
of this matter (e.g. air or water).
For instance, consider the air over a desert. As the surface
of the desert heats up from the sun, it warms the air that
touches it (this is conduction). This warm air, which is
lighter than cooler air, then rises. As it rises, it pushes (displaces) the air above and on the sides away, forcing the cool
air back down to the earth. This cool air warms, and then follows the path of the warm air before it, upwards (convection). Hence, you get a warming effect, or a thermal, developing. Birds, hang-gliders and airplanes use these “thermals” to soar high in the sky without using hardly any energy to stay aloft.
236
Back to our iguana example, in the jungle, where it is
very hot, the warm air that blows across the animal while it
is basking, exposed, on the end of a branch, is an example of
convective heating.
Radiant heat is the last type of heat transfer. Radiation
heat transfer involves the flow of thermal energy by electromagnetic waves. In contrast to conductive heating, where
objects must be touching, or convective heating, where the
matter (gas or water) must touch the object to be heated, radiant heat does not have to have any matter involved (no
touching needed for heat transfer).
The classic example here is the fast-food hamburger under the red heat lamp. The lamp does not need to touch the
burger to keep it warm, and likewise, there does not need to
be a wind current or water flow over the lamp and the burger in order to keep the food hot.
The obvious example here is the iguana basking in the
sunlight. It is soaking up the electromagnetic radiation produced by the sun’s rays. In captivity, this source of electromagnetic radiation is replaced by any number of artificial
means - usually a heat lamp or a ceramic bulb.
So, in review, this apparently simple equation of an iguana sitting on a branch to get warm, really is a lot more complicated than it looks. The iguana in the wild gets its warmth
three ways:
1. Radiant heat - The lizard absorbs the electromagnetic
radiation from the sun.
2. Convective heat - The warm air that blows across the
animal.
3. Conductive heat - from sitting on a branch that has
been warmed by the sun. The branch then acts as a conductive heat source, passing the warmth back into the animal
resting on it.
The best type of heat source for a captive pet will depend
on the type of animal being housed. As mentioned, a small
heat rock would be inappropriate for a large snake. These animals do better with convective or radiant heat. Likewise, a
big heat lamp would not be proper for an arboreal animal
which would normally get its heat from either conduction or
convection.
There are several other variables that play important
roles in heat transfer and warming. A big factor is humidity.
Moist air, or high humidity, tends to hold heat much better
than dry heat. When figuring temperatures and thermal gradients careful attention should be paid to humidity. A hot,
humid cage will be much more stifling than a hot dry cage.
Ventilation is very important in any cage design. A well
designed cage will have good ventilation. Stagnant air, especially in hot humid cages, leads to build up of pathogens, or
disease-causing bacteria and fungi. Proper ventilation will
dilute out any potential problem before it reaches concentrations that may be dangerous.
However, for all the good that proper ventilation does, it
does have its drawbacks. A well ventilated cage tends to lose
heat and humidity (it gets exhausted outside). There is really nothing wrong with this, except that the heat and humidity needs to be replaced, and, in the overall scheme of design,
it ends up costing more to maintain a steady state of temperature and humidity.
HEAT AND TISSUE INJURY
Of the three types of heat transfer, the two that cause the
most injuries are radiant heat and conductive heat. Over the
years, I have seen several hundred burns caused by hot
rocks. These crude heating devices have variable heat output, often unevenly distributed over the surface of the rock,
and can reach temperatures that will sear the flesh off any
animal that rests on it.
In addition, I have personally seen many hot rocks that
have “shorted out.”. In one case where a hot rock shorted
out, it caught fire, setting the owner’s bedroom ablaze.
Humans have a withdrawal reflex. When we touch something hot, without any cognizant thought, we automatically,
immediately, withdraw our hand. Even young children and
mammals display this reflex. I have touched some brand new
hot rocks, and their surface has been so hot, that I have experienced the same withdrawal reflex. They are so hot, I
could not physically keep my hand on their surface.
Why then, when a reptile rests on such a “hot” hot rock,
don’t they also immediately jump off?
Nobody seems to have an easy answer for that. It is not
uncommon for a snake to wrap its coils around a bare light
bulb because it is attracted to the warmth that the light emits.
So, it must feel the warmth, why then, does it not feel the
burning heat?
One answer is that the nerve receptors that sense heat
and the receptors that sense pain are different. It is possible
that, since in the wild, such pain receptors have no evolutionary significance (reptiles do not come into contact with
intensely hot objects in the wild). Therefore, evolutionarily, there is no reason that a reptile should have a hot-pain
withdrawal reflex.
Other theories put forth suggest that since reptiles do not
reason in the same fashion that people do, or other mammals
for that matter, even though they may feel pain, they do not
associate it with the object that they are touching. Hence,
they do not realize that they need to move in order for the
pain to subside.
Bottom line is, nobody really knows. So, until we understand why these animals are so prone to burns, the best
thing to do is make every effort to prevent the burns in the
first place.
TYPES OF BURNS
Burns are classified by the type of burn and by the
severity of the injury or extent of the body surface area affected. There are three basic classifications of burns in
mammals. These categories can also be used in reptiles.
Understanding the nature of the burn will help you assess
the need for intervention. Is it something that you can handle at home, or, should it be hospitalized for competent
medical care?
The extent and severity of a burn is related to several factors. Obviously the temperature of the heat source plays a
significant role. Touching a stove burner set on “warm” will
result in a far less severe burn than touching the same burner set on “high.”
Duration of contact also affects the severity of the burn
wound. Again, touching a stove burner set on “warm” only
briefly may result in a minor burn. Whereas, holding one’s
hand on the same burner for several minutes may result in
much more severe tissue damage. This is perhaps why we
see such intense damage in reptiles that have fallen asleep
on what seems like only a mildly hot heating element like a
hot rock.
Lastly, the heat conductance characteristics of the material touched also plays a role in the severity of the burn.
For instance, touching a hot piece of metal would cause a
more severe burn than touching a piece of wood at the same
temperature.
Types of burns include thermal, electrical, chemical and
radiation. Thermal burns include all the categories that we
have discussed so far, such as burns by hot rocks and heat
lamps. An electrical burn, although not common in reptiles,
can be seen where there is direct contact with an electrical
current, such as when there is a short in a wire that has electrical arcing, or when an animal bites through an electrical
cord that is plugged into a live socket.
Chemical burns are caused by strong acids or alkalis,
such as cleaning supplies like pure bleach (an alkali agent).
These are also uncommon in reptile patients, but may occur,
especially when chemicals are spilled or agents are not thoroughly rinsed after cleaning a cage.
Radiation burns in reptiles are extremely uncommon.
These are usually related to the use of radiation therapy
when treating certain types of cancers. Since radiation therapy has been used in reptile patients, this type of burn is
possible.
In older terminology, burns used to be classified as first,
second or third degree, depending on the severity of the
damage. In more recent classification, the terms partial
thickness and full thickness burns, are more commonly used.
“Thickness” refers to the outer layer of skin.
First degree burns are superficial, or partial thickness injuries that only involve the epidermis (outer skin). These
burns are painful. In mammals there may be damage to the
hair or fur (singing). The skin is reddened, and in severe first
degree burns there may be blisters (such as in a severe sun
burn).
In reptiles, you rarely see blisters, although they may occur, and occasionally, you may see singing of the scales, depending on the type of exposure. Usually, you will see reddening of the skin, and often what looks likes “bruises” under the scales, especially in white, pale or clear scales.
These burns usually heal well and rarely leave a scar. In
an otherwise healthy reptile, healing takes about one month
and a good shed for the burn to completely resolve.
Second degree burns are deeper partial thickness injuries with usually full destruction of the epidermis, and
variable damage to the underlying dermis (inner, deep layer). In mammals, although there is more damage to the dermis, the fur or hair may not necessarily be damaged. The
burns are very painful, and extensive subcutaneous swelling
does occur. In reptiles, blistering and oozing of serum from
the burn site are seen. There is extensive bruising and discoloration of the tissue. These injuries lead to the formation
of a scab-like covering over the burn.
237
Healing occurs from the margins of the wound inward. In
these wounds, especially in burns that cover a large surface
area, healing may be prolonged and significant scarring may
occur.
In third degree burns, the entire thickness of the skin is
destroyed. The burn is actually painless (all the pain sensing
nerves are destroyed), and the tissue takes on either a whitish
or charcoal black appearance. In mammals the hair and fur
fall out or are destroyed. Third degree burns are four times
as serious as second degree burns of similar size.
Healing of third degree or full thickness burns occurs by
contraction of the wound (shrinking) and epithelialization
(re-growth and migration of new skin from the margins of
the wound toward the center). In some cases of third degree
burns, skin grafting may be necessary. These burns may take
many months (4 - 6) to heal completely. Severe scarring is a
hallmark of third degree burns.
The classification of a fourth degree burn is occasionally used to describe a third degree burn that not only involves
the full thickness of the skin, but also the underlying tissue
such as muscle and bone. These injuries carry a grave prognosis.
BURN TREATMENT
Reptiles are amazing animals. They have a penchant for
healing far greater than any mammal. Some of the wounds
that I have seen in reptiles would have spelled doom for most
other animals. Incredibly, I have also seen scars on wild reptiles that bore the legacy of previous severe wounds. Wounds
that healed without the benefit of veterinary intervention.
That does not mean that we should ignore wounds in captivity, that they will heal without help, but, it does give us hope
when we see a bad wound, knowing that with proper care
and time, it should heal fine.
Minor burns will often do well with first aid. However,
severe burns will require medical attention and possible hospitalization in order to provide pain relief, infection control
and treatment for shock.
In general, first degree burns, unless affecting extensive
portions of the body, can be treated at home. If the burn is recent, apply cold water rinses or cold compresses (not ice!)
for no more than twenty minutes. This helps reduce swelling
and pain to the affected area. Applying ice to the tissue can
cause frost bite, actually causing freeze damage to the tissue.
If blisters are present, they should NOT be broken. Doing so damages down the body’s natural barrier against infection. Let the blisters either resolve or break on their own.
Infection is a common, and potentially serious complication of burns. When the skin is compromised, as with broken
blisters, always pay careful attention to contamination, keeping the affected area as clean as possible. A non-irritating antibacterial soap, such as Nolvasan, or even a gentle hand
soap, such as Ivory or Dove, will work well.
If there is damaged skin, then application of a topical
burn dressing, after gentle wound cleansing, is appropriate.
The burn should then be dressed, or covered, with a sterile
non-stick bandage. This can be tricky, especially when the
burn is on the underside of a snake.
238
In animals where there are extensive burns, I recommend
keeping them in a glass or Plexiglas enclosure without substrate. Even though this is not a natural way to house a reptile, these cages are easy to clean and disinfect, thus minimizing the risk of infection. Their benefits outweigh the disadvantages of the temporary housing.
Second degree burns, because of the extensive tissue
damage, need veterinary attention. If for no other reason,
pain is a hallmark of second degree burns, and the veterinarian can provide medications for pain relief.
If the animal is in shock, therapy must be initiated to
counter the effects. Wounds must be cleaned and debrided.
Topical burn creams, such as Silvadene, are applied, and the
patient is started on antibiotics to prevent infection at the
burn site. Injectable cephazolin or oral cephalexin (20
mg/kg/day) are my first drugs of choice.
Fluids, either intravenous, oral or otherwise, must be administered to counter the effects of shock and fluid loss from
the burn. Daily cleansing of the wound and sterile bandage
changes are needed to effect rapid healing. These may take
several weeks to months to fully heal.
Third degree, or full thickness burns may require intensive care at the outset. For human patients, there are entire
burn centers dedicated to the care of burn victims.
Depending on the extent of the burn, the owner of the
reptile should be appraised of the potentially grave prognosis. Treatment involves all the care involved for the second
degree burn, plus more. As the tissue starts to heal, the pain
can be intense. The pain from the daily cleanings and debridements can also intensify as the patient recovers feeling
to the burn area.
Antibiotic therapy may be protracted, often lasting for
several months. Wound care can get expensive, considering
that the bandages may need to be changed daily for many
months. As a veterinarian, it is important to consider all the
costs of return visits, bandage materials, follow-up laboratory sammpling and other miscellaneous costs when quoting
estimates to the clients. Even in the face of such odds, many
people do elect to treat their pets that are suffering from extensive burns.
Even some of the fourth degree burns, where not only the
skin is destroyed, but also the underlying tissue, has potential to heal if cared for properly. A blue tongue skind that I
treated had a full thickness burn through its abdominal wall
which left a completefistula into the coelomic cavity. This
animal was taken to surgery after it was stabilized and treated for shock. The dead (burned) tissue was removed, and the
healthy tissue was attached to the healthy tissue on the opposite side of the burn. There was so much tissue damage
that after the dead part was removed, the patient looked like
an hour-glass when the sides were pulled together.
After extensive wound care, bandage changes and antibiotic therapy, the patient recovered, nearly six months later. Other than the tremendous scar, the animal was back to normal.
Although not discussed, many patients exposed to heat
may not actually be burned, but, may suffer from smoke or
other toxic fume inhalation. Many melted glues and plastics
produce noxious fumes, as well as smoke that can damage
delicate lung tissue. Although initially these patients may
appear to be uninjured, they may develop a fatal fluid buildup within their lungs, and could potentially die if not treated
properly in a timely fashion.
Summary
Understanding the reason why reptiles are so prone to
burn injury remains a mystery. But, understanding the causes of burns and the mechanics of tissue injury will help us
prevent such occurrences, and in the unfortunate event that
they do happen, better manage their care.
The most important take home message from this article
is this - when dealing with burns in reptile patients, be diligent, be clean and, above all, be patient!
239
Shell repair in turtles
Douglas R. Mader
Surgical techniques utilized in turtles and tortoises are,
for the most part, similar to those employed in mammals.
However, there are a few techniques which are unique to
these hard shelled reptiles which warrant special consideration. These majority of these special procedures center
around the opening and closing of the plastron or carapace,
the major components of the shell.
There are less than twelve routine procedures that this
author performs in private practice on a regular basis. Some
of these can be executed with little to no anesthesia, some
with light tranquilization, and some require full general
anesthesia.
There are many different ways to perform the following
techniques which will be discussed. The methods vary depending on where the surgeon was trained, their level of expertise and the equipment and facilities available. This manuscript will discuss the techniques which have proven successful in clinical practice at this author’s hospital.
Minor Surgical Procedures
A few of the minor surgical procedures can be easily
accomplished with either manual restraint or mild tranquilization. These include placement of jugular catheters, aural abscess drainage, beak trimming, repairs of minor lacerations or minor shell damage, and amputations of digits to
name a few.
Abscesses
It is not uncommon for turtles and tortoises to develop
abscesses subcutaneously, behind the tympanic membrane,
on the neck and in the joints (osteoarthritis). Many of the
subcutaneous abscess are easily lanced and drained with just
manual restraint.
Tympanic, or aural abscesses are a frequent presentation
in this author’s practice. Many can be treated by making a
simple curved incision along the ventral margin of the tympanic membrane from the 4-O:clock to the 8-O:clock position. The starting and finishing point are then connected with
a straight incision which effectively removes the inferior
third of the tympanic membrane. This technique leaves a
nice window for flushing and drainage.
The technique should be performed in a sterile fashion so
that when the abscess is encountered a culture and sensitivity can be obtained to help identify the cause and aid in future treatment. The abscess material in turtles and tortoises
is caseated and needs to be curetted out. After it is removed
the cavity should be flushed with dilute betadine. On occasion the eustacean tube may be affected. If this is the case it
should also be flushed with the betadine solution. As a final
step the cavity should be painted with full strength betadine.
Daily flushing for five to seven days is usually sufficient
to cure the problem. This author rarely puts that animal on
systemic antibiotics unless the abscess is refractory to conservative therapy or there is concurrent disease. The incision
in the tympanic membrane typically heals well after the abscess is resolved.
Beak Trimming
Although beak trimming is not necessarily a surgical
procedure a brief mention of the proper technique is warranted. Under natural conditions the beaks, which are made
of keratin, have a normal wear pattern which allows the
maxillary beak to ride slightly over the mandibular ridge. In
captivity the diet is not always appropriate and often times
either the upper, lower, or both beaks will grow in grossly
aberrant fashions.
In gentle or tractable animals the head and neck can be
easily extended for shaping. A Dremmel Moto-Tool® (Dremmel, Racine, WI) with a small burr works well for this procedure. The person doing the shaping should be familiar
with the normal morphology of the species being treated.
MAJOR SURGICAL PROCEDURES
Limb Amputation
Joint abscesses may require general anesthesia for treatment. Radiographs of the affected limb are encouraged. In
severe cases where osteomyelitis has developed it may be
necessary to amputate the limb.
Limb amputation is performed much the same way as is
done in mammals. Amputation at the scapulohumeral joint
or the coxofemoral joint prevents a stump from developing
into a problem at a later date by dragging on the ground as
the animal ambulates.
240
To amputated the limb, two curvalinear incisions should
be made in the skin from cranial to caudal around the proximal portion near the articulation. This will allow ample skin
to remain to act as a flap which can be used to cover the
deficit left by the amputated appendage. Muscles and soft
tissue should be gently dissected from the bone with blunt
techniques and retracted proximally. Vital structures such as
vessels and nerves should be ligated as they are encountered.
The muscles can then be sutured over the amputation site to
act as padding over the disarticulated bone.
Subcutaneous dead space should be closed with a strong
absorbable suture such as polydioxinone. The skin tends to
invert as it heals, so to promote primary intention healing an
everting pattern should be employed. The author recommends using either a monofilament nylon or a light gauge
stainless steel suture in the smaller animals, and heavy gauge
stainless in the larger animals.
Sutures should be left in place for at least four weeks.
Aquatic turtles should not be allowed back in the water for
at least one to two weeks. Fluid needs can be met by oral
tubing or intracoelomic injections. After two weeks short
soaks or brief episodes of swimming to allow for eating may
begin, but only in clean water. Fecal contaminated water can
easily lead to contamination of the wound with subsequent
dehiscence and infection.
Intestinal Prolapse
Another common presentation of chelonians, especially
the tortoises, is prolapse of the terminal colon. A number of
causes have been implicated including intestinal parasites,
bacterial and/or fungal enteritis and fecaliths. Whole body
radiographs and a fecal examination for ova and parasites
should be performed in an attempt to determine the cause of
the prolapse.
In minor prolapses of the colon or rectum cleansing with
a mild soap and gentle reduction may suffice for treatment.
Often times it may be necessary to place a loose pursestring
suture around the cloacal vent for five to seven days.
It is imperative that the prolapse be reduced shortly after
it happens to prevent toxemia and shock. If the prolapsed
segment is damaged or necrotic, or if the prolapse continues
to happen repeatedly, amputation of the distal section may
be required. The procedure should be done under general
anesthesia.
The distal intestine should be cleansed and enough gentle traction should be applied to expose viable intestinal tissue. Identify the structures of the urodeal area and avoid
them during the amputation. A small diameter tube is
placed into the everted intestine to make it rigid. A clean syringe case works well for this. Two small gauge hypodermic
needles are then placed through the tissue, the plastic tube,
and out the opposite side of the tissue perpendicular to each
other. This will stabilize the tissue and prevent it from slipping back inside the body cavity during the amputation procedure.
A circular incision is made through the prolapsed tissue
in a 360 degree arc. An absorbable suture material, such as a
3 to 4-0 monofilament polyglyconate (Maxon™, DG®, Manati,
PR)
, in a simple interrupted pattern is used to anastomose the
two viable ends. When the suturing is completed the stay
needles are removed and the intestinal tract is allowed to return into the coelomic cavity.
The author routinely puts the patient on antibiotics for
this type of procedure. Ideally, an aminoglycoside should be
administered prior to commencing the procedure and continued on for an additional two weeks into recovery.
The patient should be fasted for at least two weeks following the amputation. Hydration can be maintained by either subcutaneous or intracoelomic fluids or an intravenous
catheter.
Penile Prolapse
The causes of penile prolapse are many. Uroliths, bacterial, parasitic and fungal infections, foreign bodies and nutritional secondary hyperparathyroidism have all been implicated. Overengorement during copulation can sometimes
prevent the organ from returning to its resting position.
The male chelonian has a single copulatory organ retracted into the cranioventral portion of their tail base, unlike
snakes and lizards which have a paired structure tucked into
the caudal portion of their tails. During copulation this organ
is extruded from the cloacal vent. For whatever reason, the
animal is sometimes unable to retract it and it may become
damaged, avulsed or infected and necrotic.
If the damage is not severe, or if it has not been displaced for a prolonged period, a thorough cleansing and
manual reduction may be all that is required. An engorged
penis can be reduced by soaking it in a hypertonic solution of dextrose, or applying DMSO to its surface. After
it reduces to its approximate normal size the penis can be
inverted and tucked back into the tail base. A loose purse
string suture may be required to maintain its position until it has healed.
If the penis is damaged beyond repair then amputation is
mandated. Once removed the animal will still be able to urinate but will no longer be reproductive.
The base of the penis is grasped with a Doyen intestinal
clamp. Two to three through-and-through absorbable horizontal matress sutures are placed parallel and distal to the
clamp. The penis is then amputated distal to the suture line.
If the penis was infected or necrotic then systemic antibiotics are warranted for two weeks post-operatively.
Celiotomies
There are a number of medical conditions which require
celiotomies for correction. Gastric or intestinal foreign bodies, retained eggs, cystic calculi, fecaliths, neoplasia, etc. to
name a few. A thorough pre-operative physical examination
which includes radiographs and a complete blood analysis
should be performed on the patient. If the patient is weak or
debilitated then an intravenous catheter should be placed prior to starting the procedure. Alternative methods of correcting the problem should be attempted prior to the celiotomy
procedure.
If foreign bodies are high in the gastrointestinal track
it may be possible to retrieve them by using an endoscope.
Some of the smaller cystic calculi and fecaliths can be removed manually through the cloacal vent using small
mosquitos or an Allis tissue forceps. If the more conservative methods prove to be ineffective then the celiotomy is
in order.
The animal should be anesthetized as described above. It
is prudent to perform the surgical procedure on a heating
pad. The patient should be positioned on its back and stabilized between sandbags. The plastron should be thoroughly
scrubbed and prepped in the same fashion as is done in
mammals.
A pre-operative radiograph will help determine the position of the celiotomy site. A high speed hand held motor tool
or a flexible motor shaft with a small circular saw is sterilized and used to cut through the shell. The operator and assistants should wear protective eye gear during this cutting
procedure. The cutting procedure creates a lot of heat and
the saw blade should be continuously cooled with sterile
saline to prevent the underlying bone from thermal damage.
When making the actual cut the saw blade should be
beveled in on all four sides. This will prevent the removed
piece from falling inside the opening when it is time for it to
be replaced.
The large piece of bone should be gently elevated using
a periosteal elevator. Care should be taken to separate the underlying coelomic membrane from the inside of the shell.
There are two large ventral venous sinuses which need to be
avoided.
The removed piece of plastron should be wrapped in
saline soaked gauze and placed to the side during the procedure. Care should be taken to make sure that it does not dry
out during the procedure.
If the plastron piece can be removed without disrupting
the coelomic membrane then it should be incised longitudinally and reflected back to expose the coelomic cavity. The
venous sinuses should not be in the way of the procedure. If
so, they can be gently retracted to the side.
Once inside of the coelomic cavity the soft-tissue techniques are similar to those in mammals. Commonly performed procedures are cystotomies, enterotomies, salpingotomies and exploratories.
In chelonians the mesovarium and mesosalpinx are
short and broad based. For “spay” procedures, or removal
of the reproductive tract, this anatomical variation makes
the technique a bit more difficult than the same procedure
in a mammal.
The mesovarium and mesosalpinx are short and broad.
There are many vessels which run the course of the ligaments and nourish the elongated ovary, oviduct and shell
gland. Unlike in mammals, where the ovarian pedicle can be
ligated with a single suture, each of these vessels must be
ligated and severed individually. In smaller animals this can
be accomplished with electrocautery.
After the soft tissue procedure is finished the shell needs
to be properly closed. Carefully unwrap the plastron piece
from its gauze. Make sure that the piece is placed back in its
hole in its original position. The beveled cuts prevent the
piece from dropping inside.
241
The plastron should be cleaned of all blood and surgical
debris. The shell should then be dried with clean gauze pads
to prepare it for the resin. Wiping the area with ether or acetone helps dry the shell and makes it more suitable for the
resin to gain purchase.
When the plastron is ready a thin layer of resin should be
applied over the plastron piece and extended two centimeters
beyond all of its margins. A pre-fitted, autoclaved piece of
fiberglass cloth is then applied to the layer of resin.
After this double layer starts to harden, a second layer of
resin is applied to the entire area. The remainder of the procedure is the same as was previously described for traumatic shell repair.
Once the patch has hardened to the touch a thin layer of
lubricating jelly can be applied to the resin to prevent it from
adhering to the cage liner after the animal is righted. The lubricating jelly can be wiped off the next day.
In certain situations a celiotomy may be performed by
making the approach through the prefemoral area of soft tissue in front of either of the back legs. One study on 56 different species of turtles reported good results on exploratory
celiotomies, surgical sexing, salpingotomies, enterotomies,
ovarian biopsies and orchidectomies.
This author has used the soft-tissue celiotomies approach
on numerous tortoises for cystotomy procedures. Pre-opertive radiographs indicate the position and size of the urinary calculus. Even calculi which have a diameter larger
than the actual space between the carapace and plastron are
removable by this approach.
The patient is placed in dorsal recumbency and the limbs
are extended straight behind. The prefemoral area is aseptically prepared and the surgical area is draped with sterile
towels.
The incision is made in a horizontal line midway between the carapace and plastron, extending from just cranial
to the leg to the margin of the soft tissue and the marginals.
The subcutaneous fat is bluntly dissected away and the underlying abdominal oblique muscles are exposed. These are
also incised along the same line as the skin. The next layer
of muscles (which may also be obscured by fat) is the transverse abdominus muscle. This is also incised in the same
fashion. The coelomic membrane is associated with the inside of the transverse abdominus muscle. Incision of the
coelomic membrane gains entrance to the coelomic cavity.
Once entrance to the coelomic cavity is attained visualization may be aided with the use of either a flexible or rigid
endoscope. An ovariohysterectomy hook is useful in gently
moving or exteriorizing internal organs.
The first structures encountered are the ovary and shell
gland. Once these are retracted the bladder is easily visualized.
For cystotomies the bladder is localized and a portion of
it is exteriorized. Stay sutures are placed into the serosa and
tacked to the surgical toweling or stabilized by an assistant.
The bladder wall is incised to gain access to the stone.
If the stone is small is can be retrieved using a lens loop
or small forceps. Larger stones can be grasped with Allis tissue forceps and broken in situ. Most of the stones are layered
and can be broken down by chipping away at their masses
with the jaws on the Allis forceps. Once the stone is dismantled to a manageable size its pieces can be exteriorized.
242
Care must be taken not to injure any of the soft tissue within the coelomic cavity during the procedure.
After the stone is out the bladder should be copiously
flushed with sterile saline. The bladder is then closed with 40 monofilament absorbable suture, such as polydioxinone, in
a double layered closure, rinsed one final time and returned
to the body cavity.
The coelomic membrane, abdominal muscles and fat are
all closed with a single layer of absorbable sutures. The skin
is closed in the previously described fashion. The cutaneous
sutures are removed in approximately four weeks.
This technique allows for complete healing in just three
to four weeks, as opposed to one to two years as in the ventral celiotomy approach through the plastron. One can surmise that there is considerably less discomfort to the patient
when using this technique.
Shell Repair
Traumatic wounds to the shell can be caused by various
factors. Commonly seen injuries include being run over by
automobiles, dropped on a hard surface, attacked by dogs
and hit by lawnmowers. The lesions encountered can be as
slight as a minor crack to as severe as a major shell deficit.
Minor damage to the shell can be repaired with manual restraint. More extensive trauma which invades the coelomic
cavity may need sedation or anesthesia.
The procedure for shell repair depends on a number of
factors. Age of the injury, size of the deficit and physical
condition of the patient. An assessment of the patient should
be performed before attempting to correct the shell. If there
are signs of shock or other life threatening conditions they
should be cared for immediately.
If the wound or shell damage is freshn and the tissue is
contaminated, but not infected, then the wound should be attended to immediately and cleaned and then closed as one
would do with a mammalian soft tissue wound. If the wound
is old or infected the infection absolutely must be controlled
before attempting to cover the damaged shell. Systemic antibiotics and wet-to-dry bandages should be utilized until all
of the infection is removed.
The edges of the shell along the defect should be debrided. If there are large pieces of shell which have broken free
they should be retrieved and cleaned to use in rebuilding the
defect. If the wound is a compression fracture then the concaved pieces should be elevated back to normal position. In
some cases it may be necessary to use orthopedic wire to fasten pieces of fractured shell together.
The surface of the shell should be cleaned and then prepared for the resin repair with either ether or acetone, being
careful not to get any of the agents into the deficit. Fiberglass
cloth should be prepared by autoclaving round or oval pieces
which have been pre-cut to the size of the defect. Round
edges on the cloth prevent it from unraveling.
The cloth should extend 1.5 to 3 cm beyond the margins
of the wound. In cases of line cracks the cloth should extend
on either side by the same margins.
A rapid setting epoxy resin is prepared (eg. Devcon® 5Minute Epoxy Cement, Devcon Corp, Danvers, MA)) and
placed along the immediate margins of the defect. Care must
be taken to prevent epoxy from entering the wound itself as
it will impede healing.
The pre-fitted fiberglass cloth is then pressed into the
now tacky resin and stretched into place, taking care to
smooth out all of the wrinkles. After the margins of the patch
have polymerized a second coat of resin can be applied to
the entire patch area. The new coat should not be so thick
that it drips through into the wound. It is best to apply several thin coats of resin rather than one or two very thick
coats.
The resin will dry to the touch within five to ten minutes,
and will set hard by 24 hours. The patch usually dries
smooth, however, an occasional smoothing with some fine
sand paper may aid in the finished appearance.
Depending on the size of the defect under the patch compete wound healing may take up to two years. Very large
deficits may never bridge, but the animal will still be able to
function properly as long as the patch remains intact.
In an adult animal the patch can remain in place for the
rest of the animal’s life. However, in a growing chelonian the
patch may cause shell growth irregularities. If a problem develops then the resin can be routed away with a motorized
burr at the margins of the growth plates.
243
Reproductive procedures in the green iguana and
common surgical procedures in lizards
Douglas R. Mader
It has been recently estimated that there are over 7.3 million reptile owning households in the United States. Compare this, if you will, with the 50 - 55 million households
having dogs and cats as pets. It is clear to see that reptiles are
fast becoming a favorite amongst pet owners. Of interest,
and it is of no surprise, that the green iguana (Iguana iguana) is currently the most popular reptile pet.
MEDICAL AND SURGICAL MANAGEMENT
OF THE FEMALE IGUANA
When an iguana presents for egg-binding, first determine
if it pre- or post-ovulatory. If pre-, and the animal is in good
condition, consider sending it home with husbandry instructions for observation only. I always send the gravid iguana
home with a calcium supplement, specifically, Neocalglucon
(calcium glubionate - Sandoz). The recommended dose is 1
cc/kg, PO bid. This is a grape flavored liquid, and the patients generally take it voluntarily.
I have the owners estimate how long the animal has been
anorectic (this is usually the presenting complaint), and then
calculate out how far off four weeks from that date will be.
If the animal either gets worse before the four weeks are up,
or starts eating (a sign that the female has resorbed her ova),
I have them come back in for a recheck. If by the four week
mark there is no change in appetite, and no eggs have been
produced, then I have them come back for either medical
management (necessitates a repeat radiograph to determine
if the eggs are now post-ovulatory), or surgery.
If they are post-ovulatory and the patient doesn’t respond
to the protocol in Table 1, or if they are still pre-, or, you still
can’t tell, then, I recommend surgery.
The animal is anesthetized and instrumented for proper
monitoring. I have found the best method for monitoring
anesthesia in the reptile patient is the pulse oximeter. This
instrument provides information on pulse rate, pulse
strength and arterial hemoglobin saturation.
A standard surgical prep is used (eg. chlorhexidine). I recommend starting the animal on antibiotics since it is difficult to
thoroughly prepare reptile skin (because of the scales). I routinely use cephalexin at 20 mg/kg, PO q24 for 7 days.
A ventral midline approach is made. Do not worry about
the ventral midline vessel. It is large, and lies within a membrane and can displace to either side, so even when making
a paramedian incision you still have a 50:50 chance of
knicking it. Not only that, but cutting through muscle is
painful for the patient, produces more bleeding, and makes
for a prolonged convalescence. I perform all of my lizard
coeliotomies using a ventral midline incision.
If you do accidentally cut the ventral midline vessel,
don’t panic, just ligate it. There are ample collateral vessels
to compensate for this if you need to ligate the vein.
In post-ovulatory cases, the salpinx, filled with eggs, is
the first structure you will encounter. Carefully exteriorize
this structure from the fimbria to the “cervix,” or the junction
of the oviduct with the urodeum. This entire tissue will need
to be removed, and there are several vessels within the
mesosalpinx that must be ligated. I recommend using a blue
handled Hemoclip. These “V” shaped clips come in various
sizes. I have found that the blue handle is the most convenient size for most exotic surgeries, making the procedures
much easier, saving time and frustration. The applicator handles also come in two lengths, allowing easy access to vessels deep within the body cavity or otherwise inaccessible
areas, or areas where an instrument ligation is difficult. The
oviductal tissue at the urodeum is ligated and transfixed if
necessary, using a monofilament absorbable suture material.
The second half of the reproductive tract is also removed
in a similar fashion. Once both shell glands have been removed then the ovaries must be located. The right ovary is
attached to the vena cava, and the left ovary is attached to a
branch of the renal vein. Interposed between the left ovary
and the renal vein is the left adrenal gland, a elongated, pink,
granular tissue. It is best not to remove or damage this gland
when ligating the vessels. If it is accidentally removed, the
patient will survive. However, make sure that you don’t remove the opposite side. Fortunately, the adrenal gland on the
right is opposite the vena cava from the ovary, and it is unlikely that you will damage it during the procedure.
In post-ovulatory cases the ovaries are small with
diminutive vessels. The ovaries must be removed. There are
about 3 - 4 veins on each ovary, and a single artery. Each of
these must be ligated or clipped. Use extreme caution when
handling these ovaries. It is not difficult to avulse the smaller vessels from the vena cava, resulting in substantial hemorrhage. Always preload your hemoclips prior to handling the vessels!
The most important take home message here is this:
Never just remove the gravid shell glands in post-ovula-
244
tory cases - the female is still capable of ovulating, which
will result in ectopic ova free in the coelomic cavity!
After the ovaries have been removed, double and triple
check for hemorrhage. When satisfied, then flush the
coelomic cavity with warmed saline prior to closing.
In pre-ovulatory cases, the ovaries complete with the attached ova are the first structures encountered when you enter the coelomic cavity. These can be quite fragile, so extreme care must be taken when exteriorizing the gonads.
The vascular supply is engorged in these cases, and identifying, ligating these vessels is mush easier than in the postovulatory cases. Of particular importance in pre-ovulatory
cases, only the ovaries need to be removed. It is not necessary to remove the shell glands in pre-ovulatory cases as it is
in the post-ovulatory cases.
In reptiles the skin is the holding layer. The skin is apposed using a horizontal mattress, everting pattern. I like to
use a non-absorbable suture. After finishing the closure the
skin will be everted. When the animal recovers and is returned to the sternal position, the raw skin will rub on the
cage bottom, so it is a good idea to protect this area. Cyanoacrylate tissue adhesive applied to the incision just prior to
recovering the animal works well for this. Otherwise, a light
body wrap will suffice.
It is unknown whether or not reptiles experience pain as
do mammals. However, I routinely use flunixen meglumine
at 2 mg/kg, IM q 24 hrs for two treatments. Butorphenol has
also been used at 0.05 mg/kg, IM q 24 hrs for two to three
days.
Sutures should be removed in four weeks. It is not uncommon for animals to shed off their sutures prior to that
time, and this should be of no concern. You should warn
your clients of this possibility so as not to cause alarm
should this happen.
MEDICAL AND SURGICAL MANAGEMENT
OF BEHAVIOR PROBLEMS IN THE
SEXUALLY MATURE MALE IGUANA
I have neutered over fifty Green Iguanas for various reasons - some because the owners did not want them to breed
with their females and some because they were aggressive.
In addition, I have tried to keep track on how this procedure
has affected the animal’s ultimate behavior.
It is important that you and the owner are able to distinguish the difference between the types of aggression displayed by male iguanas. First, there is the defensive aggression present in most all iguanas, even the most docile animals. This occurs when an animal is startled, such as when
you walk up to it while it is sleeping, or when you stick your
hand in its cage. The iguana will stand erect on all four legs,
turn sideways and puff up (they do this in an attempt to visually increase their body size - apparently to intimidate
their opponents). They will often accompany this behavior
with tail whips, but will rarely bite unless you grab for them.
In contrast, offensive aggression occurs when the owner
is sitting on the couch, minding their own business, and the
iguana runs across the room, jumps up on the couch, and
takes a chunk out of the person’s arm. In other words, the
difference between the two is that defensive aggression is
provoked (entering the animal’s private space), and the offensive aggression is not. That distinction is important because when evaluating the effects of castration it is important to be able to distinguish between the two.
I have tried to follow up on all of my post-castration
iguanas to evaluate their behavior modification. Because of
various circumstances, I have only been able to contact
about one-third of the owners after one year post-surgery.
From my observations it has been apparent that there has
been no effect on either defensive or offensive aggression
immediately after the surgery. In the animals that I have
checked on a year later, the owners have had various reports,
ranging from being somewhat less aggressive, to having no
change. The aggression has been mostly defensive, but the
offensive component was still there.
For the record, I have also talked with other veterinarians
who have castrated some iguanas. I have heard completely
opposite reports in a few cases, where the DVM states unequivocally that “the once mean iguana is now as docile as a
kitten.” The problem with any of these reports is that they are
anecdotal. There have been no controlled studies to rule out
other possibilities for the aggression (such as other male animals in the same house, exposure to sunlight [always good
for stimulating aggression], presence of female conspecifics,
ambient temperature, and day-length).
As any experienced iguana owner can tell you, there is
no way that you can predict whether or not an iguana will be
nice or mean. I have seen baby iguanas, raised as an only
child, being dotted with attention 24 hours a day, grow up to
be as “docile as a kitten.” I have also seen animals raised in
an identical fashion grow up to be little T-rex’s. Likewise, I
have seen adult wild-caught males that were harness trained.
Aside from castration to calm aggressive male iguanas, a
number of other methods have been tried. For instance, female progestational hormones can be given during the
breeding season. These come either as pills or injections.
But, just as with the castration, the effects are variable and
unpredictable. You can also attempt to temper aggression by
decreasing day-length (turning the lights off early) and cooling the animal. Remember, eventually you will have to warm
it back up or turn on the lights. You can’t deliberately keep
the animal locked up to prevent it from being aggressive.
That would be cruel. Remember, most of these behaviors are
normal for these animals. If the owner does not like the behavior, perhaps this is the wrong animal for them to keep as
a pet.
One last note on castration. I have castrated a limited
number of males pre-puberty. So far, and keep in mind that
this is not a scientific finding, these animals have yet to become aggressive. But, by castrating these animals before
they reached puberty, they never developed the large crests,
the massive jowls and the beautiful scales that the males are
known for. So, the end result might be a friendly pet, but you
lose the majestic look of a mature male green iguana.
I think the jury is still out whether or not you will be able
to predict post surgical behavior. This needs to be clearly articulated to your clients prior to performing the surgery. I also suggest that you document your conversations in the medical record.
The approach to the castration is identical to that of an
ovariectomy. The gonads are tightly adhered in the mid-dorsal coelomic cavity, making surgical access difficult. Exposure is of paramount importance, so don’t be concerned
about making a large incision. It is a good idea to start the
coeliotomy just cranial to the pubis and extend it to the
xyphoid.
Each testicle has a rich vascular supply. The right gonad
is attached to the vena cava by very short vessels (approximately one mm). The left testicle has its own blood supply,
the testicular vein and artery, which are branches of the renal vein and artery. As seen in the female, the adrenal gland
is interposed between the left testicle and the vessel. The
right adrenal gland is opposite the vena cava from the testicle, and it is unlikely that you will damage it during the procedure.
The testes are covered by a capsule which gives them
some rigidity, but if aggressively handled the capsule will
rupture. Although the capsule has a minimal vascular supply,
and bleeding from a ruptured capsule is minute, rupturing it
makes manipulating the gland during the procedure difficult.
It is necessary to gently elevate the testes to allow visualization and ultimately ligation of the blood supply. Although it is possible to manually ligate these minuscule vessels, it is highly recommended to use a vascular clip.
245
To facilitate elevation of each testis a suture can be
placed through the top of the capsule and gently retracted,
or, alternatively, if the testicle is small, it can be grasp with
an Allis tissue clamp.
Once the vessels are readily identified the vascular clips
are gently inserted between the supply vessel and the gonad.
You must be extremely careful not to tear the vascular supply or the veins attaching the testis to the vena cava or the
testicular vein. These will hemorrhage extensively, and the
blood will rapidly occlude your surgical area. If either of
these major vessels are damaged, the vascular clips can be
applied across the top of the rent, parallel to the vein. This
will cause changes to the hemodynamics of the blood flow
through each of these vessels, but you have no other choice.
Depending on the severity of the damage, the patient should
heal fine.
If possible try to double ligate (clip) all vessels. Sever the
vessel adjacent to the capsule and remove the gonad. Always
double check for hemorrhage before closing the coelomic
cavity. Irrigation is generally not necessary, but lavaging
with warm saline does help preserve the patient’s body temperature. Closure of the surgical site is similar to closure previously described for the ovariectomy.
Post-operative care is the same as it is for the female.
Again, attention to analgesia is suggested.
Table 1. Medical management of the ova-retained iguana
On presentation:
- Warm the animal to 90 - 95oF
- Tube feed a high calorie/carbohydrate meal, approximately 0.5% of the
- ICe fluids as necessary (crystalloid, 15 ml/kg, warmed)
- If hypocalcemic, 100 mg/kg Calcium Gluconate, IM, repeated q 6 hrs
- Vitamin D, 100 IU/kg, IM one time only
- Radiograph, VD/Lateral
animal’s body weight.
until the tetany ceases.
After being Stabilized:
- If pre-ovulatory condition, continue with supportive care
- consider surgical correction (ovariosalpingotomy) if critical
- if post-ovulatory, decide on medical or surgical management
For medical management:
- Calcium Gluconate, 100 mg/kg, IM q 6 hrs, followed by
- Oxytocin, 10 U/kg, IM q 6 hrs, 1 hr after each calcium injection
- provide a nest box
- if no oviposition within 24 hrs, take to surgery
REMEMBER - NOT ALL GRAVID, ANORECTIC IGUANAS ARE EGG-BOUND! WHAT YOU ARE SEEING ON
PRESENTATION MAY BE NORMAL FOR THE STAGE OF THEIR CONDITION.
247
The reptilian patient:
special pre-operative considerations
Douglas R. Mader
R. Avery Bennett
DVM, DAVCS, University of Pennsylvania, School of Veterinary Medicine
A variety of clinical situations may result in a need to
perform surgery on a reptile patient. It is vital to have a basic understanding of the unique anatomy and physiology of
the particular reptile species prior to undertaking surgery.
The clinician is referred to the sections of this book that provide information about the body system requiring surgery.
Some points of particular relevance to soft tissue surgery
will be reviewed prior to discussions concerning specific
conditions.
ANATOMY
Most reptiles lack discrete lymph nodes but lymphoid
aggregates are present within the gastrointestinal system and
the spleen. They do have lymph vessels, and lymph is propelled through the lymphatic system by lymph hearts, which
are dilations within the major lymphatic channels containing
smooth muscle. In some species, the spleen and pancreas are
closely associated, forming a splenopancreas. The location
and structure of thymic tissue is variable in reptiles.
Reptile kidneys are metanephric in origin and are generally lobulated. They may have one or more renal arteries, and
in some species, there is a separate branch of the ureter
draining each lobule. The kidneys of many lizards are located caudally in the coelomic cavity. In green iguanas, the kidneys are located within the pelvic canal, and in order to gain
access to the kidneys, it may be necessary to split and separate the pelvis.
Chelonians and some lizards have a urinary bladder; however, some lizards, snakes, and crocodilians do not. In those
species with a urinary bladder, the bladder is connected to the
cloaca by a short urethra. Generally, urine formed in the kidneys flows through the ureters into the cloaca, and then refluxes into the urinary bladder. In species without a bladder,
urine refluxes into the terminal colon. Some water reabsorption occurs in the bladder or terminal colon prior to the urine
being excreted through the cloaca. It is important to note that
the ureters do not connect directly to the urinary bladder.
The digestive organs of reptiles are similar to those of
mammalian species.1 Most reptiles except for snakes have a
cecum. Many reptiles ingest stones, which are believed to
aid in digestion. All reptiles have a gallbladder. Many reptiles have pigments within the liver creating black spots or
streaks on its surface. In general, reptiles do not store fat in
the subcutaneous space. Fat storage occurs in discrete masses within the caudal coelomic cavity.
The anatomic location of the internal organs of snakes
has been described in relation to their snout—cloaca length.
A knowledge of their relative positions is useful for surgical
approaches and localization of internal masses.
The skin of reptiles is unique. The skin is dry and devoid
of glands, with few exceptions, such as the femoral gland of
some lizards. It contains scales and scutes, which are large
scales that usually occur along the ventral surface of the animal. These are tough, hard structures composed of living
tissue with a keratinized surface. Between the scutes and
scales the skin is very soft and pliable. Some reptiles, such
as the soft-shelled turtles and some lizards, do not have
scales but rather have a smoother, leathery type of skin.
Crocodilians and some lizards have calcified plates called
osteoderms located within the dermis. Osteoderms are a protective adaptation that can make incision of skin difficult.
The epidermis is composed of three layers: the stratum
corneum, the stratum germinativum, and the intermediate
zone. The stratum germinativum is the deepest layer and is
composed of a single layer of cuboidal cells. This germinative layer undergoes mitosis to form the intermediate zone,
which is composed of daughter cells of the stratum germinativum in various stages of development. The outer stratum
corneum is heavily keratinized and acellular. At rest there is
little activity going on in these tissue layers; however, during
ecdysis, the stratum germinativum undergoes mitosis to
form a new intermediate zone and stratum corneum. It is
during ecdysis that the skin is metabolically active and
geared toward healing.
Chelonians are unique in their surface structure. The surface of their shell is living tissue. It is composed of kera-
248
tinized epidermal shields covering bony dermal plates. The
bone of the carapace contains 10 fused thoracic, lumbar, and
sacral vertebrae as well as the ribs. In most chelonians, there
are 38 epidermal shields on the carapace and 16 on the plastron. The bridge is the location where the plastron and carapace join.
WOUND HEALING
It appears that wound healing in reptiles occurs through
phases similar to those observed in mammalian species. This
has been studied in snakes. Initially, proteinaceous fluid and
fibrin fill the defect to form a scab. A single layer of epithelial cells migrates beneath the scab. This single layer then
proliferates to restore the thickness of the normal epithelium. Additionally, macrophages and heterophils migrate into
the tissue below the scab to clean up bacteria and debris. A
transversely arranged fibrous scar is produced by fibroblasts
that migrate into the area. Heterophils are present within the
scar tissue matrix until maturation has occurred. This is a
slow process in reptiles. Consequently, suture removal is
generally recommended 4 to 6 weeks following suture
placement. It appears that the activity of the dermis and epidermis during ecdysis promotes healing. If suture removal
can be delayed until the subsequent ecdysis, wound strength
is likely to be better.
Environmental temperature has an effect on wound healing. Maintaining the patient in the upper end of its optimum
range (30–36_C [85–95_F]) has been shown to promote
healing. The orientation of the wound also influences the
rate of healing, with cranial to caudal oriented wounds healing faster than transverse wounds. When treating open
wounds such as those occurring from lamp burns, good environmental hygiene is important. These wounds do heal
well by second intention with a relatively low incidence of
secondary infections.
SUTURE MATERIALS
In general, the skin of reptiles is very strong and acts as
the primary holding layer for maintaining wound closure.
For example, with coelomic surgery, the coelomic membrane and body wall are very soft and do not hold sutures
well. The success of wound closure relies on strong, wellplaced skin sutures. Since the skin is tough, it is unlikely that
sutures will tear through. Additionally, most reptiles do not
traumatize their incisions, making closure with a continuous
pattern appropriate.
In most situations, steel suture is not necessary and softer materials such as nylon or polypropylene are more comfortable for the patient. Although it is believed that synthetic, absorbable materials are eventually absorbed by reptile
patients, it appears that their absorption is prolonged. If
these materials are used for skin closure, removal is required. Chromic catgut does not appear to be an appropriate
suture for use in the reptile patient. In a rhinoceros viper
(Bitis nasicornis), the material was still present 12 weeks after placement in both the pleuroperitoneum and subcuta-
neous tissues. Other absorbable materials not dependent on
proteolysis are recommended for deeper tissue closures.
Suture removal is generally scheduled 4 to 6 weeks postoperatively. In squamates, it is often advantageous to delay
suture removal until after the subsequent ecdysis. Frequently, the shed skin will stick to the incision site but is easily removed with gentle assistance. Following suture removal, the
skin may stick to the site of the incision for one or two more
sheds but normal ecdysis resumes quickly.
Incised reptilian skin has a strong tendency to invert. If
the skin is closed in such a manner that scales oppose scales,
the healing will be delayed since the cut edges are not in apposition. It is recommended that skin closure be accomplished with an everting suture pattern such as horizontal or
vertical mattress. Skin staples marketed for use in human
surgery are applicable to reptile patients. Not only are they
strong, but they also cause eversion of the skin allowing the
incised edges to be maintained in apposition for primary
healing.
INSTRUMENTATION
The small delicate nature of many reptile patients necessitates the use of small, fine-tipped instruments. Some form
of magnification is recommended for patients weighing less
than 1 kg. With the small size and blood volume of many patients, hemostasis is very important. With magnification,
vessels are much more easily identified for coagulation.
Though an operating microscope is indicated for small patients, binocular magnification loupes of 2.5x to 8x are adequate for most procedures (Orascopic, Dimension-3, Orascopic Research, Inc.; Surgitel, General Scientific, Inc.).
Some ophthalmic instruments are well-suited for magnification surgery. Iris scissors, iris forceps, micro mosquito
hemostats, iris hooks, eyelid retractors, retinal forceps, jeweler’s forceps, spring-handled scissors, and Castroviejo needle holders are particularly useful. Numbers 15 and 11
scalpel blades are most appropriate for surgery. Gauze pads
(2 x 2) can be cut from the standard 4 x 4 sponges. Sterile
cotton tipped applicators should also be available. Surgical
spears are small, wedge-shaped, very absorbent, synthetic
sponges attached to the end of a stick (Weck-Cell Surgical
Spears). They are useful for absorbing accumulated blood or
fluid in cavities. Absorbable gelatin sponges (Gelfoam, Upjohn) are used for controlling hemorrhage. Hemostatic clips
(Ligaclip, Pitman Moore, or Hemoclip, Weck), are available
in various sizes and are used to provide hemostasis for vessels in body cavities where it is difficult to apply ligatures.
Using the applier, the clip is placed across the lumen of the
vessel and clamped in place.
The eyelid retractors work well as wound retractors, and
the iris hooks can be utilized to manipulate delicate tissues.
A Heiss blunt retractor (Weck) combines quick, easy application, small size, good strength, and adequate spread. The
blade extends 6.5 mm with a 3.3 mm hook that is less likely
to snag sutures. A small Alm retractor with short blunt teeth
(Weck) is also effective, but slightly larger.
Electrosurgery such as with the Surgitron (Ellman International) is also extremely useful in reptile patients. The
bipolar ophthalmic forceps have application for abdominal
surgery in reptiles as they allow coagulation of vessels deep
within the coelomic cavity. Minimizing blood loss is critical
because many patients are very small. The electrosurgical
unit may be utilized for skin incision, body wall incision, organ biopsies, and a variety of other procedures.
For coelomic surgery in chelonians, some type of burr or
saw is necessary to cut through the osseous plastron. An orthopedic saw is ideally suited for this procedure, as it can be
autoclaved; however, they are often prohibitively expensive.
A rotary woodworking tool (Dremmel) may be used, but
most bits cut a wide gap, resulting in delayed bone healing.
Small circular saw blades are available for these woodworking tools (Micromark, Berkeley Heights, NJ). These blades
cut a very narrow osteotomy in the plastron, allowing for
faster bone healing. Such a tool cannot be autoclaved but
may be gas sterilized or covered with a sterile stockinette.
The bits may be gas or steam sterilized, but steam sterilized
bits corrode quickly. Some type of restorative material
should be available for repairing shell defects (Five Minute
Epoxy, Devcon, or Technovit, Jorgensen Laboratories).
PATIENT PREPARATION
Prior to surgery, nutritional and hydration status of the
reptile patient must be assessed. Malnourished patients are
thin with an abundance of loose, saggy skin. Dehydrated patients often have sunken eyes and a decrease in skin turgor.
Certainly the risks with major surgery are increased when
dealing with this type of patient. If surgery can be delayed
until the nutritional and hydration status are improved, it is
to the patient’s benefit.
Balanced electrolyte solutions can be given subcutaneously (SC), intracoelomically (ICe) or intraosseously
(IO). The intravenous (IV) route is also acceptable for fluid
administration; however, in many reptiles, it is difficult to
place and maintain an IV catheter. Sites for venipuncture
have been described. IO cannulation provides rapid access to
the vascular space and is applicable for even very small reptile patients. Fluids containing dextrose may be beneficial
for anorectic patients.
Reptiles are susceptible to a wide range of microbial infections and cutaneous infections often result in systemic
disease with visceral granuloma formation. It is generally
recommended to maintain the patient in a warm environment
postoperatively. At such temperatures bacterial proliferation
is potentiated. Most bacteria isolated from reptile patients
are gram-negative.
Creating a sterile field can be a challenge with reptile patients, especially those that are very small or legless. With
small patients positioned in dorsal recumbency, tape may be
used around the legs and adhered to the operating table to
provide traction to the limbs. For legless reptiles, the body
can be secured to a restraint board. Chelonians have a tendency to roll around when placed in dorsal recumbency. For
small chelonians, a towel may be rolled and placed in ring
configuration to control this rolling.
Clear plastic drapes (VSP, Boca Raton, FL; Barrier Incise Drape, Surgikos) provide visual assessment of the pa-
249
tient intraoperatively. The majority of clear plastic drapes are
of a small size. In order to create a large sterile field, a paper
drape with an opening cut large enough to accommodate the
patient’s size is placed over the clear plastic drape. Using
this technique, the entire operating table is covered with the
sterile paper drape that has a window for observation of the
patient. The patient is maintained in an aseptic field covered
with the clear plastic drape. Paper drapes may be reused two
or three times following autoclaving. Sterile spray adhesives
(Vi-Drape Adhesive, Deseret Medical) may be used with
cloth and paper drapes, so that the drapes stick to the patient
without the need for towel clamps. This is especially important with chelonians where towel clamps are not applicable.
Care must be taken when these adhesive-type materials are
removed from the patient to avoid damaging the skin. Alcohol or adhesive remover applied to a cotton swab may be
used at the skin adhesive junction to soften the adhesive and
aid in removal.
For snakes, draping can be accomplished using a sterile
stockinette rolled over the prepared patient. The snake, now
inside the stockinette, can be placed over the sterile drape
providing an aseptic field.
Though reptiles generally have a slower metabolic rate
during periods of hypothermia, it is recommended that supplemental heat be provided during surgery and anesthesia.
Major body functions of reptiles are dependent on temperature. Especially with ill or debilitated patients, lowering their
body temperature substantially reduces the efficiency of major body functions, including the immune system. A variety
of techniques for maintenance of body temperature during
anesthesia and surgery are available. Radiant heat through
light sources; circulating warm-water blanket, hot-water bottles, instant heat (Safe & Warm, Safe & Warm Incorporated,
Seattle, WA) and other sources are applicable.
Standard patient preparation solutions should be used for
reptile patients. Povidone-iodine and chlorhexidine have
been used. Chlorhexidine provides the advantages of broader spectrum of activity and increased residual activity. When
shell repair is required for chelonian patients, the surface of
the shell must be prepared by cleansing and degreasing the
surface in order that the restorative material stick to the shell.
Acetone, ether, or trichlorotrifluoroethane (Freon Skin Degreaser, Miller-Stevenson Chemical) may be used for this
purpose.
POSTOPERATIVE CARE
Following anesthetic recovery, the patient should be
maintained in a clean, warm, dark, quiet environment.
Swimming should be prevented for a period of 7 to 14 days
following surgery to allow a scab to form and desiccate. It is
best to prevent hibernation for approximately 6 months to allow healing to proceed. The nutritional and hydration needs
of the patient must be assessed and maintained. Fluid therapy is indicated to maintain the hydration status of the patient.
Many patients become anorectic following surgery requiring
tube or force-feeding. In some cases, pharyngostomy tube
placement may be necessary to provide long-term alimentation for the patient.
251
Reptile anesthesia
Douglas R. Mader
Geraldine Diethelm
Dr. vet. Med., Marathon Veterinary Hospital, USA
There are books written on the subject of anesthesia in all
the different species. However, in private clinical practice,
you don’t need to know fifty ways to anesthetize a hamster.
What you need is a standard protocol for the average patient.
You need standard protocols for all the different patients that
you work with. Whether the anesthesia is performed by a
veterinary technician or by the veterinarian, it is important
that these protocols are followed. Once you get used to a
particular drug or anesthetic protocol, you can learn what to
expect, and will be better able to deal with problems should
they arise.
GENERAL CONSIDERATIONS
Fasting
Reptiles do not have a problem with regurgitation during
anesthesia. Therefore, It is usually not necessary to fast these
animals prior to surgery unless you are planning on a gastric
procedure.
Pre-operative
All of the general principles of anesthesia an pre-operative evaluation that apply to mammal patients also apply to
exotic pets. A thorough pre-operative physical examination
by the surgeon, appropriate laboratory screening, radiographs etc., should all be performed, or at least recommended to the client. Patients should always be classified as
to their risk of anesthesia (healthy pet, elective procedure vs.
patient with major health problems), and the potential surgical risk (simple restraint for laboratory sample collection vs.
prolonged procedure with potential for major blood loss).
Caution should be taken with patients having a low PCV,
as these animal’s do not have a lot of blood to start with, so
even minor hemorrhage can be lethal in a small pet. Consider pre-operative transfusions in those animals at risk, have
blood ready for intra-operative transfusions, or at least premedicate patients with fluids prior to the procedures.
Since hypothermia is of paramount concern in these little patients, the fluids should always be pre-warmed prior to
administration. In addition, due to the generally higher metabolic rates in these little animals, it is wise to use a 5% dextrose solution, or a 2.5% dextrose in a balanced electrolyte
solution either pre-operatively, intra-operatively, or immediately post-operatively.
Most of the exotic pets that we deal with have a relatively large surface area to volume ratio (in general, the smaller
the pet, the larger the ratio). As mentioned, this larger surface area means that these patients are prone to hypothermia.
Some form of supplemental heating is mandatory for these
patients. Circulating warm water blankets, water filled
gloves, warmed anesthetic gasses (tube warmers), heated
fluids, heated lavage fluids, and for surgical prep, the use of
chlorhexidine rather than alcohol.
Reptiles, being ectothermic, can be totally unpredictable
in their response to anesthesia. To better control this, it is
best to eliminate temperature as a variable. Every reptile
group has its own preferred optimal temperature. For instance, a garter snake thrives at temperatures around the high
70’s to the low 80’s, whereas the green iguana needs temperatures in the low 90’s to flourish. So, when performing
anesthesia in these patients, where a garter snake may do just
fine at 80 degrees, the iguana may be slower to induce, may
be more difficult to maintain, and may take much longer to
recover.
Induction and Anesthesia
Injectable anesthetics are used frequently in reptiles.
However, the agents are used more for restraint than for
anesthesia.
Ketamine and Telazol (tiletamine/zolazepam) are my
drugs of choice. Telazol gets more use in my clinic, as I use
it on a daily basis. However, it needs to be reconstituted, and
252
if not used within 14 days, goes bad. It has the advantage
over ketamine in that the dose is much smaller, being especially useful in larger patients (large constrictors, tortoises).
Ketamine, due to its acidic pH, has a tendency to cause
discoloration to the scales in reptiles when injected superficially. These marks usually result in permanent discoloration,
so, it is prudent to advise your client prior to using it.
Although I have little experience with Propofol, reports
from England suggest that it makes an excellent pre-medicant in iguanids. At a dose of 1 ml/kg, IV in the tail vein
provides 10 - 15 minutes of anesthesia, allowing for intubation or minor procedures. Keep in mind that Propofol does
not produce analgesia.
As with the other exotics, for prolonged procedures, it is
wise to maintain the reptile patient with a volatile anesthetic. Again, isoflurane is the agent of choice as it permits rapid
induction and compared to the other agents, a more rapid recovery. It has the additional advantage of virtually no metabolism by the patient.
In reptiles, the glottis is always closed except when they
are taking a breath. So, the anesthetist must be patient and
not try to force the endotracheal tube into a closed glottis.
Reptiles are usually easy to intubate due to their rather
cranial placement of the glottis. Snakes are usually intubated directly without the benefit of pre-anesthetics. Lizards are
easily masked down prior to intubation, and turtles are variable. The large or powerful species may need to be premedicated with some sort of tranquilizer in order to facilitate intubation.
Post-operative
The most important thing to remember post-operatively
is to maintain the patient’s warmth. The pet should be moved
to a warmed recovery cage or incubator. In addition, fluid
balance must be addressed, as dehydrated patients will have
a more difficult time metabolizing or eliminating the anesthetic.
Post-operative analgesia should always be a consideration. Few analgesia studies have been done in reptiles, but
substantial work has been done in small mammals due to
their extensive use in laboratory research. I usually use flunixen meglumine at 2 mg/kg, IM, q 24 hrs for 2 to 3 days.
PATIENT MONITORING
ANESTHESIA OF THE REPTILE
Pre-operative
PE
Lab work (blood, radiographs, E.C.G., etc)
IV, Fluids prn
Antibiotics prn
Pre- meds (glycopyrrolate, 0.01-0.02 mg/kg SC, IM)
Induction
ketamine = 50 mg/kg, IM
- or Telazol = snakes, lizards, water turtles, 5 mg/kg, IM
tortoises, 10 - 20 mg/kg, IM
- orface mask induction = lizards
Maintenance
isoflurane via mask or endotracheal tube (preferable)
Anesthetic monitoring
monitoring reflexes
Doppler
Pulse Oximeter
Recovery
keep warm and quiet
Analgesia
butorphenol, 0.1 - 0.5 mg/kg SC, IM, IV, q 2-4 hrs
- or flunixin megulime, 1 - 2 mg/kg, SC, IM, q 12-24 hrs
Over the years several monitoring devices have been employed to evaluate anesthetized patients. The electrocardiogram has been the gold standard. Although the significance
of the tracings may not be fully understood for all the
species, it usually provides reliable indication of the patient’s pulse rate. In addition, to the observant anesthetist, it
may also provide clues toward impending changes in the patient’s condition. Many of the smaller patients, and most of
the reptilian patients, are impossible to monitor with an
E.C.G. due to either their rapid heart rates, or the small electrical potential produced.
Ultrasonic Dopplers detect pulsatile blood flow in the patient. It produces an audible signal for each pulse wave. It is
considered very accurate, but has the disadvantage of not being able to provide any clues on the patient’s physiological
changes. In addition, the noise that the Doppler produces is
grating to listen to, and is usually best when attached to
headphones.
The stethoscope, regular bell type or esophageal, is an
excellent monitoring device providing that it is used. However, they are usually ineffective in reptiles.
Recent advances in anesthetic monitoring in human medicine have seen the introduction of the pulse oximeter to veterinary anesthesia. Specifically, the pulse oximeter has been
used to monitor pulse and oxygenation during anesthesia
and critical care settings. The pulse oximeter employs noninvasive technology and is user-friendly, requiring minimal
training for proper and accurate usage by even lay staff.
These attributes make its use in anesthetic monitoring for exotic patients an attractive adjunct to the more conventional
electrocardiogram or Doppler ultrasonic flow detectors.
The pulse oximeter is a spectrophotoelectric device that
is applied typically via means of a clamp, preferable over a
pulsating vascular bed to glabrous areas of the skin. The
probe contains a diode that emits light in both the red and infra-red wavelengths. This dual-wavelength emitted light
then passes through the pulsating vascular bed adjacent to
the diode, and then is registered in a photodetector. The percent transmittance of the light is calculated within the unit
and further equated to an oxygen saturation estimate.
Reptiles, unlike mammals which maintain respiratory
drive based on many factors, including blood CO2 and pH,
regulate their respiratory rate by careful balance of oxygen
partial pressure (PO2) and body temperature. At higher temperatures, the tissue demand for oxygen likewise increases.
The increase demand is not met by an increase in respiratory rate, but rather an increase in tidal volume.
Of particular clinical significance here is the ability to
monitor the delivered oxygen to the tissues of anesthetized
reptiles. It is not uncommon for reptiles post-procedure to
remain anesthetized for prolonged periods. By monitoring
SPO2 it may be possible to more accurately assess the state of
the reptilian patient. In mammalian anesthesia the tendency
is there to frequently bag the patient during recovery, whereas, in the reptilian patient, this increased oxygen may actually be inhibiting the return to spontaneous respiration.
The sensor traditionally has been incorporated into a finger or “clothespin-like” clamp positioned either over the patient’s finger (human) or tongue (veterinary patient). There
are several new probes available for use with exotics. Aside
from the standard tongue clips, there are now C-clamps, tail
wraps and esophageal/rectal probes. Of all the species, the
birds are probably the most difficult to monitor, however, it
253
is usually possible, using one of the probes, to monitor most
any patient. The esophageal probes seem to be the most effective in the avian patient.
Reptilian patients have been difficult to monitor due to
their thick skin and oftentimes heavy pigment, making
placement of any kind of clamp-on type of sensor ineffective. The rectal or esophageal probe make the measurement
of pulse rate and arterial oxygen saturation more feasible
even in these patients.
Placement of the esophageal probe is best when the spectrophotometric diodes are positioned adjacent to the internal
carotids/jugular vein complex, which is readily accessible
through the oral cavity in an anesthetized patient. In patients
where this is not logistically feasible (oral surgery), a membranous sheath can be applied over the probe so that it can
be inserted rectally, with the diodes directed dorsally so that
it can sense the caudal aorta and renal arteries. This is not as
efficient in the avian patients. In these cases, using the Cclamp over the thigh has been effective.
Summary
Regardless of the instrumentation employed, there is no
substitute for an alert, attentive anesthetist. Heart rate, respiratory rate, mucous membrane color, capillary refill time and
reflexes are all reliable, useful parameters for monitoring the
anesthetized patient. Don’t forget your medicine that you
learned in dogs and cats. Don’t be afraid to apply the principles to your exotic patients.
255
Fracture management in reptiles
Douglas R. Mader
Fractures in captive reptiles are common, usually being
secondary to primary nutritional deficiencies. Specifically,
pathological fractures frequently occur as a result of Nutritional Secondary Hyperparathyroidism (NSHP), which is a
general lack of dietary calcium, excessive phosphorus or deficiency in exposure to ultraviolet light/vitamin D3. Even
traumatic fractures, which under normal conditions with
healthy bones would not occur, are more likely due the generalized osteopenia associated with NSHP.
Extremity fractures are rarely compound or comminuted.
As a result, most fractures are readily treated with external
coaptation. In addition, since most fractures are often associated with demineralization and softening of the bones, internal fixation is usually not indicated. In the unlikely event
of a traumatic fracture involving normal bone, internal fixation can be utilized.
Regardless of the etiology, nutrition and diet should be
thoroughly evaluated in all fracture cases. Before attempting
any repair calcium homeostasis should be established. The
medical management in these cases is equally as important
as the surgical attention.
GENERAL CONSIDERATION
Frye states that most fractures occur as a result of low
impact forces, thus making the incidence of comminuted
fractures uncommon. In addition, due to their relatively inelastic skin, open or compound fractures are infrequent.
Little information is available on fracture healing in reptiles. No controlled studies have been conducted. Most of the
information that is known comes from anecdotal reports relating treatment successes/failures in cases of NSHP. It is
generally accepted that reptilian bone heals slower that either mammalian or avian bone, requiring from two to eighteen months to completely heal.
When planning fracture repair in reptiles general principles of orthopedic management apply. Proper alignment,
rigid stabilization, minimal disruption of soft tissue and conservation of the blood supply is paramount. The forces acting on the fracture (bending, rotation, compression and
shear) must be evaluated and neutralized to promote rapid
healing. In general, the more forces that must be neutralized
by the type of fixation, the higher the incidence of complications and failures.
Additional considerations when deciding upon type of
fracture repair include the patient’s functional requirements
(pet lizard in a terrarium vs. a Komodo dragon being returned to the wild), cost limitations set forth by the client,
the cost and availability of the required materials and the experience of the veterinarian.
Most long bone fractures will heal in time with nothing
more than strict cage rest. Although there may be some severe malunions, these complications do not seem to affect
captive reptiles in an adverse manner.
The size of the patient and its nutritional state may have
a direct impact on the type of fixation required. Large, heavy
bodied lizards and turtles may require internal fixation,
whereas small, delicate lizards may do well with a light
splint.
The general condition of the patient often plays a major
factor in the selection of fixation methods. In many of these
NSHP animals it is physically impossible to utilize any type
of internal fixator, as the bones just are not physically strong
enough for the implant to gain purchase.
As in anything in veterinary medicine, the dollar is often
the deciding factor in final determination of fixation technique. Internal fixation carries a higher price tag due to the
cost of the materials, the time necessary for application and
the training of the surgeon. Although internal fixation may
be the best for the patient, it is not always an option.
EXTERNAL COAPTATION
External coaptation involves the use of splints, slings,
casts and any other technique needed to immobilize a fracture. This is by far the most commonly utilized technique in
reptilian fracture repair. In general, the best splints/casts are
those that are lightweight and comfortable for the patient. If
the patient’s activity is restricted lightweight splints/casts are
effective.
When treating pathological fractures secondary to nutritional disease external fixation is the treatment of choice.
NSHP is the most common disease presenting to reptilian
veterinarians, and most frequently seen in the Green iguana.
Bone is a dynamic organ, undergoing constant remodeling. During prolonged hypocalcemia/hypovitaminosis D, the
mineralization process lags behind the formation of organic
bone matrix, resulting in the formation of hypomineralized
256
bone. When this occurs in young, growing animals it is
called rickets, and in adults, it is known as osteomalacia.
Pathological fractures occur when the calcium content decreases to approximately one-third of its baseline. Aside
from pathological fractures of the long bones and appendicular skeleton, soft, swollen mandibles and long bones (fibrous osteodystrophy), stunted growth, deformed heads and
abnormalities in ambulation are common.
These bones are too soft to provide support to the implants used in internal fixation techniques. IM pins, cerclage
wires and bone screws all penetrate, crush and pull out when
used in these wax-like bones. An IM pin may be utilized for
alignment in long bone fractures, but when used, it should be
in conjunction with external coaptation.
Once the calcium homeostasis is corrected the healing
progresses rapidly, with a bony callous forming in about
three to four weeks. Correcting management and husbandry
deficiencies and providing proper dietary and supplemental
calcium is needed. In addition, treating the patient with synthetic salmon derived calcitonin helps speed recovery by inhibiting the actions of parathyroid hormone, blocking the actions of the osteoclasts, stimulating the osteoblasts and providing bone analgesia. 50 IU/kg of calcitonin, IM in the triceps, administered q 1 week for two treatments is the recommended dosage. It is important that the patient is eucalcemic prior to the administration of the calcitonin.
There have been numerous methods reported in the literature for external coaptation in reptiles. There is no one right
way. Whatever technique works best in your practice situation is the best method to use. The most important thing to
remember is that the best splints/casts are the lightest and
most comfortable to the patient.
When applying external coaptation remember that the
patient is most likely in pain. Anesthesia or sedation is recommended for patients that struggle or if extensive manipulation of the fracture(s) is required.
The initial padding around the limb can be performed
with many different types of bandage material (Specialist
Cast Padding, Johnson & Johnson, New Brunswick, NJ;
Conform, Kendall Co., Boston, MA). Make sure that the
padding is cut to the appropriate width to prevent bunching
of the padding around the joints.
Tape stirrups should be incorporated into the padding
when applying the splint/cast to prevent slippage. It is not
uncommon for the splint/cast to slide down the leg after the
cast padding compresses.
This padded limb can now be reinforced by adding aluminum rods, tongue depressors and light weight casting material. It is important to conform the shape of the splint/cast
to the natural angles of the limb. This will prevent the development of fracture disease, or periarticular fibrosis, in the
immobilized joints.
Veterinary Thermoplastic (IMEX Veterinary, Inc.,
Longview, TX), Hexcelite (Hexcelite Medical, Dublin, CA)
and Orthoplast (Johnson & Johnson, New Brunswick, NJ)
are rigid at room temperature, but malleable when heated in
a water bath. The Veterinary Thermoplastic is easy to apply
when heated and cools to make a rigid splint. It comes in different sizes and thicknesses, making it convenient for different size patients.
Splints/casts can be easily applied to any of the long
bones in lizards. When applying splints/casts it is important
to follow general principles of fracture stabilization. The
joints both proximal and distal to the fracture should be immobilized.
For both humeral and femoral fractures a modified spicatype splint must be used. The splint should incorporate the
distal joint, and then have a portion that crosses over the
body. For the femur, the band should cross cranial to the vent
so that it does not interfere with elimination. In humeral
fractures, the band can cross diagonally across the chest,
passing between and under the front legs.
Chelonians can also be splinted, but modifications in
technique are required. It is usually not possible to apply a
splint to a proximal long bone (humerus/femur). These
bones can be reduced (with sedation/anesthesia as needed)
and then taped into the leg opening in the shell. I recommend
covering the limb with cast padding to add stability to the
“set limb” before taping over the opening. I also recommend
taking a radiograph of the leg folded up within the shell to
make sure that fracture alignment is appropriate.
Splints/casts do not provide rigid fracture fixation. As a
consequence, fracture healing is not as rapid as it would be
with a plate or external fixation device. However, the bone
will heal.
I recommend re-checking the fit of any splint/cast within one week of the initial application. You should always
check for slippage, swelling of the distal extremities and
pressure sores. Splints/casts are usually left on for a minimum of four, and usually six to eight weeks. Follow-up radiographs should be taken at four weeks, and again when the
cast is removed.
INTERNAL FIXATION
Internal fixation is warranted for long bone fractures in
reptiles where external coaptation is not a practical option.
Large, heavy, active and otherwise healthy reptiles all do
well with internal fixation. Internal fixation techniques utilized in mammals and approaches to the long bones are similar to those employed in reptiles.
Steinmann pins, Kirschner wires, spinal needles and
stylets can all be used as IM pins in reptiles. In addition,
these devices can all be used as parts for External Skeletal
Fixation (ESF). ESF can be used in a variety of fracture
types in reptiles of all sizes.
When using these delicate implants as a part of the ESF,
the external connecting bar and clamps are replaced by a
methylmethacrylate polymer. This is inexpensive, easy to
use and light.
Pin loosening is a common problem with ESF. Whenever possible it is recommended to use threaded pins. The
threads should be applied to the outside of the pin, not cut
into it.
Bone plating can be utilized, but in general requires a
larger patient. Cuttable plates (Synthes, Paoli, PA) with 1.5
mm diameter screws can be applied to bones as small as 3
mm diameter. Finger plates are also applicable in certain situations.
In general, plates do not need to be removed. IM pins and
ESF should be removed when there is radiographic evidence
of bone healing. In some cases a fibrous union may be all
that is needed to ensure eventual healing, thus allowing the
removal of loose pins as needed.
AMPUTATION
When there is severe tissue trauma, loss of blood supply or granulomatous infection in the limb, fracture repair
may not be a viable option. Amputation of either the foreor hind limbs is a viable option in reptiles, as they do quite
well with three limbs. Amputation of digits or limbs can
be accomplished with excellent cosmetic and functional
results.
257
Digits should be amputated at their base. The plantar/palmar flaps should be longer than the dorsal flaps so that the
incision is sutured above the substrate. This keeps the incision clean.
When amputating limbs it is best to remove the entire
appendage. Disarticulation at either the scapulohumeral or
coxofemoral joints is recommended. Limb muscles are transected distally and then elevated proximally. The joint is exposed and the limb removed. The muscle bellies are then sutured over the joint space to provide soft-tissue padding.
Nerves can be transected with a scalpel and injected with
bupivicaine to provide local analgesia post-operatively.
In chelonians after a limb amputation it may be necessary to provide some sort of prosthesis. A block of wood, a
plastic skid or a furniture roller can be glued to the plastron
to aid in locomotion.
259
Soft tissue surgery
Douglas R. Mader
R. Avery Bennett
DVM, DAVCS, University of Pennsylvania, School of Veterinary Medicine
A variety of clinical situations may result in a need to
perform surgery on a snake patient. It is vital to have a basic
understanding of the unique anatomy and physiology of the
particular reptile species prior to undertaking surgery.
CELIOTOMY
The approach for celiotomy in reptiles varies with the
family of reptile to which the patient belongs.10 Celiotomy
provides access to all the coelomic organs of reptiles and has
a wide range of applications. It will provide access to thoracic structures such as the heart and lungs and abdominal
structures such as the gastrointestinal system and major
body organs.
Indications include reproductive disorders, gastrointestinal disease, urinary system dysfunction, and exploration for
obtaining organ biopsies.
In snakes, it is best to perform a celiotomy at the lateral
margin of the body where the scutes and scales are in apposition. The advantage of making the incision between the
first two rows of lateral scales is that when the incision is
closed with an everting pattern it does not distort the flat
conformation of the ventral scutes. The incision should be
made between the scales, resulting in a scalloped configuration. This will enhance healing since the incision is made
through the softer portion of the skin between the scales. The
incision should be made along the body in a position that
provides access to the structure being approached. Once the
incision has been made through the skin, the body wall must
be incised. Keeping in mind that one pair of ribs is associated with each scute to the level of the vent, it is best to avoid
any trauma to the ends of the ribs.
Reportedly, there is no difference in exposure gained by
a ventral midline incision compared with this lateral approach; however, the lateral approach is easier to keep clean,
as it is not in direct contact with the substrate during the
postoperative period and the incision is less stressed by the
snake’s crawling movements.
Snakes do have a large ventral midline abdominal vein
present just inside the body wall in the caudal portion of the
body. If a ventral midline approach is used, care must be taken to avoid this vessel. Closure is generally in two layers:
one in the body wall (simple continuous) and the second in
the skin (an everting pattern).
DYSTOCIA
There is considerable variation among reptile species regarding their reproductive physiology. The approach to the
reproductive system of female reptiles is generally by celiotomy as described previously. Surgery is indicated when
noninvasive medical techniques have failed to relieve dystocia or if there is evidence that natural passage of the eggs or
fetuses is not possible. A decision on when to perform
surgery may be difficult to make. In some cases, however,
the egg densities are more radiodense than would be expected. Typically, reptilian eggs are not very densely calcified
and an increase in calcific density indicates that the eggs
have been in the shell gland an excessive period of time. This
may be the result of infection, resulting in delayed transit
through the oviduct and shell gland. In this situation, surgery
is recommended. Additionally, if the eggs are of abnormal
size and shape precluding passage through the pelvic canal,
surgery is indicated.
In general, the uterus, oviduct, and ovaries of reptiles are
fairly mobile within the coelomic cavity. In snakes, it may be
necessary to make more than one incision through the skin
and body wall in order to gain access to the long reproductive structure of the female. In many cases, by the time
surgery is elected, the eggs or fetuses have begun to deteriorate and are adhered to the uterus, which is often very thin
and friable.
260
Salpingotomy or hysterotomy incisions are generally repaired using an inverting suture pattern of an absorbable
synthetic suture material. It is always important to get samples for diagnostic evaluation at the time of surgery. In many
cases, bacterial infections are causative and with successful
treatment, reproductive viability may be regained.
The reproductive physiology and the feedback loop between the ovary and oviduct/shell gland of reptiles is not
well understood. It does, however, appear that both organs
are required for normal reproductive activity. If the ovaries
are removed, it appears that the oviduct and shell gland begin to atrophy. However, if the oviduct and shell gland are
removed, the ovaries may remain active. Therefore, it is imperative that the ovaries are always removed at the time of
the saplingotomy or hysterectomy.
There are some anecdotal reports of yolks being released
into the coelomic cavity following removal of the oviduct
and uterus or shell gland. Because of this, if time and patient
condition permit, removal of both the ovaries and oviduct
and shell gland are recommended. In cases where patient
condition does not permit a lengthy surgery, the ovaries only may be removed.
In cases of preovulatory egg binding, the ovaries must be
removed; however, if the oviduct and shell gland are left intact, they appear to atrophy and are not especially susceptible to infection and other medical conditions. In cases of
postovulatory egg binding, where the eggs are within the
oviduct and shell gland, these structures should be removed,
which then allows better access to the underlying ovaries.
The oviduct and shell gland are richly supplied by large
blood vessels, especially when reproductively active. These
vessels are most easily controlled using hemostatic clips,
transecting between two closely applied clips. The process is
initiated at the infundibulum and vessels are ligated and transected, progressing caudally towards the junction of the shell
gland with the cloaca. At this location, two clips are applied
to the shell gland, which is then transected and submitted for
diagnostic analysis.
In performing an ovariectomy, it is important to note that
the right ovary is very close anatomically to the vena cava.
The right ovary is elevated and hemostatic clips are applied
between the ovary and the vena cava. These will control hemorrhage from the artery and vein supplying the ovary. The
ovary can then be removed following transection of the tissues between the ovary and the clips.
Though the left ovary is not anatomically close to the vena cava, the artery and vein that supply it are adhered to the
left adrenal gland and care must be taken to avoid damaging
the gland. Again, the hemostatic clips are applied just below
the ovary and the tissue between the ovary and the clips is
transected, allowing removal of the left ovary.
Egg peritonitis may be the result of yolks being released
from the reproductive tract into the coelomic cavity. In some
cases, well-formed eggs rupture through the oviduct and
may also be found within the coelomic cavity. This may be
the result of turning the animal on its back during the
process of egg production, allowing the egg to fall dorsally
and not be picked up by the infundibulum. Another reported
cause for egg peritonitis is the presence of cystic calculi,
which may traumatize the developing eggs within the reproductive tract, allowing them to escape into the abdomen. The
presence of yolk within the coelomic cavity induces a severe
inflammatory reaction with deposition of fibrin and thickening of the serosal surface of the viscera. Generally the prognosis for such patients is grave. Treatment consists of removal of the offending material and copious irrigation of the
coelomic cavity. Systemic antibiotic therapy and maintenance of hydration and nutritional balance are also vital.
GASTROINTESTINAL PROCEDURES
The basic principles for gastrointestinal surgery in
snakes are similar to those for mammals. Surgery is indicated for removal of foreign bodies that may cause obstruction,
for resolution of intussusception, or for intestinal impaction.
Gastrointestinal abnormalities induce clinical signs such as
regurgitation, obstipation, weight loss, anorexia, and abdominal distention. Foreign body removal, resection-anastomosis, and anastomosis for colorectal atresia have been successfully performed in reptiles.
In small reptile patients, the intestine is quite thin walled,
making the use of fine suture and atraumatic needles important. The mesentery that suspends the gastrointestinal tract
of reptiles is quite variable in length. It is preferable to exteriorize the affected section of bowel in order to prevent contamination of the coelomic cavity. If this cannot be accomplished, the area to be incised should be isolated with gauze
sponges packed within the coelomic cavity of the patient.
Following closure of the incision in the gastrointestinal tract,
copious irrigation should be performed.
TRACHEAL RESECTION FOR CHRONIC
OBSTRUCTIVE LESIONS IN SNAKES
Cartilaginous granuloma arising from the tracheal cartilage may cause a gradual onset of dyspnea in snakes. Affected snakes present with open-mouth breathing, depression, and anorexia. The lesion is usually visualized on plain
radiographs as a soft tissue dense mass within the air dense
tracheal lumen. Endoscopy confirms the presence of a nonmoveable mass within the tracheal lumen.
The trachea is approached as described for celiotomy in
snakes based on the radiographic location of the lesion. The
entire section of affected trachea is removed, and the trachea
is anastomosed using a fine, monofilament absorbable suture. Suture should encompass one or two tracheal rings on
each side of the tracheotomy.
The patient is generally able to breathe without discomfort immediately postoperatively. As much as 2.5 cm of trachea has been removed without adverse affect.
261
Influence of physiotherapy on articular cartilage
Denis J. Marcellin-Little
DEDV, Diplomate ACVS, Diplomate ECVS, Department of Clinical Sciences
College of Veterinary Medicine, North Carolina State University - 4700 Hillsborough St, Raleigh, NC 27606-1499
INFLUENCE OF PHYSICAL THERAPY ON
ARTICULAR CARTILAGE
JOINT MOTION
Immobilization is detrimental to joint health. Cartilage
nutrition is promoted by the displacement of synovial fluid
that occurs during joint motion. Joint motion and weight
bearing promote the diffusion of nutrients into articular
cartilage. Also, synovial fluid production is reduced with
joint immobilization.
Partial immobilization (i.e., casting) is less detrimental
than complete immobilization (i.e., external skeletal fixation). With joint immobilization, the cartilage becomes
softer (42% softer in an 11-week-long canine study) and
thinner (9% in the same study).1 Joint immobilization in
flexion is less detrimental than joint immobilization in extension. While immobilization in extension leads to
changes resembling degenerative joint disease, immobilization in flexion leads to the atrophy of articular cartilage
without degenerative joint disease. Remobilization after
immobilization will lead to cartilage regeneration. This
restoration appears more complete after immobilization in
flexion than after immobilization in extension. The recovery of cartilage after immobilization may never be complete. In a canine study including 11 weeks of immobilization and 50 weeks of remobilization, the biomechanical
properties of the articular cartilage at the end of study remained 15% below control level (p=0.05).2 Intense exercise during that period will prevent restoration of normal
cartilage thickness and proteoglycan concentration. It is
therefore important to increase exercise moderately and
progressively after joint immobilization. Cartilage regeneration after immobilization may be improved by the intraarticular administration of hyaluronic acid. In a study of
cartilage regeneration after 4 weeks of immobilization of
the stifle joints in dogs, remobilization combined with
hyaluronic acid (HA) therapy improved histochemical
staining and reduced structural damage to articular cartilage when compared with remobilization alone.3 It is important to note that immobilization may protect cartilage
during the period immediately following an injury. After
chemically induced cartilage injuries in guinea pigs, immobilization in the short term (for 3 weeks) had definite
protective effects on the cartilage.4
Postoperative immobilization in a plaster cast for six
weeks and early mobilization in an ankle brace for one to
two weeks were compared in a prospective, randomized
study of patients undergoing surgery and internal fixation to
repair ankle fractures. Ten weeks after surgery, muscle
torque and range of motion were less impaired in the early
mobilization group. Also, 12 months after surgery, range of
motion in flexion was increased in the early mobilization
group compared to the plaster cast group.5 Another prospective, randomized study evaluated early mobilization of distal
radial fractures and confirmed an increase in grip strength
and joint range of motion in the group with early mobilization compared to the group with a short arm cast.6
PRACTICAL APPLICATIONS
Treating patients after arthrotomies
Arthrotomies are commonly performed in dogs to treat
cranial ligament injuries, luxations, to excise osteochondral
flaps secondary to osteochondritis dissecans, bone fragmentation, or incomplete ossification, to repair articular fractures, perform partial arthrodeses, or to stabilize collateral
ligament tears. The conventional postoperative management
after these arthrotomies is widely variable, based on surgeons’ preferences and the perceived need to postoperative
joint stabilization after repair. For example, some surgeons
place limbs in splints for four weeks after tibial crest transposition, some place these limbs in a soft padded bandage
for a couple of weeks, while others do not use bandage or
splints. Few clinical studies have evaluated the effects of
various modalities on dogs after arthrotomies were performed. The most common joint operated in our hospital, at
North Carolina State University, is the stifle joint. Stifle are
operated to treat to cranial cruciate ligament injuries and
patellar luxation, and less often, to treat osteochondritis dissecans, intra-articular fractures, avulsion of the tendon of
origin of the long digital extensor muscle, or collateral ligament ruptures. The recovery after stifle arthrotomies is slow,
262
especially when cranial cruciate ligament-deficient stifles
are stabilized. Millis evaluated the influence of cranial cruciate ligament transsection and immediate stabilization on
the muscle mass and found a significant decrease in muscle
mass. Ten weeks after resection, muscle loss was most pronounced in the quadriceps femoris, biceps femoris, and
semimembranosus muscles.7 Johnson evaluated effects of
electrical muscle stimulation on clinical parameters after
experimentally-induced cranial cruciate ligament transsection and surgical stabilization.8 Twelve dogs were included
in the study (6 dogs treated 5 times a week for 4 weeks, 6
control dogs). Electrical muscle stimulation was successful
in promoting faster return to function of the operated limb,
slowing osteophyte development in the stifle joint, and increasing the circumference of thigh muscles. Electrical stimulation, however, did not appear to lead to a statistically significant increase in peak vertical force or caudal propulsive
forces. Also, meniscal damage appeared increased in the
treated group suggesting that early return to function before
peri-articular fibrosis is complete may place dogs at risk of
meniscal injuries. Electrical muscle stimulation has been
used successfully in man after repair of anterior cruciate ligament injuries. Practically, dogs likely benefit from cold
therapy, massage, early mobilization through range of motion exercises, hydrotherapy, and low-impact exercises
during their postoperative rehabilitation.
Treating patients with articular fractures
The postoperative management of articular fracture
often presents a dilemma. On the one hand, anatomic
joint alignment must be maintained despite the relative
lack of strength of most repairs that rely on Kirschner
wires and bone screws. On the other hand, early mobilization is very beneficial to the joint. Hinged external
fixation and articulated braces allow joint movement
while protecting the joints. Their use, however, is very
limited in veterinary medicine. We are using hinged external fixation to protect joints after such surgeries. These
hinged external fixators may be locked when joint movement should be avoided, for example when the pain perceived is high. When these fixators are not used, a careful
postoperative plan may be designed that includes cold
packs, massages, and early mobilization through range
of motion exercises, in the immediate postoperative period. Weight bearing activities should be strictly limited
during the bone healing period. Underwater treadmill or
whirlpool therapy may be used since they allow physiologic joint motion without high impacts.
References
1.
Treating patients with degenerative joint
disease
Little is know about the benefits of exercise and physical
modalities in the management of degenerative joint disease
(DJD) in dogs. Millis wrote that active and passive exercises,
swimming, massage, heat therapy, cold therapy, and electrical
stimulation could have beneficial effects on joints with DJD in
dogs.9 Exercise may protect against the development of DJD.
This may be due indirectly to the fact that obesity is less likely in active animals and that obesity predisposes dogs to DJD.9
Oosterveld reviewed the scientific basis for treatment of
arthritis with locally applied heat or cold in vitro, in animals,
in healthy subjects, and in patients.10 The results were inconsistent. In general, locally applied heat increased and locally
applied cold decreased the temperature of the skin, superficial
tissues, deeper tissues, and joint. Most studies reported beneficial effects. Because higher temperatures may increase
breakdown of articular cartilage and tissues that contain collagen, Oosterveld concluded that when treating actively inflamed arthritic joints the goal of physical therapy should be
to decrease intra-articular temperature.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Jurvelin J, Kiviranta I, Tammi M, et al. Softening of canine articular cartilage after immobilization of the knee joint. Clin Orthop
1986;207:246-52.
Haapala J, Arokoski J, Pirttimaki J, et al. Incomplete restoration of
immobilization induced softening of young beagle knee articular
cartilage after 50-week remobilization. Int J Sports Med
2000;21:76-81.
Keller WG, Aron DN, Rowland GN, et al. The effect of trans-stifle
external skeletal fixation and hyaluronic acid therapy on articular
cartilage in the dog. Vet Surg 1994;23:119-128.
Williams J, Brandt K. Immobilization ameliorates chemically-induced articular cartilage damage. Arthritis Rheum 1984;27:208-16.
Tropp H, Norlin R. Ankle performance after ankle fracture: a randomized study of early mobilization. Foot Ankle Int 1995;16:79-83.
Millett P, Rushton N, Millet P. Early mobilization in the treatment
of Colles' fracture: a 3 year prospective study. Injury 1995;26:671675.
Millis D. Changes in muscle mass following transsection of the cranial cruciate ligament and immediate stifle stabilization. Proc Int
Symp Rehab Phys Therap Vet Med. Corvallis, Oregon 1999:155.
Johnson JM, Johnson AL, Pijanowski GJ, et al. Rehabilitation of
dogs with surgically treated cranial cruciate ligament-deficient stifles by use of electrical stimulation of muscles. Am J Vet Res
1997;58:1473-1478.
Millis D, Levine D. The role of exercise and physical modalities in
the treatment of osteoarthritis. Vet Clin North Am Small Anim Pract
1997;27:913-30.
Oosterveld F, Rasker J. Treating arthritis with locally applied heat
or cold. Semin Arthritis Rheum 1994;24:82-90.
263
Influence of physiotherapy on bone
In humans, physiotherapy (PT) has a definite positive influence on the recovery rate after surgical treatment of fractures and chronic bone and joint diseases. The specific benefits of PT (i.e., exercises, manipulation, or physical agents)
on bone metabolism is harder to quantify. PT may influence
the bone in several ways: 1.) It may help maintain bone composition and density in patients at risk of osteoporosis or osteopenia, 2.) It may promote fracture healing, and 3.) It may
promote bone regeneration during bone lengthening procedures. The purpose of this review is to present the specific
effects of PT on these aspects of bone metabolism and to use
this information to make practical recommendations.
BONE METABOLISM
The effect of physical exercise on bone composition has
been evaluated in postmenopausal women. Ballard evaluated 50 women and found that high physical activity significantly increased the bone mineral composition compared to
low physical activity (0.834 g/cm versus 0.721 g/cm,
p<0.01). Estrogen therapy also had a positive influence on
bone mineral composition in these women (0.907 g/cm with
therapy versus 0.809 g/cm without therapy, p < 0.027).1 Surprisingly, another study involving 2025 peri- and postmenopausal women documented higher bone mineral density in the women that had performed recreational and competitive sporting activities as adolescents than the women
that did not perform such activities as adolescents.2 Once adjusted for age, weight, time from menopause to densitometry, and duration of estrogen replacement therapy, the bone
mineral density was 1.4% higher (p = 0.015) in the women
who exercised during their adolescence. This shows that
physical activities have a very long-term positive influence
on bone metabolism.
Manipulation has also been shown to influence bone
metabolism. Wilson evaluated whether manipulation
techniques generate potentially osteogenic levels of strain
within mammalian bone.3 In that study, manual levered
bending created levels of compressive strain similar in
magnitude to those created by mechanical devices used in
previous animal experiments to induce new bone formation (osteogenesis).
When the influence of physical agents on bone is considered, most of the scientific work has focused on the influence of electrical currents on bone metabolism and fracture healing. Bone formation was induced in rabbits by
placing a cathode within the medullary canal of bone with an
anode encircling the femoral shaft and applying a direct current of 20 µA during six weeks.4 When direct currents (ranging from 0.02 to 0.2 µA/mm2) were applied for 21 days in
rabbits, bone production was increased by approximately
50%. Platinum appears to be the most stimulatory metal
compared to cobalt-chrome, silver, stainless steel, and titanium.5 Bone ingrowth into porous implants is also enhanced
by the application of electrical stimulation. Colella reported
that interfacial shear strength between porous titanium implants and cortical bone was consistently greater in dogs
treated with electrical stimulation compared to control
dogs.6 Electrical stimulation may also affect the cellular behavior of growth plates. In a three-week-long, in-vivo study
of the effect of direct-current stimulation (8 µA) on the distal femoral growth plate of young rabbits, characteristic
thickening of the growth plate caused by the accumulation of
hypertrophic cells was found in the group stimulated for two
weeks.7 Electricity also may have a protective effect on osteoporosis. In a report evaluating the influence of pulsed
electromagnetic fields on the progression of osteoporosis in
the ulna of turkeys (one hour per day of pulsed electromagnetic fields), an osteogenic dose-response to induced electrical power was observed, with a maximum osteogenic effect
between 0.01 and 0.04 tesla per second.8 Another study in
turkey confirmed these findings and found optimal osteogenesis with a 15 Hz sinusoidal electric field.9 The effects of
electrical muscle stimulation on bone density have been
evaluated in patients with spinal cord injury. Electrical muscle stimulation does not seem to have a positive effect in the
short term and appears to have a positive effect, albeit minor,
when used over longer periods of time. In a short-term study,
electrical muscle stimulation did not influence bone mineral
content or bone density. During a 32-week-long exercise period four paraplegic men volunteered for an exercise program in which their paralyzed quadriceps muscles were
stimulated by means of computer-regulated electrical impulses applied through external electrodes.10 Another sixmonth study evaluating the effects of functional electrical
stimulation (FES) cycle ergometry on bone mineral density
(BMD) was investigated in six quadriplegic men, failed to
264
show changes in femoral bone mineral density.11 A longerterm study found that an electrical stimulation exercise program used on the lower limb of 37 patients with spinal cord
injury significantly decreased bone loss over time (0.2 and
3.3% reduction in loss per year, p < 0.05).12
FRACTURE HEALING
Early and continued mobilization (manipulation, exercises) has profound beneficial effects on all the healing
process of all musculoskeletal tissues. Also, prolonged rest
or immobilization may delay recovery or adversely effect
tissues. Buckwalter recently reviewed the effects of early
motion on healing of musculoskeletal tissues.13 He wrote:
“Experimental studies, of the past several decades confirm
and help explain the deleterious effects of prolonged rest
and the beneficial effects of activity on the musculoskeletal
tissues. They have shown that maintenance of structure and
composition of normal bone, tendon and ligament, articular
cartilage and muscle, requires repetitive use and that
changes in the patterns of tissue loading can strengthen or
weaken normal tissues. Although all the musculoskeletal
tissues can respond to repetitive loading, they vary in the
magnitude and type of response to specific patterns of activity. Furthermore, their responsiveness may decline with
increasing age. Skeletal muscle and bone demonstrate the
most apparent response to changes in activity in individuals
of any age. Cartilage and dense fibrous tissues also can respond to loading, but the responses are more difficult to
measure. The effects of loading on healing tissues have
been studied less extensively but the available evidence indicates that repair and remodeling tissues respond to loading and that, like immature normal tissues, repair tissues
may be more sensitive to cyclic loading and motion than
mature normal tissues. Early motion and loading of injured
tissues is not without risks, however. Excessive or premature loading and motion of repair tissue can inhibit or stop
healing. Unfortunately, the optimal methods for facilitating
healing by early application of loading and motion have not
been defined. Nonetheless, experimental studies and newer
clinical investigations document the benefits of early controlled loading and motion in the treatment of musculoskeletal injuries, and show that optimal restoration of
musculoskeletal function following injury or surgery requires early controlled activity”.13 Bone fragment motion
influences fracture healing. While axial micromotion stimulates bone healing, 14 shear is detrimental to fracture healing. Circular external fixators help ensure the absence of
shear while allowing axial micromotion. This may be the
most significant factor responsible for the enhanced fracture
healing associated with circular external fixation used to
treat long bone fracture in dogs compared to plate or conventional external fixation.15
Electrical stimulation with direct current has wide applications in the stimulation of fracture healing, especially in
the treatment of non-unions and delayed unions. The electrodes may be implanted in the bone or, more recently, have
been placed on the surface of the skin.16,17 Electrically stimulated titanium cathodes (current density: 0.33 µA/mm2) enhanced bone formation in a model of canine delayed union.18
In a ten-year review of patients treated with implanted electrodes, all fractures had remained united and normal bone
remodeling had occurred. This ten-year review supported
the long-term safety and effectiveness of this technique in
treating nonuniting fractures.19 Non-invasive methods (steel
plates placed on the skin across the fracture site) have shown
excellent results in the treatment of non-unions in man. Scott
evaluated 21 patients with non-unions, six of ten treated with
electrical capacitive coupling healed; none of the patients
left untreated healed (p=0.004).20 Abeed reported on the use
of 40-mm-diameter stainless steel plates providing capacitively coupled electrical stimulation (63 kHz, 6V peak-topeak sine wave) for up to 30 weeks in 16 patients. He found
that a distance of 80 mm or less between the electrodes resulted in healing in all cases. He also found that healing was
not affected significantly by any of the following factors:
whether or not the non-union had been treated surgically
prior to stimulation, whether or not it had been infected,
whether or not the patient bore weight after treatment, or by
the presence or absence of metal at the fracture site from
previous surgery. He concluded that the dependence of healing on the interplate distance suggests that maintaining sufficient current across the plates is necessary to allow healing,
which for larger bones may be achieved by increasing the
area of the plates, the applied voltage, or the excitation frequency of the stimulation signal.21
BONE HEALING AND CLINICAL RESULTS
AFTER LIMB LENGTHENING
Physical therapy is an important component of the success of limb lengthening. Coglianese wrote that limb lengthening by distraction osteogenesis and external fixation is
used increasingly in the United States for a variety of orthopedic conditions. Maintenance of joint motion critical for
successful outcomes can be difficult to achieve.22 In a clinical review of limb lengthening, Greene wrote that the patient
must be encouraged to bear weight on the lengthening limb,
lest the newly formed bone fail to mature and corticalize
properly.23
PRACTICAL RECOMMENDATIONS
Clinically we know that limb use is important after limb
trauma and fracture repair. Disuse osteoporosis will result
from prolonged immobilization or absence of weight bearing. In fact, limb immobilization alone has been shown to
have detrimental effects in experimental dogs including loss
of bone size and weight, 24 and contracture of the quadriceps
femoris muscle. Although the causes of osteoporosis are not
well known, a lack of muscular activity, increased blood
supply, and a decrease in piezoelectric action of bone crystals on bone cells from the absence of weight bearing are
considered to be important factors.25
THESE PRINCIPLES SHOULD ALWAYS
BE FOLLOWED:
• Orthopedic fixation methods should never interfere
with the normal range of motion of adjacent joints. Intramedullary pins should not interfere with the hip joint
or sciatic nerve. Plates should not contact articular surfaces. External fixators should be compact enough to
avoid restriction in limb function.
• Casts should be avoided after fracture treatment.
• If a soft padded bandage is placed on a limb after
surgery, it should not remain in place for more than a
few (possibly three to five) days. The limb immobilized
in a bandage should always be placed in a functional
weight bearing position and hyperextension should be
avoided.
• Controlled range of motion manipulations should be
started immediately after surgery with simultaneous
pain management. Controlled weight bearing activities
should follow.
• Suspected complications (osteoporosis, contractures)
should be identified early and treated aggressively.
• Physical therapy must be considered in all high risk patients, including limb lengthening procedures.
265
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
References
1.
2.
3.
4.
5.
6.
Ballard JE, McKeown BC, Graham HM, et al. The effect of high level physical activity (8.5 METs or greater) and estrogen replacement
therapy upon bone mass in postmenopausal females, aged 50-68
years. Int J Sports Med 1990;11:208-14.
Puntila E, Kroger H, Lakka T, et al. Physical activity in adolescence
and bone density in peri- and postmenopausal women: a populationbased study. Bone 1997;21:363-7.
Wilson AW, Davies HM, Edwards GA, et al. Can some physical therapy and manual techniques generate potentially osteogenic levels of
strain within mammalian bone? Phys Ther 1999;79:931-8.
Lagey CL, Roelofs JM, Janssen LW, et al. Electrical stimulation of
bone growth with direct current. Clin Orthop 1986;303-12.
Spadaro J. Electrically enhanced osteogenesis at various metal cathodes. J Biomed Mater Res 1982;16:861-73.
Colella S, Miller A, Stang R, et al. Fixation of porous titanium im-
19.
20.
21.
22.
23.
24.
25.
plants in cortical bone enhanced by electrical stimulation. J Biomed
Mater Res 1981;15:37-46.
Sato O, Akai M. Effect of direct-current stimulation on the growth
plate. In vivo study with rabbits. Arch Orthop Trauma Surg
1990;109:9-13.
Rubin C, McLeod K, Lanyon L. Prevention of osteoporosis by pulsed
electromagnetic fields. J Bone Joint Surg [Am] 1989;71:411-7.
McLeod KJ, Rubin CT. The effect of low-frequency electrical fields
on osteogenesis. J Bone Joint Surg 1992;74A:920-9.
Pacy P, Hesp R, Halliday D, et al. Muscle and bone in paraplegic patients, and the effect of functional electrical stimulation. Clin Sci
1988;75:481-7.
Leeds E, Klose K, Ganz W, et al. Bone mineral density after bicycle
ergometry training. Arch Phys Med Rehabil 1990;71:207-9.
Hangartner T, Rodgers M, Glaser R, et al. Tibial bone density loss in
spinal cord injured patients: effects of FES exercise. J Rehabil Res
Dev 1994;31:50-61.
Buckwalter J. Effects of early motion on healing of musculoskeletal
tissues. Hand Clin 1996;12:13-24.
Kenwright J, Richardson JB, Cunningham JL, et al. Axial movement
and tibial fractures. A controlled randomised trial of treatment. J Bone Joint Surg 1991;73B:654-9.
Marcellin-Little DJ. Fracture treatment with circular external fixation. Vet Clin N Am Sm Anim Pract 1999;29:1153-1170.
Clark DM. The use of electrical current in the treatment of nonunions. Vet Clin N Am Sm Anim Pract 1987;17:793-798.
Mason DR, Renberg WC. Postsurgical enhancement of fracture repair: biophysical alternatives to bone grafting. Comp Cont Ed Pract
Vet 2001;23:423-430.
Collins P, Paterson D, Vernon -RB, et al. Bone formation and impedance of electrical current flow. Clin Orthop 1981;196-210.
Cundy P, Paterson D. A ten-year review of treatment of delayed union
and nonunion with an implanted bone growth stimulator. Clin Orthop
1990;259:216-22.
Scott G, King J. A prospective, double-blind trial of electrical capacitive coupling in the treatment of non-union of long bones [see comments]. J Bone Joint Surg Am 1994;76:820-6.
Abeed RI, Naseer M, Abel EW. Capacitively coupled electrical stimulation treatment: results from patients with failed long bone fracture unions. J Orthop Trauma 1998;12:510-3.
Coglianese D, Herzenberg J, Goulet J. Physical therapy management
of patients undergoing limb lengthening by distraction osteogenesis.
J Orthop Sports Phys Ther 1993;17:124-32.
Green S. Postoperative management during limb lengthening. Orthop
Clin North Am 1991;22:723-34.
Geiser M. J Bone Joint Surg 1958;40B:282-311.
Leighton RL. Quadriceps contracture In: M. Bojrab, ed. Disease mechanisms in small animal surgery. Philadelphia: Lea & Febiger,
1993;1076-1078.
267
Principles and clinical applications
of goniometry in dogs
Goniometry is the measure of the angles formed by
joints. These angles may be measured either in a standing
position or in flexion or extension.1-3 Goniometry is performed using a measuring device, in general a transparent
plastic goniometer. Goniometry is a simple, affordable,
and non-invasive method to quantitate the range of motion
of joints. The accuracy and reproducibility of goniometry
in humans have been documented and various goniometric
methods have been compared. Goniometry is used extensively by orthopedic surgeons and physical therapists in
human medicine to quantify baseline limitation of joint
motion, to decide on appropriate therapeutic interventions,
and to document the effectiveness of these interventions.
Goniometry has been similarly used in canine orthopedics
to assess treatment efficacy for problems involving the
carpal,1 elbow,4-8 stifle,9 or coxofemoral joints.2,10,11 In
dogs, however, goniometry has not been validated and only scant information is available regarding goniometric
methods and reference values. 12-15 The reported ranges of
motion in dogs have been based on measurements made
on 10 mixed breed dogs in one report and 15 mixed breed
dogs in another report.13-15
We conducted a study that intended to 1) validate goniometry in Labrador Retrievers by comparing measurements made with a plastic goniometer to measurements
made on radiographs, 2) evaluate intertester reliability, 3)
evaluate intratester reliability, 4) evaluate the effects of
sedation on the range of joint motion, and 5) establish
normal parameters for joint range of motion in adult
Labrador Retrievers free of orthopedic diseases. We hypothesized that goniometry was valid and reliable and
that the maximal range of motion evaluated under sedation was not statistically different from the pain-free
range of motion evaluated in awake dogs. We hypothesized that less variation between measurements was present when distal joints (carpus and tarsus) were evaluated
than when proximal joints (shoulder and coxofemoral
joints) were evaluated. We also hypothesized that less
variation was present for the last five dogs evaluated compared to the first five dogs evaluated in this study. To test
these hypotheses, three investigators blindly and independently examined 16 Labrador Retrievers.
Sixteen Labrador Retrievers were randomly selected
from our local breed club for inclusion in the study. The
sample size was determined prior to the onset of the study by
conducting a statistical power analysis to determine the minimal number of dogs necessary to conduct statistical comparisons between study groups. The criteria for inclusion in
the study were being at least 18 months of age, being registered by the American Kennel Club, having no direct blood
relationship to other dogs included in the study, having no
lameness nor history of orthopedic disease or trauma, having
a normal orthopedic examination, and having no radiographic evidence of joint disease. All dogs were evaluated
within a one-week period. One randomly selected front limb
and ipsilateral pelvic limb were evaluated from each dog.
The 14 joint positions evaluated included carpal, elbow,
shoulder, tarsal, stifle, and coxofemoral flexion and extension, carpal valgus, and carpal varus. The three investigators
independently made goniometric measurements of each dog
awake and under sedation for a total of 4032 measurements.
To assess intratester variation, five sets of three goniometric
measurements were performed for all joint positions on one
dog by one investigator with an interval of 15 minutes or
more between each set of measurements.
Sixteen Labrador Retrievers (6 males and 10 females)
were included in the study. The median age of the dogs in
the study was 3 years (range, 2 to 7 years) and median
weight was 32 kg (range, 27 to 46 kg). The goniometric
measurements did not differ statistically from radiographic
measurements. The investigators had 2, 10, and 12 years of
professional experience, respectively. The measurements
made by the three investigators did not differ statistically
from each other (P ranging from 0.22 to 0.99). The median
variance present within the 15 measurements made by one
investigator for all joint positions was 3° (range, 1 to 6°).
The measurements made awake did not differ statistically
from the measurements made under sedation. Statistical differences were not present between the first and last five dogs
evaluated (P = 0.11 for dogs awake and P = 0.90 for dogs sedated). The mean of the variances present in distal joints was
smaller than the mean of the variances present in proximal
joints (P = 0.002 for dogs awake and P = 0.02 for dogs sedated). Since sedation and investigators did not affect the go-
268
Table 1. Range of motion of 16 normal Labrador Retrievers.
Joint
Position
Carpus
Flexion
Extension
Valgus
Varus
Flexion
Extension
Flexion
Extension
Flexion
Extension
Flexion
Extension
Flexion
Extension
Elbow
Shoulder
Tarsus
Stifle
Hip
Low normal†
High normal†
Mean
Median
31°
194°
11°
6°
34°
164°
54°
164°
37°
162°
40°
160°
48°
160°
34°
197°
13°
8°
38°
167°
59°
167°
40°
166°
43°
164°
52°
164°
32°
196°
12°
7°
36°
165°
57°
165°
39°
164°
42°
162°
50°
162°
32°
196°
12°
7°
36°
166°
57°
165°
38°
165°
41°
162°
50°
162°
niometric measurements, the mean, median, and 95% confidence intervals for all investigators and for awake and sedated dogs were averaged to calculate the combined mean, median, and 95% confidence interval for joint range of motion
in normal Labrador Retrievers (Table).
6.
While this study validates goniometry in normal dogs,
additional research is needed to provide objective information regarding the ranges of angles present at rest or during
locomotion of normal dogs and to provide information about
the changes present in ranges of motion in dogs with various
orthopedic diseases. The standing joint angles in the canine
pelvic limbs of 15 mixed breed dogs, 16 Labrador Retrievers, and 16 Greyhounds have been reported.13,16 Information
regarding joint angles is particularly important when planning joint arthrodeses or the correction of limb deformities.3,17 More complete information regarding the range of
motion during locomotion has been collected in several
kinematic studies.18
8.
References
1.
2.
3.
4.
5.
Marcellin-Little DJ, Ferretti A, Roe SC, et al. Hinged Ilizarov external fixation for correction of antebrachial deformities. Vet Surg
1998;27:231-45.
Marcellin-Little DJ, DeYoung BA, Doyens DH, et al. Canine uncemented porous-coated total hip arthroplasty: results of a long-term
prospective evaluation of 50 consecutive cases. Vet Surg 1999;28:1020.
Collins KE, Lewis DD, Lanz OI, et al. Use of a circular external skeletal fixator for stifle arthrodesis in a dog. J Sm Anim Pract
2000;41:312-315.
Huibregtse BA, Johnson AL, Muhlbauer MC, et al. The effect of
treatment of fragmented coronoid process on the development of
osteoarthritis of the elbow. J Am Anim Hosp Assoc 1994;30:190-195.
Roy RG, Wallace LJ, Johnston GR. A retrospective long-term evaluation of ununited anconeal process excision on the canine elbow.
Vet Comp Orthop Traumatol 1994;1994:94-97.
7.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Bouck GR, Miller CW, Taves CL. A comparison of surgical and medical treatment of fragmented coronoid process and osteochondritis
dissecans of the canine elbow. Vet Comp Orthop Traumatol
1995;8:177-183.
Sjöström L, Kasström H, Källberg M. Ununited anconeal process in
the dog. Pathogenesis and treatmetn by ostotomy of the ulna. Vet
Comp Orthop Traumatol 1995;8:170-176.
Cook JL, Tomlinson JL, Reed AL. Fluoroscopically guided closed reduction and internal fixation of fractures of the lateral portion of the
humeral condyle:prospective clinical study of the technique and results in 10 dogs. Vet Surg 1999;28:315-321.
Johnson JM, Johnson AL, Pijanowski GJ, et al. Rehabilitation of dogs
with surgically treated cranial cruciate ligament-deficient stifles by
use of electrical stimulation of muscles. Am J Vet Res 1997;58:14731478.
Prostredny JM, Toombs JP, VanSickle DC. Effect of two muscle sling
techniques on early morbidity after femoral head and neck excision
in dogs. Vet Surg 1991;20:298-305.
de Haan JJ, Goring RL, Beale BS. Evaluation of polysulfated glycosaminoglycan for the treatment of hip dysplasia in dogs. Vet Surg
1994;23:177-181.
Newton CD. Normal joint range of motion in the dog and cat. Appendix B In: C. D. Newton and D. M. Nunamaker, eds. Textbook of
Small Animal Orthopaedics. Philadelphia, PA: Lippincott,
1985;1101-1106.
Mann FA, Wagner-Mann C, Tangner CH. Manual goniometric measurement of the canine pelvic limb. J Am Anim Hosp Assoc
1988;24:189-194.
Riegger-Krugh C, Millis D. Canine anatomy and biomechanics. I:
Forelimb In: C. Wadsworth, ed. Basic science for animal physical
therapists. La Crosse, WI: Orthopedics Section, APTA, Inc., 2000;227.
Riegger-Krugh C, Weigel J. Canine anatomy and biomechanics. II:
Hindlimb In: C. Wadsworth, ed. Basic science for animal physical
therapists. La Crosse, WI: Orthopedic Section, APTA, Inc., 2000;228.
Wilke VL, Conzemius MG, Benson T, et al. Tibial plateau angle with
respect to the ground in the normal Labrador Retriever and
Greyhound. Proc Vet Orthop Soc 2001;28:7.
Cofone MA, Smith GK, Lenehan TM, et al. Unilateral and bilateral
stifle arthrodesis in eight dogs. Vet Surg 1992;21:299-303.
DeCamp CE. Kinetic and kinematic gait analysis and the assessment
of lameness in the dog. Vet Clin N Am Small Anim Pract
1997;27:825-840.
269
Update on the diagnosis of elbow dysplasia
GONIOMETRY
A goniometer may be used to measure the range of motion of the elbow joint. In normal Labrador Retrievers, the
range of motion of the elbow ranges from 34 to 38° (mean
and median, 36°) in flexion and from 164 to 167° (mean,
165° and median, 166°) in extension. Based on preliminary
results of a study ongoing in our Teaching Hospital,the range
of motion of the elbow of Labrador with elbow dysplasia
ranged from 45 to 76° (mean, 56° and median 53°) in flexion and from150 to 165° (mean, 161° and median, 162°) in
extension (Table 1).
Table 1. Range of motion of the elbow joint in Labrador
Retrievers.
Dysplastic elbow
joints
Normal elbow
joints
Flexion
Mean, 56°
Range, 45 to 76°
Mean, 36°
Range, 34 to 38°
Extension
Mean, 161°
Range, 150 to 165°
Mean, 165°
Range, 164 to 167°
projections have been used to image the MCP: mediolateral,
flexed mediolateral, extended 15°-supinated mediolateral,
craniocaudal, craniolateral caudomedial 15- to 50°-oblique,
and medio-15°-caudal laterocranial oblique projections.2,7-12
The sensitivity of the conventional radiographic projections
to image the MCP is suboptimal and has been estimated to
only range from 10 to 62% at a specificity of 100%.12,13 Additional diagnostic imaging methods used in the identification of fragmentation of the MCP include linear tomography, xerography, computed tomography (CT), and magnetic
resonance imaging (MRI). CT and MRI have a higher accuracy, sensitivity, and specificity than radiography.13,14 These
methods, however, are more costly than radiography and
have a limited availability.
We conducted a study aimed at describing and evaluating
a new radiographic view that would potentially enhance visualization of the MCP in dogs. We hypothesized that the
medio-35°-distal lateroproximal oblique (MEDLAP) radiographic view would enhance the diagnosis of fragmentation of the MCP in dogs. In order to test this hypothesis, we
conducted a pilot anatomic study on 20 cadaver limbs and a
blinded, prospective clinical study on 100 elbow joints.
Table 2. Identification of the medial coronoid process in
20 cadaver limbs.
RADIOGRAPHY
Positive identification
Radiographic view
Elbow dysplasia is the most common developmental
anomaly of the elbow joint in dogs and one of the most common orthopedic problems affecting large and giant breed
dogs.1 The manifestations of elbow dysplasia may include an
abnormal medial coronoid process (MCP), osteochondritis
dissecans of the trochlea, the failure of the anconeal process
to unite with the olecranon process, and incongruity of the
joint surfaces.2 Fragmentation of the MCP appears to be the
most common manifestation of elbow dysplasia.3-5 Early diagnosis of fragmentation of the MCP is critical to provide
optimal treatment before the development of degenerative
joint disease and for early selection of healthy breeding
stock. The MCP is unfortunately the most difficult portion of
the joint to image on radiographs.6 Multiple radiographic
Examiner 1
Examiner 2
Examiner 3
Mediolateral
Flexed
mediolateral
60%
25%
0%
95%
45%
20%
Craniocaudal
20%
5%
5%
Cranio-15°-lateral
caudomedial
oblique
80%
35%
50%
Medio-35°-distal
lateroproximal
oblique
100%
100%
100%
270
For the anatomic study, the identification rate of the
MCP varied widely depending on readers and views (Table
2). The MEDLAP view allowed positive identification of the
MCP in all joints and was more sensitive than the craniocaudal and cranio-15°-lateral caudomedial oblique views
(Table 2). Fifty-three dogs were included in the clinical
study. Six dogs had unilateral arthroscopy and 47 dogs had
bilateral arthroscopies for a total of 100 arthroscopies. Thirty-four dogs were male (64%) and 19 were female (36%).
Twelve breeds and one mixed-breed dog were included and
23 dogs were Labrador retrievers (43%). The median age
was 9 months (range, 5 months to 11 years). The median
weight was 31 kg (range, 16 to 49 kg). On arthroscopic examination of the MCP, 18 were normal, 45 MCP were fractured (19 fractures were displaced), 35 were fissured, and
two had chondromalacia. Forty-seven elbows had pathology
of the trochlea with 11 dogs having osteochondritis dissecans. Forty-six of 47 dogs with pathology of the trochlea had
an abnormal MCP. At a specificity level of 90%, the median
sensitivities to detect anomalies of the MCP were 0.35 for
the craniocaudal view, 0.39 for the cranio-15°-lateral caudomedial oblique view, 0.43 for the mediolateral view, 0.54 for
the flexed mediolateral view, and 0.80 for the MEDLAP
view and the median sensitivities to detect fractured MCP
were 0.29 for the craniocaudal view, 0.34 for the cranio-15°lateral caudomedial oblique view, 0.30 for the mediolateral
view, 0.41 for the flexed mediolateral view, and 0.55 for the
MEDLAP view.
of the curve shapes (Pearson’s correlation=0.9 in most cases). The fraction of accurate diagnosis of fractured MCP (defined as the sum of true positives and true negatives divided
by the total number of cases) and the fraction of accurately
positive diagnosis of fractured MCP (defined as the number
of true positives divided by the total number of cases)
demonstrated that only the MEDLAP and mediolateral
views could statistically differentiate fractured and non-fractured MCP using Fisher’s exact tests. The kappa agreement
between the radiographic and arthroscopic diagnosis of fracture of the MCP was 0.17 for the mediolateral, 0.16 for the
flexed mediolateral, 0.02 for the craniocaudal, 0.16 for the
cranio-15°-lateral caudomedial oblique, and 0.32 for the
MEDLAP view.
The findings of this study indicate that the MEDLAP radiographic view allows better visualization of the MCP than
several previously described views used to diagnose pathology and fragmentation of the MCP. The MEDLAP view
seems to be particularly advantageous to diagnose the presence of an abnormal MCP, even in the absence of a separate
MCP fragment. This may make the MEDLAP view particularly suited as a screening radiographic view when suspecting the presence of elbow dysplasia in young dogs.
References
1.
Table 3. Areas under ROC curves for five radiographic
views used for detection of an abnormal or fractured
medial coronoid process in 100 elbow joints.
Radiographic
view
Mediolateral
Flexed mediolateral
Craniocaudal
Cranio-15°-lateral
caudomedial oblique
Medio-35°-distal
lateroproximal
oblique
Abnormal
MCP
Fractured
MCP
0.731
0.788
0.738
0.646
0.712
0.693
0.754
0.645
2.
3.
4.
5.
6.
7.
8.
0.896
0.798
9.
10.
ROC curves representing the detection of an abnormal
and fractured MCP using the median value of the examiners
for each view were drawn (Table 3). For detection of abnormal MCP, the area under the MEDLAP curve was statistically higher than the areas under other views (P < 0.05) except for the flexed mediolateral view (P = 0.09). Statistics
could not be performed to compare the craniocaudal and
MEDLAP views due to degenerate data and a high Pearson’s
correlation (r=0.9). ROC curves were also drawn for patients
with fracture of the MCP. Statistical analyses could not be
performed to compare these curves due to high correlations
11.
12.
13.
14.
Morgan J, Wind A, Davidson A. Bone dysplasias in the labrador retriever: a radiographic study. J Am Anim Hosp Assoc 1999;35:33240.
Kirberger RM, Fourie SL. Elbow dysplasia in the dog: pathophysiology, diagnosis and control. J S Afr Vet Assoc 1998;69:43-54.
Olsson SE. General and aetiologic factors in canine osteochondrosis.
Vet Quart 1987;9:268-278.
Wind AP. Elbow incongruity and developmental elbow diseases in the
dog: Part II. J Am Anim Hosp Assoc 1986;22:725-730.
Van Ryssen B, van Bree H. Arthroscopic findings in 100 dogs with
elbow lameness. Vet Rec 1997;140:360-362.
Hornof WJ, Wind AP, Wallack ST, et al. Canine elbow dysplasia. The
early radiographic detection of fragmentation of the coronoid process. Vet Clin North Am Small Anim Pract 2000;30:257-266.
Berzon JL, Quick CB. Fragmented coronoid process: anatomical, clinical and radiographic considerations with case analyses. J Am Anim
Hosp Assoc 1980;16:241-251.
Robins GM. Some aspects of the radiographical examination of the
canine elbow joint. J Sm Anim Pract 1980;21:417-428.
Voorhout G, Hazewinkel HAW. Radiographic evaluation of the canine elbow joint with special reference to the medial humeral condyle
and the medial coronoid process. Vet Radiol 1987;28:158-165.
Miyabayashi T, Takigushi M, Schader SC, et al. Radiographic anatomy of the medial coronoid process of dogs. J Am Anim Hosp Assoc 1995;31:125-131.
Boulay JP. Fragmented medial coronoid process of the ulna in the
dog. Vet Clin N Am Sm Anim Pract 1998;28:51-74.
Wosar MA, Lewis DD, Neuwirth L, et al. Radiographic evaluation of
elbow joints before and after surgery in dogs with possible fragmented medial coronoid process. J Am Vet Med Assoc 1999;214:52-58.
Carpenter LG, Schwarz PD, Lowry JE, et al. Comparison of radiologic imaging techniques for diagnosis of fragmented medial coronoid
process of the cubital joint in dogs. J Am Vet Med Assoc
1993;203:78-83.
Snaps FR, Balligand MH, Saunders JH, et al. Comparison of radiography, magnetic resonance imaging, and surgical findings in dogs
with elbow dysplasia. Am J Vet Res 1997;58:1367-1370.
271
Guidelines for a correct approach
to the critical patient
Yves Moens
DVM, PhD, Dipl. ECVA, Department of Clinical Veterinary Medicine,
Veterinary Faculty, University of Berne, Switzerland
ASSESSMENT AND PREPARATION
All patients must be assessed prior to anaesthesia. The risk
of aspiration and the ease of intubation should be checked.
The results of medical and surgical evaluation should be discussed and the availibility of blood and blood products should
be assessed. The result of necessary investigation i.e. blood results should be available prior to anesthesia except a life
–threatening condition needs immediate anesthesia. Absolutely minimally hematocrit, total protein, glucose and blood urea
should be known. Hypovolemia and -if known- electrolyte
disturbances (especially hyperkalemia), should be treated before commencing anesthesia. FIRST STABILIZE!!
If pain exists treat pain (preferably an opiate or a regional
technique) and provide a comfortable and warm environment.
CONDUCT OF ANAESTHESIA
Draw up the anesthetic required and prepare all emergency drugs such as adrenaline, atropine and vasopressors if
indicated. All monitoring should be switched on before inducing anesthesia. Capnography, pulsoximetry, ecg, noninvasive blood pressure or invasive blood pressure preferably
available. Suction devices must be ready (vomiting or regurgitation during induction). In most ill patients pre-oxygenation with 100% oxygen for 3 minutes will decrease risk of induction. Induce ad effect with careful clinical observation.
Consider the combination of regional anesthetic techniques
with general anesthesia to diminish the concentration of anesthetic agent. Ensure the adequate intravenous access even during surgery, two access lines can be useful. Always ensure the
port for giving emergency drugs to be in good reach. Some
very critical patients will benefit of the placement of a central
venous catheter to monitor fluid therapy and heart function
during and after operation. Do everything to limit hypothermia. Perform and carefully titrate postoperatieve pain therapy.
Induction can be done with thiopentone, propofol. Alpha-agonists should not be use in urethral obstruction as
they induce urination. Use minimal dose of ketamine in FUS
(< 2mg/kg). Renal blood flow (RBF) and Glomerular filtration rate (GFR) are decreased, depending on depth of anesthesia, fluid status, cardiovascular systems and anesthetic
agents.
Autoregulation of renal blood flow exists between 60160 mmHg, try to maintain blood pressure in this range.
Treat hypotension first with decreased anesthetic concentration, then fluids and finally vasopressors. Check urine postoperative urine output and ureum/creatinine.
CARDIAC DISEASE
In principle heart medication should not be withdrawn
before anesthesia.Tachycardia may be detrimental to patients depending on the cardiac output i.e. hypertrophic
CMP or atrial fibrillation. Tachycardia increases cardiac
oxygen demand. Prevent tachycardia, prevent excitement,
ketamin, anticholinergics. Sedation: not necessasry if profoundly depressed. ACP decrease blood pressure and provokes hypothermia.
Useful for afterload reduction in PDA and mitral insufficiency. It is also anti-arrhythmogenic. Contra-indication:
epilepsy, hypovolemia, hepatic desease, heart failure, aortic
or pulmonary stenosis. Induction can be done with an opiate-benzodiazepine mixture ad effect iv (fentanyl+valium)
or with etomidate (for the very compromised cases) preceded by iv valium or midazolam always after preoxygenation!
ECG monitoring, capnography and pulsoximetry as soon as
possible post induction. Limit fluid therapy during anesthesia in congestive heart failure. Maintain anesthesia with iv
opiate (fentanyl) and a low concentration of isoflurane.
Monitor blood pressure if possible.
PULMONARY DISEASE
Renal disease-obstruction
If possible treat anemia before anesthesia (blood tranfusion), oxygen carrying capacity is otherwise decreased.
Treat hyperkalemia (do not anesthetise before K < 5).
Most anesthetics depress respiratory function. If possible
delay surgery in patients with pulmonary edema, pneumothorax, lung contusions or hydrothorax. Try to improve the situation (punction, analgesia). A mild sedation can be helpful
272
in controlling stress. ACP has minimal effect on ventilation.
Opioid agonists-antagonist are less respiratory depressive
than pure agonists (ACP 0,03 mg/kg + Butorphanol 0,2
mg/kg).
Always pre-oxygenate 3-5 minutes. A rapid induction is
necessary to gain control of the airway and be able to use IPPV. In case of recent pneumothorax it can be better to try to
maintain spontaneous respiration (or ventilate with high frequency and low tidal volume). Monitor oxygenation with
pulsoximetry. In principle do not use N2O. PEEP (positive
end expiratory pressure) can be considered if oxygen satura-
tion remains low despite ippv with 100% oxygen (5 to 10 cm
H2O) if cardiac output is sufficient. Provide postoperative
oxygen (oxygen cage, nasal canula, elisabethan collar).
CRANIAL TRAUMA
In principle ketamine should be avoided and barbiturate
induction is a good choice. Isoflurane maintenance. Avoid hypoventilation, rather hyperventilate to reduce cerebral vasodilatation (PCO2 30 mmHg). Avoid acp, opiates controversial.
273
Principles and techniques of locoregional
analgoanesthesia (perispinal, brachial plexus ...)
Yves Moens
A combination of local or locoregional anesthesia with a
general anesthesia has several very important advantages:
1) a satisfactory surgical plane of anesthesia can be obtained with much lesser doses of general anesthetics
(volatile or intravenous agents).
2) With the combination of the local techniques and a
general (light) anesthesia the postoperative analgesia will be
better/longer or at least easier to control with additional
medication in this phase (less CNS sensitization).
Off all this techniques topical application, tissue infiltration, ring blocks and epidural anesthesia are easy to do in
practice. Subdural (in the cerebrospinal liquid) anesthesia
and particular nerve blocks like the plexus brachialis block
are somewhat more difficult. Lidocaine (1-2%) and bupivacaine (0.2-0.7%) remain the products of choice.
1. TOPICAL APPLICATION
Application of local anesthetic ointments, liquid solutions or sprays (lidocaine) on nasal and oral mucous membranes, esophagus, trachea, urogenital mucosae is possible.
Intrapleural analgesia following introduction of a local anesthetic in the pleural cavity (thoracotomy, via thorax drain).
The intact skin is not penetrated except following application of a special formula of prilocaine (emla).
2. TISSUE INFILTRATIONS
A very simple and to often a neglected possiblity (eg linea alba and skin for cesarean section, laparatomy).
10 minutes in all tissues distal to the tourniquet/cuff that last
as long as they stay in place; sensibility returns within minutes after release of the tourniquet or cuff.
4. PLEXUS BRACHIALIS BLOCK
This is a block of the n.axillaris, n.medianus, n.ulnaris,
n.musculocutaneus, n.radialis following succesful infiltration of the area of the plexus brachialis situated at the level of the shoulder joint at the medial side of the scapula
(e.g. 2-20 ml lidocaine 1 or 2%, or mixture of lido and
bupi). Excellent method for radius/ulna surgery. Complications are pneumothorax, nerve trauma, bleeding and intravascular injection.
Technique (mostly performed on the anesthetised animal):
1. direct an injection (long) needle medial from the
shoulder joint in the direction of the first rib (palpate) and
proceed to the level of the bone-cartilage junction.
2. Aspirate (air? blood?) and infiltrate the area.
3. If succesful there will be analgesia and motoric paralysis (not detectable when this block is performed under
anesthesia which will be normally the case). Analgesia extends from the elbow to distal. Succesful block will be apparent when conducting general anesthesia: low concentration of inhalation agent and /or analgesics necessary, stable
vital parameters.
A new method consists in locating the nerve truncs of the
plexus with a nerve stimulator and a special needle („electrolocation“). The closer the needle point is to the nerve the
lower the current will be that is needed to elicit a twitch from
the distal leg. This increases succes rate of plexus brachialis
block and reduces the amount of local anesthetic needed.
3. INTRAVENOUS REGIONAL ANESTHESIA
(BIER’S BLOCK)
5. INTERCOSTAL BLOCKS
Although a simple and effective technique for distal extremity surgery not exceeding 1.5 hrs this anesthetic technique is not always favoured by some surgeons because of
the lack of bleeding in the operated area. In principle a rubber tourniquet or an inflattable cuff is applied above the area
to be operated upon, punction of a vene and iv injection of
0.5-1% lidocain. This realises an effective analgesia after 5-
These are used before thoracotomies or when starting to
close the thorax; this can also be used for analgesic support
with rib fractures. Inject in the intercostal muscles close to
the origin of the rib at its caudal border 0.2 to 1 ml 2% lidocain and this in two intercostal spaces before and two spaces
after the thoracotomy incision.
274
6. SPINAL ANESTHESIA
b) Doses: 1ml/4,5 kg bw effect up to L1, 1ml/3,5 kg bw
effect up to Th4; 1ml/6 kg bw for sectio cesarea
Mostly used is epidural anesthesia. The combination of
an epidural anesthesia and general anesthesia is a very good
technique for surgery caudal to the ribs (orthopedics, soft tissues, cesareans..). It allows a light level of general anesthesia, a stable plane of anesthesia, and post operative pain relief. A more advanced technique is to introduce an epidural
catheter (via a Tuohy needle) in the spinal canal if the need
for very prolonged postoperative analgesia is foreseen.
- Hypotension (especially with hypovolemic or shocky
patients). Epidural anesthesia is best performed in presence
of an IV line and the possiblity of fluid administration
- Temporary bladder paralysis: empty the bladder after
the end of surgery if necessary
a) Technique:
Most often this will be done when the patients are already anesthetised or at least heavily sedated in lateral or
sternal recumbency using spinal needles at the level of the
foramen lunbosacrale.
c) Combinations!!
The local anesthetic can be combined with an opioid
(methadone, morphine 0.1 mg/kg) for epidural injection.
They have an important synergistic analgesic effect very
practical for prolonged analgesia (up to 10 hrs).
c) Complications epidural (expected: <1%)
275
Assisted and controlled centilation
Yves Moens
If respiratory arrest or severe hypoventilation occurs artificial ventilation is indicated. Rhytmic compression of the
thorax is insufficient and can be but a very temporary measure. The most practical way to do perform efficient artificial
ventilation is by instituting a means of IPPV= intermittent
positive pressure ventilation.
Practical means of performing IPPV are
a) the use of an AMBU – bag
b) the use of a „demand „ valve and a source of pressurised air or (better) oxygen
c) the use of an anesthetic circuit/machine and manual
compression of the breathing bag
d) the use of a mechanical ventilator, independent, or incorporated into an anesthetic machine.
The connection with the patient is by far best done via an
endotracheal tube
How to know how to ventilate: volume / frequency?
When no monitoring available (a manometer indicating
airway pressure is the minimum) one has to relie on guidelines. Simple is: frequency of 12 to 15/min with an inspiratory peak pressure of 12 to 15 cm H2O. A spirometer measuring tidal and minute volume is an interesting apparatus to
control the amount of ventilation providedspecially when no
capnograph is available. A tidal volume of 10 to 15 ml /kg
and a minute volume of 100 to 150 ml /kg will realise (in
principle!) a normocapnia. The part of the minute-ventilation that regulates the PaCO2 is the so called „alveolar
minute ventilation“. This is minute ventilation minus dead
space ventilation. Dead space ventilation is ventilation of apparatus dead space (connectors, etc..), anatomic dead space
(constant) and alveolar dead space. A large alveolar dead
space occurs during shock or with a pulmonary embolus. In
the latter case the normal minute ventilation indicated by the
spirometer will not be sufficient to realise normocapnia!.
Ideal is the measurement of the efficacy of the ventilation by
using capnography (measuring end-tidal CO2 as an indication of PaCO2). Unfortunately with large alveolar dead
space the end-tidal CO2 is much lower then arterial CO2 and
hypoventilation may remain undetected. Therefore the ultimate control of the efficiency of artificial ventilation is
blood-gas analysis and the control of PaO2, PaCO2, pH.
Side effects of artificial ventilation
The veterinarian must be aware of the side effects to decide wether or not and how to ventilate. IPPV diminishes
cardiac output (up to 50%) by reduced venous return depending on the mean intrathoracic pressure generated (especially in hypovolemic patients). When cardiac output is
low due to decreased venous return extreme caution with
IPPV is necessary. IPPV must not be done in presence of a
tension pneumothorax. Barotrauma occurs at high airway
pressures (> 50 cm H2O) in normal lungs but in diseased
lungs (ruptured alveoli, bullae) maintenace of spontaneous
respiration might be prefererd. If IPPV is necessary low
airway pressure can be obtained with small tidal volumes
and a high frequency.
Veterinary use of ventilators and ventilatory patterns
Most useful is IPPV = “conventional” mechanical
ventilation and this can be „pressure“ controlled or “volume” controlled. Negative Pressure Ventilation has not
many applications.
“Assisted” ventilation means that the patient triggers by
the light negative pressure that he generates an inspiration
given by the ventilator. This way he determines the frequency whereas „automatic „ means that the operator determines the frequency. The „assist“ possibility is not essential.
Normally the pressure cycle during IPPV is positive-zero. When there is a positive expiratory pressure this is called
PEEP. This is obtained with special valves adapted to ambu
–bags or anesthetic systems. PEEP is used during ventilation when PaO2 remains low despite high inspired O2 fraction due to certain lung pathology. PEEP increases alveolar
size, lung volume, compliance, etc and is used to treat atelectasis (which causes shunting of blood) in certain causes
of lung pathology to „open“ closed alveoli. PEEP increases
also mean inthrathoracic pressure and hence decreases cardiac output. The result of the latter can in fact cause a decrease! of PaO2. There is thus an „optimum“ peep. Usual a
PEEP pressure of 5 to 10 cm H2O is used.
For veterinary use a simple ventilator is the best. It is
important to understand advantages and limitations of
“pressure” and “volume” controlled and the clinical
consequences.
a) pressure controlled: operator chooses a peak pressure
to be reached and a frequency (12 / min and 15 cm H2O is
an example). The machine will give flow (thus a volume) until this pressure is reached. If the compliance is very low (eg
hernia diafragmatica, abdominal tympanism) this pressure
will be reached very quickly and a low (insufficient) volume
276
administered. Additional monitoring is thus useful, at least
airway pressure must be read but capnography and/or
spirometry are better.
b) Volume controlled: operator chooses a volume and a
frequency; this volume will be administered also when the
compliance is low. This way in certain cases a very high airway pressure will be reached. Barotrauma can occur > 50
cmH20.
Inthrathoracic pressure will be high and the cardiovascular side effects are pronounced. Airway pressure monitoring
is essential.
277
Impiego di antistaminici in dermatologia felina
Chiara Noli
Dip ECVD
Studio Dermatologico Veterinario, Milano
Gli antistaminici possono essere utili complementi per la
terapia della dermatite atopica nei carnivori domestici, anche
se gli effetti benefici si osservano solo in alcuni animali, e
probabilmente nella minoranza di quelli trattati. La risposta
è molto variabile, a seconda del soggetto e del farmaco, e
non c’è ancora consenso su quale farmaco funzione meglio,
perciò è necessario che sullo stesso paziente sia condotta una
serie di prove con molecole diverse.
L’importanza dell’istamina come mediatore del prurito è
molto controversa nei piccoli animali. Non si sa se questo
mediatore sia importante per la reazione infiammatoria e per
la sensazione di prurito, poiché altri mediatori potrebbero
essere coinvolti nella risposta allergica. Questo potrebbe
spiegare, almeno in parte, lo scarso successo degli antistaminici nella dermatite atopica del cane e del gatto. Inoltre
l’efficacia, anche se parziale, di alcuni antistaminici con effetto antiserotoninico suggerisce che la serotonina sia un
mediatore di rilievo nei carnivori domestici.
I mastociti dei soggetti atopici sono più reattivi e rilasciano istamina, ed altri mediatori, più facilmente rispetto a
quelli normali. Alcuni antistaminici sono capaci di inibire in
vitro la degranulazione mastocitaria nell’uomo e nel cane.
Nessuno studio è stato finora condotto su mastociti felini,
tuttavia non si può escludere che questo meccanismo avvenga anche nel gatto.
È risaputo come gli antistaminici di prima generazione, e
forse anche gli antidepressivi triclicici (amitriptilina e dossepina), abbiano anche effetti sedativi sul comportamento
dei soggetti che li assumono, particolarmente se il comportamento di leccamento eccessivo ha una componente psicogena. Altri effetti antiallergici degli antistaminici potrebbero
includere una diminuita migrazione, accumulo e attivazione
di cellule infiammatorie e una diminuita espressione di molecole di adesione, portando ad un blocco della fase ritardata della risposta infiammatoria, che si sviluppa in corso di
dermatite atopica.
Classe
Nome
Effetto
anti-His
Effetto
sedativo
Effetto
anti-Ser
antistaminici
di prima
generazione
idrossizina
clorfeniramina
difenidramina
clemastina
si
si
si
si
si
si
si
si
si
antistaminici
di seconda
generazione
ossatomide
terfenadina
loratidina
cetirizina
ketotifen
si
si
si
si
si
Antidepressivi dossepina
triciclici
amitriptilina
ciproeptadina
si
si
si
Inibitore
Inibitore late
degranulazione phase reaction Dose
2 mg/kg bid
0,5-1 mg/kg bid
0,5 mg/kg bid
0,15 mg/kg bid
1-2 mg/kg bid
si
si
si
si
si
si
si
si
si
si
1-2 mg/kg bid
0,5 mg/kg sid
2-3 mg/kg bid
0,5-1 mg/kg
279
Farmacologia dei farmaci antiinfiammatori
non steroidei
Rosangela Odore
DVM, PhD, Dipartimento di Patologia Animale, Settore Farmacologia e Tossicologia,
Università di Torino, via L. da Vinci 44, 10095 Grugliasco (TO)
Giovanni Re
DVM, PhD, Dip.ECVPT, Dipartimento di Patologia Animale, Settore Farmacologia e Tossicologia,
Università di Torino, via L. da Vinci 44, 10095 Grugliasco (TO)
INTRODUZIONE
MECCANISMO D’AZIONE
L’utilizzo di sostanze ad azione antiinfiammatoria in terapia risale all’antichità, infatti già gli antichi egizi (3500
a.C.) utilizzavano piante contenenti acido salicilico per alleviare il dolore, Ippocrate nel V secolo a.C. usava succo di
corteccia di salice quale rimedio per febbri e dolori di diversa natura. In Inghilterra verso la metà del ‘700 il reverendo
Edmund Stone riferiva alla Royal Society del successo degli
estratti della corteccia del salice nella cura delle febbri. Nel
1829 Leroux purifica per primo il glicoside salicina dalla
corteccia del salice, mentre l’impiego degli antiinfiammatori
su larga scala risale al 1875, anno in cui è stato introdotto il
salicilato di sodio, da cui successivamente (1899) è stato sintetizzato l’acido acetilsalicilico1. Da qui inizia la storia moderna dei farmaci antiinfiammatori in seguito alla sintesi ed
all’introduzione in terapia numerose nuove molecole.
La conoscenza del meccanismo d’azione dei FANs risale
agli anni ’70 con la scoperta che le azioni svolte dall’aspirina sono dovute all’inibizione della produzione di prostaglandine (PGs) mediante l’inibizione dell’enzima che ne catalizza la sintesi, la cicloossigenasi (COX)3. La COX è un’endoperossidasi che promuove la conversione dell’acido
arachidonico in endoperossidi (PGG2 e PGH2), intermedi instabili, che innescano la cascata di reazioni responsabili della sintesi di prostaglandine (coinvolte nei fenomeni vasomotori della fase acuta) e di trombossani (coinvolti nell’aggregazione piastrinica). Viene quindi inibita unicamente la
via cicloossigenasica, mentre la lipoossigenasica non è inibita dai FANS, che non interferiscono con la sintesi dei leucotrieni, mediatori che intervengono nell’infiammazione,
nello shock e nella broncocostrizione2. Recentemente sono
stati scoperti composti appartenenti alla famiglia dei diarilpirazoli (es. tepoxalin) in grado di inibire anche l’attività
della perossidasi e della lipoossigenasi estendendo e potenziando il grado di inibizione della sintesi dei prostanoidi4.
Negli anni ‘90 sono state identificate almeno due isoforme
dell’enzima, definite COX1 e COX2, responsabili di funzioni
differenti5. L’isoforma COX1 è normalmente presente nelle cellule che costituiscono la parete dei vasi, lo stomaco e il rene ed
è responsabile della sintesi di PGs coinvolte nel mantenimento
del trofismo cellulare. Ad esempio, nello stomaco, le PGs sono
indispensabili per la produzione del muco che svolge funzione
protettiva sulla mucosa gastrica. L’isoforma COX2 al contrario
non è normalmente presente a livello cellulare, la sua sintesi è
generalmente indotta da citochine e da altri mediatori dell’infiammazione ed è responsabile della sintesi delle PGs che intervengono nella fase acuta del processo infiammatorio2. Questa
scoperta ha dato il via ad una serie di esperimenti volti all’identificazione di principi attivi dotati di maggior selettività
d’azione nei confronti della COX2 rispetto alla COX1, selezionando composti dotati di un potente effetto antiinfiammatorio,
ma caratterizzati da minori effetti collaterali.
CARATTERISTICHE CHIMICHE
E CLASSIFICAZIONE
In base alle loro caratteristiche chimiche i farmaci antiinfiammatori non steroidei o FANS possono essere suddivisi principalmente in due gruppi: acidi carbossilici e acidi
enolici. Ciascun gruppo è diviso a sua volta in sottogruppi:
tra gli acidi carbossilici sono compresi i salicilati (es. acido
acetilsalicilico), gli acidi propionici (es. carprofen), gli acidi antranilici (es. acido meclofenamico), gli acidi acetici
(es. diclofenac) e gli acidi aminonicotinici (es. flunixin),
mentre gli acidi enolici comprendono pirazolonici (es. fenilbutazone) e ossicamici (es. meloxicam). Esistono poi altri gruppi di sostanze, utilizzate nel settore umano, ma attualmente di scarsa importanza per la medicina veterinaria,
come ad esempio i derivati del paraminofenolo (es. paracetamolo), gli alcanoni (es. nabumetone), i diarilfuranoni (es.
rofecoxib), i diarilpirazoli (es. celecoxib) e le sulfonanilidi
(es. nimesulide)2.
280
Altro aspetto interessante riguardo il meccanismo d’azione
dei FANS è da ricercarsi nel tipo di inibizione operata a carico della COX, che può essere di tipo reversibile o irreversibile. La durata d’azione di un inibitore irreversibile
(l’unico finora conosciuto è l’aspirina) è legata alla velocità
con cui l’organismo è in grado di operare il turn-over della
COX, mentre quella degli inibitori reversibili dipende unicamente dalle loro caratteristiche chimiche e farmacocinetiche
(es. tempo di eliminazione dall’organismo, durata di permanenza nel focolaio infiammatorio).
Nonostante la ricerca abbia recentemente compiuto evidenti progressi riguardo la conoscenza del meccanismo
d’azione dei FANS esistono ancora diversi punti da chiarire.
Sembra infatti che questi composti possano agire attraverso
meccanismi più complessi rispetto alla sola inibizione delle
COX. Infatti non per tutti i FANS esiste una correlazione diretta tra potenza di inibizione delle COX ed attività antiinfiammatoria. Ad esempio l’indometacina, potente antiinfiammatorio, non è un altrettanto potente inibitore delle COX1.
Un ultimo aspetto riguardante il meccanismo d’azione
può essere rappresentato dal confronto tra FANS e glicocorticoidi. I glicocorticoidi, come noto, sono in grado di inibire
la sintesi di prostaglandine, ma il meccanismo d’azione è
differente. Infatti, i glicocorticoidi inducono la sintesi di una
proteina, la lipocortina, in grado di inibire la fosfolipasi A2
enzima che promuove la liberazione dell’acido arachidonico
dai fosfolipidi di membrana in seguito all’insulto cellulare.
L’azione dei glicocorticoidi si esplica, quindi a monte rispetto alla tappa inibita dai FANS e implica l’inibizione della
sintesi di prostaglandine e trombossani (via mediata dalle
COX), ma anche di leucotrieni (via mediata dalla lipoossigenasi). Per questo motivo l’attività antiinfiammatoria dei
corticosurrenalici risulta di intensità superiore rispetto a
quella dei FANS6,7.
ATTIVITÀ ANTIINFIAMMATORIA
Le PGs vengono prodotte dalle cellule in risposta a stimoli lesivi di diversa natura ed in seguito alla loro liberazione svolgono ruoli diversi nelle varie fasi della flogosi.
Ad esempio la PGE2 e la PGE1 incrementano gli effetti
edemigeni e iperemici delle chinine e di altri autacoidi. In-
oltre, alcune prostaglandine favoriscono la vasodilatazione,
facilitando l’infiltrazione leucocitaria e la formazione di essudato. I leucotrieni, prodotti dalla via lipoossigenasica, aumentano la permeabilità vasale, svolgono attività chemiotattica per i leucociti e inducono la liberazione di istamina e altri autacoidi dai mastociti. Come già detto i FANS, al contrario dei glicocorticoidi, non interferiscono con questa via
enzimatica2,6. È stata al contrario sostenuta l’ipotesi che in
seguito a somministrazione di FANS si possa osservare un
aumento dei livelli di leucotrieni per la maggior disponibilità di acido arachidonico non più convertito dalle COX8.
Un’ulteriore differenza tra azione dei FANS e dei glicocorticoidi riguarda la velocità e la durata d’azione: i FANS
agiscono più rapidamente perché il loro meccanismo d’azione
prevede l’inibizione diretta della COX, l’azione dei glicocorticoidi, che si basa sull’induzione alla sintesi di nuove proteine
risulta più duratura. Tuttavia la potenza d’azione dei FANS
varia a seconda del composto e del tessuto interessato in quanto sembrano esistere piccole differenze nella struttura delle
COX presenti nei diversi distretti, differenze che interferiscono con l’affinità del farmaco per l’enzima.
Un esempio è dato dal paracetamolo che esercita una
notevole inibizione sulle COX presenti a livello di sistema
nervoso centrale, mentre è scarsamente efficace sulle COX
dei tessuti periferici. Ne deriva una potente attività analgesica e antipiretica, ma uno scarso effetto antiinfiammatorio. Al
contrario il fenilbutazone è poco attivo come analgesico centrale, ma è molto efficace come antiinfiammatorio e analgesico periferico9.
ATTIVITÀ ANALGESICA
La sensazione di dolore che compare nel corso dei processi flogistici è provocata dalle prostaglandine che da un
lato, tramite un meccanismo AMPc dipendente, stimolano
le fibre sensitive periferiche e i nocicettori e dall’altro
provocano un aumento dell’eccitabilità neuronale a livello
centrale1. L’effetto analgesico dei FANS è quindi principalmente dovuto all’inibizione della produzione di
prostaglandine, anche se probabilmente esistono meccanismi diversi correlati tra loro e legati all’azione di alcune
citochine (IL e TNF).
L’azione dei FANS a livello centrale non è sicuramente
mediata dall’interazione con i recettori per le endorfine,
come invece succede per gli analgesici narcotici. Quindi la
loro azione di controllo su dolori intensi, acuti e viscerali
profondi non è altrettanto efficace, non sono in grado di alterare le funzioni mentali, non determinano ipnosi e non
provocano tolleranza o assuefazione10.
ATTIVITÀ ANTIPIRETICA
Figura 1. Schema semplificato del meccanismo d’azione dei
farmaci antiinfiammatori non steroidei.
Le citochine liberate nel corso dei processi flogistici stimolano la liberazione di PGE2 a livello dell’area periventricolare e preottica ipotalamica che induce una stimolazione
del centro termoregolatore con conseguente aumento della
temperatura corporea. I FANS esplicano la loro azione antipiretica inibendo la sintesi di PGE2, per questo motivo sono
in grado di esercitare effetto antipiretico ma non ipotermizzante2.
FARMACOCINETICA
La farmacocinetica dei FANS è condizionata dalle loro
caratteristiche chimiche (sono infatti generalmente acidi deboli con pKa compreso tra 3 e 6.5) e dalla liposolubilità della forma non-ionizzata.
I FANS vengono bene assorbiti dal tratto gastrointestinale, specialmente a livello gastrico e del primo tratto dell’intestino, dove a causa del pH acido la quota di farmaco in
forma non-ionizzata risulta maggiore. La somministrazione
per via parenterale di sali idrosolubili garantisce un rapido e
totale assorbimento. Viste le loro caratteristiche di acidi deboli i FANS si trovano nell’organismo per la maggior parte
in forma ionizzata. La frazione non-ionizzata è veicolata in
alta percentuale dalle albumine. I FANS contraggono un
forte legame anche con le proteine tissutali, comprese quelle
presenti negli essudati, che giustificano la loro concentrazione nei focolai infiammatori.
La distribuzione dei FANS, a causa della elevata ionizzazione, si limita generalmente al comparto extracellulare
con volumi di distribuzione medi attorno a 0.1-0.3 l/Kg. La
frazione non ionizzata di farmaco è tuttavia in grado di attraversare le membrane plasmatiche.
Per quanto riguarda la biotrasformazione i FANS vanno
incontro sia a reazioni di fase I (ossidazioni, idrolisi) sia di
fase II (glucuronazione) dando generalmente luogo a
metaboliti inattivi, ma non mancano gli esempi in cui il
metabolita è attivo (es. fenilbutazone => ossifenilbutazone).
I metaboliti sono più idrosolubili del composto di partenza e
quindi più facilmente eliminabili. Il gatto è particolarmente
sensibile agli effetti indesiderati dei FANS a causa della
scarsa capacità di glucuronazione, specialmente dei composti aromatici (es. salicilati).
L’escrezione dei FANS avviene principalmente attraverso l’emuntorio renale in parte per filtrazione glomerulare, in
parte per secrezione tubulare. L’acidità delle urine influenza
il riassorbimento tubulare, per questo motivo nei carnivori
(urina più acida) sono eliminati più lentamente rispetto agli
erbivori (urina più alcalina). Ne consegue che i tempi di
emivita della fase di eliminazione sono molto diversi a seconda della specie e si rende indispensabile una regolazione
dei dosaggi e delle modalità di somministrazione a seconda
della specie.
281
Gli effetti a carico dell’apparato digerente possono essere imputabili all’acidità dei composti somministrati per via
orale, ma compaiono anche in seguito a somministrazione
per via parenterale. Il meccanismo è da ricercarsi nell’inibizione della sintesi di PGs, specialmente di PGI2 e
PGE2, che svolgono un’azione citoprotettiva a carico della
mucosa gastrica, inibendo la secrezione acida dello stomaco,
promuovendo la circolazione ematica della mucosa e favorendo la secrezione di muco. Tutti i FANS che esplicano
azione non selettiva sulle COX, causano questo tipo di
azione tossica, seppure con notevoli differenze di intensità,
che si manifesta con la comparsa di vomito e ulcerazioni a
carico della mucosa dello stomaco o del duodeno.
L’azione sull’aggregazione piastrinica, è provocata dall’inibizione della sintesi di trombossano A2 da parte delle piastrine. La tossicità a questo livello si esplica attraverso un
aumento del tempo di sanguinamento. L’aspirina è particolarmente potente, in quanto inibitore irreversibile delle COX
e in quanto le piastrine dispongono di scarse possibilità biosintetiche, non sono quindi in grado di rimpiazzare le COX
acetilate dall’aspirina1. Questa azione non rappresenta solamente un effetto collaterale, al contrario può rappresentare
un’utilizzazione terapeutica, già sfruttata nel settore umano,
e parzialmente nella clinica dei piccoli animali.
I FANS possono provocare una riduzione del flusso renale e della filtrazione glomerulare particolarmente evidente
in animali con insufficienza cardiaca congestizia, affezioni a
carico del fegato con ascite, disturbi renali cronici con ipovolemia. Tali soggetti sono più sensibili ad una riduzione dei
livelli ematici di PGs ad azione vasodilatatoria e la possibilità di insorgenza o del peggioramento di una insufficienza
renale acuta è più probabile.
Bibliografia
1.
2.
3.
4.
5.
TOSSICITÀ
Gli effetti tossici dei FANS, che ne limitano l’utilizzo
particolarmente nel cane e nel gatto, comprendono disturbi
gastro-enterici con comparsa di lesioni emorragiche e ulcerative, alterazioni della circolazione a livello renale (soprattutto nei soggetti anziani o nefropatici) e alterazioni dell’aggregazione piastrinica. I FANS vanno somministrati con
cautela in soggetti affetti da alterazioni a carico del rene e
del fegato, disidratati, debilitati, con carenze proteiche che
portano a ipoproteinemia e ipoalbuminemia.
6.
7.
8.
9.
10.
Insel PA, (1996), Analgesic-antipyretic and antiinflammatory agents
and drugs employed in the treatment of gout. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics 9th ed, McGrawHill, New York, 617-657.
Jackson-RobertsII L, Morrow JD, (2001), Analgesic-antipyretic and
antiinflammatory agents and drugs employed in the treatment of
gout. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics 10th ed, McGraw-Hill, New York, 617-657.
Vane JR, (1971), Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature, 231:232-235.
Lee DHS, Macintyre JP, Taylor GR et al., (1999) Tepoxalin enhances
the activity of an antioxidant, pyrrolidine dithiocarbamate, in attenuating tumor necrosis factor a-induced apoptosis in WEHI 164 cells. J Pharmacol Exp Ther, 289: 1465-1471.
Lecomte M, Leneuville O, DeWitt D.L, Smith WL, (1994), Acetylation of human prostaglandin endoperoxide synthase-2 (cyclooxigenase-2) by aspirin. J Biol Chem, 269:13207-13215.
Higgins AJ, (1985), The biology, pathophysiology and control of eicosanoids in inflammation. J Vet Pharmacol Therap, 8:1-18.
Flower RL, (1988), Lipocortin and the mechanism of action of the
glucocorticoids. Br J Pharmacol, 94:987-995.
Abramson SR, Weissmann G, (1989), The mechanisms of action of
non steroidal anti-inflammatory drugs. Arthritis Rheum, 32: 1-9.
Lees P, May SA, McKellar QA, (1991), Pharmacology and therapeutics of non-steroidal antiinflammatory drugs in the dog and cat: 1 General pharmacology. J Small Anim Pract, 32:183-193.
Gebhart G.F., McCormack K.J. - Neuronal plasticity. Implication for
pain therapy. Drugs, 47:1-47; 1994.
283
Farmacologia dei principi attivi utilizzati
nelle turbe del comportamento
Maria Cristina Osella
DVM, PhD, Libero Professionista, Professore a Contratto presso la Facoltà di Medicina Veterinaria di Torino,
Via Basso 2, 10034 Chivasso-TO
Giovanni Re
DVM, PhD, Dip. ECPT, Dipartimento di Patologia Animale, Settore Farmacologia e Tossicologia,
Università degli Studi di Torino Via Leonardo da Vinci 44, 10095 Grugliasco-TO
Paola Badino
MSc, PhD, Dipartimento di Patologia Animale, Settore Farmacologia e Tossicologia,
Università degli Studi di Torino Via Leonardo da Vinci 44, 10095 Grugliasco-TO
INTRODUZIONE
BENZODIAZEPINE
L’intervento farmacologico è uno dei cardini del trattamento dei disturbi comportamentali del cane e del gatto
unitamente all’applicazione delle tecniche di modificazione del comportamento1. Prima di prescrivere un farmaco è
necessario che il veterinario raccolga un’accurata anamnesi clinica e comportamentale al fine di proporre un intervento mirato nell’ambito del piano diagnostico. La diagnosi comportamentale deve essere sempre di tipo differenziale e supportata da accertamenti clinici approfonditi, mirati
alla valutazione di eventuali fattori strettamente organici. I
disturbi comportamentali sono in genere ad eziologia multifattoriale e i meccanismi neurofisiologici che stanno alla
base sono spesso di difficile individuazione e possono essere tra loro correlati2.
Per questo motivo la terapia farmacologica non presenta
caratteri di univocità e deve essere adattata al singolo caso.
Nel caso in cui il clinico utilizzi un farmaco dotato di specificità d’azione molto elevata, il trattamento farmacologico
può inoltre fornire un ausilio nel ricusare o confermare l’ipotesi diagnostica iniziale.
Attualmente esistono modelli diagnostici, proposti da diverse scuole di pensiero1,3, che utilizzano protocolli terapeutici differenti, ma le categorie farmacologiche utilizzate sono sostanzialmente le stesse e comprendono i tranquillanti
minori o ansiolitici (benzodiazepine), i fenotiazinici (tranquillanti maggiori o neurolettici), gli antidepressivi triciclici,
gli inibitori delle monoaminoossidasi (I-MAO), gli inibitori
selettivi della ricaptazione della serotonina (SSRI) e alcuni
ormoni steroidei (progestinici, antiandrogeni)1.
Tra le benzodiazepine più frequentemente utilizzate nel
trattamento dei disturbi comportamentali è possibile annoverare il diazepam, il clordiazepossido, il clorazepato, il clonazepam e l’alprazolam. È comunemente ritenuto che la
maggior parte degli effetti prodotti da questi farmaci siano
dovuti alla loro interazione, a livello di sistema nervoso centrale, con i recettori per un neurotrasmettitore endogeno inibitorio, l’acido γ-aminobutirrico (GABA). In realtà, si conoscono due diversi recettori per il GABA (GABAA-R e GABAB-R), ma le benzodiazepine sono in grado di interagire
solo con il GABAA-R, un canale ionico transmembranario
che permette l’ingresso degli ioni Cl-. Tali farmaci si legano
al recettore in un sito diverso rispetto quello occupato dal
mediatore endogeno e ne potenziano gli effetti facilitando il
legame del GABA con il proprio recettore4. Ne consegue un
aumento della frequenza di apertura del canale che provoca
l’inibizione neuronale in seguito ad iperpolarizzazione causata da un aumentato ingresso di Cl- nella cellula. Dal punto
di vista clinico, questo si traduce in un’azione ansiolitica o
ipnoinducente, anticonvulsivante e sedativa. Nell’ambito del
trattamento dei disturbi comportamentali le benzodiazepine
vengono generalmente somministrate per via orale. Tale via
consente un rapido e pressoché completo assorbimento, anche se esistono notevoli differenze a seconda del composto
considerato, ad esempio il diazepam e il clorazepato vengono assorbiti rapidamente, mentre clordiazepossido e alprazolam sono assorbiti più lentamente. Il legame con le proteine plasmatiche è elevato e, grazie alla loro elevata liposolubilità, attraversano facilmente la barriera ematoencefalica di-
284
stribuendosi rapidamente nel tessuto cerebrale5. Le benzodiazepine possono essere metabolizzate tramite reazioni di
ossido riduzione, che danno luogo alla formazione di metaboliti attivi, in seguito coniugati con acido glucuronico e
quindi eliminati per lo più per via urinaria, oppure direttamente coniugate ed inattivate. È molto importante conoscere il destino metabolico di questi farmaci, in quanto l’emivita plasmatica dei metaboliti attivi è spesso superiore rispetto
a quella del composto di partenza e da questo dipende la loro durata d’azione7. Ad esempio il diazepam presenta un
tempo di emivita che supera nell’uomo le 24 ore e viene
quindi classificato come benzodiazepina a lunga durata d’azione, tuttavia è necessario considerare le differenze tra specie che, in questo caso, sono molto evidenti. Infatti, l’emivita plasmatica del diazepam nel cane è pari a 2.5-3.2 ore e nel
gatto a 5.5 ore, mentre l’emivita del suo principale metabolita, il nordiazepam è pari a 3 ore nel cane e a 21 ore nel gatto6.
Al contrario l’alprazolam è una benzodiazepina a breve durata d’azione (nell’uomo l’emivita plasmatica è inferiore alle 4
ore)7, ma non sono riportati in letteratura dati riguardanti la
farmacocinetica di questo composto nel cane e nel gatto. Le
benzodiazepine sono generalmente ben tollerate e gli effetti
collaterali di questi farmaci sono rappresentati per lo più
un’accentuazione delle loro proprietà farmacologiche, in tal
senso possono evidenziarsi eccessiva sedazione, astenia e ridotta attività psicomotoria e cognitiva6. Nel gatto la potenziale tossicità delle benzodiazepine è stata più volte riconosciuta1,8 ed è associata alla carenza dei sistemi enzimatici che presiedono alla glucuronazione dei composti aromatici caratteristica di questa specie1. È stato ampiamente riportato che la
somministrazione di benzodiazepine interferisce negativamente sui processi della memoria, in particolare questi farmaci riducono la capacità di apprendere nuove informazioni6 e
per questo motivo potrebbero essere di ostacolo alla contemporanea terapia comportamentale1. Le benzodiazepine vengono utilizzate per il trattamento dei disturbi fobici e ansiosi sia
nel cane sia nel gatto, nel caso in cui si desideri un effetto farmacologico di rapida insorgenza. Ad esempio, sono utilizzate
con successo nel controllo delle fobie da tuono e da rumori.
La limitazione d’uso è rappresentata, in questo caso, dal fatto
che per essere efficace, il farmaco dovrebbe essere somministrato almeno 3-4 ore prima della comparsa dell’evento scatenante9. Questi farmaci possono essere associati alla somministrazione di altri psicotropi, quali ad esempio la clomipramina
cloridrato1,3. È necessario tenere conto che in caso di assunzione per periodi prolungati di queste sostanze possono comparire fenomeni di tolleranza1.
FENOTIAZINICI
I fenotiazinici (acepromazina, clorpromazina) rivestono,
nel campo della terapia comportamentale, soprattutto un’importanza di tipo storico. Attualmente vengono utilizzati altri
neurolettici definiti “atipici”2,3 quali ad esempio il risperidone e la clozapina.
I fenotiazinici sono dotati di azioni molto complesse a livello del sistema nervoso centrale, di cui la principale è l’antagonismo nei confronti dei recettori dopaminergici. Oggi è noto che la dopamina riveste una notevole importanza a livello di
sistema nervoso centrale non solo nella modulazione dell’attività psichica e motoria, ma anche nel tono dell’umore, nella secrezione di alcuni ormoni ipofisari e, molto probabilmente, in
alcune componenti dei processi cognitivi10. I recettori per la
dopamina fanno parte del gruppo di recettori funzionalmente
accoppiati alle proteine G e vengono comunemente classificati in due famiglie (D1 e D2). I recettori D1 e D2 sono distribuiti
in maniera differente nei neuroni cerebrali e nelle cellule endocrine. Le azioni farmacologiche associate ad una attività
neurolettica, come quella tipica dei fenotiazinici, sono dovute
al blocco dei recettori dopaminergici di tipo D211.
Il loro impiego prolungato può comportare la comparsa
di effetti collaterali quali disturbi a carico dell’apparato cardiovascolare e sintomi extrapiramidali. Si dimostrano, inoltre, decisamente inadatti nel trattamento dell’aggressività,
poiché inibiscono indifferentemente sia il comportamento
normale sia l’anormale e non trattano selettivamente la causa dell’aggressività. L’acepromazina, inoltre, provoca reazioni esagerate a stimoli ambientali e il comportamento dell’animale diventa meno prevedibile12.
ANTIDEPRESSIVI TRICICLICI
La struttura chimica degli antidepressivi triciclici (TCA)
è simile a quella dei fenotiazinici e di conseguenza ne ricalcano alcuni degli effetti quali l’azione antiistaminica, simpaticolitica e sedativa. Il capostipite di questo gruppo di farmaci è l’imipramina a partire da cui sono state sintetizzate
altre molecole che conservano la struttura triciclica. Da un
punto di vista chimico possono essere classificate in amine
terziarie (imipramina, amitriptilina, clomipramina) e in amine secondarie (desmetilimipramina, desipramina)13.
I TCA agiscono aumentando la disponibilità di catecolamine (noradrenalina e dopamina) e serotonina a livello di sinapsi bloccandone la ricaptazione neuronale. Ne consegue
un prolungamento della loro azione fisiologica a livello dei
siti recettoriali postsinaptici corrispondenti. La potenza e la
selettività d’azione variano a seconda della molecola considerata, ad esempio la desmetilimipramina è tra i più potenti
inibitori della ricaptazione della noradrenalina, mentre il suo
analogo, la clorimipramina, è particolarmente potente e selettivo nel bloccare il reuptake della serotonina. In generale
le amine terziare sono inibitori più potenti della ricaptazione
della serotonina, mentre le secondarie agiscono prevalentemente sulla ricaptazione della noradrenalina13.
I TCA vengono comunemente utilizzati, in medicina
umana, per il trattamento della depressione, degli attacchi di
panico, degli stati fobici ed ossessivi. Possono essere inoltre
utilizzati nei deficit dell’attenzione in quanto favoriscono
l’azione delle catecolamine13.
Le amine terziarie vengono metabolizzate in vivo ad
amine secondarie e rappresentano la classe di farmaci che
agiscono a livello del sistema nervoso centrale più sicura e
più comunemente utilizzata nella terapia del comportamento degli animali da compagnia12.
Dal punto di vista cinetico, i TCA, essendo dotati di elevata liposolubilità, vengono assorbiti completamente e rapidamente in seguito a somministrazione per via orale, ma sottostanno ad un effetto di primo passaggio che ne limita la
biodisponibilità. A livello ematico si legano alle proteine per
il 90% e la quota di farmaco disponibile varia, nell’uomo,
notevolmente da individuo ad individuo (dal 5 al 23%)13,
purtroppo non esistono a questo riguardo dati relativi agli
animali. Generalmente i metaboliti dei TCA presentano un
maggiore effetto inibitorio sulla ricaptazione della noradrenalina, mentre i composti di partenza agiscono prevalentemente sulla serotonina. I metaboliti spesso hanno un tempo
di emivita simile, se non superiore, rispetto ai composti di
partenza. La conoscenza della caratteristiche cinetiche di
questi composti è molto importante per una corretta somministrazione in base alla loro durata d’azione13.
Gli effetti collaterali dei TCA sono legati all’affinità che
questi farmaci possiedono per alcuni sistemi recettoriali (colinergici, istaminergici, α1-adrenergici) e conseguono principalmente al blocco del sistema nervoso simpatico e parasimpatico. L’attività anticolinergica può causare problemi
alla vista (midriasi), secchezza delle fauci, ritenzione urinaria, tachicardia e aritmie, ipotensione ortostatica, atassia, disorientamento, depressione generalizzata e anoressia. Questi
sintomi generalmente scompaiono o almeno si riducono, in
seguito alla sospensione del trattamento. La somministrazione dei TCA è controindicata in animali con precedenti di ritenzione urinaria e gravi aritmie. Particolare attenzione deve
essere posta nel trattamento dei soggetti anziani, in quanto è
stato riscontrato che alte dosi di TCA possono provocare alterazioni nei livelli di enzimi epatici. Sempre ad alte dosi,
questi farmaci possono determinare ripercussioni sulla funzionalità tiroidea e interferire con la terapia dell’ipotiroidismo. Può comparire una sindrome serotoninergica caratterizzata da stato confusionale, irrequietezza, ansia, mioclonie, atassia, iperreflessia, tremori, diarrea e diaforesi1. In base a dati recenti, sembra che nel cane compaiano raramente
effetti collaterali in seguito al trattamento con TCA e che
questi siano per lo più rappresentati da irritazione del tratto
gastroenterico. Più raramente compare aumento dell’appetito e tachicardia14. Rispetto al cane, il gatto risulta essere più
sensibile all’azione dei TCA, soprattutto per quanto riguarda gli effetti cardiaci. Questo sembra essere dovuto al fatto
che i TCA vengono metabolizzati per coniugazione con acido glucuronico e come noto, il gatto presenza carenza per
quanto riguarda questa via metabolica1.
I TCA sono molto efficaci nel trattamento dell’ansia da
separazione e dell’ansia generalizzata, ma anche nelle sindromi compulsive. La clomiprimina viene utilizzata, in medicina umana, nel trattamento dei disordini ossessivo-compulsivi e degli attacchi di panico13. In uno studio condotto
nel cane, si è mostrata efficace nel trattamento della dermatite acrale da leccamento. Come già detto in precedenza, la
clomipramina è anche un inibitore selettivo della ricaptazione della serotonina, per questo motivo una risposta positiva
al trattamento con questo farmaco viene considerata indicazione diagnostica di disturbo ossessivo-compulsivo12.
INIBITORI DELLE MONOAMINOOSSIDASI
(I-MAO)
Le monoaminoossidasi (MAO) sono enzimi che catalizzano la deaminazione ossidativa delle monoamine (adrenali-
285
na, noradrenalina, dopamina, serotonina e istamina). I metaboliti prodotti sono fisiologicamente inattivi e quindi la funzione delle MAO è quella di ridurre l’azione dei neurotrasmettitori monoaminergici. Sono substrato di questi enzimi
anche altre monoamine di origine endogena o che vengono
introdotte con la dieta (octopamina, tiramina). Sono presenti due isoforme enzimatiche, MAO-A e MAO-B, che si distinguono per specificità di substrato. Ad esempio la MAOA ossida prevalentemente l’adrenalina, la noradrenalina e la
serotonina, mentre la MAO-B ha come substrato la feniletilamina13.
Gli I-MAO aumentano i livelli di neurotrasmettitori a livello cerebrale inibendo i sistemi enzimatici deputati al loro
catabolismo (MAO) e conseguentemente provocano un miglioramento dell’umore1,13. Questi farmaci vengono generalmente classificati come inibitori irreversibili (es. pargilina,
iproniazide, clorgilina) e reversibili (es. selegilina).
Questi farmaci vengono utilizzati raramente nella terapia
farmacologica dei disturbi comportamentali degli animali da
compagnia, rappresenta un’eccezione l’impiego della selegilina, un inibitore selettivo delle MAO-B, utilizzata nel trattamento di una patologia descritta come disfunzione cognitiva
del cane anziano1,12. La selegilina viene anche utilizzata in
associazione alla terapia comportamentale, nel trattamento
delle turbe di origine emozionale quali la sindrome ipersensibilità/iperattività, la sindrome da privazione e le fobie generalizzate ed anche nell’ansia da separazione3.
INIBITORI SELETTIVI DELLA
RICAPTAZIONE DELLA SEROTONINA
(SSRI)
Gli SSRI sono una categoria eterogenea di composti che
presentano la stessa efficacia dei TCA, ma con minori effetti collaterali rispetto a questi ultimi. Sono farmaci che potenziano specificamente la trasmissione serotoninergica e
comprendono la fluoxetina, la paroxetina, la sertralina, il citaloparam e la fluvoxamina13.
Si tratta di potenti e selettivi inibitori della ricaptazione
della serotonina, mentre tale effetto su noradrenalina e dopamina si verifica solamente a concentrazioni molto alte,
praticamente non raggiungibili in seguito a somministrazione di dosi terapeutiche. Gli SSRI possono presentare caratteristiche diverse se si considerino la potenza e la selettività
d’azione. Ad esempio, il citalopram presenta una maggiore
selettività d’azione, mentre la paroxetina è l’inibitore più potente. Un’altra caratteristica degli SSRI è rappresentata dal
fatto che questi farmaci sono praticamente sprovvisti di
azione bloccante su altri recettori, quali ad esempio i recettori muscarinici e i recettori α1-adrenergici. Di conseguenza,
non presentano alcuni effetti collaterali sul sistema nervoso
autonomo, caratteristici dei TCA e dovuti alla loro affinità
per tali recettori13.
I dati relativi alla farmacocinetica di questi composti sono più scarsi rispetto a quelli sui TCA anche in medicina
umana e sono praticamente assenti negli animali da compagnia. Le caratteristiche farmacocinetiche dei SSRI variano
molto da composto a composto. In generale vengono bene
assorbiti dal tratto gastroenterico e, nell’uomo, il picco pla-
286
smatico viene raggiunto in 4-6 ore. Il citalopram presenta
una biodisponibilità orale pari al 100%, mentre gli altri composti sottostanno all’effetto di primo passaggio (la biodisponibilità della paroxetina è pari al 50%). Il legame alle proteine plasmatiche varia dal 95% per la paroxetina, fluoxetina e sertralina al 50% per il citalopram. I composti di partenza vengono per lo più eliminati per via fecale, mentre i
metaboliti sono eliminati prevalentemente per via urinaria. I
metaboliti della fluoxetina, della sertralina e del citalopram
sono attivi e quindi in grado di inibire la ricaptazione della
serotonina13.
La fluoxetina può essere efficacemente utilizzata nel trattamento dell’aggressività, dei disturbi ossessivo-compulsivi,
nell’ansia da separazione e negli attacchi di panico. La paroxetina è efficace nel trattamento degli stati depressivi,
mentre la sertralina è particolarmente utile nel trattamento
dell’ansia generalizzata12.
SOSTANZE CHE INTERFERISCONO CON
I RECETTORI PER GLI ORMONI SESSUALI
Appartengono a questa categoria i progestinici (medrossiprogesterone acetato) e gli antiandrogeni (ciproterone acetato).
I progestinici venivano in passato utilizzati nella terapia
dell’aggressività in virtù del loro effetto deprimente sul sistema nervoso centrale e poiché riducono gli atteggiamenti
comportamentali dimorfici maschili. Oggi il loro impiego
nell’ambito della terapia comportamentale veterinaria è molto limitato. Infatti i trattamenti prolungati con progestinici
possono presentare effetti collaterali anche gravi quali insorgenza di diabete, ginecomastia, iperplasia della ghiandola
mammaria, adenocarcinomi, iperplasia dell’endometrio,
piometra, ipofunzionalità surrenalica e inibizione dell’emopoiesi1.
Attualmente, tra le sostanze che interferiscono con i recettori per gli ormoni sessuali l’unico farmaco utilizzato nella terapia delle turbe comportamentali è il ciproterone acetato. Si tratta di un antagonista selettivo per i recettori degli androgeni, il suo meccanismo d’azione consiste nel legarsi al
recettore bloccandolo ed impedendo allo steroide endogeno
di esplicare la sua azione. In medicina umana questi farmaci vengono utilizzati per il trattamento della sessualità aggressiva del maschio15, in terapia comportamentale veterinaria trova unica applicazione per il trattamento dei disturbi
aggressivi legati ai conflitti gerarchici del cane3.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
Overall KL, (1997), Clinical behavioral medicine for small animals,
Mosby, St. Louis, 293-322.
Dodman NH, Shuster L (1998), Psychopharmacology of animal
behavior disorders, Blackwell Science, Malden.
Pageat P, (1998), Pathologie du comportement du chien, Editions du
Point Vétérinaire, Maisons-Alfort.
Mehta AK, Ticku MK (1999), An update on GABAA receptors, Brain
Res. Rev., 29:196-217.
Charney DS, Mihic SJ, Harris RA (2001), Hypnotic and sedatives. In
“Goodman and Gilman’s The Pharmacological Basis of Therapeutics” Hardman JG, Limbird LE eds., McGraw-Hill, New York, 399427.
Plumb DC (1999), Veterinary Drug Handbook, Iowa State University
Press, Ames.
Biggio G, Concas A., Serra M, Torta R. (1998) Gli ansiolitici. In
“Neuropsicofarmacologia”, UTET, Torino, 279-296.
Hugues H, Moreau RE, Overall KL (1996), Acute hepatic necrosis
and liver failure associated with benzodiazepine therapy in cats.
JVECC, 6:13-20.
Shull-Selcer EA, Stagg W (1991), Advances in understanding and
treatment of noise phobias. Vet. Clin. North Am: Sm. Anim. Pract.,
22:353-367.
Spano PF, Memo M, Missale MC (1996), Trasmissione catecolaminergica. In “Farmacologia Generale e Molecolare”, UTET, Torino,
205-230.
Janssen PA, Awouters FHL (1999), Farmaci antipsicotici. In “Principi di Farmacologia”, Piccin, Padova, 289-308.
Overall KL (2001), Pharmacological treatment in behavioural medicine: the importance of neurochemistry, molecular biology and mechanistic hypotheses. Vet. J., 162:9-23.
Brunello N, Popoli M., Racagni G (1998), Gli antidepressivi. In
“Neuropsicofarmacologia”, UTET, Torino, 256-271.
King JN, Simpson BS, Overall KL et al. (2000), Treatment of separation anxiety in dogs with clomipramine: results from a prospective,
randomised, double-blind, placebo-controlled, parallel-group, multicenter clinical trial. J. Appl. Anim. Behav. Sci., 67:255-75.
Hiipakka RA, Liao S. (1999), Steroidi androgeni ed anabolizzanti e
loro antagonisti. In “Principi di Farmacologia”, Piccin, Padova, 851864.
287
Current antibiotic therapy for small animal patients
Mark G. Papich
DVM, MS, Professor of Clinical Pharmacology
College of Veterinary Medicine, North Carolina State University
Therapy of bacteria in small animals requires an understanding of the most common bacterial pathogens, their virulence factors, and likelihood of drug resistance. Many bacteria follow a susceptible susceptibility pattern and can be
treated with first-line antibiotics, such as penicillins (amoxicillin, ampicillin, amoxicillin-clavulanate), trimethoprimsulfonamides, tetracyclines, or chloramphenicol. Examples
of these infections are Pasteurella, Streptococcus, many
anaerobes, Actinomyces, and most anaerobic bacteria.
(Some Bacterioides can be a resistant anaerobic bacteria.)
Staphylococci., for example Staphylococcus intermedius, also shows a predictable susceptibility pattern in small animals. It is usually is sensitive to 1st generation
cephalosporins, fluoroquinolones, and penicillin-beta lactamase inhibitor combinations (for example, amoxicillinclavulanate). The cephalosporins often used as first-line
treatment for staphylococcal infections include cefadroxil or
cephalexin because there is a very low rate of resistance
documented. Anaerobic bacteria causing infections in small
animals also have a relatively predictable susceptibility pattern. Most anaerobic bacteria are sensitive to penicillins
(penicillin, ampicillin, amoxicillin, and derivatives), metronidazole, clindamycin, chloramphenicol, and the cephamycin
class of cephalosporins. Some Bacteroides in small animals
can become resistant to some of these drugs, however.
On the other hand, gram-negative bacilli encountered in
small animals can develop resistant and show an unpredictable susceptibility to common antibacterial drugs. These
bacteria include the Enterobacteriaceae such as Escherichia
coli, Klebsiella pneumoniae, Proteus, Enterobacter, and
Pseudomonas aeruginosa. These bacteria can cause urinary
tract infections, wound infections, and pneumonia. Drugs
needed to treat these infections may include extended-spectrum cephalosporins, fluoroquinolones, or aminoglycosides.
The extended-spectrum cephalosporins that have been used
in animals include cefotaxime and ceftazidime. The aminoglycosides used in veterinary medicine include gentamicin,
amikacin, and tobramycin. Amikacin is more active than
gentamicin against resis

44° SCIVAC

Transcription

Similar documents

Scaricare - Fisiokinesiterapia

Definition Definition a flut atrial flutter CABG coronary artery bypass

antlo brochure + sch..

Publication - Red Bluff Bull and Gelding Sale

Copertine EXTRA - Life EX-TRA

Malattia di Pompe Inquadramento clinico

Trattamento e prevenzione delle recidive nei pazienti con trombosi

Microangiopatia trombotica dopo trapianto di cellule staminali

59° Congresso Internazionale Multisala SCIVAC Rimini, 30 Maggio

scarica pdf qui

Epatologia Medica e Chirurgica