ZBORNIK REFERA ZBORNIK REFERATOV XXIII. SIMPOZIJ O

Transcription

ZBORNIK REFERA
TOV
REFERATOV
XXIII. SIMPOZIJ O AKTUALNIH BOLEZNIH MALIH @IVALI
Dolenjske Toplice, 22. - 24. april 2010
1
ZBORNIK REFERA
TOV
REFERATOV
2
ZBORNIK REFERA
TOV
REFERATOV
S L OV E N S KO Z D R U @ E N J E V E T E R I N A R J E V Z A M A L E @ I VA L I
S L O V E N I A N S M A L L A N I M A L V E T E R I N A RY A S S O C I AT I O N
ZBORNIK REFERATOV
XXIII. SIMPOZIJA O AKTUALNIH
BOLEZNIH MALIH @IVALI
http://www.zdruzenje-szvmz.si/
3
ZBORNIK REFERA
TOV
REFERATOV
VSEBINA
Hackett T: The critical cat – Triage, vascular access and emergency treament ............................ 7
Hackett T: Feline shock – The unique challenges of treating cats .............................................. 11
Romagnoli S: Feline pediatrics ................................................................................................. 13
Romagnoli S: Techniques for neonatal resuscitation and critical care ....................................... 18
Hackett T: Managing the dyspneic cat – Case studies in feline respiratory distress ................... 23
Hackett T: Feline trauma ......................................................................................................... 26
Romagnoli S: Practical use of hormones in feline reproduction ................................................ 29
Romagnoli S: Ovarian remnant syndrome in the queen: Clinical approach
to a surgeon’s dilemma ........................................................................................................... 38
Domanjko Petri~ A: Sr~no popuš~anje pri ma~ki ....................................................................... 41
Knez V: Zgodnja sterilizacija in kastracija ma~k ........................................................................ 43
Kogovšek J: Kirurško zdravljenje zlomov stegnenice pri ma~kah ............................................. 46
Bourdeau P: Fungal diseases of the skin in cats ...................................................................... 49
Bourdeau P: Skin condition in cats: parasitic or not? .............................................................. 56
Brlo`nik M, Zaninovi} P, Zdovc I: Pristop k diagnostiki bolezni spodnjih se~il pri ma~ki ............. 60
Rejec A, Jeraj M, Butinar J, Fidel JL: Pospešeni protokol obsevanja pri zdravljenju
ploš~atoceli~nega karcinoma smr~ka in ustne votline pri ma~kah ............................................. 61
Firm I, Rejec A, Butinar J: Sindrom »okna na kip« in akutne ledvi~ne odpovedi
pri doma~i ma~ki ..................................................................................................................... 62
Pogorevc E, Celinšek B: Diagnostika pankreatitisa pri ma~kah ................................................. 63
Zajc R: Dihalna stiska pri ma~ki – stabilizacija, diagnostika in pogosti vzroki ............................. 65
Porenta K: Rehabilitacija in fizioterapija psa po operaciji kolka – klini~ni primeri ....................... 67
Firm I: Osnove EKG za tehnike ............................................................................................... 69
Lukanc B: Pooperacijska oskrba ma~ke .................................................................................... 71
Seliškar A: Ma~ka in analgetiki ................................................................................................ 74
Celinšek B: Odvzem biološkega materiala pri ma~ki ................................................................. 78
Nemec Svete A, Tozon N: Ravnanje z vzorci za izvajanje testov za ugotavljanje
ku`nih bolezni ma~k ............................................................................................................... 80
Knez V: Krvne skupine ma~k .................................................................................................. 84
Pavlin D: Rokovanje s katetri in sondami ................................................................................ 87
Erjavec V: Razlika med ma~jo in pasjo ustno votlino ................................................................ 89
Suhadolc Scholten S: Majhne skrivnosti za boljše po~utje ma~k ............................................... 93
Izdalo:
Slovensko zdruènje
veterinarjev za male ìvali
Fotografija:
Arhiva Term Krka
Krofi~ M, Mlakar N, Tomsi~ K, Pavlica Z, Seliškar A, Tozon N: Celostna obravnava
geriatri~nega stomatološkega pacienta – klini~ni primer ........................................................... 94
Nemec Svete A, Lukanc B, Tomsi~ K, Seliškar A: Kvantitativno dolo~anje
koncentracije CRP pri psih z uporabo nove imunokemijske metode .......................................... 97
Ravnik U, Suhadolc Scholten S, Tozon N: Hemobartoneloza pri ma~ki – klini~ni primer .......... 100
Oblikovanje:
AKTA DESIGN
www.akta-sp.si
Naklada:
250 izvodov
Plavec T: Hiperaldosteronizem pri ma~kah – pogostejši kot si mislimo? ................................... 102
Marhold C, Slavec B, Ra~nik J, Zadravec M, ôn~ M, Dov~ A: Diagnostika
klamidijskih oku`b pri ma~kah .............................................................................................. 104
Oman M, Dov~ A, Kvapil P, Kastelic M, Miheli~ B: Zdravstvena problematika
zapuš~enih ma~k v mestni ob~ini Ljubljana. ........................................................................... 106
4
2
ZBORNIK REFERA
TOV
REFERATOV
UPRAVNI ODBOR SLOVENSKEGA ZDRU@ENJA VETERINARJEV ZA MALE @IVALI SZVM@
ORGANIZACIJSKI IN UREDNI[KI ODBOR
Doc. dr. Alenka SELIŠKAR, dr. vet. med. (predsednica), Ljubljana
Prof. dr. Nata{a TOZON, dr.vet. med. (podpredsednica – bodo~a predsednica), Ljubljana
Igor FIRM, dr. vet. med. (blagajnik), Mozirje
Sara SUHADOLC SCHOLTEN, dr. vet. med. (tajnica), Ljubljana
Mag. Jure PIPP, dr. vet. med. (~lan), Ljubljana
Mag. Iztok VALENTINÎ^, dr. vet. med. (~lan), Maribor
ÂSTNA ^LANA ZDRU@ENJA:
Prof. dr. Vjekoslav SIMÎ^, dr. vet. med., Ljubljana, Slovenija in
Prof. dr. Jones R. BOYD, Dublin, Irska.
WORLD SMALL ANIMAL VETERINARY ASSOCIATION - WSAVA
OFFICERS
President:
Dr. David WADSWORTH ( U.K. )
President elect:
Dr. Jolle KIRPENSTEIJN ( The Netherlands )
Secretary:
Dr. Walt INGWERSEN ( Canada )
Vice president:
Dr. Peter J. Ihrke ( USA )
Treasurer:
Dr. Diane SHEEHAN ( Australia )
Immediate past president:
Dr. Brian ROMBERG ( South Africa )
FEDERATION OF EUROPEAN COMPANION ANIMAL VETERINARY ASSOCIATIONS FECAVA
OFFICERS
President:
Dr. Johan Van TILBURG ( Belgium )
Vice president:
Dr. Simon ORR ( U.K. )
Past president:
Dr. Andrew BYRNE ( Ireland )
Secretary:
Dr. Monique MEGENS ( The Netherlands )
Treasurer:
Dr. Jerzy GAWOR ( Poland )
EJCAP Editor:
Dr. Keith A. DAVIS ( U.K. )
5
3
ZBORNIK REFERA
TOV
REFERATOV
Generalni pokrovitelj:
PFIZER LUXEMBOURG SARL PODRU@NICA ZA SVETOVANJE S PODRO^JA FARMACEVTSKE DEJAVNOSTI,
LJUBLJANA, Letališka 3c, 1000 Ljubljana
Simpozij so omogo~ili še:
ABBOTT LABORATORIES D.O.O., PODRU@NICA LJUBLJANA, Dunajska 22, 1000 Ljubljana
BTL MARKETING D.O.O., Zalo`nikova ulica 43, 1351 Brezovica pri Ljubljani
DIPROS D.O.O., Gorenjesavska cesta 54, 4000 Kranj
FECAVA - THE FEDERATION OF EUROPEAN VETERINARY COMPANION ANIMAL ASSOCIATIONS
INTERVET INTERNATIONAL B.V., BOXMEER podru`nica Ljubljana, Kri`na ulica 10, 1000 Ljubljana
IRIS MEDNARODNA TRGOVINA D.O.O., Cesta v gorice 8, 1000 Ljubljana
KEMOFARMACIJA VELETRGOVINA ZA OSKRBO ZDRAVSTVA D.D., Cesta na Brdo 100, 1000 Ljubljana
KRKA, TOVARNA ZDRAVIL D.D., Šmarješka cesta 6, 8501 Novo mesto
MM SURGICAL DRU@BA ZA TRGOVINO IN ZASTOPANJE D.O.O., Galjevica 81, 1000 Ljubljana
NOVARTIS VETERINA D.O.O., Verovškova 57A, 1000 Ljubljana
SALUS d.d., Mašera Spasi}eva ulica 10, 1000 Ljubljana
SCHERING - PLOUGH CENTRAL EAST AG LUZERN, ŠVICA PREDSTAVNIŠTVO V SLOVENIJI, Dunajska 22,
1000 Ljubljana
SANOLABOR D.D., Leskoškova cesta 4, 1000 Ljubljana
TOSAMA TOVARNA SANITETNEGA MATERIALA D.D., Šaranovi~eva cesta 35, 1230 Domàle
UNIVERZA V LJUBLJANI VETERINARSKA FAKULTETA, Gerbi~eva 60, 1000 Ljubljana
VETCONSULT PHARMA TRGOVINA IN MARKETING D.O.O., Gerbi~eva 50, 1000 Ljubljana
VET PET TRGOVINA D.O.O., Letališka 29, 1000 Ljubljana
VETERINA PLUS D.O.O., Dunajska 51, 1000 Ljubljana
VETPROMET, ZASTOPANJE D.O.O., Cesta na Brdo 100, 1000 Ljubljana
ZOO MARKET PREIS MARKETING, TEHNOLOGIJA IN IN@ENIRING D.O.O., Eipprova 3, 1000 Ljubljana
6
4
ZBORNIK REFERA
TOV
REFERATOV
P
XXIII. SIMPOZIJ
SOBOTA, 24. april 2010, velika dvorana KKC
Moderator: Kogovšek J
09.00 – 09.30
Domanjko Petri~ A: Sr~no popuš~anje pri ma~ki
09.30 – 10.00
Knez V: Zgodnja sterilizacija in kastracija ma~k
10.00 – 10.30
Kogovšek J: Kirurško zdravljenje zlomov
stegnenice pri ma~kah
10.30 – 11.00
ODMOR
Moderator: Kotnik T
11.00 – 11.45
Bourdeau P: Fungal diseases of the skin in cats
11.45 – 12.30
Bourdeau P: Skin condition in cats:
parasitic or not?
12.30 – 14.00
KOSILO
Moderator: Valentin~i~ I
14.00 – 14.15
Brlo`nik M, Zaninovi} P, Zdovc I: Pristop k
diagnostiki bolezni spodnjih se~il pri ma~ki
14.15 – 14.30
Rejec A, Jeraj M, Butinar J, Fidel JL: Pospešeni
protokol obsevanja pri zdravljenju
ploš~atoceli~nega karcinoma smr~ka in ustne
votline pri ma~kah
14.30 – 14.45
Firm I, Rejec A, Butinar J: Sindrom »okna na
kip« in akutne ledvi~ne odpovedi pri doma~i
ma~ki
14.45 – 15.00
Pogorevc E, Celinšek B: Diagnostika
pankreatitisa pri ma~kah
15.00 – 15.15
Zajc R: Dihalna stiska pri ma~ki – stabilizacija,
diagnostika in pogosti vzroki
15.15 – 15.30
Porenta K: Rehabilitacija in fizioterapija psa po
operaciji kolka – klini~ni primeri
15.30
ZAKLJUÊK SIMPOZIJA
O AKTUALNIH BOLEZNIH
rogram
MALIH @IVALI
ÊTRTEK, 22. april 2010, velika dvorana KKC
PREDKONGRESNI DAN - DERMATOLOGIJA
(dermatološke parazitoze)
08.00 – 09.00
PRIJAVA UDELE@ENCEV
09.00 – 09.15
Kotnik T: Otvoritev
09.15 – 10.00
Bordeau P: Differential diagnosis of the
alopecic dog
10.00 – 10.30
Bourdeau P: New aspects in canine
leishmaniosis
10.30 – 11.15
ODMOR
11.15 – 12.00
Predstavitev klini~nih primerov
12.00 – 12.30
Skupš~ina Dermatološke sekcije
12.30 – 14.00
KOSILO
14.00 – 14.15
Pipp J: Pozdravne besede
14.15 – 15.00
Convert G: Cat scratch disease, a
dermatological issue?
15.00 – 15.45
Bourdeau P: The variety of skin
conditions due to mites (and ticks) in dogs
15.45 – 16.15
ODMOR
16.15 – 17.00
Bourdeau P: Dermatoses due to fleas or other
insects: A challenge for the clinician
17.00 – 17.45
Bourdeau P: Internal parasites in dogs:
How to control them? - some key points from
Dirofilaria to Leishmania
17.45 – 18.30
Razprava
20.00
VEÊRJA (Merial)
SOBOTA, 24. april 2010, mala dvorana KKC
PROGRAM ZA VETERINARSKE TEHNIKE
08.00 - 09.00
PRIJAVA UDELE@ENCEV
Moderator: Seliškar A
09.00 – 09.30
Firm I: Osnove EKG za tehnike
09.30 – 10.00
Lukanc B: Pooperacijska oskrba ma~ke
10.00 – 10.30
Seliškar A: Ma~ka in analgetiki
10.30 – 11.00
ODMOR
Moderator: Knez V
11.00 – 11.30
Celinšek B: Odvzem biološkega materiala pri ma~ki
11.30 – 12.00
Nemec Svete A, Tozon N: Ravnanje z vzorci za
izvajanje testov za ugotavljanje ku`nih bolezni
ma~k
12.00 – 12.30
Knez V: Krvne skupine ma~k
12.30 – 14.00
KOSILO
Moderator: Pavlin D
14.00 – 14.30
Pavlin D: Rokovanje s katetri in sondami
14.30 – 15.00
Erjavec V: Razlika med ma~jo in pasjo ustno
votlino
15.00 – 15.30
Suhadolc Scholten S: Majhne skrivnosti za boljše
po~utje ma~k
15.30
ZAKLJUÊK SIMPOZIJA
PETEK, 23. april 2010, velika dvorana KKC
08.00 – 09.00
PRIJAVA UDELE@ENCEV
09.00
OTVORITEV SIMPOZIJA
Moderator: Seliškar A
09.00 – 09.45
Hackett T: The critical cat – Triage, vascular
access and emergency treament
09.45 – 10.30
Hackett T: Feline shock – The unique
challenges of treating cats
10.30 – 11.00
ODMOR
Moderator: Tozon N
11.00 – 11.45
Romagnoli S: Feline pediatrics
11.45 – 12.30
Romagnoli S: Techniques for neonatal
resuscitation and critical care
12.30 – 14.00
KOSILO
Moderator: Pipp J
14.00 – 14.45
Hackett T: Managing the dyspneic cat – Case
studies in feline respiratory distress
14.45 – 15.30
Hackett T: Feline trauma
15.30 – 16.00
ODMOR
Moderator: Knez V
16.00 – 16.45
Romagnoli S: Practical use of hormones in
feline reproduction
16.45 – 17.30
Romagnoli S: Ovarian remnant syndrome in the
queen: Clinical approach to a surgeon’s dilemma
17.30 – 19.00
SKUPŠÎNA SZVM@
20.00
VEÊRJA (Pfizer)
POSTERJI
Krofi~ M, Mlakar N, Tomsi~ K, Pavlica Z, Seliškar A, Tozon N: Celostna obravnava geriatri~nega
stomatološkega pacienta – klini~ni primer
Nemec Svete A, Lukanc B, Tomsi~ K, Seliškar A: Kvantitativno dolo~anje koncentracije CRP pri psih
z uporabo nove imunokemijske metode
Ravnik U, Suhadolc Scholten S, Tozon N: Hemobartoneloza pri ma~ki – klini~ni primer
Plavec T: Hiperaldosteronizem pri ma~kah – pogostejši kot si mislimo?
Marhold C, Slavec B, Ra~nik J, Zadravec M, ôn~ M, Dov~ A: Diagnostika klamidijskih oku`b pri
ma~kah
Oman M, Dov~ A, Kvapil P, Kastelic M, Miheli~ B: Zdravstvena problematika zapuš~enih ma~k v
mestni ob~ini Ljubljana
7
5
ZBORNIK REFERA
TOV
REFERATOV
8
6
ZBORNIK REFERA
TOV
REFERATOV
The Critical Cat
Triage, Vascular Access and Emergency Treatment
Tim Hackett
Triage
Veterinarians must understand the unique problems
related to feline size and physiology that require special
attention in emergencies. With a basic understanding of
feline emergency medicine these small patients that can
be managed in most veterinary hospitals.
Each new patient should be evaluated in an orderly
and systematic manner. Problems that interfere with vital
physiological functions should receive the highest priority. These are generally disorders of the respiratory system, cardiovascular system, or neurological system.
Disability--Is there evidence of neurological injury? Sei
zures? Subcutaneous emphysema over nasal sinus
es? Broken teach? What is the posture of the animal?
Is the animal bright, alert and responsive? Does the
animal respond to painful stimuli? Are the pupils di
lated, constricted, of equal size, and responsive to
light? Is there an extremity fracture that might threaten
a peripheral nerve?
Management of the life-threatening problems identified during the primary survey is continued as shock therapy begins. The secondary survey identifies all other problems related to the trauma. The entire animal's body is
examined again from head to toe. Necessary diagnostic
samples are collected and submitted. Only when the patient is stable are indicated radiographs taken. In-depth
management of the patient's less life-threatening problems is undertaken in the definitive care phase.
Initial Assessment
Do an initial assessment of the critical feline to identify life-threatening physiological problems. Whenever a
problem is identified immediate therapy is begun. This
"primary survey” follows the ABC (and D's) of triage and
resuscitation:
Cardiovascular System
Airway--Is the cat having difficulty moving air? Is
there an airway obstruction? This can create a highpitched sound heard best over the obstruction.
Breathing--Is the cat dyspneic? What is the color of
the mucous membranes? Pulmonary contusions, pneu
monia, pulmonary edema, pneumothorax, diaphrag
matic hernia, and broken ribs can all result in a rapid,
shallow (restrictive) breathing pattern.
Circulation--Is there evidence of hemorrhage, fluid loss
or heart disease? Are the mucous membranes pale
and dry? Are the femoral pulses weak and rapid?
Are the extremities cold? Is the abdomen distended?
External blood loss is and a venous catheter is inserted. Blood samples are collected for analysis of the packed
cell volume and serum total solids. The remainder of the
sample can be saved for a complete blood count and
biochemical analysis. The initial intravenous solution can
be any crystalloid fluid, such as normal saline, Hartmann's
lactate, or Normosol-R. Crystalloid fluids should be titrated to each patient. Cats are extremely sensitive to
overhydration and aggressive fluids can easily create more
problems with pulmonary edema. Our technique is to
administer one fourth of a shock volume (Shock volume
in cats is 45 ml/kg of crystalloid fluid) in the first 10
minutes. We give the dose in 10 ml/kg test doses to avoid
iatrogenic fluid overload. Most case that are volume depleted will show improvement with only modest fractions of the total shock volume. Titration cannot be overemphasized. Serious problems can develop if too much
fluid is given to quickly.
Tim Hackett D.V.M., M.S.
Diplomate, American College of Veterinary Emergency & Critical Care
Associate Professor and Small Animal Medical Chief of Staff
After the initial bolus, we assess for evidence of shock
(rapid heart rate, tachopnoea, weak pulses, cool extremities, slow capillary refill time), and then give another
quarter shock volume over the next 20 minutes. At thir-
James L. Voss Veterinary Medical Center
Colorado State University
Fort Collins, CO 80523
[email protected]
9
7
ZBORNIK REFERA
TOV
REFERATOV
ty minutes the patient is again assessed and a packed cell
volume and total solids is evaluated. Packed cell volume
and total solids are rechecked thirty minutes after beginning fluid therapy. If the packed cell volume drops
below 25 to 30% and the patient is still showing signs of
shock, whole blood is given. If the serum total solids
drops below 45 gm/L a colloid should be used to maintain intravascular volume. We tend to use hydroxyethyl
starch at doses of 5-10 ml/kg. Colloids like crystalloids
can cause volume overload. Take care when giving these
fluids quickly.
Other variables include fluid balance (body weight, central venous pressure), serum electrolytes, urine production, coagulation function and patient comfort.
Fluid Balance. Because of increased capillary permeability and decreased systemic vascular resistance, critically ill cats can experience large fluid movement from
the vasculature into the tissues. Crystalloid fluids can lower
protein levels causing a drop in the oncotic pressure.
With increased vascular permeability and abnormal distribution this may cause interstitial edema. If fluid accumulates in the lungs, gas exchange is impaired and oxygen delivery reduced. Cerebral edema will cause progressive changes in mentation. Frequent checks of the body
weight, central venous pressure, mentation and urine
production are vital. Respiratory rate and thoracic auscultation should be repeated listening for changes associated with pulmonary edema. Excessive fluid losses (vomiting, diarrhea, polyuria) should be measured or estimated and replaced with crystalloid fluids as they occur.
Respiratory system
Respiratory distress in cats is a therapeutic dilemma.
Critical cats can be so compromised that diagnostics and
treatment can cause respiratory and cardiac arrest. A diagnosis should not come at the expense of the patient.
An induction chamber for cats works well to give the cat
added oxygen while observing them in an attempt to localize the respiratory problem. Try to determine the nature of the problem first with observation. A rapid shallow respiratory pattern suggests restrictive disease while
a slow deep inspiratory pattern is seen with airway obstruction. With the restrictive pattern, auscultation can
help differentiate pleural space disease (pneumothorax,
hydrothorax) from parenchymal diseases (pneumonia,
pulmonary edema).
Vascular Access for the Critical Cat
Since fluid therapy requires close attention to prevent
overhydration, variables like packed cell volume, total
protein, glucose, and electrolytes should be checked several times a day. For this reason it is important to have
reliable vascular access. This is best accomplished with a
jugular, or medial saphenous central intravenous.
Cats will become more and more distressed as they struggle for oxygen. A stressed animal will need more oxygen
so the problem can get worse. Mild sedation with very
low doses of a diazepam or a narcotic can allow the anxious dyspneic cat to relax and breathe more efficiently.
Restraint for catheterization, radiographs and physical
examination should wait until the patient is relaxed and
breathing easier. In the case of pleural effusion or pneumothorax, a thoracocentesis can provide a diagnosis at
the same time it is providing the life-saving treatment.
Veterinarians and veterinary technicians that can reliably gain vascular access in the sickest cats are valuable
members of the patient care team. Often, the patients
most in need of vascular access are the hardest to catheterize.
Catheterization Basics
Secondary Survey and Hospitalization
Intravenous catheters are invasive devices and their
use must be managed with potential complications in mind.
Direct access can also allow infectious agents a means of
bypassing defenses to colonize the host. These “foreign”
materials can also cause a variety of inflammatory complications from mild vasculitis to serious thrombosis and
vascular occlusion.
Cats dealing with critical illness develop a variety of predictable complications. These patients are at risk of organ failure. Hypothermia, acute respiratory distress (pulmonary edema), sepsis, disseminated intravascular coagulation, renal failure and liver disease are just some of
the problems seen regularly in our feline critical care practice. By anticipating multiple organ dysfunction, monitoring critical hemodynamic and respiratory variables and
treating abnormalities that are identified, these patients
may be supported throughout hospitalization.
A surgical preparation of the skin over the catheter
site, and sterile handling of catheter and connection tubing will minimize infectious complications. Hair should
be clipped within 2 to 4 cm of the site. The area should
then be cleaned and disinfected with antiseptic surgical
scrub for 3 minutes. While it is not necessary to wear
sterile gloves when placing intravenous catheters, the
person handling the catheter should have clean hands.
We recommend wearing disposable vinyl or latex gloves
Intensive, serial monitoring is the core of critical care
medicine. Readily obtainable physiologic variables are used
for screening, early warning and hopefully, early correction of life threatening problems. Packed cell volume, total protein, oxygenation parameters (mucous membrane
color, oxygen saturation) have already been discussed.
10
8
ZBORNIK REFERA
TOV
REFERATOV
travascular catheters, this procedure is easily mastered
using fresh cadavers. People anticipating a need for this
skill would be wise to learn it before they need it. Unfortunately this route can only be used for giving fluids, not
for drawing blood.
when scrubbing the skin, then drying or changing the
gloves when handling catheters and tubing.
After the catheter is in place, the site should be covered with a clean dressing. The catheter needs to be held
securely, however think about how you will remove or
change connections when you are applying the bandage.
Incorporating “T-port” connectors in the final bandage
will take the strain of movement off the catheter. These
connections are also easily replaced without having to
replace the entire dressing.
Hematologic and Physiologic Variables to
Monitor and Address in Critical Cats
Catheters and the local site should be checked every
24 to 48 hours. The bandage should be removed, and
the vessel palpated. The catheter should be removed and
a new one placed in another site if there is any evidence
of inflammation or thrombosis.
Oncotic pressure. Serum albumin when low should
be addressed with appropriate nutrition and colloidal fluids (blood or hetastarch). Total solids should be monitored and kept above 35 g/L. Persistent hypoalbuminemia is associated with increased mortality in critically ill
animals.
Central intravenous catheterization
A large-bore, teflon, jugular venous catheter can be
maintained for days. Incorporated into a bandage around
the cat's neck, these catheters tend to stay dryer, cleaner
and can remain in longer than peripheral catheters. Central venous catheters are useful in obtaining a central
venous pressure (CVP). The CVP provides important information about fluid loading and the hearts ability to
pump the fluids forward. Large central catheters can also
be useful for repeated blood sampling. By drawing 3 cc
of blood back into a syringe pre-loaded with 0.5 cc-heparinized saline (1 U heparin/ml 0.9% saline flush), any
volume of blood can then be sampled. The heparinized
blood can then be returned to the patient and the line
flushed. This “Three-syringe” technique will minimize
patient discomfort and iatrogenic blood loss.
Electrolytes and glucose. Calcium, sodium, chloride
and potassium should be maintained within normal limits. Potassium should be added to maintenance fluids to
avoid iatrogenic hypokalemia. Potassium containing fluids should never exceed a rate of 0.5 mEq/kg body weight/
hour of additional potassium. Blood glucose should be
maintained between 100 and 200 gm/dL (5.5 11 mmol/
L). Hypokalemia that does not rapidly correct with high
levels of supplemental potassium may respond to magnesium supplementation. Hypomagnesemia is common
in the critically people and animals. Unfortunately, serum
magnesium represents only a small fraction of whole body
magnesium and is not a reliable measure. Magnesium
can be replaced at 0.75 - 1 mEq/kg/day by constant rate
infusion in 5% dextrose in water. After 24 hours the dose
is lowered to 0.3 to 0.5 mEq/kg/day or the animal can be
switched to a magnesium containing maintenance crystalloid fluid.
Central venous catheters should be avoided in patients
with bleeding disorders, seizures or hypercoagulable states
(hemolytic anemia, hyperadrenocorticism, DIC, protein
losing nephropathy).
Urine production. Urine output and urine specific gravity tells us about renal blood flow and function. Recumbent and azotemic patients, and those at risk for multiple
organ dysfunction should have an indwelling urinary catheter in place with a sterile closed collection system. Low
urine output (< 1 ml/kg/hour) in a hydrated patient may
represent acute renal failure. A low urine output with
elevated urine specific gravity is an indication of inadequate fluid intake (IV fluids or drinking). Quick intervention with fluids, and diuretics (furosemide 1-2 mg/kg)
may start urine flow and prevent permanent renal damage. It is important to withhold furosemide until dehydration is corrected. Patients that are hypotensive following fluids may benefit from a positive inotrope like dobutamine to offset any drops in cardiac output as a result
of furosemide.
Intraosseous catheterization
The smallest and sickest cats are often the most difficult to catheterize although they may be the most in need
of intravenous fluid therapy. Rather than struggle with a
small, peripheral catheter, or the trauma of a vascular
cut-down procedure, an intraosseous catheter can provide short-term access. Placed in the medullary cavity of
any long bone, the intraosseous space rapidly absorbs
crystalloid fluids, colloids and drugs. Any needle with a
stylet can be used. We will usually use an 18-gauge bone
marrow needle or a 20 to 22-gauge 1” spinal needle. The
needle is usually placed in medullary space of the femur
in cats.
Intraosseous catheterization is a worthwhile skill for
feline emergency and critical care practitioners. The intraosseous space is always available regardless of the
degree of hypovolemia or dehydration. Unlike other in-
11
9
ZBORNIK REFERA
TOV
REFERATOV
Coagulation. Disseminated intravascular coagulation
(DIC) is a common component of systemic illness. Daily
examination of a blood smear for decreased platelets and
fragmented red blood cells is inexpensive and easy. Tests
of factor function (prothrombin time) should be considered if bleeding is occurring with normal platelet numbers. The most important treatment for DIC is to remove/resolve the underlying cause. Specific therapy is
directed toward decreasing microthrombi (heparin), providing missing factors (fresh frozen plasma) and improving perfusion (fluid/colloid support).
Pain control. Cats in constant stress will become immunosuppressed. It is vital to the care of the patient that
it be made as comfortable as hospitalization will allow.
The appropriate use of analgesics, padding, bandage
changes and personal contact will have positive effects
on the patients overall sense of well-being.
Physiologic Variable
Optimal Values
Intervention
Systemic arterial pressure
Central venous pressure
Urine output
Blood Glucose
Packed Cell Volume
Total Serum Solids
Albumin
Arterial blood gasses
>90 mmHg
<3 cmH20 (5-10 cm H2O if loading)
>1 ml/lb/hr
>3.9 mmol/L
25-35%
>35 g/L, < 50 g/L
>10 g/L
PaO2 > 70 mmHg
Sa02 > 92%
PaCO2 < 35 mmHg
HCO3 > 14, < 24
pH > 7.3, < 7. 5
>70, <150 BPM
Normal range varies with equipment
Fluids, inotropes
Diuretics, venodilators
Diuretics, dopamine
Nutrition, dextrose
Transfusion
Plasma, colloids
Plasma
Supplemental oxygen
Supplemental oxygen
Ventilatory support
Fluids, perfusion
Fluids, perfusion
Fluids, analgesics, anti-arrhythmics
Blood, plasma, heparin
Heart rate
Prothrombin time
12
10
ZBORNIK REFERA
TOV
REFERATOV
Feline Shock
The unique challenges of treating cats
Tim Hackett
Introduction
Baseline information
Shock, in it's most basic form, is an inadequate delivery of oxygen. If we look at oxygen delivery as an equation we can address all the variables involved can correct
those we can.
When deciding on rates, volumes, and types of fluids
for our sick feline patients, it is especially important to
know about the electrolytes, and the cat's normal body
weight. If there are acute decreases in body weight, most
of these losses can be attributed to water loss. This will
allow a more accurate assessment of dehydration. If ideal weight is not known and the animal is clinically dehydrated (poor skin turgor, dry mucous membranes, sunken eyes) the degree of dehydration can be estimated at
approximately 10%.
DO2 ml/min (oxygen delivery) = CaO2 (oxygen
content) x CO (cardiac output)
CO = Heart rate x Stroke volume
CaO2 = SaO2 (Oxygen saturation) x Hgb (hemoglobin
concentration) x 1.34 + (PaO2 x 0.003)
Circulatory shock is divided into 3 major classifications; hypovolemic shock, cardiogenic shock or pump
failure, and distributive shock. Though the mechanisms
for each are distinctly different, each results in reduced
oxygen delivery (DO2) to tissues through low blood flow
or uneven distribution of flow. In actual feline practice
we usually deal with issues of blood volume and poor
cardiopulmonary function. A single patient may have several pathologic processes simultaneously resulting in reduced perfusion of tissues.
A thorough physical examination should be performed;
assuming fluid losses are not life threatening. If however, your quick assessment suggests life-threatening complications (abnormal mucous membrane color, abnormal
capillary refill times, tachycardia, tachopnoea, weak pulse,
cool extremities, obvious blood loss, etc.), then your first
goal of fluid therapy will be to save the life of the animal
and your thorough physical examination will have to be
postponed and fluid therapy to stabilize the patient's condition must be started first.
Third-space losses involve the accumulation of large
fluid volumes in cavities such as the pleural or peritoneal
space and intestinal or gastric lumen, or in tissues around
fracture or trauma sites. These losses result relative hypovolemia without predictable changes in body weight.
Cats are notoriously bad at shock. Instead of compensating for low volume with a faster heart rate, the cat
in shock is often bradycardic. Cats also have issues with
cardiopulmonary function leading to problems handling
shock rates of fluids. Close attention is required to prevent iatrogenic pulmonary edema when giving large volumes of fluid to feline patients.
Mucous membranes are good indicators of hydration.
Color and refill time, as well as moistness, should be
assessed. The color of the mucous membranes will vary
considerably. A septic patient often has red, injected,
mucous membranes, while a severely hypovolemic patient may have pale to gray mucous membranes. Because many factors will govern the color of mucous membranes, this feature alone cannot be used to assess hydration.
Decreased skin turgor, sunken eyes, dry mucous membranes are other subjective observations that suggest clinical dehydration.
[email protected]
13
11
ZBORNIK REFERA
TOV
REFERATOV
The Emergency Phase
The Replacement Phase
When a patient is excessively hypotensive and has clinical signs of shock, the blood volume must first be restored. If there are no clinical signs of shock, one can
proceed to the second phase of fluid replacement.
The volume of fluid administered during the rehydration/replacement phase is based on an assessment of fluid
needs for (1) returning the patient's status to normal (deficit volume), (2) replacing normal ongoing losses (maintenance volume), and (3) replacing continuing abnormal
losses (continuing losses volume).
The volume of fluid required is based on the patient's
weight, but you should be prepared to administer a plasma volume each hour if crystalloid solutions are being
used. In the cat this is 45-50 ml/Kg/hr.
By dividing the total fluid volume into 1/8-1/4 test
doses and titrating to effect (frequently monitoring of endpoint variables), one may determine when it is appropriate to move to the second phase of fluid resuscitation
(rehydration phase). If the clinical signs of shock resolve
after the first bolus, there is no need to proceed with
another bolus of fluid. Move on to the rehydration phase.
One must be cautious about overhydration and hemodilution. Overhydration during the emergency phase
is most likely to occur when large volumes are administered to cats with pulmonary contusions, preexisting
pulmonary edema, aspiration pneumonitis, hypoproteinemia, brain injuries, and underlying heart disease.
Hypovolemic Shock
The primary defect in hypovolemic shock is an inadequate circulating volume. This can be from sudden massive blood loss as in surgery or trauma or fluid loss from
vomiting, diarrhea or renal disease. Because cardiac output relies on stroke volume and heart rate, the patient
with inadequate volume will be tachycardic in an attempt
to compensate. Neurohormonal pathways detecting a
drop in blood pressure will lead to increased vascular
tone in an attempt to shunt circulation from the periphery to vital tissue beds. This results in cool extremities,
tachycardia, prolonged capillary refill, oliguria and weakness.
Treatment should be directed at the primary source
of fluid loss while correcting the fluid deficit. Crystalloid
fluids can be used initially to restore circulating volume.
Crystalloids will improve cardiac output and should not
be withheld for fear of diluting the red blood cell mass.
Oxygen delivery is a function not only of oxygen content
but of cardiac output as well.
Maintenance volumes are normal ongoing losses.
Ongoing losses are divided into sensible and insensible
losses. Sensible losses can be measured and are water
losses in the urine and feces. Insensible losses are normal but are not easily quantitated. These water losses
occur with metabolism, and from the respiratory tract.
One-third of the maintenance volume is made up of the
insensible volumes and two-thirds, sensible volumes.
Traditionally, maintenance volumes have been estimated
at about 66 ml/kg/day.
The Maintenance Phase
The last phase of fluid therapy is the maintenance
phase. At this point the patient has received enough
fluid to compensate for shock (if necessary) and has had
a partial replacement of any deficit volume. Chronologically, this phase begins no sooner than 24 hours after
fluids were begun. Objective signals that the patient is
ready to be placed in the maintenance phase are an absence of clinical signs of shock or dehydration, and the
body weight will have increased by at least the percentage of dehydration already corrected. During the maintenance phase, you will be providing both maintenance
volumes and continuing losses volumes.
Oxygen delivery to the tissues is one of the primary
functions of the cardiopulmonary system and of primary
importance to the patient manifesting signs of circulatory failure. If the defect in the transport of oxygen to the
vital tissues can be identified and removed while the patient is supported, recovery is possible.
With a treatment goal of improving oxygen delivery to
the tissues we can increase cardiac output by increasing
stroke volume (fluids). Oxygen content can be increased
by increasing the hemoglobin concentration (Red cell
transfusion) and increasing oxygen saturation (Oxygen
supplementation).
14
12
ZBORNIK REFERA
TOV
REFERATOV
Feline pediatrics
Stefano Romagnoli
The success of neonatal care depends on normality of
pregnancy as well as parturition, as abnormal pregnancy
and/or dystocia may easily predispose neonates to develop pathological conditions or transient hypoxia which may
threaten their survival during the first few hours/days of
life. Sadly, it is inevitable that some kittens will die, and a
low level of loss is to be expected, even in the best run
breeding cattery. It is generally found that pedigree cats
have higher levels of neonatal mortality than non-pedigree. In one study, pedigree cats had an average kitten
mortality of 34.5% from birth to one year of age (range
of 8-40%), compared to 10-17% in non-pedigree cats.
These higher levels of mortality may reflect inbreeding
within pedigree cats. However, there may also be bias in
the non-pedigree data as it is difficult to get accurate
figures for pet cats.
Normal kittens eat or sleep 90% of the time for their first
2 weeks. Unfortunately, neonates tend to show limited
responses to disease, so their presenting signs are rarely
indicative of a particular condition. Regardless of whether they are hungry or ill they typically cry excessively,
and/or fail to suckle. The most common signs of illness
are weakness, hypothermia, lethargy, restlessness, and/
or regurgitation of milk. Sick kittens respond poorly to
their environment, and typically have either very thin abdomens from lack of food or very swollen abdomens
from swallowing air. They often lay separated from the
other kittens and are ignored by the queen. Sick kittens
need to be treated immediately as they cope very poorly
with anorexia or hypothermia.
Approximately 15-40% of kittens die between birth and
3 months of life, with the majority of these losses occurring at birth or within 4-5 weeks of age. Deaths occurring at birth or within the first 2 weeks in otherwise normal neonates are generally referred to as “fading syndrome”. The 2-week distinction is rather arbitrary, and
most clinicians will consider as fading kittens all those
newborns that die within 12 weeks of age. Kitten losses
up to 12 months of age are due to problems acquired in
utero, at birth (birth to 2 weeks) or around weaning time
(5 to 12 weeks of age). Neonatal kittens may die suddenly or “fade” within a few days. Unfortunately, the clinical
signs of many neonatal diseases are very similar and vague.
While normal kittens tend to cuddle together and sleep
contentedly between feeds, sick kittens tend to lie separately, are generally more restless, are not keen to suckle, and cry frequently (if still strong enough to do so).
Neonates are vulnerable because their thermoregulatory
mechanisms are poorly developed, they are at increased
risk of dehydration and hypoglycaemia, and they are immunologically immature. Therefore, regardless of the
initiating cause, neonates rapidly become hypothermic,
hypoglycaemic, dehydrated, hypoxic, and die. They are
predisposed to hypothermia because they cannot thermoregulate, lack insulating fat and thermogenic brown,
cannot induce peripheral vasoconstriction, cannot react
to cold by shivering, and have a large surface area to
volume ratio over which to loose body heat. Hypothermia then triggers ileus and reduced intestinal absorption,
increases susceptibility to infection, and eventually leads
to cardiopulmonary failure. Neonates are predisposed to
hypoglycaemia because they have high energy requirements (2-3x the metabolic rate of adults/kg body weight),
but have no energy reserves and their immature livers
are inefficient at generating energy. This can then be exacerbated by hypothermia-induced reduction of intestinal absorption. The neonatal risk of dehydration is because they have a higher percentage of body water (82%)
than adults, while incurring greater loses through their
immature kidneys, lungs and skin. The most important
causes of “fading” or sick kittens are 1) birth/queen-related factors, 2) Congenital abnormalities; 3) Low birth
weight; 4) Inappropriate environment; 5) Inappropriate
nutrition; 6) Neonatal isoerythrolysis; 7) Infection.
Stefano Romagnoli, DVM, MS, PhD, Dipl. ECAR
President, European Board of Veterinary Specialisation
Dept. of Veterinary Clinical Sciences, Faculty of Veterinary Medicine, Agripolis, Legnaro,
35020 (PD)
University of Padova, Italy
[email protected]
1) Birth / queen-related factors - Kittens that suffer dystocia have a significantly increased risk of death within
the first few weeks of life. In fact, prolonged labour or
dystocia are probably the most significant causes of neo-
15
13
ZBORNIK REFERA
TOV
REFERATOV
natal death. This results from the effects of hypoxia and/
or trauma. Dystocia occurs in ~6% of pregnancies (range
0-18%). Studies have shown that cats with extremes of
conformation, such as the Siamese and Persians, experience much higher levels of dystocia (7-10%) than cats
with normal conformation (generally <5%). Hypoxia
during birth can result in stillbirth, or the birth of weak,
slow, kittens that fail to suckle. These kittens usually die
within the first week of life or, due to failing to ingest
sufficient colostrum, have an increased risk of infectious
disease. Kitten mortality is usually highest in the first
litter born to a particular queen and after her fifth litter.
The high death rates in kittens from first-time queens
probably relates to inexperience, trauma and cannibalism. Older queens tend to have smaller litters and tend to
produce more kittens with congenital defects. The negative effect of extremes of litter size is seen as reduced
survival of single kittens, and of kittens from litters of 7
or more. Kitten mortality also increases with increasing
maternal obesity, and with other queen-related causes,
including a lack of milk, mastitis, or maternal neglect.
2) Congenital abnormalities - Obvious physical defects
may be seen in 10-20% of stillborn kittens. However, the
prevalence varies considerably; from 1-10% of kittens born
to research cats, to 1-31% of kittens born to pedigree
cats. Congenital disorders are present from birth, and
can affect any body system. They may result from genetic disorders or teratogenic factors. Because inbreeding
increases the risk of genetic disease, congenital disorders are seen more frequently in pedigree cats. In addition, certain defects are seen more frequently in some
breeds than others. Congenital defects resulting from
exposure to teratogenic substances may be seen in cats
of any breed. For example, cleft palates may result from
treatment with griseofulvin, corticosteroids, or excessive
amounts of vitamin A; skeletal deformities may result
from the administration of organophosphate anti-flea
products. It has also been suggested that overheating, in
some pregnant cats, may result in an increased risk of
skeletal deformity in their kittens. Severe defects usually
result in stillbirth or early neonatal death. Milder disorders may result in fading kittens, or only become apparent later in life.
3) Low birth weight - Underweight kittens have a significantly increased risk of neonatal death. They are physiologically immature compared to normal-weight kittens,
and they may be too weak to nurse adequately. In addition, they lack insulating fat and thermogenic brown fat,
and they have weak thoracic muscles and immature lung
development. They are particularly susceptible to hypothermia, dehydration, respiratory failure, and sepsis. Kittens may be born underweight because of maternal malnutrition or ill-health; congenital disease; in utero infections; or any condition that results in poor placental blood
supply. The average birth weight for most breeds of cat
is 100g ± 10g. However, it is normal for some breeds to
have significantly smaller kittens (Oriental; ave. 80g); while
others (Maine Coon) have significantly larger kittens
(ave.120 g). It is therefore very important to know what
the average weight for kittens of a particular breed is
when trying to decide whether or not a particular kitten
is underweight. As a general guideline newborn kittens
<75 g are likely to have very high death rates.
4) Inappropriate environment Environmental factors, such
as extremes of temperature and humidity, poor hygiene,
overcrowding, or over-handling, all result in increased
kitten mortality. Ideally, the kittening room should be well
ventilated, draft free, and maintained at a fairly constant
18-24oC temperature, 55-60% humidity. This will allow
the dam to be comfortable, and she can supply any additional heat required by the offspring. Where kittens have
to be hand-reared it is necessary to supply additional
heating. Ideally the temperature in the box should be
maintained at 29-32oC, but the box should be large enough
for the kittens to move away from the heat if they become too hot. The temperature is gradually reduced to
27oC by 7-10 days and 22oC by the end of the first month.
Overcrowding will lead to increased infectious disease
and disease resulting from competition at the mother’s
nipples (which can in turn result in inadequate nutrition
[see below]). Over-handling will not only limit the kitten’s
feeding time, but with nervous queens, may result in cannibalism of her kittens.
Providing kittens with a suitable environmental temperature is essential. A kitten that has ceased to suckle regularly will quickly become cold and hypoglycaemic. Since
neonates cannot shiver and are unable to control their
own body temperature hypothermia will result, and this
will lead to a further reduction in activity and suckling.
The rectal temperature of new-born kittens ranges from
35-37oC in the first week, to 36-38oC in the second and
third weeks, and reaches normal adult levels of 38-39oC
by the fourth week. Hypothermia is particularly harmful
as it can initiate a number of other problems. For example: a week-old kitten should have a temperature of 3537oC and a heart rate of 200-250 bpm. However, if its
temperature falls to 30oC, its heart rate will fall to 40-50
bpm. While this is initially a protective response, if sustained, it can lead to a decrease in respiratory rate, which
may in turn lead to cardiopulmonary failure. Also, a hypothermic kitten will not suckle effectively, its gastrointestinal motility will become depressed, and it will have an
increased susceptibility to infection. It is therefore important to check the temperature of any potentially weak
or ill kittens. However, if their rectal temperature remains
<34oC for prolonged periods of time the kitten is likely to
die.
16
14
ZBORNIK REFERA
TOV
REFERATOV
5) Inappropriate nutrition - Care should be taken to feed
the queen an appropriate diet. Incorrect nutrition of the
queen can affect the quality of the milk she produces.
Generally, when the queen is healthy and producing adequate milk the kittens should have no problems with inappropriate nutrition. Inadequate milk production may
be associated with an inexperienced or overly nervous
queen, old queens, sick or malnourished queens, dystocia, certain familial traits, systemic illness or mastitis.
Inadequate milk uptake by the kitten can also result from
anything causing kitten ill-heath or weakness, from competition and bullying by siblings, or any environmental
factor that distracts or upsets the queen-kitten bond.
Normal kittens should suckle within 2 hours of birth as
they can only adsorb colostrum in the first 16-24 hours
of life. Since any kitten not gaining sufficient weight has
an increased risk of neonatal death it is important to weigh
kittens regularly (at birth, daily for the first week, then at
least twice weekly until after weaning). A loss of <10%
may be expected in the first 24h, but after that there
should be daily weight gain (~10-15g/day; 5-10%); they
should double their birth weight by 1-2 weeks of age and
weight gain should be steady and progressive. Failure to
gain weight over 24 hr requires attention and any weight
loss should be investigated, as kittens losing more than
10% body weight are unlikely to survive. It is essential
that kittens gain adequate nutrition as they have a greater
risk of developing hypoglycaemia than adults. This is
because they are metabolically less able to generate glucose than adults, while having a much larger requirement for it. Any kitten that is ill or stressed may develop
hypoglycaemia. This may be seen as weakness, hypothermia, crying, difficult breathing, seizures, coma and,
eventually, death.
Neonatal kittens are also very susceptible to dehydration.
This may result from inadequate consumption of milk,
or excessive fluid losses (usually associated with overheating, excessively low humidity, or diarrhoea). Kittens
contain relatively more body water than adults and their
water turnover rate is twice that of adults. Neonatal kitten maintenance fluid requirements are ~130-220ml/kg/
24h, compared to 50-65ml/kg/24h for a mature cat. This
is because kittens have greater fluid losses through their
skin, lungs and kidneys, which are all immature. Since
the kittens derive all of their food and water in the form
of milk, when the supply is inadequate, supplemental feeding is needed. Where the kittens have been orphaned or
the queen is unable to feed them they will need total replacement feeding. Weaning should begin at 3-4 weeks
of age. It is important to ensure that all of the kittens gain
sufficient food at this time. In large litters competition at
the food bowl can lead to weaker kittens being bullied
and so eat less.
6) Neonatal isoerythrolysis - Neonatal isoerythrolysis (NI)
is relatively common is certain purebred kittens. Cats
have 3 blood groups; Type A, B, and AB. Type A is genetically dominant to Type B. Genetically, a Type A cat
may therefore be A/A or A/B. The rare blood type AB is
inherited slightly differently, and is recessive to Type A
but dominant to Type B. AB cats are only found in breeds
in which the Type B has been identified, usually increasing in frequency as the percentage of Type B cats increases. The frequency of Type A, B and AB blood types
varies between breeds (Table 1), and also, to some extent, between countries. Generally, most domestic short
and longhaired cats (DSH/DLH) are Type A (75-100%
Type A; 0-25% Type B; 0-10% Type AB). Interestingly,
the Bengal breed appears to have a particularly high number of AB cats, although actual prevalence data are not
yet available. Unlike puppies, kittens have naturally occurring antibodies against the other blood types in their
plasma. Antibodies of the IgG class (and to a lesser
extent of the IgM class) are acquired by kittens with colostrum. Kittens with blood type A have weak anti-B
antibodies, while kittens with blood type B have strong
anti-A antibodies. Since these antibodies occur naturally, the queen does not need to be sensitized by previous
pregnancies or blood transfusions. Since the highest proportion of Type B cats are seen in British Short Hair (BSH)
cats, NI is seen most frequently in this breed of cats.
During the first 16 hours of life maternal antibodies are
transferred to the kitten through colostrum ingestion. If
the kitten has blood type A or AB and the mother has
blood type B, colostral antibodies will lyse the kitten’s
red blood cells. Haemolysis can be intravascular and/or
extravascular, causing severe anemia, nephropathy, multiple organ failures as well as disseminated intravascular
coagulopathy. Since all blood type B cats have high antibody titers, even primiparous mothers can have litters
with NI. Clinical signs develop more often in blood type
A or AB kittens born to blood type B mothers. As the
fetus is protected from maternal antibodies, kittens at
risk are born healthy and nurse vigorously, but will start
showing clinical signs within hours to days after colostrum ingestion. Clinical signs will include either a) sudden death; b) progressive failure to nurse and to thrive
during the first 3 days (with presence of dark, brownred urine caused by haemoglobinuria, icterus, anemia)
with death occurring during the first week; some kittens
may survive and develop a tail-tip necrosis between the
first and second week of life, which may then slough
between 3 days and 2 weeks of age. or c) no clinical sign
except for presence of tail-tip necrosis, positive direct
Coombs’ test and moderate anemia.
17
15
ZBORNIK REFERA
TOV
REFERATOV
100% Type A
~80% Type A
75-100% Type A
60% Type A
40% Type A
Siamese
Somali
Domestic Short-Hair
Domestic Long-Hair
Devon Rex
British Short Hair
Burmese
Abyssinian
Persian
Tonkinese
Birman
Oriental
Maine Coon
Norwegian Forest Cat
Table 1: Breed prevalence of feline blood types
Where NI is seen, all sexually active cats should be bloodtyped to prevent further inappropriate mating. In addition, it is recommended that all BSH cats should be bloodtyped prior to breeding. This can be done using a simple
in-house test card (Rapid Vet-H, dms laboratories). It is
important to ensure that Type B queens do not mate with
Type A toms. Where an unknown mating has occurred,
placental blood can be used to determine a kitten’s blood
type. If the queen’s blood-type is known to be Type B,
and a kitten is found to be a Type A, it can be prevented
from suckling the queen, at least until it is >24h old.
While this procedure will prevent the occurrence of NI,
the lack of colostrum will leave the kitten at risk of infectious disease.
Kittens showing signs of NI, if <24h old, should be immediately removed from their mother to prevent further
absorption of anti-A antibodies. In kittens, most colostral antibodies are absorbed by 12-24h of age. Once removed, the kittens can either be fostered to a Type-A
queen, or fed milk replaced formula for 24 hours. After
this time it is generally safe for them to be returned to
their dam. If the anaemia is severe a blood transfusion
will need to be performed. However, despite removing
the kittens as soon as clinical signs are noted, most affected kittens die within their first week of life.
7) Infection - In general, infections are involved in relatively few early neonatal deaths. However, they can result in significant mortality from 3-4 weeks of age onwards. Since neonatal kittens have immature immune
systems, and gain <5% of their maternally derived antibodies (MDA) transplacentally, they need to gain protection from infectious disease via transfer of MDA in the
colostrum. The passive protection of the intestines by
MDA continues for the entire duration of suckling as IgA
antibodies resist gastric degradation and can bind potential pathogens in the gut lumen, preventing them from
attaching to or penetrating the intestinal mucosa. The
ability of neonates to absorb MDA begins to decline 6h
after birth, and is no longer possible after ~48h. The
majority of neonatal infections are caused by agents to
which vaccines are not available; it is therefore important
that neonates are born into the same environment as their
dam has been living since she will then have raised anti-
bodies against its resident infectious organisms. The protective effect of systemically absorbed MDA usually begins to wane from 3-4 weeks of age. The kittens’ natural
immunity is still developing at this time, and since most
vaccine regimens do not start until ~8 weeks of age, this
can leave a period of time when the kittens are particularly at risk from these infectious diseases.
A healthy kitten should be able to cope with a low level of
infectious organisms within its environment. It will generally experience no more than occasional mild and brief
clinical signs. However, if the kitten’s immune system
becomes suppressed serious disease or fatal infections
may occur. Factors which may contribute to an inadequate immune response include inadequate colostrum
intake, inadequate nutrition, low birth weight, peri-natal
hypoxia, congenital disorders (especially of the immune
system), previous trauma or infection, a low environmental temperature, or an unhygienic environment leading to a build up of contamination with infectious agents.
Respiratory and gastrointestinal infections are seen most
frequently.
Viruses
• The cat flu viruses (feline calicivirus [FCV] and feline
herpes virus [FHV-1]) are perhaps the most commonly
seen viral infections of kittens. While in healthy kittens
infection may be mild and brief, weak kittens may develop more severe clinical signs or secondary bacterial infections. FHV-1 infection may also be associated
with abortion.
• Feline coronavirus infection (FCoV), like the cat flu
viruses, is hard to eliminate from breeding catteries.
When present, infection may be associated with an
increased incidence of reproduction failure, abortions
and stillbirths. Affected kittens may show signs of
diarrhoea, malaise, or “fading”, and occasional cases
of more classical effusive feline infectious peritonitis
(FIP).
• Feline panleukopenia virus (FPV) is usually seen in catteries that fail to vaccinate properly. It is occasionally
seen in kittens from vaccinated queens, possibly resulting from severe environmental contamination. In-
18
16
ZBORNIK REFERA
TOV
REFERATOV
fection may result in abortions, stillbirths, fading kittens, diarrhoea, panleukopenia, septicaemia, cerebellar ataxia, and/or death.
• Feline leukaemia virus (FeLV) has been almost eliminated from the pedigree breeding population in many
countries. Neonatal disease caused by this infection is
therefore seen mainly in rescue catteries. In this situation it may result in reproductive failure, abortions,
stillbirths, fading kittens, a panleukopenia-like syndrome, septicaemia or death.
• (In puppies canine herpes virus is a common cause of
puppy loss, and can result in abortion, or neonatal
death associated with abdominal distension and pain
at <3weeks of age. Other common viral infections of
puppies include canine distemper virus, canine parvovirus, canine coronavirus [which appears to be
changing in significance], canine adenovirus-2, and
parainfluenza).
Where infectious disease is suspected it is important to
ensure that the queens’ vaccination programme is up to
date. Since kittens gain some protection from infectious
disease in the form of MDA passed in the colostrum, it
may help to give booster vaccines prior to mating. In
some cases it may be appropriate to instigate an isolation
breeding and early weaning programme.
Bacteria - In kittens, bacterial infections are often seen
secondary to viral infection. However, bacterial infections
can also be seen without prior viral infection. In most
cases the bacteria originate from the queen’s birth canal
(beta haemolytic Streptococcus sp. [Strep. G infection]),
gastrointestinal tract (E. coli, Salmonella sp., Campylobacter sp., many normal enteric bacteria), or respiratory
tract (Bordetella sp., Pasturella sp., Mycoplasma sp.).
Clinical signs depend on the site, nature, and severity of
the infection. They may include diarrhoea, coughing, dyspnoea, polyarthritis, omphalophlebitis, or dermatitis, as
well as the less specific signs more typical of fading kittens. Ultimately, many of these infections may result in
septicaemia and death. The increased risk of sepsis in
neonates results from the factors listed above, especially
failure of passive transfer of MDA. In addition, neonatal
propensity to develop hypoglycaemia and intestinal ileus
(especially when cold), significantly increases the risk of
translocation of enteric bacteria into the blood stream.
This is exacerbated by sepsis further predisposing to
hypothermia and hypoglycaemia (possibly resulting from
impaired liver function, depletion of glycogen, and peripheral utilisation of glucose by bacteria and leucocytes).
Disease may be very sudden or may run a more protracted course. While the clinical signs are varied, they frequently result in bradycardia, dyspnoea, dehydration,
weakness, crying, seizures, coma and death. Sepsis often occurs as the final stage of other conditions, and is
particularly associated with systemic viral infections. The
most common cause of sepsis are gram-negative bacteria, but can include; Streptococcus, E. coli, Staphylococcus, Klebsiella, Enterobacter, Enterococcus, Pseudomonas, Clostridium, Bacteroides, Fusobacterium, Pasteurella
and Salmonella.
Parasites - In well-run catteries parasite infestation should
not be a problem. Where queens are not dewormed, heavy
kitten infestations can result in a poor body condition,
soft or bloody stools, lack of appetite, a pot-bellied appearance, weight loss, and occasionally death. A severe
flea, tick or hookworm infestation can result in significant anaemia. Gut parasites, such as Giardia, Tritrichomonas foetus, Isospora or Cryptosporidia may cause diarrhoea and a failure to thrive. Toxoplasma infection may
result in abortion, stillbirths and fading kittens.
References and suggested readings
·
·
·
·
·
·
·
Blunden AS (1998) The Neonate: Congenital Defects and Fading Puppies. BSAVA Manual of Small Animal Reproduction &
Periparturient Care, p 143-152
Feline Advisory Bureau Manual of Cat Breeding (2006), FAB Publications, Tisbury.
Feldman DC and Nelson RW (1987) Feline reproduction. In: Canine and Feline Endocrinology and Reproduction. Ed. Feldman
DC and Nelson RW, WB. Saunders, Philadelphia. pp. 525-548 (or the 2004 edition).
Hoskins JD (1995) Fading puppy and kitten syndrome. Kirk’s Current Veterinary Therapy XII, eds. RW Kirk and JD Bonagura,
WB. Saunders, Philadelphia. pp. 30-33
Hotston Moore P and Sturgess CP (1998) Care of Neonates and Young Animals. BSAVA Manual of Small Animal Reproduction &
Little S (2004). Breed Specific Reproduction Projects; Heritable Aspects of Cat Breeding; Feline Reproduction: A Manual for Cat
Breeders and Veterinarians (CD ROM); www.catvet.homestead.com , [email protected]
Sturgess CP (2006) Feline paediatric medicine. Eur J Comp An Pract 16(1): 83-94
19
17
ZBORNIK REFERA
TOV
REFERATOV
Techniques for Neonatal Resuscitation and Critical Care
Stefano Romagnoli
When a neonate is in critical condtions treatment must
be instituted immediately, after which the clinician may
concentrate on the kitten, the rest of its litter, their mothers health, and the overall health and management of the
other cats in the cattery. In fact, it is only through a
complete history that the true nature of the problem can
be determined. If sick kittens are not to die, they must
be detected and treated early as their health status can
deteriorate rapidly. This paper will focus on perinatal
reviival as wel as on some of the most common health
problems in young kittens such as hypothermia, hypoglycaemia and dehydration and their clinical approach in a
practice situation. The following protocol should be adopted and the following information collected for each critical neonatal patient:
Physical exam - Weight and body condition should be
assessed, presence of signs of trauma, congenital defects, or disease should be carefully investigated. While
some congenital defects, such as cleft palate or atresia
ani are readily evident, others, like congenital heart defects, are only evident on a post mortem examination. It
is important to be aware of normal age-related changes
and not over-interpret normal findings e.g. neonatal joint
instability or cardiac murmurs. The coat should be
checked for quality, cleanness and parasites. The thorax
and head should be checked for normal shape and feel;
normal heart rate is ~200-220 beats per minute; normal
respiration is ~15-35 breaths per minute. The abdomen
should feel gently full, not swollen, tight or empty. The
intestines and bladder should feel soft, mobile and nonpainful. The extremities should be pale pink (extremity
erythaemia is often associated with sepsis). Eyes and nose
– Kittens should open their eyes between days 5-14; a
mild cloudiness is normal and should resolve quickly. While
a small amount of sticky discharge is not of major concern, closed eyelids that are swollen or matted with pus
is. Gums - Until about a week old healthy neonates have
35020 (PD)
[email protected]
dark pink or red gums. However, sick neonates often
have pale, grey or bluish gums. Umbilical cord – This
should be dry and free of discharges, and normally falls
off between 3-7 days of age. It is of concern if it is still
moist, painful, inflamed or discharging. Defaecation and
urination – Since stimulation of the perineal area in kittens of <3 weeks of age results in defaecation and urination this technique can be used to look for the presence
of diarrhoea or constipation (present in ~60% of sick kittens), and to check urine colour (see below).
Blood sampling: The small size of kittens makes collection difficult. It is usually only possible to take very small
volumes of blood (0.3-0.5 ml, rarely up to 1.5 ml). Total
blood volume is ~75ml/kg, so at 1 week a kitten of 200g
only has ~15ml total). Blood should be collected from
the jugular vein. Care should be taken not to induce a
large haematoma. This can result in significant loss of
circulating volume, and can, if severe, obstruct the airway. Collect samples into 0.5 ml EDTA and heparin tubes,
run glucose on a single drop using a glucometer, and run
packed cell volume (PCV) and total protein (TP) on a micro-haematocrit tube. It is often only possible to assess
PCV, TP, urea, glucose, and blood smear cytology. In
order to correctly interpret the results it is important to
know what is normal for kittens of that age (Chandler
1992; Hotston Moore and Sturgess 1998). For example,
normal neonatal kittens have mild normochromic normocytic anaemia, and blood urea and creatinine levels in
kittens are considerably lower than adults. Few biochemical and haematological results are specific for a particular disease. Severe anaemia may be seen with NI, or a
heavy flea or hookworm infestation. Panleukopenia may
be seen with FPV, FeLV, or sepsis. Hypoglycaemia is common, regardless of the cause of illness. Hyperbilirubinaemia may be seen in NI or liver disease. Hyperammonaemia may occur with hepatic encephalopathy and a
congenital portosystemic shunt.
Urine collection: Stimulating the kitten’s perineum with a
warm moist cotton ball is a useful method for collecting
a urine sample. Urinalysis can be helpful in the diagnosis
of NI, where brown-staining urine results from haemoglobinuria. Pyuria is suggestive of a urinary tract infection, while a specific gravity of >1.017 indicates dehydration. Glucosuria is not abnormal in neonates.
20
18
ZBORNIK REFERA
TOV
REFERATOV
Further investigations: More specific tests include serology (e.g. FeLV, FIV), slide agglutination or Coombs’ test
for NI, pharyngeal swabs for the cat flu viruses, or ocular swabs for chlamydophila felis. If a bacterial infection
is suspected swabs, blood or urine can be taken for culture and sensitivity. In cases of septicaemia, it is difficult
to obtain sufficient blood to perform blood culture. It is
usually more rewarding to sacrifice a moribund kitten,
and then send fresh samples of heart blood, heart tissue,
liver, lungs, etc. for culture. Survey radiography or ultrasound examination may be considered, but there is little
radiographic contrast in kittens (so reduce the kV by half
of that used in an adult of the same body thickness), and
ultrasound examination may require a “stand-off” for the
probe. Faecal cultures can be examined for the presence
of pathogenic bacteria, Giardia spp., Tritrichomonas foetus, coccidia, and intestinal parasites.
Peri-natal kitten revival
Hypoxia related to dystocia is probably the single most
significant factor in neonatal mortality. Since the healthy
mother cat will generally make a good job of nursing her
kittens, it is important not to interfere unless necessary.
However, intervention is recommended when a kitten is
not breathing, or on the few occasions when maternal
instinct appears to be lacking. The aim is to imitate the
cat’s own methods; she ensures that the kitten’s nose
and mouth are clear, then, with a nipping/licking action,
she chews through the umbilical cord. This, and more
vigorous licking of this area, provides stimulation of respiration. The cat then gives the kitten a more general
drying lick, then concentrates on the perineal area in order initiate bowel and bladder functions. If something
goes wrong of the mother does not have any maternal
instinct, the following intervention should be put in place:
• Severe the umbilical cord - If the umbilical cord has
not broken on delivery, separate it using 2 haemostats
>2 cm from the kitten’s abdominal wall. Complicated
cutting and tying are not usually necessary. Dipping the
stump in chlorhexidine is a common procedure, although
there is no need for disinfection if the kitten is born in a
clean environment.
• Clear the airways: Tear the membranes from the nose,
wipe the nose and open the mouth, tilt the kitten’s head
down and clear away any fluid. If the kitten is not breathing, or if it has come tail first and possibly inhaled fluid,
it is necessary to clear debris and fluid from the airway. If
suction equipment is available this can be done by sucking the debris out of the airway. This can also be achieved
using a Jackson cat urinary catheter attached to a 5-10
ml syringe as a gentle suction apparatus. The catheter
can also be used to induce the kitten to sneeze and cough
by stimulating its nose/throat. One of the traditionally
used methods involves swinging the kitten. To do this,
place the kitten in the palm of your hand, its back to-
wards your palm and neck between your forefinger and
third finger, its head protruding between your fingers.
Enclose the kitten in your fingers and, turning your hand
palm downwards with your arm extended, give a gentle
swing several times; make quite sure first that you are
not too near any protruding edges or disaster will follow.
The swing will have the effect of forcing fluids out of the
kitten’s airway and a further wipe of its nose and mouth
will clear any debris away. Keeping some absorbant paper on the nostrils of the kitten during the procedure will
allow to detect minute quantities of liquid coming out.
The swing will also serve to stimulate respiration. Take
care; if performed too vigorously this method can result
in brain haemorrhage.
• Stimulate respiration: If the kitten is still not breathing, some form of artificial respiration may be necessary.
Mouth-to-mouth respiration can be useful, but only if
very carefully performed. There are several points to remember. It is of no use blowing fluids and debris further
down the airway; these must be cleared away first (see
above). Secondly, the capacity of kitten lungs compared
to humans is minute. Blow very gently and allow a pause
for expiration. Repeat this cycle every 3-5 seconds. Breathing into the kitten’s airway through a small endotracheal
tube or drinking straw may help to reduce the risk of
over-inflating the kitten’s lungs, and be more hygienic
than direct mouth-to-mouth. Various methods have been
used to make the new-born animal gasp, including the
administration of brandy or other spirits to the kitten’s
tongue, flicking its chest sharply but gently with a fingertip, alternate warm and cold water applications, or the
insertion of a 25-g needle into the nasal philtrum. However, it is more reliable to apply a drop of doxopram
hydrochloride (20 mg/ml) sublingually. A strong regular
heart beat should be easily palpable; if not, external cardiac massage can be attempted. It is important to note
that unlike adults neonatal heart rates fall in a protective
response to hypoxia, and this should not be misinterpreted. If the dam was given opioids prior to delivery
naloxone hydrochloride (0.4 mg/ml) can be administered
to the offspring (1 drop sublingually) to reverse respiratory depression. If in doubt persist with stimulating the
kitten; some can still be revived after >30 minutes from
birth. That said, the longer the duration before breathing
the higher the risk of hypoxia causing brain damage or
blindness. Hypoxic bradycardic puppies may respond to
the administration of atropine into the umbilical vein. While
no information is available on the use of this method in
kittens, it may be worth considering. Since premature
kittens often have very poor pulmonary development the
administration of dexamethasone (0.1mg) may help to
stimulate surfactant production. Supplementary oxygen
should be given until the kitten is breathing regularly and
is obviously vigorous. This can be done using a small
face mask, an oxygen box, or using a fine urinary catheter to administer intranasal oxygen (the adapter to a 3
21
19
ZBORNIK REFERA
TOV
REFERATOV
French endotracheal tube can be used to connect the
oxygen supply to the catheter). The kittens tongue is a
reliable indicator of respiration. If the kitten is receiving
sufficient oxygen its tongue will be pink, if not it will have
a bluish tint.
Critical Care of Neonatal Kittens
Sick kittens need to be treated immediately. Supportive
therapy is aimed at re-warming, maintaining blood glucose levels, correcting dehydration and, when required,
supplying additional oxygen.
Hypothermia - Neonatal kittens cannot thermo-regulate,
they lack insulating fat and thermogenic brown, and they
cannot react to cold by shivering. They loose heat rapidly, especially if left wet. Body temperature generally falls
from ~36oC at birth, to 30oC within a few hours, then
increases to 38oC over the first week. It is important that
these temperatures are maintained as hypothermia can
initiate a number of other problems: e.g. a week-old kitten should have a temperature of 35-37oC and a heart
rate of 200-250 bpm, but if its temperature temporarily
falls to 30oC, its HR will fall to 40-50 bpm. While this is a
protective mechanism, if persistent, it can results in a
decrease in respiratory rate that may in turn leads to cardiopulmonary failure. Also, a hypothermic kitten will not
suckle effectively; it may develop gastrointestinal ileus,
and will have an increased susceptibility to infection. It is
important to check the temperature of any potentially weak
or ill kittens, however, if their temperature is maintained
at <34oC for a prolonged period of time they are likely to
die.
The kitten should then be rubbed all over with a clean
towel. This further stimulates respiration and dries the
kitten. It should then be kept warm. If the mother is ill or
uncooperative, place the kittens in contact with a warm,
well-covered hot water bottle and conserve the heat by
covering the bed with a blanket. Great care must be taken not to inflict contact burns on the kittens by having
the bottle too hot. When attempting to re-warm hypothermic kittens it is important to do so gradually, ideally
over 1-4h, depending on the severity of chilling. Rapid
re-warming can lead to cardiovascular collapse and death.
Importantly, overheating can also be detrimental, and can
quickly lead to dehydration and death. Because hypothermia can markedly reduce the absorptive ability of the
intestines concurrent hypoglycaemia and dehydration
cannot be corrected using oral solutions; parenteral fluids are needed.
sions and death. If a kitten refuses to feed, prompt action
is required. Kittens have no energy reserves and will deteriorate rapidly. If a kitten is showing signs of hypoglycaemia, a few drops of glucose syrup placed on its gums
can be life saving. However, if the kitten is cold, glucose
solution should not be given by mouth as it will not be
adsorbed from hypothermic intestines. More severe cases can be corrected by the parenteral administration of
isotonic glucose solutions. It is important to correct any
hypothermia at the same time. When giving supplemental glucose it is important to monitor glucose blood concentrations as kittens can easily become hyperglycaemic.
Once recovering the kitten can be fed a small amount of
glucose solution, and either the amount and/or frequency of routine feeding should be increased. Note: the nutritional requirements of a septic kitten are increased
(~1.5x maintenance) so in these cases it may be necessary to provide nutritional support by tube feeding (see
later).
Tube feeding: If kittens are too weak to suckle for themselves, then tube feeding is perhaps the cleanest and most
efficient method by which to deliver nutrition. However,
it requires proper equipment and good technical skills.
Also, as the kittens have no control over how much they
are fed, they can easily be given too much (or too little).
Stomach tubes must be soft, flexible, blunt-ended and
generally not more than 2-3 mm wide. A premature human infant feeding tube is ideal (6-10 French feeding tube
for neonates and 8-10 French for kittens over 300g), or a
soft rubber canine urethral catheter may also be used.
The tube must be measured to the correct length (from
the kitten’s nose to the last rib), and an indelible mark
should be made on the tube at this point. The tube should
be lubricated with K-Y jelly before it is used. To place the
tube the kitten’s mouth must be opened by pressing gently at the corners, and, keeping the head flexed downwards, the tube is then slid along the roof of the mouth
and down the back of the kitten’s throat into the oesophagus. The tube is passed down the oesophagus until the
mark on the tube is level with the kitten’s nose. The other
end of the tube will then be in its stomach. A syringe
containing pre-warmed milk can then be attached, and
the milk can be delivered slowly, directly into the stomach. If the kitten’s head is kept flexed forward, it is quite
difficult to miss the oesophagus and so pass the tube
into the airway by mistake. Many kittens mew loudly
throughout the whole procedure, and it is useful to note
that they cannot do this if the tube is in the airway. If the
tube does not pass easily or if coughing occurs withdraw
the tube from the kitten’s mouth and try again.
Frequency of feeding:: 0-2 weeks:
Hypoglycaemia - This results from inadequate or infrequent feeding and if protracted can cause severe depression, muscle twitching and occasionally lead to convul-
22
20
6-10 feeds/24h at 2-4h intervals.
2-4 weeks:
4-5 weeks:
ZBORNIK REFERA
TOV
REFERATOV
Diarrhoea and dehydration - Diarrhoea is common in
kittens, particularly those fed milk replacement formula.
It may also be caused by over feeding; giving too concentrated a solution of milk replacement formula; or as a
result of infection (usually caused by poor hygiene). Treatment must be prompt as dehydration can develop rapidly, followed by collapse, hypothermia, and death. Looking for skin tenting is an unreliable method of assessing
dehydration in neonates. Instead, dehydration should be
assessed by weight loss, dryness of mucus membranes,
and urine specific gravity (>1.017).
• Mild cases respond well to dilution of the milk replacement formula 50:50 with boiled water, which can
then be given until the diarrhea stops. Treatment with
SQ fluids may be required (see below, but starting
with ~1ml/30g is reasonable).
B
• Severe cases should be given no milk at all. Instead
they can be given oral support with 5-10% glucose
solution, glucose-saline, or isotonic electrolyte solution until the diarrhoea stops. While oral supplementation may help, it is generally better to give parenteral fluids. If the neonate is cold, do not give any oral
medication/fluid.
• Intravenous (IV) or intraosseous (IO) routes are used
most frequently for parenteral access. IV access can
often be gained using a 23-25-g catheter placed in the
cephalic or jugular vein. However, kittens’ short legs
can make catheter placement difficult and flow hard
to maintain. IO access can be easily gained using the
proximal femur (Figure 1). Subcutaneous (SQ), intramuscular and intraperitoneal (IP) routes are less advisable as the absorption is slower and less reliable
than in adults, especially if dehydration or shock is
present. In addition, the IP route requires strict asepsis, and carries a small risk of puncturing viscera. If
the IP route is to be used the daily fluid requirement is
calculated (see below) then the volume is divided, and
given 2-3x daily.
Figure 1. Placement of the IO needle in the bone marrow. A) The proximal femur is preferred in the cat while
the wing of the ileum can be useful in dogs. Picture:
Slatter D, Textbook of Small Animal Surgery, third Edition, 2000, WB Saunders, Philidelphia. B) Detail of the
placement of the IO needle within the bone marrow of
the proximal femur. IO needles can be left in place for up
to 72 hours, although their use is often limited by clotting within the needle. To try to reduce this risk, the needle should be flushed regularly with heparinised saline,
usually every 6 hours.
Picture: http://courses.vetmed.wsu.edu/samdx/bm.asp.
• Use fluid pumps, syringe pumps, or a burette with a
paediatric giving set (60 drops/ml) to reduce the risk
of over-hydration to which all neonates are particularly susceptible (in part because of their immature
kidneys).
• Fluid requirements per kg are higher in neonates than
• While sick neonates are often acidotic their reduced
adults but total volumes required are low. Immature
kidneys lack the ability to concentrate urine so fluid
losses cannot be controlled, especially if there is concurrent vomiting and/or diarrhoea. Maintenance fluid
rates in kittens <2 weeks of age are 130-220ml/kg/
24h (ave. 180ml/kg/24h), by weaning ~120ml/kg/24h,
and adult levels of ~50-65ml/kg/24h from 6 months.
hepatic ability to metabolise lactate to bicarbonate
means that lactated Ringer’s should not be given. Saline or Ringer’s are better choices in kittens <7 weeks
of age. In severe acidosis bicarbonate can be given as
per known acid-base status, or ~2mmol/kg can be
given over 10-15 mins. Hypoglycaemic kittens should
be given 5% dextrose solution mixed 50:50 with saline, or 1-2 ml of 10-25% glucose in very severe cases. All fluids should be carefully warmed prior to administration and kittens should be closely observed
for signs of over-hydration.
Example: 1 week old kitten, 200g, needs 36ml fluid/24h
maintenance; 1.5ml/h (~1 drop/40 seconds using a paediatric giving set). If 7% dehydrated, the estimated deficit is 14ml. Therefore, the fluid rate should be ~2.5ml/h
over 6h (1 drop/20sec), then reduce to ~2ml/h (1 drop/
30sec); but always monitor for over-hydration.
• Once the kitten has been warmed up and given fluid
therapy it must be allowed to recover quietly. Feeding
can only begin once the kitten is warm and able to
suck. Stomach tubing is not helpful here, since when
23
21
ZBORNIK REFERA
TOV
REFERATOV
a kitten is cold and collapsed its intestines stop functioning, so stomach contents can be easily regurgitated and then aspirated. As soon as the kitten is able to
suck, it should be given isotonic glucose or Lectade
solution (~1.0 ml/100 g body weight) given every 15
minutes until it is rehydrated and can urinate when
massaged. If all goes well, diluted milk replacement
formula can then be introduced after 24 hours, and
full strength milk 24 hours after that.
• The administration of antibiotics is not recommended, particularly for the treatment of diarrhoea. Antibiotics severely disrupt the process of normal colonisation of the gut by harmless bacteria, and can therefore make the situation worse. Antibiotics cannot be
used as a substitute for colostrums and good hygiene.
References
·
·
·
·
·
Cave TA, Thompson H, Reid SWJ, Hodgson DR and Addie D (2002) Kitten mortality in the UK: histopathological examinations
(1986-2000). Vet Rec 151: 497-501
Chandler LM (1992) Pediatric normal blood values. Kirk’s Current Veterinary Therapy XI, eds. RW Kirk and JD Bonagura, WB.
Saunders, Philadelphia. pp. 981-984
Hoskins JD (1995) Fluid therapy in the puppy and kitten. Kirk’s Current Veterinary Therapy XII, eds. RW Kirk and JD Bonagura, WB.
Saunders, Philadelphia. pp. 34-37
Hotston Moore P and Sturgess CP (1998) Care of Neonates and Young Animals. BSAVA Manual of Small Animal Reproduction &
Sturgess CP (2006) Feline paediatric medicine. EJCAP 16(1): 83-94
24
22
ZBORNIK REFERA
TOV
REFERATOV
Managing the Dyspneic Cat
Case studies in feline respiratory distress
Tim Hackett
Introduction
As we discussed in the first lecture on triage, respiratory
distress in cats is a therapeutic dilemma. Critical cats can
be so compromised that diagnostics and treatment can
cause respiratory and cardiac arrest. Try to determine
the nature of the problem first with observation. A rapid
shallow respiratory pattern suggests restrictive disease
while a slow deep inspiratory pattern is seen with airway
obstruction. With the restrictive pattern, auscultation can
help differentiate pleural space disease (pneumothorax,
hydrothorax) from parenchymal diseases (pneumonia,
pulmonary edema). With an understanding of the factors
that increase the work of breathing we can narrow our
list of possible problems.
Work of breathing
For gas exchange, fresh air must be brought into the
alveoli through the process of alveolar ventilation. The
O2 cost of quiet breathing is extremely small, being less
than 3% of total resting O2 consumption. With voluntary
hyperventilation it is possible to increase this to 30%,
probably greater with respiratory disease. For animals
with obstructive or restrictive lung disease, the O2 cost
of breathing can limit their exercise ability.
Muscles of the respiratory system must overcome several forces: Elastic recoil and airways resistance. The elastic forces opposing inhalation are a combination of elastic properties of the lung and alveolar surface tension.
Elastic forces were described above as they effect pulmonary compliance.
Airway resistance is the pressure difference between the
alveoli and the mouth divided by flow rate and is determined Poiseuille's law:
Where R = airway resistance, n = viscosity, l = length
and r = radius. Note the critical importance of tube radius; if the radius is halved, the resistance increases 16fold. However doubling the length only doubles resistance.
Airways resistance is determined by lung volume, bronchial smooth muscle tone and dynamic airway compression. At reduced lung volumes (expiration), radial traction supporting the bronchi is lost and airway caliber is
reduced. Dynamic airway collapse is seen with forceful
respiration. Sudden changes in intrathoracic pressure can
affect the large airways.
Minimizing the work of breathing
Cats will adopt respirations to minimize the work of
breathing. Those with upper airway obstruction will have
a slower, deeper inspiratory effort with stridor (whistling
sounds) heard loudest over the point of narrowing. By
decreasing the speed of airflow past an obstruction this
breathing pattern will favor maximal flow through narrowed airways with minimal energy expenditure. It's easy
to understand the problems of airway obstruction by trying to breathe through a straw.
Intrathoracic airway collapse (thoracic trachea and bronchi) will have increased expiratory effort. Tracheal collapse will often have a loud snap, bronchitis/asthma patients will have pronounced expiratory wheezes.
Animals with pleural effusions, pulmonary edema or pulmonary fibrosis will adopt a restrictive breathing pattern.
By minimizing the change in volume while increasing the
respiratory rate they can maintain alveolar minute ventilation despite decreased pulmonary compliance.
[email protected]
25
23
ZBORNIK REFERA
TOV
REFERATOV
Observation
Try to determine the nature of the respiratory problem first with observation. A rapid shallow respiratory
pattern suggests restrictive disease while a slow deep
inspiratory pattern is seen with airway obstruction. With
the restrictive pattern, auscultation can help differentiate
pleural space disease (pneumothorax, hydrothorax) from
parenchymal diseases (pneumonia, pulmonary edema).
Imaging
Cats presenting with upper or lower respiratory signs
should have a thoracic radiographs when it is safe to
restrain. Bronchial patterns develop as the peribronchiolar tissues become inflamed (as would be seen with bronchitis or bronchial asthma). Interstitial patterns develop
with thickening of the fibrous structures of the lung. Alveolar patterns characterized by “Air bronchograms” are
caused by fluid accumulation in the alveoli (pulmonary
edema or pneumonia). Thoracic and cervical radiographs
can be used to diagnose collapsing trachea, tracheal or
laryngeal foreign bodies, and tracheal or laryngeal masses.
The clinical signs and physical examination abnormalities associated with near drowning, smoke inhalation,
are similar with electric cord bites with the exception of
oral burns and can usually be ruled in or out with the
history.
Adult respiratory distress syndrome (ARDS) results from
a variety of pulmonary insults and can be thought of as
organ failure of the lung. The clinical criteria for a diagnosis of ARDS include hypoxemia, pulmonary infiltrates
(fluid accumulation in the lung tissue) without evidence
of heart failure and decreased pulmonary compliance. The
primary pathogenesis of this edema is an increased alveolar capillary permeability. Problems associated with the
development of ARDS include aspiration of stomach contents, traumatic pulmonary contusion, inhalation of noxious gases, oxygen toxicity and a variety of infectious
diseases. Secondary lung diseases associated with the
development of ARDS include gram-negative sepsis, trauma (not just chest trauma), pancreatitis, transfusion reactions and toxins. Removal of the primary causes and
administration of oxygen support preferable with positive end expiratory pressure are the principle treatments.
Pulmonary Thromboembolism
Pulmonary Edema
Noncardiogenic pulmonary edema occurs occasionally in
cats secondary to electric cord bites, sepsis, following
near drowning or choking, uremia, smoke inhalation, and
the acute respiratory distress syndrome (ARDS).
Most cats that chew on electric cords are presented with
acute onset of dyspnea and oral burns, which may or
may not be associated with dysphagia or ptyalism. The
syndrome occurs most commonly in the young. Pulmonary edema develops rapidly, generally within hours.
Common physical examination abnormalities include oral
burns, dyspnea, and pulmonary crackles. Thoracic radiographs show mixed interstitial and alveolar patterns
that are most prominent in the dorsal portions of the
caudal lung lobes. The pathogenesis of edema is thought
to be increased pulmonary capillary hydrostatic pressure
and increased alveolar-capillary permeability. Increased
pulmonary capillary hydrostatic pressure is likely due to
a centrally mediated burst of sympathetic activity, which
causes constriction of resistance and capacitance vessels
leading to a shift of blood from the splanchnic viscera
into the circulation. This ultimately results in overcirculation of the pulmonary vasculature. Increased peripheral
vascular resistance increases pulmonary capillary hydrostatic pressure and pulmonary venous pressures increase
as the left ventricle pumps against increased outflow resistance. Treatment includes supplemental oxygen, morphine (0.05 mg/kg by subcutaneous injection) to reverse
the sympathetic tone. If morphine is unavailable, other
narcotic agonists and agonist/antagonists may also be
beneficial.
Pulmonary thromboembolism (PTE) is the occlusion of
the pulmonary vasculature by products of the coagulation cascade. Thrombosis of pulmonary vasculature results in an ischemic condition. This commonly results in
tachopnoea, dyspnea, and potentially, cyanosis. PTE occurs through 3 major mechanisms, damage to vascular
endothelium, altered pulmonary blood flow, and hypercoagulability. Diseases commonly associated with damage to vascular endothelium include dirofilariasis, neoplasia, valvular heart disease, endotoxemia, and any cause
of vasculitis including pancreatitis and immune mediated
disease. Altered pulmonary blood flow occurs most commonly with cardiomyopathy, partial venous occlusion by
granulomatous disease or neoplasia, valvular heart disease, vascular tumors, any form of shock, polycythemia,
and hyperviscosity syndromes. Syndromes of hypercoagulability can be either primary or secondary. People
develop primary antithrombin III (ATIII), protein C, plasminogen, and plasminogen activator deficiency as well
as dysfibrinogenemia that predisposes to thrombus formation. Acquired hypercoagulability occurs with many
diseases resulting in decreased production of ATIII, lost
of ATIII, increased concentration of some coagulation
factors, platelet hypersensitivity, or thrombocytosis.
The most common clinical signs associated with PTE include acute onset dyspnea or tachopnoea with or without cough and hemoptysis. Auscultation generally reveals
increased bronchial sounds; crackles are rare. Split second heart sound may occur due to pulmonary arterial
hypertension.
26
24
ZBORNIK REFERA
TOV
REFERATOV
Diagnosis can be difficult. Thoracic radiographic findings are dependent on the primary disease but can include increased interstitial densities, increased size of the
pulmonary arteries, mild right heart enlargement, alveolar lung disease, and pleural effusion. Occasionally, thoracic radiographs are completely normal. These cases
are often oxygen dependent but respond well to supplemental oxygen (noticeably better oxygenation, reduced
respiratory rate, and decreased anxiety). Diagnosis is often by compatible underlying disease and a positive response to oxygen.
Feline Bronchial disease
There is no clear terminology for the bronchial obstructive diseases in the cat. Bronchitis is inflammation
of the airways. Asthma generally implies a reversible
bronchoconstriction related to hypertrophy of smooth
muscle in airways, hypertrophy of mucous glands, and
infiltrates of eosinophils. Asthma in cats is a Type I hypersensitivity reaction, often without an obvious cause.
Cats with bronchitis not due to asthma generally have
infiltrates of neutrophils or macrophages as well as hypertrophy of mucous glands, hyperplasia of goblet cells,
excessive mucous, and ultimately fibrosis secondary to
chronic inflammation. Causes include bacterial infection,
(including mycoplasmosis) viral infection and parasitic
infections.
Cats with bronchitis can be of any age. There is no
obvious breed or gender predilection. Primary presenting complaints include cough, dyspnea, and wheezing.
Physical examination abnormalities include cough, dyspnea, and crackles, and wheezes in the pulmonary tissues. Increased bronchovesicular sounds may be the only
abnormality noted on auscultation. If dyspnea occurs, it
commonly has a pronounced expiratory component. Open
mouth breathing or panting commonly occurs during
periods of stress.
Cats presenting dyspneic as an emergency are often
to distressed to handle. Physical examination, intravenous catheterization and diagnostics could prove fatal.
The best approach is to place them in an oxygen cage
while obtaining a history and observing their respiratory
efforts.
Pleural Cavity
Diseases of the pleural space cause a decreased tidal volume and a restrictive breathing pattern. Characterized by
the rapid, shallow respirations and dull lung sounds, fluid and air in the pleural space can be diagnosed and treated
by rapid thoracocentesis. Once removed, fluid can be
examined to determine the likely cause. Thoracocentesis
is performed using a 20 or 21g needle attached to a short
piece of extension tubing. Alternatively a larger (19g)
butterfly catheter may be used. The needle and tubing
are attached to a 20-60 cc syringe through a 3-way stopcock. A 2x2 cm area over the lateral chest wall between
the 6th and 10th intercostal spaces is surgically prepared.
With the animal comfortable in either sternal or lateral
recumbency, the needle is advanced into the thoracic cavity. It is helpful to mark the location of the needle's bevel
before advancing into the chest. Once either air or fluid
start flowing, the needle can be laid flat against the chest
wall with the bevel facing in toward the lungs. This will
allow complete re-inflation without lacerating the lung
on the needle.
A negative thoracocentesis may be due to fibrous adhesions and small pockets of fluid. It is usually not necessary to evacuate all fluid or air so a negative tap should
not be pursued by re-directing the needle or repeated
attempts. Radiographs may be helpful to decide if further
attempts are warranted. Diaphragmatic hernias may also
cause significant pleural restriction but yield a negative
tap. These patients should be given supplemental oxygen while radiographs are taken.
Thoracic radiographs reveal primarily a bronchial pattern. Overinflation and air trapping is seen in some dyspneic cats with chronic disease. Cytology of transoral
airway wash samples reveals increased mucus with variable numbers of eosinophils, neutrophils, and macrophages. Bacteria may or may not be visualized. Aerobic and
Mycoplasma culture as well as antibiotic susceptibility
testing should be performed regardless of the type of
inflammatory cell and whether or not bacteria are seen.
Cats with eosinophilic airway cytology should be assessed for dirofilariasis using adult antigen detection tests
or newly developed antibody tests. Fecal flotation (Toxocara and Toxascaris in kittens), Baermann examination
of feces (Aelurostrongylus), and fecal sedimentation (Paragonimus) should be performed in cats with eosinophilic
airway cytology particularly if indoor-outdoor and from
parasite endemic areas.
27
25
ZBORNIK REFERA
TOV
REFERATOV
Feline Trauma
Tim Hackett
Introduction
As we learned in the first seminar, each emergent
patient should be evaluated in an orderly and systematic
manner. This is especially true in trauma. It is the job of
the triage team to evaluate and treat injuries interfering
with vital physiological functions. While trauma by its very
nature is a polysystemic disease, pulmonary complications present one of the most common, and life-threatening aspects of trauma triage. It is the purpose of this
lecture not to review trauma triage, but to concentrate
on the pathophysiology, diagnosis, and treatment of traumatic injury to the respiratory tract. These injuries require immediate recognition and treatment, as aggressive fluid therapy can make some of these injuries worse.
It is important to assume some degree of thoracic and
pulmonary injury in all veterinary trauma patients. In a
canine study, thoracic injuries were present in 58% of
patients presented for treatment of orthopedic injures.
Pulmonary contusions, pneumothorax, and fractured ribs
were most commonly observed. These findings have also
been noted in cats falling from great heights and suffering other forms of trauma.
Pulmonary Contusions
Lung contusion is the most common acute pulmonary complication of blunt chest trauma. Due to the compliant nature of the feline thorax, severe injury may be
present without external signs of trauma. Such a contusion may occur under the site of a flail chest or independent of obvious external injury. A large bruise in a very
bad place, the contused alveoli fill with blood, and fluid
resulting in atelectasis. Hypoxemia will result from pulmonary shunt as blood flows through these non-venti-
lated portions of lung. With time, pulmonary contusions
appear radiographically as a diffuse interstitial to alveolar
lung pattern. The location varies with the injury. It is important to note that contusions may not be evident on
radiographs for several hours after the injury so a radiograph taken on admission may not reveal the severity of
the injury.
Complicating trauma management is evidence that respiratory insufficiency following pulmonary contusion may
be iatrogenic. The use of large volumes of rapidly administered crystalloid solutions can exacerbate the fluid
loss into damaged tissues worsening the hypoxemia associated with the contusions. Maintaining plasma colloid
oncotic pressure with the use of plasma or other colloid
solutions may lessen the occurrence of respiratory insufficiency by preventing water loss into the injured lung.
We use even more conservative fluid replacement in trauma patients with pulmonary contusions. Using a combination of crystalloid fluids (5-10 ml/kg, 1/8 to 1/4 of a
typical shock volume) and colloid solutions (whole blood,
or hydroxyethyl starch) we strive to maintain a minimally
acceptable blood pressure (mean pressure of 60 mmHg)
while avoiding iatrogenic pulmonary fluid overload. Patients with severe contusions may present with or develop hemoptysis. Blood from the mouth, agitation and respiratory distress are all indications that pulmonary parenchymal hemorrhage is ongoing and aggressive treatment is necessary. These patients are quickly restrained
(fast acting anesthetic or a paralytic) and intubated. Ventilating with 100% oxygen and 5-10 cm H20 positive endexpiratory ventilation will help keep remaining alveoli
open, and open catalectic lung units. Patient tidal volume
should be monitored closely as positive pressure ventilation and damaged lungs can lead to a tension pneumothorax.
Pneumothorax
Simple pneumothorax occurs when gas accumulates
in the pleural space but pleural pressure does not significantly exceed atmospheric pressure. Gas can enter the
space either from outside the chest wall, as occurs with
bite wounds, sharp objects, or weapons, or via the lung
through a tear in the lung parenchyma. Small amounts
[email protected]
28
26
ZBORNIK REFERA
TOV
REFERATOV
of gas cause pleural pressure to increase slightly, but it
remains sub atmospheric during inspiration because it is
in equilibrium with the negative alveolar pressure. Although pleural and alveolar pressures become positive
during forced expiration, slight separation of the pleural
spaces does not compromise ventilation. If the pneumothorax is small and the pleural leak seals itself, the
gas will be absorbed as a result of partial pressure differences between gas in the pleural space and in the blood.
Tension pneumothorax is characterized by a progressive
increase in pleural pressure sufficient to impair circulation. This occurs as gas enters the pleural space and
remains there during expiration because tissue or fluid
occludes the pulmonary parenchyma. While tension pneumothorax can occur during spontaneous negative pressure inspiration, it is more likely with intubated patients
receiving positive pressure ventilation. The accumulating
gas not only collapses the lungs but also interferes with
venous return to the right atrium. Thoracocentesis is
preferred in the initial evaluation of thoracic injury. With
a 20-gauge needle attached to an intravenous extension
set, 3-way stopcock, and 60 ml syringe, one will aspirate
air, fluid, or both. It is advisable to aspirate from both
right and left sides of the thorax.
A thoracostomy tube allows rapid, continuous evacuation of air or fluid from the pleural space. If it becomes
necessary to use needle thoracocentesis more than twice
to alleviate dyspnea, placement of the thoracostomy tube
is necessary. Before placing the tube, a sterile preparation of the thorax is provided. Insertion is best accomplished with a stylet enclosed in the tube in order to avoid
unnecessary dissection of subcutaneous tissues the thoracostomy tube can be either intermittently drained with
a syringe, or continuously evacuated using controlled
suction. Intermittent syringe evacuation is the only way
to quantify the volume of air removed.
The thoracostomy tube is removed when the pleural
leak has sealed and the lungs have re-expanded and/or
when fluid drainage has decreased in blunt trauma this is
usually one to three days. Physical examination and chest
roentgenograms are used to determine suitability of drain
removal. Additionally, daily cytological evaluation of the
thoracic effluent should be monitored for incidence of
infection.
Fractured Ribs
Rib fractures are painful and limit diaphragmatic and
chest wall motion. Failure to adequately expand the lungs
results in atelectasis of the underlying lung and hypoxemia. Flail chest occurs when three or more ribs, or the
junction of ribs and the sternum, are each fractured at
two points. This results in paradoxical inward movement of the flail segment during inspiration when the
rest of the thoracic cage expands. Because the hypoxemia associated with flail chest results from atelectasis
due to pain and contusions of the lung underlying the
flail segment, therapy is aimed at relieving pain through
analgesics and local blocks, supplemental oxygen, and
supportive measures while the contused lung heals.
As we saw in the last seminar, each trauma patient should
be evaluated in an orderly and systematic manner. Injuries that interfere with vital physiological functions should
receive the highest priority. These are injuries that involve the respiratory system, cardiovascular system, or
neurological system. Serious injuries that are not immediately life threatening includes: fractures, luxations, and
intra-abdominal injuries (ruptured spleen, liver or damage to the urological system). Minor injuries may merely
require observation, monitoring, and serial evaluations
to assure they do not slip to a more serious status.
Initial Assessment
Using our standard triage scheme, the initial assessment of the trauma patient identifies life-threatening physiological injuries. Whenever a problem is identified immediate therapy is begun. This "primary survey” follows
the ABC (and D's) of triage and resuscitation (see the
first lecture “The Critical Cat”)
Management of the life-threatening problems identified during the primary survey is continued as shock therapy begins. The secondary survey identifies all other problems related to the trauma. The entire animal's body is
examined again from head to toe. Necessary diagnostic
samples are collected and submitted. Only when the patient is stable are indicated radiographs taken. In-depth
management of the patient's less life-threatening injuries
is undertaken in the definitive care phase. The fractures
are stabilized, and careful inspection for "hidden" injuries
is begun.
Abdominal Trauma
Abdominal injuries are occult. Injuries caused by blunt
trauma include lacerations of the liver and/or spleen, urological trauma, infarcted bowel, or reproductive organ
damage during pregnancy. Penetrating injuries from gunshot, impalement injuries, and bite wounds are more
obvious. The wounding potential of missiles is related
both to velocity and mass of the bullet. High velocity
missiles produce cavitation within the abdomen that is
sufficiently energetic to disrupt hollow organs, break
bones and spread contamination. Physical examination
findings and diagnostic studies are required in deciding
which abdomen should be surgically explored following
penetrating injury. This decision is generally based upon
signs of peritoneal penetration, unexplained shock, ileus,
organ evisceration, free gas on radiographic examination
or evidence of bacteria or plant debris following abdominocentesis or peritoneal lavage. Blunt abdominal trauma cases are challenging diagnostic problems because
the clinical manifestations may be delayed for hours or
days. Abdominal tenderness is an important clinical signs
29
27
ZBORNIK REFERA
TOV
REFERATOV
of peritoneal irritation by blood or intestinal contents.
Less life-threatening emergencies
Ultrasound is the most sensitive means to identify and
locate peritoneal fluid. If unavailable, a four quadrant abdominocentesis is our preferred means for confirming
blunt abdominal injury. From the fluid obtained, a packed
cell volume, total solids, cytology, billirubin, and creatinine can be evaluated. If the packed cell volume of centesis fluid exceeds the peripheral packed cell volume, very
likely there is either a splenic, hepatic or renal parenchymal laceration. In the dog or cat our approach is to treat
these patients as conservatively as possible. With an abdominal pressure bandage and individualized fluids therapy, it is unusual to require surgery for a splenic or hepatic laceration. Caution should be employed in applying
an excessively tight bandage when thoracic injuries are
also present.
Fractures and luxations of the bony pelvis and extremities are not considered life-threatening emergencies.
Of greater importance is the damage to associated neural, vascular, and soft tissues surrounding these bony
injuries. In fractures of long bones, blood loss may exceed 25% of the total blood volume. This blood is often
not obviously lost but rather sequestered about a fracture site.
With major biliary tree or common bile duct injury,
the clinical signs of icterus are often delayed 4 to 6 weeks.
If the abdominal fluid bilirubin is approximately 30 times
greater than peripheral bilirubin, then surgical exploratory will be required to close the lacerated organ and lavage the abdomen. This surgery is not considered an
emergency procedure. With urological injury, the packed
cell volume of the abdominal fluid will be lower than the
peripheral packed cell volume due to hemodilution with
urine. The diagnosis is confirmed by comparison of abdominal fluid urine nitrogen or creatinine to peripheral
blood values collected at the time of the abdominocentesis.
Emergency management of intraperitoneal rupture of
the bladder, urethra, and/or ureters involves drainage of
the abdominal fluid via an indwelling catheter until the
patient is sufficiently stable to undergo anesthesia and
surgical repair. Prior to surgery, contrast studies of the
kidneys, ureter, and bladder should be performed to assess the severity of injury using an excretory urogram.
If there is evidence of lower urinary tract injury, positive
contrast urethrography and cystography may be necessary.
Fractures are classified as either open or closed. Most
closed fractures pose no immediate threat should remain
partially exposed for assessment of color, pain, swelling,
discharge, odor, and temperature. Open fractures require
a thorough cleansing and covering of the wound along
with appropriate antimicrobial therapy. Contaminated
wounds should be cultured to life and definitive repair is
generally delayed at least 24 hours. Application of a splint
will relieve pain, lessen additional swelling of the limb,
and prevent a closed fracture from becoming an open
fracture. The principle of immobilization of the joint above
and the joint below the fracture decreases the usefulness
of splints in animals. In splinting, the toes with antimicrobial sensitivity performed. The last step in the emergency management of the open fracture is the application of sterile gauze and immobilization if possible.
Bite wounds, gunshot wounds, and wounds with
massive contusions should not be closed. Early closure
of these wounds generally results in disruption and prolonged convalescence. Definitive fracture treatment is
undertaken after the animal is stabilized.
Luxation of joints requires use of principles described
for fractures. Most joint luxations are closed and are
easily managed. Following resolution of shock, the luxation is reduced and ligamentous damage investigated to
ascertain the necessity for open repair.
If plant debris or significant numbers of mixed bacteria be found with centesis of the abdominal fluid, a ruptured viscus is likely and exploratory surgery is indicated.
Use of peritoneal lavage for diagnosis of abdominal
injury should be considered if abdominocentesis is negative. If no blood, bile, urine or intestinal fluid can be
aspirated, the abdominal fluid is irrigated with 10 to 20
ml/kg of warmed crystalloid fluid. If feasible, the patient
is moved from side to side to assure the fluid reaches all
areas of the abdominal cavity. The fluid is then allowed
to drain via gravity.
30
28
ZBORNIK REFERA
TOV
REFERATOV
Practical use of hormones in feline reproduction
Stefano Romagnoli
As with other species, the use of hormonal compounds in cats requires a thorough understanding of the physiology
of reproduction, which will be briefly reviewed here. The onset of puberty in the cat occurs from 4 to 12 months of
age depending on season, day length, body weight and breed. However, onset of puberty as late as 18-21 months of
age is reported for Persian and long haired queens (Table 1). In cats, there is a critical weight which has to be reached
(2/3 of the adult body weight, or 2.3-2.5 kg) before puberty is attained. Furthermore, if the critical age and weight are
reached during the period of decreased day-length, the onset of puberty will be further delayed.
Breed
N° of queens
Mean
Range
8
11.3
7.0-14.0
Abissinian
Birman
7
11.3
10.0-18.0
45
7.7
4.0-19.0
6
13.0
9.0-18.0
33
9.6
4.0-16.0
7
12.4
9.0-18.0
Persian
40
11.2
6.0-21.0
Siamese
20
9.3
4.0-20.0
Other breeds (long –haired)
17
11.0
6.0-18.0
Other breeds (short -haired)
19
9.4
4.5-15.0
Burmese
Colourpoint
Hymalaian
Manx
Table 1 – Breed, number of females considered, age at puberty in months and range for some breeds of queens
(modified from Jemmet & Evans, 1977, and Povey, 1978)
35020 (PD)
[email protected]
The feline reproductive cycle is divided into proestrus,
estrus, postestrus, diestrus and anestrus. Proestrus is
indicated by continuous rubbing of the head and neck
against any object, some vocalization but refusal of mating, and it is reported to be very short and often not
observed (Shille et al., 1979). It lasts an average of
1.2+0.8 days. Estrus behaviour in the queen, as in other mammals, is indicative of receptivity to mating, and is
characterized by signs which are similar to those of
proestrus but more intense, more frequent vocalizing,
crouching with the forequarters pressed to the ground
and hyperextension of the back which causes lordosis,
so that the vulva is presented for mating. Unlike canine
estrus which begins with decreasing serum estradiol concentrations, estrus in the queen occurs at peak follicular
activity. Feline ovulation is induced by LH released from
31
29
ZBORNIK REFERA
TOV
REFERATOV
the pituitary in response to a neural reflex originating
from the vagina stimulated by the Tom’s penis. Occurrence of ovulation does not shorten duration of estrus
which averages 8.5+4.2 days (range 2-19 days) in bred
queens (regardless of whether or not follicle(s) ovulated). Instead, absence of coitus is associated with a shorter
duration of estrual behaviour (6.2+2.9 days). The length
of estrus may vary depending on the season, with longer
duration in the Spring (5-14 days) as opposed to other
seasons (1-6 days). The number of follicles ovulating
has been related to the number of matings, with one
mating/estrus not being sufficient to cause ovulation in
up to 50% of bred females, and >4 matings/estrus being
associated with high numbers of follicles ovulating (Concannon et al., 1980; Romagnoli, 2005).
The term Postestrus has been used to indicate the stage
which follows one estrus and precede the next in queens
which did not ovulate (Lofstedt, 1982). The term metestrus is sometime used, but may be a source of confusion as it indicates a phase of corpus luteum development which does not occur in non-ovulating queens.
Queens that ovulate show evidence of corpus luteum
development, therefore going through a normal Diestrus
whose length varies depending on occurrence of conception. Diestrus lasts approximately 35-45 days in nonpregnant queens, and approximately 60 days in pregnant
queens. Following luteolysis, cyclicity resumes with a 710 days delay both in pregnant and non-pregnant females,
although lactation and suckling may inhibit resumption
of cyclicity for 2-3 weeks post-weaning. Queens exposed
to natural photoperiod undergo Anestrus, a phase of reproductive quiescence, during late Fall and early Winter
(October-December).
As in the canine, the feline estrus cycle can be easily
staged with vaginal cytology. Exfoliated vaginal epithelial
cells can be collected with a saline-moistened cottontipped swab gently inserted for approximately 2 cm into
the vagina and then rolled onto a glass slide; or by flushing 0.5 cc of saline into the vagina with a Papanicolautype pipette, placing a drop of vaginal fluid on glass slide
and then smearing it. Any of the Romanowsky-type stains
can be used satisfactorily (Giemsa, Wright’s, New mehtylene blue, Leishman blue, Diff-Quik) to stain feline
vaginal smears whose patters do not differ greatly from
those of the bitch. Percentage of anuclear squames is
reported to be 10% on the first day of estrus, and to
increase to 40% on the fourth day of estrus, with the
percentage of intermediate cells falling from 40% to 10%
during the same period (Shille et al., 1979). Although
easy to perform also in felines, vaginal cytology is not
routinely used in queens to stage the estrous cycle (ovulation does not need to be identified as it generally occurs
when the queen mates), but rather to look for vaginal
epithelial cornification in cases of silent or prolonged heat.
During the follicular phase estradiol concentration increases rapidly from 12-15 pg/ml during proestrus to 25
pg/ml on the first day of estrus, then up to >70 pg/ml
within the following 4-6 days, then down to 20-25 pg/ml
on the following 1-2 days and finally reaches 10-15 pg/
ml (a concentration typical of postestrus) between 7 and
10 days after the onset of estrus.
Induction of oestrus and ovulation
Oestrus induction in the queen is commonly achieved
using PMSG. A variety of different treatments have been
used as shown in Table 2, but PMSG at the dose of 100150 IU a single time followed by 50-100 IU of hCG 5-7
days later is the protocol that consistently has given the
best results. Some efficacy of the antiprolactinics has
been claimed, but not substantiated so far. Although
prolactin does not seem to play a role in determining
feline anestrus, clinical evidence indicates that in previously fertile queens prolonged use of cabergoline results
in oestrus induction. This is in line with the observation
that in the bitch the lowering of prolactin due to the use
of antiprolactinic drugs is not always followed by induction of oestrus (Okkens et al., 1997). No information is
available on the use of cabergoline in queens with primary anoestrus.
On day 2 of induced oestrus, hCG (100 IU) or GnRH (50
mcg gonadorelin, or 0.8 µg buserelin) should be injected
intramuscularly (IM) before mating. However, pathological conditions like illness (progesterone-producing ovarian cysts), inadequate animal husbandry and feeding as
well as too young age have to be excluded before medical induction of oestrus and ovulation. Induction of ovulation may be necessary in case of permanent oestrus,
for induction of pseudopregnancy to prolong the interoestrus interval or in case of artificial insemination. In
these cases, ovulation can be induced by IM or SC injection of hCG or GnRH (at the above dosages) when the
queen is in oestrus or also by slightly rubbing a cotton
swab at the vaginal mucosa to achieve vaginal stimulation and to induce a LH surge mimicking the mating of a
tom. It may be necessary to repeat this procedure several times to get sufficient LH concentrations to induce
ovulation.
32
30
ZBORNIK REFERA
TOV
REFERATOV
Protocol
Dosage
Reference
PMSG
100-1000 IU, 5-7 d
Cline et al., Lab An Sci 1003, 1980
PMSG+hCG
100-150 IU on day 1 + 50-100 IU on day 5-7
Cline et al., Lab An Sci 1003, 1980; Donoghue et al., Biol Reprod
46:972, 1992; Swanson et al., Biol Reprod 57:295, 1997
FSH+hCG
2 mg/day 4-5 days + 50-250 IU
Dresser et al., Therio 28:915, 1987
FSHp+hCG
2 mg on day 1, 0.5-1.0 mg days 2-5 + 50-250 IU
Tsutsui et al., Jap J Vet Sci 51:677, 1989
huFSH + hCG
7.5 or 15 IU days 1-4 + 100 IU on day 4.5
Orosz et al., Therio 37:993,1992
hMG + hCG
15 IU days 1-5, + 100 IU on day 6.5
Orosz et al., Therio 37:993,1992
FSHp (ultra pure)
2.5-10 mg total dose, in 5 days
Verstegen et al., J Reprod Fert Suppl 47:209, 1993
Antiprolactin drugs
Cabergoline 5 mg/kg, max 15 days
Verstegen, unpublished
Table 2 – Oestrus induction protocols in the queen.
Unwanted pregnancy
Unwanted mating in privately owned sexually mature
outdoor cats is common and detection of pregnancy in
these cats is usually quite late in gestation. Fetal parameters can be measured by ultrasound to estimate the date
of parturition.5 However, if a cat is presented immediately after unwanted mating, it should be checked for evidence of mating (signs of scratching and biting, spermatozoa in a vaginal smear) first. The use of estrogens causing closure of the utero-tubal junction and therefore inhibiting the transport of the embryo is very effective, but
due to the risk of side effects (especially pyometra), injections are not recommended. Repeated injections of
prostaglandin F2 alpha (PGF2α) for induction of abortion
after day 30 have been described with significant side
effects (salivation, vomiting, diarrhea) and variable success rates (25-75 %, n=4). Dopamine-agonists have been
used occasionally in cats for induction of abortion from
day 30 onward, although the available information on
this drug in the feline is scant. Production of litters by
feral cats was prevented by addition of cabergoline to the
diet of pregnant females at a dose of 5-15 ug/kg/day for
4-12 days. In a controlled laboratory study, cabergoline
at doses of 1.7 ug/kg given i.m. daily for 5 days, starting
at day 30 of pregnancy, induced luteolysis and terminated pregnancy in 4 of 5 cats, with negligible side effects.
In another study, the oral cabergoline formulation, (Galastopä Ceva-Vetem, Italy) administered per os at a dose
of 15 µg/kg for 4 to 7 days terminated pregnancy in 8
cats when started between day 30 and 42, but failed in 2
cats when started at day 45. This failure of abortifacient
efficacy in late pregnancy is perhaps not surprising, since
the feline placenta is thought to produce progesterone
during the last 3 weeks of pregnancy. Emesis was a side
effect in some animals.
The use of antiprogestins was recently proposed for termination of the feline pregnancy. As progesterone is necessary for maintenance of pregnancy, its withdrawal or
the blockade of its receptors with antiprogestins, allows
opening of the cervix and spontaneous contractions of
the myometrium. Aglepristone treatment has been proven to be safe and effective for early, midterm and late
pregnancy termination in the queen. Success rates in
queens vary from 100% for early treatment (days 5/6
after mating), to ~ 85 % for mid-pregnancy treatment
(days 25 to 33) to <70% for late treatment (days 45).
Two injections (10-15 mg/kg BW) on consecutive days
are recommended; due to variable success rates following midterm or late termination of pregnancy, an ultrasound examination should be performed to make sure
that abortion is complete. Currently, many authors consider the use of aglepristone as the method of choice for
prevention of nidation and mid-term termination of pregnancy in the queen.
In cats, antiprogestins can also be used for:
1) open and closed-cervix pyometra – Conservative
medical treatment of bitches with pyometra can be
achieved with the administration of 10 mg/kg of aglepristone on days 1, 2, 8 and then also 15 and 28 depending on the clinical situation in bitches with both open
cervix and closed-cervix pyometra (Romagnoli et al.,
2006). The use of aglepristone should be associated with
antibiotics if necessary, and can also be associated with
PGF provided that cervical opening has occurred. Unpublished information indicates that the effect of aglepristone on pyometra in the queen (using the 15 mg/kg
dose) is probably the same as in dogs.
2) treatment of feline mammary hypertrophy - Benign mammary hypertrophy is a benign fibroglandular
proliferation of one or more mammary glands which typically occurs in young queens at their first luteal phase.
The proliferation of the mammary gland is due to an excessive response to the action of progesterone which is
present in presumably normal concentrations in affected
animals. Mammary glands will start swelling rapidly and
within 2-3 days all glands become very swollen, firm and
33
31
ZBORNIK REFERA
TOV
REFERATOV
nodular. If left untreated, the problem may disappear on
its own without any complication in most cases. Treatment with prostaglandins or antiprolactinic is not effective, while removal of ovaries or administration of aglepristone can be curative. When mammary hypertrophy
occurs following progestogen administration, signs typically do not subside immediately following neutering or
withdrawal of progestin therapy (Gorlinger et al 2002).
In such cases, surgical removal of persisting nodules
should be considered in order to perform histology and
rule out presence of neoplasia. Recently, it was shown
that the condition is responsive to aglepristone (Wehrend
et al 2001, Gorlinger et al 2002, Meisl et al., 2003), which
may be an option also for cats treated with long-acting
progestogens. Although dose regimens for aglepristone
in cats have not been reported, anecdotal treatments with
15 mg/kg are known to be effective as abortifacients or
in case of a pyometra. Dosages for mammary hypertrophy may need to be higher or prolonged in time depending on whether it is a spontaneous disease or if it is due
to progestogen administration. Recently, Muphung et al
(2009) studied the effect of aglepristone in a group of
queens treated with a high dose of medroxyprogesterone acetate (MPA - 50 mg) followed by 2 injections of 10
mg/kg aglepristone 3 weeks later. Based on histology
and immunohistochemistry, no evidence of an effect of
aglepristone on the mammary gland of treated queens
was present. Lack of effect might be due to the very high
dose of MPA used, to the rather low dose of aglepristone
(10 mg/kg instead of 15 mg/kg), to the short treatment
with aglepristone (only 2 injections) or to the long interval between MPA and aglepristone treatments.
3) Aglepristone has recently been successfully used also
for induction of parturition in term bitches. There is no
information on such use in queens.
Control of Reproduction
Surgical contraception is not any longer the only approach
requested by owners, as an increasing part of them would
appreciate to preserve a cat’s future reproductive potential. Furthermore, restrictions are being imposed on surgical castration in an increasing number of countries for
ethical reasons and animal welfare legislation. Alternative approaches are based on interference with endocrine
regulatory mechanisms and may include the use of a)
progestins causing a negative feedback on the pituitary,
b) GnRH agonist implants leading to a down-regulation
of the hypothalamo-pituitary-gonadal axis and c) melatonin implants.
Progestins - Synthetic analogues of progesterone, also
termed progestins or progestogens, are pharmaceutical
compounds commonly used in (dogs and) cats for temporary (starting the treatment shortly before prooestrus
onset) or prolonged (starting in anoestrus) postponement
of oestrus, or for suppression of oestrus (starting the
treatment after proestrus onset). The following compounds are currently available in various parts of the
world: medroxyprogesterone acetate (MPA), megestrol
acetate (MA), proligestone (PR), chlormadinone acetate
(CMA) and delmadinone acetate (DMA). From the clinical
point of view all these products act in the same way
through a block of the production and/or release of GnRH
from the hypothalamus (Romagnoli and Concannon,
2003).
Medroxyprogesterone acetate (MPA) is a long-acting
progestin, developed for human use in the 1960’s and
widely available in most countries of the world as a veterinary drug for use in dogs and cats (oral formulation)
or mostly dogs (depot formulation). As MPA is slowly
metabolized by the liver, its effective circulating levels can
be maintained for 3 to 6 months after a single intramuscular injection. Various treatment regimens have been
recommended for small animals with the minimum effective dose being approximately 2.0 mg/kg for queens
(Table 3). Higher dosages have been suggested and are
occasionally found on drug leaflets in some countries,
but their use should be discouraged because of the increasing risk of side effects at MPA doses > 3.0 mg/kg
in both bitches and queens. MPA should be administered
in anoestrus, and treatment length should not exceed 2
years (or 4 injections at 6 month-intervals). The interval
from treatment to the first spontaneous oestrus ranges
from 1.5 to 26 months after the last injection. In some
countries MPA is not recommended for use in cats (Jackson, 1984)
Megoestrol acetate (MA) is a short-acting progestin, which
is better suited than MPA for temporary postponement
and suppression. MA is typically available as an oral formulation (although parenteral formulations are marketed
in some countries) with dosages varying in the bitch depending on the cycle stage: from 0.55 mg/kg/day for 32
days in anoestrus up to a maximum dosage of 2.2 mg/
kg/day for 8 days in early prooestrus. In anoestrus queens
it should be given at the dose of 5.0 mg/cat every 2 weeks,
while this dosage can be increased to 5.0 mg/cat/day for
up to 4 days in case of a breakthrough heat. Dosing of
injectable MA formulations should be done carefully based
on body weight, keeping in mind that no dose response
data are available to demonstrate what is the most appropriate protocol for injectable MA in small animals.
Delmadinone acetate (DA) and Chlormadinone acetate
(CA) are synthetic progestins whose action on the reproductive and endocrine system is similar to that of MPA
(they are derivatives of MPA): effectiveness is reportedly
good for prolonged postponement of cycle in cats at the
dose of 2 mg/cat. Published information on both drugs
34
32
ZBORNIK REFERA
TOV
REFERATOV
is scant. Post-treatment fertility is reportedly normal for
both. DA is currently available as a veterinary drug in
some European countries.
Androgens – Like for progestins, administration of androgens in the female will suppress gonadotrophin release thanks to a negative feedback upon the hypothalamic-pituitary axis. Furthermore, androgen receptors have
been identified in oestrogen target tissues and androgen
administration may cause a decrease in the response of
oestrogen function. Natural and synthetic androgens have
been used for the control of oestrus in bitches and queens.
These drugs are commonly employed in racing Greyhound bitches, not only because of their suppressive effect on oestrus, but also because of their anabolic effects. As with progestins, treatment with androgens
should be started when the animal is in the first half of
anestrus, as delaying its administration until late anoestrus
may prove ineffective (Kutzler, 2006). In cats, the use of
androgens is not currently advised due to the incidence
of side effects (on which, however, there is little if any
scientific data available). There is no information on the
efficacy and safety of testosterone in cats, and mibolerone is not recommended in this species due to the fact
that the effective dose (50 µg/day) is close to the toxic
dose (60 µg/day).
Proligestone (PGS) is the most recent type of progestin
available for use in (dogs and) cats, which has been developed to selectively act on the hypothalamic-pituitarygonadal axis with less progestational activity compared
to other synthetic progestogens. However, based on studies performed in The Netherlands a range of side effects
has been reported also for this compound (at least in
dogs). The recommended dosage regimen in queens is
10 mg/kg repeated after 3 and 4 months, and then every
5 months. Breakthrough heats may occur during treatment, although their incidence has not been studied in
bitches or queens. Table 3 shows the suggested dosages of the most commonly used progestogen-based compounds in the queen.
Suggested Dosage
Cat
MPA
2.0 mg/kg IM every 5 months
MA
in anestrus: 5 mg/cat every 2 wk or 2.5 mg/cat/wk PO (better if divided into
2 administrations every 3.5 days)
in proestrus: 5 mg/cat/day for 4 days, then 5 mg every 2 wk, PO
DA
PO: 0.25-0.7 mg/kg, once a week. SC: 2.5-5.0 mg/kg, every 6 months. For oestrus
suppression, SC: 0.5-1.0 mg/kg, for 6 days or 2.5-6.75 mg/kg, one or two injections
24 hours apart
PGS
10 mg/kg SC every 3, 4, 5, 5 months
Table 3 – Suggested dosages of the 4 most commonly used progestogen compounds in queen for the control of
reproduction: MPA = medroxyprogesterone acetate; MA = megestrol acetate; DA = delmadinone acetate; PGS =
proligestone
GnRH agonists - A recent development in the field of the
control of reproduction in the queen is the use of longacting GnRH agonists, which have become commercially
available as veterinary drugs in Europe during 2008. Both
deslorelin (Suprelorin, Virbac) and azagly-nafarelin (Gonazon®, Intervet) have proven effective in controlling eline
reproduction in preliminary trials. Based on ongoing studies at the University of Padova in adult queens, the 4.7
mg deslorelin implant seems to be effective in inhibiting
reproductive cyclicity for >12 months, and good efficacy
has also been observed in delaying puberty in male and
female cats implanted at 2-4 months of age. Deslorelin
(Suprelorin®, Virbac is currently marketed in Europe for
use in male dogs, therefore its use in queens should be
regarded as extra-label. Azagly-nafarelin is not marketed yet anywhere in the world.
Melatonin - The cat is a seasonal breeder (long-day breeder) influenced by day light with increasing melatonin concentrations and decreasing sexual activity following decreasing photoperiod. Exogenous melatonin may mimic
this effect and has therefore been described in cats for
intravenous, subcutaneous and oral administration. Oral
administration of melatonin for 30 to 35 days (given 3 h
before lights-off) effectively and reversibly suppressed
oestrus without any side effects. Because permanent oral
administration is impractical in daily routine and clinical
practice, melatonin implants were tested for their efficacy in controlling feline reproduction. Whereas melatonin
implants containing 12 mg suppressed oestrus in 3 of 4
cats only, Gimenez et al showed that 18 g implants (Melovine®, CEVA Sante Animal, Libourne, France) were highly
effective (9/9 cats). Treatment in interoestrus resulted in
35
33
ZBORNIK REFERA
TOV
REFERATOV
a prolonged duration of efficacy compared to treatment
in oestrus (113.3 ± 6.1 days vs. 61.1 ± 6.8 days). Initial
oestrus induction for 2-3 days was observed in 3/9 cats
(interoestrus) and 7/9 cats (oestrus). Whereas in the
former study one cat suffered from uterine pathology
after treatment, no side effects were observed in later
trials. Regarding fertility all effects are fully reversible and
mating at the end of treatment resulted in pregnancy rates
of 75%; so treatment with a melatonin implant seems to
offer a new promising alternative for short-term oestrus
cycle control in the queen while preserving future reproductive potential. However, further studies with more
animals are necessary to finally evaluate the risk for side
effects.
SIDE EFFECTS OF REPRODUCTIVE DRUGS
The incidence of progestin and androgen side effects
appears to be associated with overdosing, a wrong choice
of patients and/or administration during stages of the
cycle other than anoestrus. For instance, while a dose of
2.5 mg/kg of MPA in a young, healthy bitch can be used
safely for at least 18-24 months (or for 3-4 injections at
6-month intervals, provided it is injected in anestrus), a
dose of 6.0 mg/kg is at risk of causing side effects well
before 18 months, and a dose of 10 mg/kg will cause
acromegaly and pyometra after an equal or shorter treatment period. Similarly, a dose of 3.0 mg/kg will cause
development of benign and malignant mammary tumours
in bitches if administered every 3 months for 12 consecutive treatments.
Normal dosage in healthy females
Normal dosage in females with subclinical
disease, high dosage, or prolonged treatment
Delayed onset of parturition
Benign and malignant mammary nodules
Skin reaction at inoculation sites
Cystic endometrial hyperplasia, pyometra
Masculinization of female foetuses
Acromegaly
Behavioral/metabolic changes (decreased libido; increased
appetite and body weight; polyuria/ polydipsia)
Diabetes mellitus
Adrenocortical suppression in cats (using MA)
Cushing’s disease
Table 4 – Side effects due to the use of progestins following administration of a) normal dosages in healthy females,
or b) normal dosages in females with subclinical disease, normal dosage for too long, or dosages higher than indicated. A reversible adrenocortical suppression is reported in normal cats receiving megoestrol acetate (MA) at dosages
of 5.0 mg/cat for 7 to 14 days.
A safe dosage may cause side effects if: a) administered
in dioestrus (because of the coincident endogenous
progesterone secretion adding to exogenous administration), b) given to an animal with a pre-existing disease
(such as subclinical cystic endometrial hyperplasia or diabetes), or c) administered to a pregnant female (as it will
delay perturition). An example of potential side effects
occurring following a normal or a high dosage of progestins
is reported on Table 4.
Although side effects have been reported more commonly
for MPA, CA, DA and MA than for PGS, it should be
noted that the clinical use of gonadal steroidal compounds
in dogs and cats started almost 50 years ago, at which
time very little was known on reproductive and endocrine
effects of steroids, while PGS has been introduced into
the veterinary market more recently and perhaps used
with more caution and attention to dosages. Reported
side effects of PGS include pain at the injection site and
discoloration of the hair; although earlier clinical trials
have not reported development of uterine disease or mammary tumours when PGS is used at the suggested dose
regimen, no large clinical studies have been performed in
recent years. PGS can probably be regarded as slightly
safer than MPA. However, small animal clinicians should
use the same degree of caution when using any progestin (Table 4). Fertility is generally not affected by the treatment with progestins, although the endometrial proliferative action due to these drugs may alter endometrial
status particularly in prolonged treatments.
Similarly to progestins, androgens may cause side effects if administered at too high dosages, for too long or
in the wrong patient. Reported side effects for androgens following chronic treatment with normal dosage
include the most common clitoral hypertrophy and vaginitis, and the less common virilisation, masculinisation of
female foetuses, body odor, urinary incontinence, urine
spraying, mounting behaviour, cervical dermis thickening and epiphora. Furthermore, overdosing may result in
anal gland inspissation and resulting odors. Androgens
are known to be much less harmful to fertility due to the
lack of endometrial proliferation, although endometrial
atrophy may become chronic following prolonged treatment. Reproductive side effects following chronic use of
mibolerone at efficacious dosages include ovarian fibroma, endometrial atrophy and vaginal mucosa atrophy.
Beagles (but not other breeds) treated with mibolerone
appear to have a reduced response to ACTH challenge.
In general, the use of androgens is not recommended in
36
34
ZBORNIK REFERA
TOV
REFERATOV
the following cases: a) animals intended for future breeding; b) young animals (7 months old or younger bitches,
due to early epiphyseal closure); c) Bedlington terriers
due to their genetical predisposition to chronic progressive hepatitis; d) pregnant animals; e) animals with androgen dependent neoplasms or with a history of liver or
kidney diseases
GnRH agonists appear to be much less harmful for reproductive and general health of bitches and queens when
compared to gonadal steroids, because of the fact that
their action is based on removal of endogenous steroids
from the general circulation, thereby eliminating any potential risk of hormonal related conditions. However, these
compounds may be a source of problems both in terms
of owners convenience as well as health risks for the
female being treated. GnRH agonists provide a powerful
stimulus for the pituitary, which is forced to release all its
reserves of gonadotrophins until down-regulation occurs.
The interval from treatment to onset of down-regulation
may vary from 2 to 4 weeks. During this period, ovarian
activity and secretion is typically stimulated, which may
cause induction of heat if the female is treated in anoestrus,
or a surge in progesterone secretion if treatment occurs
in dioestrus. Heat induction can be a major inconvenience
for an owner who is requesting control of oestrus for
her/his pet. Such oestrus is normally fertile; therefore, a
bitch may conceive and become pregnant, but often spontaneous abortion occurs at mid-pregnancy as soon as
pituitary down-regulation occurs. The surge in progesterone production may exhacerbate a subclinical uterine
or ovarian condition, as well as delay parturition if treatment is performed during the last trimester of pregnancy. Induction of heat is not observed when bitches are
treated in dioestrus or retreated in anoestrus (when the
previous implant is still functioning), although breakthrough heats have been observed within the last month
prior to re-treatment.
As with all treatments which are supposed to be repeated over time at regular intervals, owner compliance is an
important limiting factor. Failure of owners to bring back
their bitches or queens for successive treatments often
accounts for breakthrough heats. Treatment during a
breakthrough heat should be carefully avoided, as administration of any reproductive drug during the follicular phase is likely to carry a risk for the female. A list of
effects/side effects of progestins, androgens and GnRH
agonists is presented in Table 5.
Effect
Progestins
Increased frequency of GnRH peaks
Decreased frequency of GnRH peaks
XXX
Suppression of ovarian activity
XXX
Suppression of uterine motility
XXX
Suppression of adrenocrotical axis
XXX
Ýncreased secretion of prolactin and growth hormone
XXX
Ýnsulin resistance
XXX
Endometrial proliferation and secretion
XXX
Atrophy of endometrial lining
Cervical closure
XXX
Proliferation of mammary parenchyma
XXX
Atrophy of mammary parenchyma
Lactational arrest
XXX
Foetal developmental defects
XXX
Delayed parturition
XXX
Increased appetite and body weight
XXX
Vaginitis
Increased libido/aggressiveness/mounting behaviour
Anabolic effects
Physeal closure in prepuberal animals
Decreased libido/aggressiveness
XXX
Clitoral hypertrophy
Urinary incontinence/urine spraying
Skin decoloration
XXX
Growth of anal hepatoid glands
Thickening of cervical dermis, epiphora
Androgens
XXX
XXX
XXX
GnRH agonists
XXX (a)
XXX (b)
XXX (b)
XXX (b)
XXX (c)
XXX
XXX
XXX
XXX
XXX
XXX (d)
XXX (c)
XXX possible
XXX (possible)
XXX (e)
XXX
XXX
XXX
XXX
XXX
XXX
XXX
XXX
XXX
Table 5 – The most relevant clinical effects, including side effects, of progestins, androgens and GnRH agonists on the
reproductive system, mammary gland, body weight and behaviour of bitches and queens. (a) present only during the first 2-4
weeks following treatment, after which it disappears; (b) present only after the end of the first 2-4 weeks following treatment;
(c) present only during the first 2-4 weeks following treatment in bitches implanted with deslorelin during diestrus; (d) this
effect is maintained in bitches implanted in anestrus, while it appears at the end of the induced oestrus in bitches treated in
anestrus. (e) if implanted during the last trimester of pregnancy
37
35
ZBORNIK REFERA
TOV
REFERATOV
CLINICAL CONSIDERATIONS FOR A SAFE
USE OF REPRODUCTIVE DRUGS IN
QUEENS
The ideal candidate for a progestin or androgen treatment is an adult postpuberal female in anestrus, while
the ideal candidate for treatment with a GnRH agonist is
an adult postpuberal female in diestrus. Before a female
is treated with long acting compounds she should be
evaluated for normality of uterine and mammary conditions as well as of glucose metabolism. A minimum database of clinical information to be gathered prior to administering a long-acting compound should include a)
collecting a thorough reproductive history to rule out
occurrence of estrus within the last 1-2 months (which
would mean that the queen might have ovulated and therefore she might be in diestrus); b) a complete clinical exam;
c) palpation of the mammary gland to rule out presence
of mammary nodules; d) a vaginal smear to rule out presence of oestrus. Also, if heat occurred within the last 2
months it would be appropriate to wait a few more weeks
or assay progesterone to rule out diestrus.
In general, a progestin or androgen treatment period of
12-18 months is considered adequate in most patients,
although longer treatments can also be safe provided that
the female is given a thorough clinical check as described
above (a-d) prior to each treatment. While most bitches
and queens may tolerate well treatment periods of more
than 12-18 and up to 24 months, animals with a preexisting disease such as subclinical diabetes, small mammary nodules or cystic endometrial hyperplasia may see
their condition worsen rapidly as a result of a progestin
treatment, or may experience a temporary worsening in
case of treatment with a GnRH agonist in diestrus. A
series of considerations on patient selection and type of
presenting complaint for which a progestin treatment
should or should not be used is presented (Table 6).
Do not use progestins
… as this may cause
In pre-puberal queens (depot compounds)
feline mammary hyperplasia (a)
In pregnant females
fetal development defects or delayed parturition
In pseudopregnant bitches
pseudopregnancy to relapse and become chronic
During diestrus
side effects due to to overdosing (b)
In females with vaginal haemorrhage
Worsening of underlying condition (c)
In diabetic patients
Worsening of underlying condition (d)
In bitches with prolonged heat
Worsening of underlying condition (e)
Table 6 – Potential side effects due to the use of progestins at normal dosages depending on patient selection. (a) in
prepuberal queens it is best to use initially a short acting compound (such as MA) per os for 1-2 weeks and then
change to a long acting progestin once potential side effects have been ruled out. (b) the stage of the reproductive
cycle should always be identified using vaginal cytology and/or serum progesterone assay, and the bitch or queen
should best be treated during anestrus; diestrus should be ruled out in felines too, as 30-60% of queens ovulate
spontaneously, maintaining thereafter a 30-45 day-long diestrus. (c) prolonged sanguineous vulvar discharge following parturition in the bitch can be a critical problem which should either be treated with a uterine contractive drug (i.e.
as ergonovine) or sent to surgery. Milder bloody vulvar discharge can be caused by uterine neoplasia, cystic endometrial hyperplasia with superimposed endometrial inflammation, pyometra, metritis, none of which conditions will
benefit from administration of a progestin. (d) although not always necessary, it would be wise to measure blood
glucose before and/or after a prolonged treatment to confirm health status with regard to glucose metabolism. (e) a
prolonged heat may be due to ovarian cyst/s, a granulosa cell tumor, or may be due to a split heat (in the bitch) or to
a misinterpretation of normal estrous signs by the owner. For none of these categories is a progestin treatment
indicated.
38
36
ZBORNIK REFERA
TOV
REFERATOV
Literature and Suggested Readings on Control of Reproduction
Banks DR, Stabenfeldt G (1982) Luteinizing hormone release in the cat in response to coitus on consecutive days of estrus. Biology of
Reproduction 26, 603-611
Chakraborty PK, Wildt DE, Seager SWJ: Serum luteinizing hormone and ovulatory response to luteinizing hormone releasing hormone in
the estrous and anestrous domestic cat.. Lab An Sci 29:338-344, 1979
Concannon PW, Hodgson B, Lein D: Reflex LH release in estrous cats following single and multiple copulations. Biol Reprod 23:111117, 1980
Erünal-Maral N, Aslan S, Findik M, Yüksel N, Handler J, Arbeiter K. Induction of abortion in queens by administration of cabergolin
(Galastop TM) solely or in combination with the PGF2α analogue Alfaprostol (Gabbrosim TM). Theriogenology 2004;61:1471-5.
Fieni F, Martal J, Marnet PG, Siliart B, Guittot F. Clinical, biological and hormonal study of mid-pregnancy termination in cats with
aglepristone. Theriogenology 2006;66:1721-8.
Findik M, Maral NE, Aslan S. The use of proligestone, megestrol acetate and GnRH on queens with the aim of hormonal contraception.
Turk J Vet Anim Sci 1999;23 (Suppl 3):455-9.
Goericke-Pesch S, Georgiev P, Wehrend A. Prevention of pregnancy in cats using aglepristone on days 5 and 6 after mating. Theriogenology 2010, accepted
Georgiev P, Wehrend A. Mid-gestation pregnancy termination by the progesterone antagonist aglepristone in queens. Theriogenology
2006;65:1401-6.
Georgiev P, Bostedt H, Goericke-Pesch S et al. Induction of abortion with Aglepristone in cats on day 45 and 46 after mating. Reprod
Dom Anim 2009; doi: 10.1111/j.1439-0531.2009.01540.x, ISSN 0936-6768
Gimenez F, Stornelli MC, Tittarelli CM et al. Suppression of estrus in cats with melatonin implants. Theriogenology 2009;72:493-499.
Gorlinger S, Kooistra HS, van den Broek A, Okkens AC - Treatment of fibroadenomatous hyperplasia in cats with aglepristone. Journal
of Veterinary Internal Medicine 16, 710-713. 2002
Graham LH, Swanson WF, Wildt DE, Brown JL. Influence of oral melatonin on natural and gonadotropin-induced ovarian function in the
domestic cat. Theriogenology 2004;61:1061–76.
Gudermuth DF, Newton L, Daels P, Concannon P. Incidence of spontaneous ovulation in young, group-housed cats based on serum and
faecal concentrations of progesterone. J Reprod Fertil 1997;51 (Suppl 1):177-84.
Henik RA, Olson PN, Rosychuk RA. Progestagen therapy in cats. Compend Cont Educ 1987;7:132-41
Kutzler MA. Estrus induction and synchronization in canids and felids. Theriogenology 2007;68:354–74
Kutzler M, Wood A. Non-surgical methods of contraception and sterilization. Theriogenology 2006;66:514-25.
Jöchle W, Jöchle M. Reproduction in a feral cat population and its control with a prolactin inhibitor, cabergoline. J Reprod Fertil
1993;47:419-24.
Johnston SD, Kustritz MVR, Olson PNS. Prevention and termination of feline pregnancy. In: Johnston SD, Kustritz MVR, Olson PNS,
eds., Canine and Feline Theriogenology. Philadelphia, London, New York, St Louis, Sydney, Toronto: W. B. Saunders Company, 2001:
414-30.
Loretti AP, Ilha MR, Ordas J, Martin de las Mulas J. Clinical, pathological and immunohistochemical study of feline mammary fibroepithelial hyperplasia following a single injection of depot medroxyprogesterone acetate. J Feline Med Surg 2005;7:43–52.
Lofstedt RM: The estrous cycle of the domestic cat. Compend Cont Ed Pract Vet 4:52-58, 1982
Michael RP – Observation upon the sexual behaviour of the domestic cat (Felis catus L.) under laboratory conditions. Behaviour 8: 1-23,
1961
Meisl D, Hubler M, Arnold S - Treatment of fibroepithelial hyperplasia (FEH) of the mammary gland in the cat with progesterone
antagonist Aglepristone (Alizine). Schweiz Arch Tierheikd 145, 130-136. 2003
Muphung W, Rungsipipat A, Chatdarong K – Effects of the antiprogestin aglepristone on the uterine tissue of cats administered
medroxyprogesterone acetate. Reprod Dom Anim 44 (Suppl 2):204-207, 2009
Middleton DJ, Watson AD, Howe CJ, Caterson ID. Suppression of cortisol responses to exogenous adrenocorticotrophic hormone, and
the occurrence of side effects attributable to glucocorticoid excess, in cats during therapy with megestrol acetate and prednisolone. Can
J Vet Res 1987; 51:60-5.
Munson L, Bauman JE, Asa CS, Jöchle W, Trigg TE. Efficacy of the GnRH analogue deslorelin for suppression of oestrous cycles in cats.
J Reprod Fertil 2001;57 (Suppl 1):269-73.
Onclin K, Verstegen J. Termination of pregnancy in cats using a combination of cabergoline, a new dopamine agonist, and a synthetic
PGF2α, cloprostenol. J Reprod Suppl 1997;51 (Suppl):259-63.
Robinson R, Cox HW – Reproductive performance in a cat colony over a 10 year period. Lab Anim Sci 4: 99-112, 1970
Romagnoli S, Concannon P W. Clinical use of progestins in bitches and queens: a review. In: Concannon PW, England G, Verstegen J,
Linde-Forsberg C, eds., Recent Advances in Small Animal Reproduction. International Veterinary Information Service, Ithaca NY
(www.ivis.org)
Romagnoli S – Failure to conceive in the queen. Journal of Feline Medicine and Surgery. 7 (1): 59-64, 2005
Root MV, Johnston SD, Olson PN. Estrous length, pregnancy rate, gestation and parturition lengths, litter size, and juvenile mortality in
the domestic cat. J Am Anim Hosp Assoc 1995;31:429–33.
Rubion S, Driancourt MA. Controlled delivery of a GnRH agonist by a silastic implant (Gonazon) results in long-term contraception in
queens. Reprod Domest Anim 2009;44 (Suppl 2):79-82.
Saxena BB, Clavio A, Singh M, Rathnam P, Bukharovich EY, Reimers TJ Jr, Saxena A, Perkins S (2003). Effect of immunization with
bovine luteinizing hormone receptor on ovarian function in cats. Am J Vet Res 2003;64:292-8.
Shille VM, Lundstrom KE, Stabendfeldt GM: Follicular function in the domestic cat as determined by estradiol 17? concentrations in
plasma: relation to estrous behaviour and cornification of exfoliated vaginal epithelium. Biol Reprod 6:953-963, 1979
Shille VM. Mismating and termination of pregnancy. Vet Clin North Am Small Anim Pract 1982;12:99-106.
Verstegen J P, Onclin K, Silva LDM, Donnay I. Abortion induction in the cat using prostaglandin F2 alpha and a new anti-prolactinic
agent cabergoline. J Reprod Fertil 1993;47 (Suppl):411-7.
Wehrend A, Hospes R, Gruber AD. Treatment of feline mammary fibroadenomatous hyperplasia with a progesterone-antagonist. Vet Rec
2001;148:346-7.
Wildt DE, Guthrie SC, Seager SWJ: Ovarian and behavioural cyclicity of the laboratory maintained cat. Horm Behav 10:251-257, 1978
Wildt DE, Seager SWJ, Chakraborty PK. Effect of copulatory stimuli on incidence of ovulation and on serum luteinizing hormone in the
cat. Endocrinology 1980;107:1212–7. (A)
39
37
ZBORNIK REFERA
TOV
REFERATOV
Ovarian remnant syndrome in the queen: clinical approach
to a surgeon’s dilemma
Stefano Romagnoli
Introduction
The term Ovarian Remnant Syndrome (ORS) describes
occurrence of heat after ovariectomy or ovariohysterectomy in the bitch or queen which can be due to the presence of residual ovarian tissue not completely removed
at surgery, or to the presence of a partial or complete
separation of normal ovarian tissue during development
on the broad ligament (Wallace, 1991; Johnston et al.,
1996; Prats, 2001). As presence of ovarian tissue on the
broad ligament has been reported only in the queen and
only anecdotally (Bloom, 1954; Stein, 1975), the ORS
should not be considered as ovarian pathology but rather
as a surgical complication of ovariectomy or ovariohysterectomy (Pearson, 1973). When performing an elective
ovariectomy or ovariohysterectomy, the surgeon should
always look very carefully the broad ligament around the
ovary to rule out presence of abnormal ovarian tissue in
this location. A supernumerary ovary as such is thought
to be extremely rare and has never been reported so far.
Single or double, monolateral or bilateral nodules in the
broad ligament near the ovary are occasionally encountered in the queen, but they are generally adrenocortical
tissue which is of no clinical significance in the cat.
A less common cause of ORS can be a piece of ovarian
tissue accidentally dropped into the abdominal cavity during surgery. Such pieces of tissue can establish vascular
connections with the omentum or the serosa of abdominal viscera, and become active again thus allowing ovarian follicles to grow and reach the preovulatory stage.
Revascularization of ovarian tissue following ovariectomy has been reproduced experimentally by suturing a
sliced fragment of ovary in a serosal pouch of the stomach or under the splenic capsule (bitch), or to the mesenStefano Romagnoli, DVM, MS, PhD, Dipl. ECAR
35020 (PD)
[email protected]
tery or lateral abdominal wall (queen). Cyclic signs of
proestrus and estrus can be observed in bitches undergoing such a surgical treatment (Leroux and Venderwalt,
1977). In the queen, ovarian remnants experimentally
sutured or left free into the abdomen can revascularize
and become active in follicular growth in about 90% of
cases (Shemwell and Weed, 1970; DeNardo et al., 2001).
In women, failure to perform a complete removal of the
ovary may be due to presence of inflammation of the
ovary, ovarian bursa or periovarian tissues at time of surgery. However, this is rarely the case in small animal
medicine as bitches and queen are generally spayed electively as young individuals with little of any chance of
presence of inflammation in the ovarian or periovarian
tissues.
A practical approach to diagnosis of ovarian
remnants
Queens and bitches with ORS may display signs of
proestrus or estrus at regular or irregular intervals. Signs
of heat generally appear within weeks to months following surgery, although occasionally the delay may be longer
(several months to 1-2 years). Estrous signs are often
characterized by the normal sequence of physical changes typical of proestrus and oestrus (male attractiveness
and acceptance, cornified vaginal smear, vulvar swelling
and discharge in the bitch). Breeding can be observed
normally although pregnancy will not occur. Bitches with
an ORS may exhibit signs of false pregnancy several weeks
to a few months following estrous behaviour, or the false
pregnancy may even be the only sign if estrus was silent.
One bitch showing signs of estrus 7 years after ovariohysterectomy was reported to have a granulosa cell tumor on the ovarian remnant (Pluhar et al., 1995). In a
report describing 11 cases in the cat the interval between
surgery and return to estrus was 17 days to 9 years with
an average of 2 years (Wallace, 1991). In one case chronic vaginitis was the presenting complaint for a toy poodle
bitch with an ORS (Perkins and Frazer, 1995). In order to
advance the diagnosis or plan a diagnostic approach es-
40
38
ZBORNIK REFERA
TOV
REFERATOV
trus can be induced in both bitches and queens by oral
administration of cabergoline at the dose of 5 mg/kg daily (1.0 cc of the commercial product per 10 kg of body
weight) for 3-4 weeks, starting in anestrus (Prats, 2001).
Diagnosis of ORS requires confirmation of presence of
residual ovarian tissue through observation of a cornified
vaginal smear in a spayed female. Assaying serum estradiol may not be helpful as estradiol is secreted in a pulsatile manner, thus making confirmation of high serum levels often impossible on just a single serum sample. Vaginal cytology is more useful, although occasionally it may
not be fully consistent with estrus (Wallace, 1991). The
vaginal smear should be collected when the female shows
signs of heat as reported by the owner. A degree of
cornification >50% indicates that an estrogen source
somewhere within the organism is targeting the vaginal
epithelium. If the ovary is ruled out, the only other estrogen source is the adrenal glands. However, adrenals
are not known to be able to secrete estrogens in quantities enough to cause recurrent and cyclic estrous signs.
Ovulation induction is of pivotal importance in the queen
and can be performed in the bitch as well (although less
crucial in this species) using GnRH at 25-50 mg/queen
or 2.2 mcg/kg in the bitch, or hCG at 250-500 IU in the
queen or at 50 IU/kg in the bitch (England, 1997; Prats,
2001). Serum progesterone should be assayed on blood
sample collected 2 weeks after heat/induction of ovulation.
Differential diagnosis of ORS includes all those conditions responsible for vulvar swelling and discharge in the
spayed bitch, or for estrous behaviour and breeding acceptance in the spayed queen, such as: vaginal or uterine
(if only ovariectomy was performed) neoplasia, vaginitis,
uterine stump pyometra, exogenous estrogen therapy,
trauma, coagulopathy. Abdominal ultrasound or radiography are not considered useful techniques in cases of
ORS because of the small size of the ovarian fragment
and the fact that tissue reaction around ovarian pedicle/s
often prevents recognition of an ovarian remnant unless
an exploratory laparotomy is performed. Even on exploratory lapatoromy it may be difficult to recognize a small
piece of pinkish/red tissue among viscera, unless one or
more follicles or corpora lutea are present. For this reason it is very important that surgery is not attempted
unless a fully cornified vaginal smear is present or serum
progesterone has risen to concentrations >2.0 in the
bitch, or >1.5 ng/ml in the queen. A serum progesterone concentration above the threshold is indicative of
presence of luteal tissue which is easily identified (more
easily than follicles) because of its yellowish colour.
both ovarian pedicles or the caudal poles of both kidney
should be thoroughly checked at surgery. If nothing can
be identified upon visual inspection at this time a vast
excision of scar tissue around the ovarian pedicle/s should
be performed and all tissues submitted for histopathology. Remnants of ovarian tissue are almost always found
around the ovarian pedicle/s (Miller, 1995; Johnston et
al., 1996). Therefore it is not necessary to perform a
long and exhaustive search of the entire abdominal cavity, although the broad ligament should always be checked
as accessory ovarian tissue might be present there together with an ovarian remnant. Removal of an ovarian
remnant in diestrus in a bitch may induce pseudoprengnancy.
The only other option would be a life-long treatment with
a progestogen, which is not advisable for its side effects
and because of practical implications (twice yearly injections, costs etc.). A more recent alternative, still not commercially available, would be the use of long acting GnRH
superagonists such as Deslorelin (Romagnoli et al., 2009).
This compound is reported to inhibit the hypothalamicpituitary release of LH and FSH for up to one year in
dogs and cats, therefore preventing estrus in bitches and
queens without causing any of the progestogen or steroid-related side effects. Deslorelin comes in small cylindrical oil-based implants the size of a microchip, which
are to be placed in the subcutaneous space. Animals have
been re-implanted after the first year with prolonged effect and no negative consequences. Preliminary data from
our laboratory indicate that prolonged use of deslorelin
in queens may be a viable option (Romagnoli et al., unpublished observations).
When discussing therapeutic options for a case of ORS
with a client, it is important to highlight the fact that
recurrence of estrus after spaying is a common problem
especially in queens (Miller, 1995) and it is not related to
ability of the surgeon or conditions of the animal: no
correlation was found between occurrence of ORS and
any of the following patterns in the bitch: age of the dog
at spaying, breed, difficulty of surgery (elective vs nonelective) physical conditions of the bitch (normal weight
vs obese) or ability of the veterinary surgeon (newly graduate vs experienced veterinarian) (Wallace, 1991).
How to eliminate an ovarian remnant
Exploratory laparotomy is the treatment of choice. As
ovarian remnants can be present on one or both ovaries,
41
39
ZBORNIK REFERA
TOV
REFERATOV
References
Bloom F – Pathology of the dog and cat. Evanston, IL. American Veterinary Publications, Inc, 1954
DeNardo GA, Becker K, Brown NO, Dobbins S – Ovarian remnant syndrome: revascularization of free-floating ovarian tissue in the feline
abdominal cavity. J Am An Hosp Assoc 37:290-296, 2001
England GCW – Confirmation of ovarian remnant syndrome in the queen using hCG administration. Vet Rec 141:309-310, 1997
Johnston SD, Root MV, Olson PNS – Ovarian and testicular function in the domestic cat: clinical management of spontaneous
reproductive disease. Anim Reprod Sci 42:261-274, 1996
Leroux PH, Venderwalt LA – Ovarian autografts as an alternative to ovariectomy in bitches. J South Afr Vet Assoc 48:117-123, 1977
Pearson H – The complications of ovariohysterectomy in the bitch. J Small An Pract 14:257-266, 1977
Perkins NR, Frazer GS – Ovarian remnant syndrome in a toy poodle: a case report. Theriogenology 44:307-312, 1995
Prats A – Ovarian remnant syndrome in the queen. EVSSAR Newsletter, 4 (1):5-8, 2001
Pluhar GE, Memon MA, Wheaton LG – Granulosa cell tumor in an ovariohysterectomized dog. JAVMA 207:1063-1065, 1995
Shemwell RE, Weed JC – Ovarian remnant syndrome. Obstet Gynaecol 36:299-303, 1970
Stein BS – The genital system. In: Feline Medicine and Surgery. Santa Barbara, American Veterinary publications Inc., 1975
Romagnoli S, Stelletta C, Milani C, Gelli D, Falomo ME, Mollo - Clinical use of deslorelin for the control of reproduction in the bitch.
Reproduction in Domestic Animals, 2009 vol. 44; p. 36-39,
Wallace MS – The ovarian remnant syndrome in the bitch and queen. Vet Clin North Am 21:501-507, 1991
42
40
ZBORNIK REFERA
TOV
REFERATOV
SR^NO POPUŠÂNJE IN ARTERIJSKA TROMBOEMBOLIJA
PRI MA^KAH
Aleksandra Domanjko Petri~
Sr~no popuš~anje in arterijska tromboembolija sta še vedno slabo prepoznavni stanji v klini~ni praksi. Zlasti prvo
se pogosto zamenjuje z drugimi vzroki za dihalne teàve,
kar ima pogosto usodne posledice za ìval. Predstavljeni
bodo znaki ter najpogostejše nepravilne interpretacije v
takih primerih, pravilna diagnostika ter terapija zlasti urgentnih stanj, ki je pri ma~ki nekoliko specifi~na.
Pogosti vzroki sr~nega popuš~anja pri
ma~kah
Najpogostejši vzroki sr~nega popuš~anja pri ma~ki so
razli~ne kardiomiopatije – patološka stanja sr~ne mišice.
Poznamo ve~ vrst kardiomiopatij glede na morfologijo, tj.
hipertrofno, restriktivno, dilatacijsko ter desno-prekatno
aritmogeno.(1) Sam izgled kardiomiopatije se lahko s progresijo bolezni spremeni, zato obstaja tudi razred neklasificiranih kardiomiopatij. Za hipertrofno kardiomiopatijo
vemo, da je genetskega izvora, podobno se sumi za aritmogeno desnostransko kardiomiopatijo. Nekatere sekundarne kardiomiopatije nastanejo kot posledica nekega
drugotnega vzroka, taka je dilatacijska, ki je posledica
pomanjkanja taurina v prehrani.
Od sekundarnih vzrokov za sr~no popuš~anje pri ma~ki
je potrebno omenit nekontroliran hipertiroidizem, relativno pogost pri ma~kah starejših od 10 let. Pri tej bolezni je levi prekat lahko zmerno hipertrofiran, vendar nikoli
tako kot pri hipertrofni kardiomiopatiji. Ob hipertrofiji levega prekata pomislimo tudi na sistemsko hipertenzijo, ki
se lahko pojavi so~asno s hipertiroidizmom ali pa najve~krat kot posledica ledvi~ne bolezni.
Za klinika je predvsem pomembno prepoznat napredovanje bolezni in pravšnji ~as ko je potrebno ukrepanje.
Asimptomatska ma~ka s kardiomiopatijo zahteva druga~en
pristop kot tista v sr~nem popuš~anju.
doc.dr. Aleksandra Domanjko Petri~, dr.vet.med.
Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male ìvali, Gerbi~eva 60,
SI-1000 Ljubljana,
[email protected]
Klini~na predstavitev ma~ke v sr~nem
popuš~anju in diferencialne diagnoze
Klini~na slika ma~k v sr~nem popuš~anju je lahko dokaj
razli~na in zavajajo~a, zato klinika pogosto zavede v razmišljanje od drugih mo`nih diferencialnih diagnozah.
Ma~ka v sr~nem popuš~anju je pogosto tahipnei~na in/ali
dispnei~na. Tahipnei~na je praviloma zaradi napredovalega plju~nega edema, dispnei~na pa zaradi plevralnega izliva. Lahko je prisotna kombinacija obojega. Lahko diha z
odprtim gob~kom in na ta na~in v èlodec nabere veliko
zraka, kar je è zavedlo nekatere, da so pomislili na zasuk
èlodca. Pogost problem pri ma~kah je, da jih interpretiramo kot pse, kar pa je zavajajo~e. Zavede nas lahko tudi,
ker pri vseh ma~kah ne slišimo šuma na srcu ali aritmij.
Nekatere imajo povsem normalni sinusni ritem v okviru
normalnih frekvenc. Kadar pri ma~ki slišimo galopni ritem
ali vsaj rahlo aritmijo je to znamenje, da z njenim srcem
nekaj ni ~isto v redu. (~e pa tega ne slišimo, pa ni nujno
da je s srcem vse v redu!) Plju~ni hropci in odsotnost
šuma lahko koga zavede v razmišljanje o astmati~ni krizi,
vendar so pri astmi praviloma prisotni piski, lastnik pa
pove, da ma~ka ob~asno kašlja. Kašelj ni zna~ilen za ma~ko
v sr~nem popuš~anju kot je to pri psih. Znaki tahipneje/
dispneje se praviloma pojavijo nenadno brez predhodnih
znakov. Pridušeni toni srca in plju~ govorijo v prid plevralnega izliva, prav tako nabrekle jugularne vene. Rentgen in ultrazvok sta klju~ni diagnosti~ni metodi za ugotovitev vzroka, vendar je potrebna posebna previdnost, da
ma~ko v taki stresni situaciji ne spravimo ~ez rob. Butorphanol (0,1 mg/kg IM) omogo~i varnejše ravnanje s tako
stresno ìvaljo.(1) Na rentgenski sliki lahko vidimo plju~ne
infiltrate v primeru popuš~anja srca, ali plevralni izliv. Ma~je
srce pogosto ni tako o~itno pove~ano kot pri psih (saj
hipertrofiran prekat hipertrofira navznoter) in pove~an levi
atrij tako o~itno ne privzdigne sapnika kot pri psih v stranski projekciji, ker je ma~je srce v toraksu nekoliko bolj
leè~e. Kadar nismo prepri~ani o vzroku dihalne stiske
lahko ma~ko v sternalnem poloàju in po potrebi z dodajanjem kisika pogledamo na hitro še z ultrazvokom. V
ve~ini primerov levostranskega popuš~anja srca je levi
atrij zna~ilno pove~an. Natan~nejšo ultrazvo~no preiskavo lahko odloìmo na kasnejši ~as, ko je ma~ka stabilna,
43
41
ZBORNIK REFERA
TOV
REFERATOV
saj natan~na determinacija miokardne bolezni ni nujna za
primarno urgentno zdravljenje.
Doma~a oskrba ma~ke s sr~nim
popuš~anjem
Smiselno je ma~ki izmerit tlak, saj ~e je hipotenzivna naša
nadaljnja diureti~na terapija ne bo delovala. Ostale rutinske laboratorijske preiskave odloìmo na ~as, ko je ma~ka
stabilna. Takrat je predvsem smiselno kontrolirat elektrolite, saj ma~ke ob neješ~nosti hitro postanejo hipokalemi~ne, ter ureo in kreatinin.
Dolgoro~no èlimo vzdrèvat primeren tlak v srcu in
prepre~it ponovitev akutnega sr~nega popuš~anja, ter
tromboembolije, ob tem, da se ma~ka po~uti dobro. Prva
dva cilja doseèmo z aplikacijami furosemida ter zaviralca konvertaze. Furosemid drìmo na najni`jem mo`nem
odmerku, ki še prepre~uje zadrèvanje teko~ine v telesu
(ma~ke so nanj ob~utljivejše), npr. 1-2 mg/kg /12-24 ur
ali vsakih nekaj dni). Nekatere ma~ke po akutni krizi lahko
celo ne potrebujejo ve~ furosemida.
Diferencialno diagnosti~no pomislimo še na travmo prsnega koša (anamneza!), preveliko koli~ino infuzijske teko~ine,
nekardiogeni plju~ni edem ali hude plju~ne infekcije. Plevralni izliv je najpogosteje modificiran transudat ali pravi
hilotoraks v povezavi z obstrukcijo venskega in limfati~nega priliva (1).
Terapija ma~k v sr~nem popuš~anju
Kratkoro~ni cilj terapije ma~ke v sr~nem popuš~anju je
olajšanje hipoksemije, zmanjšanje tlaka v levem preddvoru in izboljšanje hemodimani~ne funkcije. Akutno sr~no
popuš~anje zdravimo ne glede na tip miokardne bolezni.
Kisik, diureza in venodilatacija predstavljajo pravilen pristop k ma~ki v levostranskem sr~nem popuš~anju. Plevralni izliv moramo drenirati, najbolje z metuljasto iglo
»roza barve«. Furosemid apliciramo previdno 1-2 mg/kg/
2 uri, raje pa na ve~je ~asovne razmike (npr. na 6-8 ur),
ob tem pa moramo spremljati diurezo in pitje. Ma~ke v
takem stanju ne pijejo, zato jim dajemo vodo po brizgi,
~e pa s tem povzro~imo prevelik stres pa apliciramo nekaj
teko~ine pod koò ali damo ma~ko na perfuzor na zelo
po~asno I.V. infuzijo elektrolitske raztopine. Ne apliciramo glukoze, ker s tem pove~amo kapilarni tlak in tlak v
levem preddvoru, kar pove~uje plju~ni edem.
Ma~ke v sr~nem popuš~anju in hipotenziji
Nekatere ma~ke razvijejo znake nizkega minutnega volumna skupaj s sr~nim popuš~anjem. Obi~ajno so
hipotermi~ne, bradikardne in mo~no hipotenzivne (sistoli~ni tlak >70 mmHg).(1) V takih primerih so potrebni
pozitivni inotropi, ki jih apliciramo intravensko, (dopamin, dobutamin) v odmerkih za izboljšanje tlaka (1-2 µg/
kg/min titriramo do maks. 5 µg/kg/min za dobutamin). S
tem èlimo izboljšati sistoli~ni tlak na 100 in ve~ mmHg,
normalizirati sr~no frekvenco in telesno temperaturo, zato
ma~ko tudi ogrevamo dokler je potrebno (obi~ajno 12-24
ur). S teko~inami i.v. smo zelo previdni, apliciramo s perfuzorjem ni`je odmerke od vzdrèvalne teko~ine.
V kolikor je potrebna kontrola sr~ne frekvence zaradi izboljšanja diastoli~ne disfunkcije lahko dodamo zaviralce beta,
(zlasti velja za ma~ke z obstrukcijo levega izto~nega trakta), oz. zaviralce kalcija (npr. diltiazem). Zaviralce beta
nikoli ne vpeljemo v ~asu sr~nega popuš~anja, ampak šele
v kompenziranem stanju.
Arterijska tromboembolija
Pri vseh oblikah napredovalih kardiomiopatij lahko pride
do arterijske embolije zaradi visokega tveganja za nastanek strdka, ponavadi v levem preddvoru. Le ta se v
nekem trenutku odlepi in odpotuje v arterijski sistem, kjer
se najve~krat zagozdi v razcepiš~u aorte z obema iliakama. Prizadete ma~ke so v hudi bole~ini, se oglašajo in so
pareti~ne. V~asih je epizoda embolije prvo znamenje, da
ima ma~ka bolezen srca. Klini~ni znaki so bolj nezna~ilni
pri emboliji mezenterialne, cerebralne, koronarne, renalne ali drugih arterij.
Hipotermija je slab prognosti~ni znak. Ma~ke so zaradi
bole~ine tahipnei~ne in takšne je te`ko lo~iti od tistih v
sr~nem popuš~anju (potreben RTG). Najprej poskrbimo
za bole~ino, obi~ajno z opiati, v nadaljevanju lahko damo
fentanilski obli` (1-3 µg/kg/h). Ni idealne terapije, še vedno ni enovitega sklepa o naju~inkovitejšem zdravljenju.
Uporablja se aspirin (5 mg/ma~ko vsake tri dni – nizek
odmerek se je izkazal za enako u~inkovitega z manj stranskih u~inkov kakor visoki odmerek aspirina), nefrakcioniran heparin, ali nizkomolekularni heparin kot preventiva
novemu nastajanju strdkov (ob heparinski terapiji je potrebno preverjati ~ase strjevanja). Warfarin, ki se uporablja v ta namen pri ljudeh je povezan s previsokim tveganjem za krvavitve, ma~ke je tudi te`ko spremljati v ta
namen. V preizkušanju je novo zdravilo clopidogrel, ki pa
pri nas še ni na razpolago (2).
Literatura
1. Luis Fuentes V. Management of Feline Myocardial Disease. In: Bonagura DJ & Twedt DC. Eds. Kirk’s Current Veterinary Therapy XIV.
Saunders 2009;809-15.
2. Tobias AH, Fine DM. Arterial Thromboembolism in Cats. In: Bonagura DJ & Twedt DC. Eds. Kirk’s Current Veterinary Therapy XIV.
Saunders 2009
44
42
ZBORNIK REFERA
TOV
REFERATOV
ZGODNJA STERILIZACIJA IN KASTRACIJA MA^K
Vanja Knez
Uvod
Mednarodno priznane študije
Zadnjih 10 do 15 let sterilizacija in kastracija ma~k nista
ve~ tabu, ampak veljata za osnoven servis ma~k v veterinarski mali praksi. Le-ta po protokolu zajema dehelmintizacijo, cepljenje (core, non-core priporo~ila AAFM, ABCD)
in sterilizacijo oz. kastracijo. Z omenjenim protokolom
podaljšamo ìvljenjsko dobo ma~k in tako ve~inoma
do~akajo normalno pri~akovano starost, ki je od 10 do
15 let. V tem ~asu so tako oskrbovane ma~ke za veterinarje vir stalnega dohodka. V strokovnih krogih pa se
postavlja ve~na dilema, v katerem obdobju je najbolj primerno in najla`je opraviti poseg. Stroka mora biti v tem
soglasna in zagovarjati je potrebno strokovne argumente,
ki jih bom v tem referatu podala.
Ena izmed prvih pomembnejših študij zgodnje sterilizacije in kastracije je iz leta 1993 (3-4). Študija je zajela 96
ma~k (od tega 48 samcev in 48 samic), starih od 6 do 14
tednov. Dokazali so, da zgodnja sterilizacija in kastracija
ne ogroàta ma~jih mladi~ev, ~e se drìmo predpisanega
protokola.
Zgodovina
V Severni Ameriki in Kanadi je zgodnja sterilizacija in kastracija rutinski poseg è dobrih 35 let. (1) Zgodnjo sterilizacijo in kastracijo opravljajo od starosti 6 do 12 tednov
pri teì vsaj 1 kg. Potreba po zgodnji sterilizaciji in kastraciji je izvirala iz dejstva, da so ìvali, posvojene iz zavetiš~ kljub zagotovljenim brezpla~nim posegom, dogovorom in pogodbam imele mladi~e. Ker so zaradi prenatrpanosti zavetiš~ morali prepre~iti nezaèlena rojstva, so
se odlo~ili za zgodnejšo sterilizacijo in kastracijo. Vse
posege so prestavili na ~as pred posvojitvijo.
V Evropi, predvsem v razvitih dràvah, sta bila sterilizacija in kastracija rutinska posega, vendar ~asovno postavljena v obdobje od 6. meseca dalje. V današnjem ~asu pa
nevladne organizacije, ki se ukvarjajo z zaš~ito ìvali v
dràvah EU, pozivajo h kastraciji in sterilizaciji okoli 4.
meseca starosti. Tudi zdruènje The cat group (RSPCA,
FAB, ESFM, AHT, BSAVA, CATS PROTECTION, THE
BLUE CROSS idr.) zagovarja in promovira politiko zgodnje sterilizacije in kastracije. Pomemben je njihov akt: 4
months-policy statement 1. (2)
Predsodki glede posega se porajajo predvsem v ju`nih in
nerazvitih dràvah. Z razvitostjo dràve raste tudi odgovornost ljudi do ìvali.
Vanja Knez, dr. vet. med.
Istega leta je AVMA podprla koncept sterilizacije in kastracije za pse in ma~ke pri starosti 8 do 16 tednov zaradi
preštevil~nosti populacije.
Susan Little v svojem ~lanku Zgodnja sterilizacija in kastracija ma~k poudarja, da koncept zgodnje kastracije in
sterilizacije ni nobena novost. (1) V razvitem svetu se oba
posega izvajata è dobrih 35 let. Kadar govorimo o zgodnji sterilizaciji in kastraciji, govorimo o posegih v starosti
od 8 do 16 tednov.
Opustiti moramo tradicionalno mišljenje, da je primeren
~as za sterilizacijo in kastracijo med 5-im in 7-im mesecem starosti. Mnogo veterinarjev àl še vedno najraje
opravlja posega v tem obdobju, kajti takrat se po~utijo
najbolj varne. V zgodnejšem obdobju jih skrbita predvsem protokol in anestezija.
Ostali zadr`ki, povezani z zgodnjo sterilizacijo in kastracijo,
so zaostajanje v rasti, pretirana debelost, spremembe v
obnašanju in boleznim spodnjih se~il. Iz Englove študije
iz leta 1977 (1) izhaja splošno znani mit, da so zgodnje
kastrirani samci nagnjeni k obstrukciji se~nice in boleznim
spodnjih se~il. Ta zastarela študija je bila polna napak,
vendar se nekateri še vedno sklicujejo nanjo. Novejše
raziskave so pokazale, da bolezni se~il pri kastriranih
ma~kih niso povezane s kastracijo, ampak izhajajo iz drugih faktorjev, kot so stres, dieta ter število ma~kov. (3-4)
Vzroki pretirane debelosti so ponavadi povezani s prehrano, telesno vadbo, pasmo, starostjo in statusom.
Raziskava iz leta 1996 (5) kaè, da je potreba po kalorijah
manjša za sterilizirane/kastrirane ma~ke. Za samce, kastrirane med 7 tedni in 7 meseci, je 28% manj, za sterilizirane samice iste starosti pa 33% manj. Ker je miši~ni
razvoj pri samcih odvisen od androgena, je manjša miši~na
masa posledica le-tega, ne glede na ~as kastracije.
Klinika Tristokosmatih, velika klinika za male ìvali, Kajuhova 5a, SI-1000 Ljubljana
[email protected]
45
43
ZBORNIK REFERA
TOV
REFERATOV
Ena izmed pomembnejših raziskav (6) predpubertetne sterilizacije/kastracije je dokazala, da ne prihaja do telesnih
in vedenjskih razlik (mese~no so preverjali šest vedenjskih lastnosti) med skupino ma~k, pri katerih sta bila posega opravljena zgodaj in skupino ma~k, steriliziranih/
kastriranih pri tradicionalni starosti. Dokazali pa so, da
prihaja do vedenjskih razlik med steriliziranimi/kastriranimi in nesteriliziranimi/nekastriranimi ma~kami. Sterilizirane/kastrirane ma~ke so v odnosu do ~loveka bolj
ljube~e. Tudi do ostalih pripadnikov svoje vrste kaèjo
manj znakov agresije.
V to študijo so bile zajete 3 skupine ma~k: 1. skupina:
ma~ji mladi~i, sterilizirani/kastrirani pri 7-ih tednih starosti; 2. skupina: ma~ji mladi~i, sterilizirani/kastrirani pri
7-ih mesecih starosti in 3. skupina: nesterilizirane/nekastrirane ma~ke. Predmet analize je bil tudi vpliv gonadnih
hormonov na razvoj skeleta. Distalna radialna zrast se
ponavadi zapre po puberteti v starosti od 14 do 20 mesecev. Predvidevali so, da so gonadni hormoni potrebni za
normalen razvoj simfizne zrasti. Pri prvi in drugi skupini
so ugotovili zapoznelo zaprtje distalne radialne zrasti. Na
dolgi rok pa ni bilo nikakršne razlike v dolìni kosti radius
in ulna pri vseh treh skupinah.
Druga študija zaprtja radialne zrasti pa kaè (7-8), da prihaja do razlik v dolìni opazovane kosti med steriliziranimi (ne glede na to ali so bili sterilizirane/kastrirane pri 7
tednih ali 7 mesecih) in nesteriliziranimi ma~kami.
Izsledki ameriške raziskave (9) kaèjo, da sta zgodnja sterilizacija in kastracija popolnoma varna posega glede vpliva na zdravje in vedenje ma~k. Raziskava je zajela 263
ma~k, posvojenih iz zavetiš~, ki so jih spremljali 37 mesecev.
Ciklus ma~ke in razmnoèvanje
Ma~ka je sezonsko poliestri~na ìval, pri kateri se gonitev
lahko za~ne è s štirimi meseci, odvisno od pasme, telesne
teè in vpliva fotoperiode oz. delovanja melatonina, ki ga
izlo~a ~ešarika. Ovulacija nastopi ob parjenju. Brejost
ma~ke traja v povpre~ju od 57 do 63 dni.
Pasemske ma~ke in vzreditelji
Velika ve~ina vzrediteljev prodaja svoje mladi~e, ki niso za
vzrejo, è sterilizirane/kastrirane. Poskusno smo s tem
za~eli v letu 2000. Šlo pa je predvsem za ma~ke, ki so bile
prodane za ljubljen~ke in niso bile namenjene za razplod
zaradi genetskih ali kakšnih drugih napak. Tako pri kongenitalni napaki, kot je npr. popkovna kila, korigiramo
hernijo in isto~asno ma~ko še steriliziramo/kastriramo,
ker take ma~ke ni dovoljeno uporabljati za razplod. Za
sterilizacijo/kastracijo pred prodajo smo se odlo~ili, ker
smo imeli slabe izkušnje s pogodbami in smo edino tako
lahko prepre~ili nadaljnje razmnoèvanje za razplod neprimernih ma~k.
Ma~ke gredo lahko v nov dom pri starosti 12 tednov in
ni~ prej.
Pediatri~ni protokol
Pri zgodnji sterilizaciji/kastraciji je anestezijski protokol
varen in ni potrebno imeti posebne opreme. Kirurški poseg je tehni~no nezahteven. Prednosti in koristi so
obojestranske za ìvali in praktike. Pred posegom samim
moramo pozornost nameniti: hipoglikemiji, hipotermiji,
krvavitvam in infekcijskim boleznim.
1. splošni pregled mladi~a pred posegom
Priporo~eno je da so prej dehelmintizirani in cepljeni. Pri pregledu smo pozorni na razne anomalije
(npr. kriptorhizem, hernije).
2. teà
Ma~ji mladi~ naj ima vsaj 1 kg telesne teè.
3. prepre~evanje hipoglikemije
Da prepre~imo hipoglikemijo, odstranimo hrano le 3 do 4 ure pred posegom in è 1 uro po posegu ma~jemu
mladi~u ponudimo manjši obrok.
4. pred posegom
Mladi~i iz istega legla naj bodo skupaj v mirnem in toplem prostoru, da zmanjšamo stres in razburjenje,
apliciramo i/m anestetik.
5. »koktajl« anestetikov
V literaturi je razli~no število kombinacij za pediatri~ni protokol. KDT (Ketamin-Domitor-Turbogesic) koktajl:
- 4 IE ketamina (100 mg/1ml)
- 2 IE medetomidina (Domitor 1 mg/ml)
- 2 IE butorfanola (Torbugesic 10 mg/ml)
Doza za 1 kg.
Za kastracijo je zadostna i/m aplikacija, za sterilizacijo pa po potrebi še inhalacija izoflurana (tubus 2.0).
6. omoti~ni mladi~i
Mladi~em, ki so še zelo omoti~ni, dodamo 5 % glukozo oralno.
7. prepre~iti hipotermijo
Hipotermijo prepre~imo z grelnimi blazinami, minimalnim britjem in minimalnim polivanjem z alkoholom.
Po operaciji preverimo temperaturo rektalno (normalna TT mladi~a 37,6-38°C). Mladi~e grejemo s toplimi
brisa~ami, termoforji, grelnimi lu~mi. Pri tem pa moramo biti ves ~as pozorni, da jih ne pregrejemo.
8. zbujanje
Zbujamo z Antisedanom.
9. analgetik
Metacam kapljice,1 gtt oralno (0,1-0,05 mg/kg TT ma~ke)
46
44
ZBORNIK REFERA
TOV
REFERATOV
V zadnjem obdobju je bilo izvedenih nekaj študij predvsem zaradi t.i. stranskih u~inkov in predsodkov, ki so se
porajali v povezavi z zgodnjo sterilizacijo in kastracijo.
Veterinarji, ki izvajajo pediatri~ni protokol, izjavljajo, da je
hitrejši in manj stresen za ìval. Ma~ji mladi~i še niso
predebeli, ni krvavitev, po posegu hitro okrevajo in se
hitro zbujajo iz anestezije. Z zgodnjo sterilizacijo/kastracijo
se izognemo posegom pri gone~ih ma~kah, brejih ma~kah
in ma~kah s piometro. Daljnoro~no s posegom prepre~imo
tumorje na seskih in tumorje testisov. Z uravnavanjem
populacije prepre~imo nepotrebne evtanazije ma~k v
zavetiš~ih in zmanjšujemo prenose bolezni v preštevil~ni
populaciji (npr. levkoza in ma~ji aids). Materialni stroški
so pri opravljanju posega zgodaj manjši in tudi minimalna specialisti~na oprema nam olajša delo.
Povzetek
Raziskave so pokazale, da ni ne telesnih ne vedenjskih
negativnih stranskih u~inkov zgodnje sterilizacije in kastracije ma~k.
Stroka priporo~a sterilizacijo/kastracijo ne pri tradicionalnih 6-ih mesecih, ampak pri 4-ih mesecih v izogib prezgodnji brejosti.
Sam zgodnji poseg je s poznavanjem in z upoštevanjem
pediatri~nega protokola za veterinarja enostavnejši in cenejši.
Viri
1. http://catvet.homestead.com/EarlyAlter.html
2. http://www.fabcats.org/cat_group/policy_statements/index.html
3. Faggella, A.M. and M.G. Aronsohn (1993). Anesthetic techniques for neutering 6- to 14-week-old kittens. Journal of the American
Veterinary Medical Association 202(1): 56-62.
4. Aronsohn, M.G. and A.M. Faggella (1993). Surgical techniques for neutering 6- to 14-week-old kittens. Journal of the American
Veterinary Medical Association 202(1): 53-55.
5. Root, M. (1995). Early spay-neuter in the cat: Effect on development of obesity and metabolic rate. Veterinary Clinical Nutrition 2:
132-134. ISSN: 1076-3872.
6. Stubbs, W.P., M.S. Bloomberg, S.L. Scruggs, V.M. Shille, and T.J. Lane (1996). Effects of prepubertal gonadectomy on physical and
behavioral development in cats. Journal of the American Veterinary Medical Association 209(11): 1864-1871.
7. Root, M.V., S.D. Johnston, G.R. Johnston, and P.N. Olson (1996). The effect of prepuberal and postpuberal gonadectomy on penile
extrusion and urethral diameter in the domestic cat. Veterinary Radiology and Ultrasound 37(5): 363-366.
8. Root, M.V., S.D. Johnston, and P.N. Olson (1996). Effect of prepuberal and postpuberal gonadectomy on heat production measured
by indirect calorimetry in male and female domestic cats. American Journal of Veterinary Research 57(3): 371-4.
9. Howe, L.M., M.R. Slater, H.W. Boothe, H.P. Hobson, T.W. Fossum, A.C. Spann, and W.S. Wilkie (2000). Long-term outcome of
gonadectomy performed at an early age or traditional age in cats. Journal of the American Veterinary Medical Association 217(11):
1661-1665.
47
45
ZBORNIK REFERA
TOV
REFERATOV
KIRURŠKO ZDRAVLJENJE ZLOMOV STEGNENICE
PRI MA^KAH
Joè Kogovšek
Izvle~ek
Pri ma~kah so med zlomi skeletnih kosti najpogostejši
zlomi stegnenice. Konzervativno zdravljenje je smiselno
le v primerih, ~e fragmenti niso dislocirani. Frakture z
dislociranimi fragmenti je potrebno zdraviti kirurško z
osteosintezo. Najve~krat se pri tem uporabljajo intramedualarne igle ali zunanji fiksatorji. Kadar po implantaciji igel
pri~akujemo med fragmenti nemir, je potrebno take osteosinteze kombinirati s hemicerklaàmi, zunanjimi fiksatorji, ploš~icami ali cerklaàmi. Za odprte kominutivne
frakture je najprimernejša imobilizacija z zunanjimi fiksatorji.
Abstract
Femoral fractures are the most common fractures of skeleton in cats. Conservative treatment is indicated only if
there is no dislocation of the fragments. Surgical treatment with osteosynthesis is needed for fractures with
dislocated fragments. Intramedullary needles and external fixators are most commonly used for osteosynthesis.
If instability of fracture is expected after needle implantation, osteosynthesis should be combined with hemicerclage, external fixators, lamellas and cerclages.
Najpogostejši vzroki za zlom stegnenice so travme. Med
temi prevladujejo prometne nesre~e, padci iz višine, udarci... Ve~ina lastnikov ma~k ob prihodu v ambulanto pove,
da vzroka ne pozna, da je prišla ìval s potepa po treh
nogah ali pa, da so onemoglo našli nekje ob cesti. Niso
prav redki primeri, da zlom spremljajo še druge poškodbe; zlom medenice, poškodbe v podro~ju trebuha,
prsnega koša...
NEKAJ ANATOMSKIH POSEBNOSTI
STEGNENICE PRI MA^KAH:
Diafizni del femurja je pri ma~kah oblikovan nekoliko ovalno
in je praviloma raven. Med diafiznim in vratnim delom
stegnenice je pribli`no 130 stopinjski kot.
Glavica stegnenice se prehranjuje ve~inoma iz ekstrakapsularnega krvnega pleteà, ki obkroà vrat stegnenice.
Pri mladih ma~kah se znatno oskrbuje tudi preko ìl ligamentum teresa (vrvasta vez). Oskrba preko ìl ligamenta
se pri ma~kah prekine pri starosti nad sedem mesecev.
Kondila stegnenice sta, ~e jih primerjamo s pasjo kostjo,
skoraj povsem v osi diafize. Rastna cona v distalnem
fiznem delu je znotraj sklepne kapsule, kar je pomembno
pri kirurškem zdravljenju distalnih epifizioliz (pri Salter
Harris zlomih).
UVOD
Pri ma~kah so zlomi stegnenice, glede na odstotek zlomov ostalih kosti skeleta, na prvem mestu. Fossumova
ocenjuje, da je takih zlomov ve~ kot 30 %, po naši analizi
pa kar 48 %. Ugotovili smo tudi, da je po pogostnosti
zlomov na drugem mestu tibija s 14 % in na tretjem mandibula s 4 odstotki.
Glede na mesto zloma stegnenice delimo na tiste na
proksimalne delu, diafizne in zlome v distalnem delu.
Najve~ je zlomov v diafiznem delu. Zlomi v bliìni sklepov
so posebnost mladih ìvali, pri katerih rast še ni zaklju~ena.
IMOBILIZACIJA ZLOMOV STEGNENICE
KONZERVATIVNO ZDRAVLJENJE
Konzervativno zdravljenje zlomov femurja je smiselno,
~e je zlom brez dislokacij. Pri odraslih ìvalih so te poškodbe zelo redke. Klasi~na imobilizacija z obvezami, oziroma opornicami za ma~ke praviloma ni primerna. K sre~i
ma~ki bole~e ekstremitete drìjo v fleksiji ob telesu (naravna
imobilizacija), zato pogosto zadoš~a le drànje ìvali v
zaprtem prostoru (kletki).
prof.dr. Joè Kogovšek, dr.vet.med.
SI-1000 Ljubljana
[email protected]
48
46
ZBORNIK REFERA
TOV
REFERATOV
OPERATIVNO ZDRAVLJENJE
Zunanji fiksator
Pri ma~kah zlome femurja z dislociranimi fragmenti
naravnamo v pravilno anatomsko pozicijo le z ustrezno
kirurško tehniko. Za imobilizacijo se uporabljajo implantati, ki zagotavljajo stabilnost in zato tudi hitro zraš~anje.
To pa je tudi dovolj za ~im krajšo rehabilitacijsko dobo.
Za osteosintezo femurja se uporablja ve~inoma eksterni
fiksator tipa I. Primeren je skoraj za vse vrste zlomov.
Skoraj nikoli pa niso primerni za fiksacijo intraartikularnih
kominutivnih fraktur. Le redko se aplicira zunanji fiksator
tipa II. Ta bi bil primeren predvsem za imobilizacijo Salter
Harris fraktur.
Intramedularne igle
Za osteosinteze diafiznega dela femurja pri ma~kah se
pogosto uporabljajo intramedularne igle ali èblji. Najboljši rezultati so s Steinmannovimi iglami. Kirshnerjeve
ìce so primerne za mlade ma~ke oziroma ma~ke manjših pasem. Kuntscherjevi in Rusheve èblji se precej
opuš~ajo. Primeren je tudi Schantzov vijak, ki je sicer
namenjen za imobilizacijo z zunanjim fiksatorjem.
Slaba lastnost osteosintez z iglami so pogostokrat nestabilnosti med fragmenti (rotacija fragmentov).
Premer medularnega kanala je povpre~no od 5 do 6 mm.
Za imobilizacijo se uporabljajo igle, ki izpolnjujejo pribli`no
70 % medularne odprtine ( premer 3,5 do 4,2 mm.). Po
implantaciji igel, ki izpolnjujejo le 30 do 40% medularne
votline, je zaradi pri~akovanega nemira med fragmenti,
potrebna še dodatna imobilizacija. V ta namen lahko
uporabimo enega od naslednjih antirotacijskih materialov: cerklaè, hemicerklaè, zunanje fiksatorje ali nevtralizacijske ploš~ice.
Odli~na rešitev so Steinmannove igle na zaklep. Za imobilizacijo s takim implantatom se uporabljajo igle, ki
zapolnijo medularno votlino do 70 %.
Igle lahko vstavljamo z retrogradno ali z normogradno
tehniko. Priporo~ajo normogradno tehniko, ker se tako
manj verjetno poškoduje ishiati~ni ìvec. Po izkušnjah
Montavona se je med retrogradnim vstavljanjem in zaradi
predolgega intramedularnega implantata poškodoval ta
ìvec kar pri vsakem ~etrtem pacientu. Z normogradno
tehniko, še posebej ~e je implantat tanjši, se pri ma~kah
lahko vstavljajo igle nekoliko lateralno od ishiati~nega ìvca.
Normogradna tehnika je primerna tudi za perkutano
naravnavo zlomljene stegnenice.
Dolìno igel odmerimo na osnovi rentgenskega posnetka. Za srednje velike ma~ke so primerne igle dolìne od 9
do 11 cm. Igla naj bi segala po implantaciji do proksimalnega roba patele, oziroma do višine trohanterja. Najmanj
nevarnosti, da bi implantat poškodoval ìvec, je takrat, ~e
je igla potopljena v fosso trochantearico.
Za suprakondilarne ali epiziolizne frakture je mogo~a
imobilizacija tudi z nameš~anjem igle skozi kolenski sklep
iz med~vršne jame. Boljša je retrogradna tehnika, ker
èlimo hrustan~ni del le odpreti kot pokrov~ek, ki ga po
vstavitvi igle vrnemo v prvotno lego. Sicer se epifiziolize
imobilizira z dvema Kirschnerjevima ìcama – lastovi~ji
rep.
Debelina transosalnih igel ne sme presegati 20 do 25%
premera kosti. Najprimernejše transosalne igle so s pozitivnim (izven nivojskim), notranje pa z negativnim navojem
(v nivoju). Igle vstavljamo nekoliko kavdalno (kavdolateralno) ob vastusu lateralisu. V enem fragmentu naj bosta
vstavljeni vsaj dve igli. Minimalni nemir med fragmenti
doseèmo, ~e so vstavljene tri transosalne igle.
Pogosto se nameš~a zunanje fiksatorje skupaj z intramedularnimi iglami. V takih primerih je lahko dovolj le ena transosalna igla v vsakem od fragmentov. Fossum zagotavlja
dobre rezultate, ~e sta sklenjeni povezovalna palica in intramedularna igla “tie–in povezava”.
CRIF sistem (Clamp – Rod Internal Fixator) nekoliko spominja na eksterni fiksator. Razlika je v tem, da je fiksator
prekrit z mehkimi tkivi in je verjetno metoda prihodnosti.
Zaradi visoke cene je pri~akovati, da se bo metoda ve~
uporabljala za osteosinteze pri psih.
Imobilizacija s ploš~icami
Za imobilizacijo stegneni~nih zlomov se pri ma~kah uporabljajo dinami~ne kompresijske ploš~ice, oziroma nevtralizacijske ploš~ice. Boljše so ploš~ice, ki se na dolo~enih
mestih stikajo s kostjo LCDCP (limited contact – DCP).
VCPs ploš~ice lahko med operacijskim posegom odreèmo
(rezalne) do èlene dolìne. Ker so nekoliko tanjše, jih
zato lahko oja~imo tako, da poloìmo eno na drugo (sendvi~ sistem). Najboljši rezultati so z LCDC ploš~icami za
diafizne transverzalne frakture femurjev.
Zelo dobro anatomsko repozicijo doseèmo z Uni Lock
ploš~ico (mandibularne zaklepne ploš~ice), ki sodijo med
vsestransko prilagodljive implantate. Predvsem so uporabne za zlome v distalnem delu femurja. V proksimalno
in distalno luknjo vstavljamo bikortikalne, v ostale pa
monokortikalne vijake. ê je stabilnost slabša po namestitvi ene ploš~ice, lahko drugo privijemo z druge (medialne) strani.
Med zlome proksimalnega dela sodijo zlomi glavice femurja, epifiziolize, zlomi vratu, avulzije trohanterja in subtrohanterne zlome.
Zlome vratnega dela in glavice femurja lahko po anatomski repoziciji imobiliziramo z vijakom in antirotacijsko iglo.
Pri mladih ìvalih je mogo~a osteosinteza le z dvema Kirschnerjevima iglama. Biomehaniki so dokazali, da se dosega stabilnejšo osteosintezo, ~e sta igli postavljeni paralelno. Igle se lahko vstavlja retrogradno ali antegradno. Ret-
49
47
ZBORNIK REFERA
TOV
REFERATOV
rogradno je enostavnejše za nameš~anje, vendar z antegradnim principom povzro~imo manj poškodb na mehkih tkivih. Še manj poškodb na mehkih tkivih pa povzro~imo po ventralnem pristopu.
Trohanterne frakture so za kirurga manj zahtevne. Dobre
rezultate se doseè s tehniko „zuggurtung“.
Subtrohanterni zlomi so pri ma~kah redki. Navadno so
sestavni del kominutivnih zlomov diafiznega dela. Za osteosintezo se uporabljajo zunanji fiksatorji, ploš~ice ali
tudi igle. V nekaterih primerih je potrebna kombinacija
dveh (n.pr. igla in eksterni fiksator).
Kominutivne frakture vratu ali glavice pogosto ne omogo~ajo tako solidne naravnave in fiksacije, da bi lahko
pri~akovali dobro pooperativno funkcijo prizadete noge.
V takih primerih se je potrebno odlo~iti za osteotomijo
preostalega dela glavice.
LITERATURA
1. P.M. Montavon, K. Voss, S.J. Langley–Hobbs. Feline Orthopedic Surgery and Musculoskeletal Disease.Philadelphia: Saunders, 2009.
2. Fossum TW. Chirurgie der Kleintiere. Urban & Fischer, 2007.
3. Auer J. Veterinary specialty news. The VetFix System (Clamp-Rod Internal Fixator) AO – Development News – Number 1,
2004: 2 – 4.
4. Keller M, Voss K. UniLock: Application in small animals. Locking bone plate/screw systems were developed for use in human
maxillofacial surgery. The authors describe applications of the UniLock system in small animal surgery. AO Dialogue, 15,
2002. 20 - 21.
5. Brinker WO, Piermattei DL, Flo GL. Small animal orthopedics and fracture repair. Philadelphia: WB Saunders, 1997.
50
48
ZBORNIK REFERA
TOV
REFERATOV
Fungal diseases of the skin in cats
Patrick Bourdeau
Fungi form a group of very original pathogens more or less adapted to develop in the living tissues. Amongst domestic
mammals the cat is probably the most frequently concerned by mycoses, and skin infection the most common.
Dermatophytes are the first cause of dermatomycose but a variety of other fungi can be encountered in Europe.
I Dermatophytoses
Dermatomycoses, generally superficial, due to keratinophilic fungi: Microporum and Trichophyton (+ in humans
Epidermophyton).
Synonym: ringworm.
The most important species of dermatophytes in cats is by far Microsporum canis. The second species, probably
misdiagnosed isTrichophyton mentagrophytes. Cats can be infected by other species of dermatophytes (See table I).
Table I: Most important species of dermatophytes infecting cats
Main host, source
Others species
M. canis
Cat, dog
Rabbit, horse, rodents …
M. persicolor
Rodents microtinae (voles)
Dog, cat ..
M. gypseum
Soil
Dog, horse…
T. mentagrophytes
Rodents
All species (Dog, cat…)
Human contamination
+++++
++
+
+++
Morphology of dermatophytes in lesions
-
Septate hyphae (2- 6 µm. diam.) in stratum corneum, more visible in hairshafts (in bundles).
-
Arthrospores. ± spherical (2 à 8 µm according species). (hair follicle, surface of skin…)
-
Development in hairshaft
Ectothrix (= endo-ectothrix). Hairshafts surrounded by small spores (2 µm) « mosaic » = microsporic :
(i.e : M. canis)
short chains = microïd (i .e : T. mentagrophytes)
(Microsporum persicolor do not infect hairshaft.
Clinical aspects
a) Classical annular ringworm
- The most frequent with Microsporum canis.
Prof. Patrick Bourdeau,
- Frequent in young animals, incubation 1 - 4 weeks
(2 months ?)
DVM, Dipl. ECVD, EVCP
Dermatology /Parasitology / Mycology
- Non pruritic (general situation).
Oniris: Ecole Nationale Vétérinaire de Nantes, France
- Annular alopecia (0.5 to 5 cm in diam.) spontane
[email protected]
51
49
ZBORNIK REFERA
TOV
REFERATOV
ous regrowth of hairs in the center of lesions (individ
ual spontaneously heal). Skin non reactive, thin scal
ing.
Diagnosis
- A variant in hunting or foraging animals due to
T.mentagrophytes (Microsporum persicolor or Mi
crosporum gypseum.) : Localized, slowly extensive,
generally facial and scaly lesion. May become multifo
cal and generalized.
1) History : frequent in young cats ( less than 1 year of
age) ; persians and other longhaired breeds ; colonies
(catteries) ; season (T. mentagrophytes : autumn-Winter)
; contagion : other cats, dogs, humans
b) Kerions
- Quite unfrequent in cats as compared to dogs, mainly
due T. mentagrophytes (M. canis …)
- Surelevated, rounded, inflammatory suppurative (fol
liculitis) plaques. Unique or multiple, mainly on face.
c) Diffuse alopecic dermatophytosis
Quite frequent in cats. Moderate erythema, diffuse
alopecia ± scales and crusts. Localized or extensive.
d) Feline miliary dermatitis
Pruritic
Diffuse alopecia, moderate erythema and scaling ; mul
tiple little papules and crusts.
e) Onychia and paronychia
- Rare. Mainly T. mentagrophytes or M. canis. Fragil
ity of claws, (several digits and legs)
f) Combined dermatophytoses
- Much less frequent than in dogs
- Extensive, scaly and erythematous many combina
tions of species.
g) Mycetomas
- Underdiagnosed. Mainly in persian cats. Sometimes
called « pseudomycetoma ». Deep infection (dermis
with dermatophytes that forms « grains » in a suppu
rative reaction (plaques, fistulae). Lesions quite fre
quently located on the dorsum. See below
Successsive steps are necessary to observe, isolate then
identify causal agent.
2) Wood’s light : Fluorescence from living spores of dermatophytes in anagen hairs : only Microsporum canis
(most of strains) : Modified by topical therapy. Positive
wood’s light is confirmed by microscopic examination.
2) Microscopic examination
Skin scrapings and hairshafts examined in lactophenol,
(lactic blue, KOH).
Typical aspect of parasitised hairshafts. (M persicolor do
not develops in hairshaft).
3) Optionnal : orientation test : Dermatophyte test
medium.DTM
- The growth of dermatophytes is suggested if rapid
change of color of the agar (turn to red). 7 to 14 days.
Many limits (sensitivity – specificity). False positive and
negative.
- must be confirmed by identification under microscope.
5) Fungal culture
Sample : (Mc Kenzie toothbrush method, Mariat carpet
method). Inoculation of Sabouraud medium. Condition
for development may vary with dermatophytes. Incubation 27°C.
Growth can be modified when previous antifungal treatment have been applied.
Identification depends on the technicity of the lab : in
general 3 wks (to less than 6 days).
Precise identification will help to understand epidemiology of each case, and conception for control.
6) Histopathology : Not an indication except :
Histopathological findings
- PAS stain allows a better visualisation of fungal elements (hyphae)
1) Moderate inflammation: only filaments in stratum corneum + arthrospores + invasion of infundibulum and
hairshafts.
2) Inflammatory. : Papulovesicular. Intraepidermal vesicles, spongiosis, crusts, dermal infiltrate (neutrophils,
lymphocytes, eosinophils). (Possible Confusion with autoimmune skin disease).
5) Mycetomas : granulomatous inflammation surroundig
filamaents and vesicles grouped in « grains ».
a) If interesting for differential diagnosis (histopatholgy
useful for other suspected dermatoses)
b) In case of mycetoma.
Control
- Once the diagnosis is made the infected animal(s) has
to be isolated in a place easy to clean and disinfect.
- Other animalsl shoud be separated and a fungal culture
performed (Carpet or Toothbrush). If contaminated they
will be treated.
Topical treatment
Long haired cats should be clipped before and during the
treatment (only 10% of cure in Persians if not clipped..)
Topical antifongal agents applied once or twice a week :
52
50
ZBORNIK REFERA
TOV
REFERATOV
Enilconazole rinse – antifungal containing shampoos (miconazole).
Evolution/follow up
Total duration of antifungal therapy 6 weeks (2 weeks
after « clinical » cure). Even in case of apparent cure 25
to 30% remain carriers or infected and relapse may occur.
Systemic treatment
- Griseofulvin : dosage frequently too low in labelled products. At least 25 mg/kg bid (oral) is necessary. Contraindicated in pregnant females and immunosuppressed cats.
- Ketoconazole : 5-10mg/kg (oral) daily. Control liver parameters.
Environmental disinfection
- It is important to clean the environment of infected cats
(vacuuming, washing at high temperature…)
- Itraconazole : 5 mg/kg/day. Treat very other week 3
times (total of 6 weeks). Well tolerated in general.
- Enilconazole in spray (Clinafarm may help to treat potentially infected surfaces. Some authors propose the use
of fumigation although no demonstration support the
efficacy of such protocol).
II Malassezia
- The importance of Malassezia yeasts has been initially demonstrated in human (Malassezia furfur) then in cdog
(Pityrosporyum canis). In cats the knowledge is much more recent and limited.
- A group or yeasts (13 species described) lipophilic, morphologically similar.
Amongst these species only one species : M. pachydermatis, the most common species in dogs and cats, do not need
lipids to grow in culture. All other species are said lipodependant.
Malassezia furfur is mainly anthopophilic (75-78 % of healthy people, 46 % of normal fungal flora of hairs). Occasionally isolated from animals (pig, sheep, elephant…). Agent of pityriasis versicolor in humans.
- Malassezia pachydermatis
Zoophilic. Isolated in numerous species of mammals and birds : Ear canals, skin, mucosae (perianal, oral…). Accidental transient contamination have been described: M. furfur in animals, M. pachydermatis in humans : hands, ears,
eye. (+ vaginal, urines, fungemias)
Characteristics of major species of Malassezia (adapted from de Hoog)
Malassezia
Buds
growth
CremophorEL
SGA
40°C
growth
Esculin
Catalase
Tween 80 Tween 40 Tween 20
pachydermatis
Wide
+
+
-
+
+
-
V
v
furfur
Wide
-
+
+
+
+
+
+
V
sloffiae
Wide
-
+
-
+,V
+
+
+
-
sympodialis
Wide
-
+
-,V
+
+
+
+
+
obtusa
Wide
-
-
-
-
-
-
-
+
globosa
Narrow
-
-
-
-
-
-
-
+
restricta
Narrow
-
-
-
-
-
-
-
-
- Rapid growth in culture (1 mm at D1–D2) .
- Elongated yeasts (cylindrical to globose) (2 - 7 µm in size ).
- Budding (blastoconidia) wide or narrow with cicatricial marks. Thin capsule.
- Typical shape « foot-print… »
- Lipophilic ( olive oil 1% - medium or Dixon)
- Optimal growth 35 -37°C ; in practice rapid growth at 27-32°C,
- Not inhibited by cycloheximide .
53
51
ZBORNIK REFERA
TOV
REFERATOV
Malassezia dermatitis is a superficial infection (skin and
mucocutaneous junctions) due to the proliferation of several species of Malassezia
III Crytococcosis
(terminology : malasseziosis is not recommanded )
A systemic mycosis due to Cryptococcus neoformans
A breed predisposition has been shown in dogs (Basset
hound, Teckel, West Highland White Terrier, Shar Pei),
but nor really in cats.
Proliferation favourized by many conditions: hypersensitivities, endocrinathies, immunodeficiencies.
It is mostly observed in cats (other species : dog, cattle,
horses...exceptionnal in birds).
- An important disease in immunocompromised humans
(transplant, neoplasia, AIDS).
The agent is very common and has a Worldwide distribution.
Cryptococcosis is likely underdiagnosed.
Malassezia otitis
- Erythemato-ceruminous, generally bilateral.
- Pruritus (positive auditopedal reflex) abundant (± liquid), brownish cerumen.
Malassezia dermatitis
- Rapid growth in culture (opt. 32 °C). Inhibited by Actidione.
- Spherical yeast 4-6 µm. (2-25 µm in lesions); Unipolar
to multiple budding ; Thick Capsule (visible in indian ink)
- Erythema, diffuse alopecia, greasiness of skin, scaling
variable.
- Other species of Cryptococcus do not grow at 37°C.
(non pathogenic) : C. albidus, C. laurenti, C. terreus, C.
uniguttulatus.…
- Typically on ventral part of neck (±oval), chin, skin folds
and periorificial areas.
- A major source is dejections of birds (digestive tract),
fruits, milk…
- Generalized seborrhoea.
Malassezia pododermatitis : ± paronychia (brownish
deposit at the base of claws).
Diagnosis
Observation of numerous Malassezia in skin smears or
acetate tape tests: Look for Malassezia on a least 5
microscopic fields (X 400 or 1000).
Interpretation: carriage is normal ;
- Huge number in otitis or high number in dermatitis
- MOG (= Malassezia OverGrowth = microcolonies associated to corneocytes) in stained smears, associated
with suspicion for hypersensitivity.
Fungal culture (both lipid-rich and non lipid-rich medium
in case of suspicion)
Many possible methods for sampling.
Histopathology : Malassezia can be eliminated from
biopsies at the beginning of the process for fixation.
Non specific perivascular pattern associated, to occasional
spongiosis. Lymphohistiocytic infiltrate.The presence of
Malassezia within infundibulum could be a criteria for
pathogenicity.
Contamination is mainly by inhalation, (possible inoculation in cat). Dissemination via blood and lymph and tropism for CNS. Not contagious
- Defects of cellular immunity facilitate the development.
(FeLV), corticotherapy). FIV+ cats have an increased carriage, more severe clinical signs and respond less to treatment.
Clinical signs
- Many subclinical infections
- In general a chronic disease. Several forms may coexist
on the same individual
Rhinosinusal form
The most common. Chronic nasal discharge, respiratory
distress, proliferations at nares openings, ulcers of the
nose. Pseudotumoral mass on the nose occasionally fistulized. Enlarged lymph nodes. May extend to eyes (chorioretinitis) or CNS (meningitis).
Respiratory : Rare in carnivores . Dyspnoea and cough.
Neurologic
Ocular Photophobia, uveitis ( uni or bilateral)
Skin lesions
Very frequent ( > 50% of cases), mainly located on the
face and extremities
Secondary to dissemination, possibly primitive ( inoculation)
54
52
ZBORNIK REFERA
TOV
REFERATOV
Papules, nodules (2 cm), plaques, ulcers reddish and
purulent. In general multiples.
Disseminated forms
Lesions
Little inflammatory reaction. Viscous aspect due to the
very abundant yeasts in lesions (capsule material that
inhibits phagocytosis).
Diagnosis
- Yeasts in general very abundant in lesions ; observed
from direct smears (diluted indian ink, Diff quick): shape,
thick capsule.
- Fungal culture (Growth at 37°C + inhibited by cycloheximide)
- Diagnosis :
Direct examination of pus (filaments ± irregular ± vesicles) difficult to observe. Possible stains of smears.
Histopathology: epithelioid or purulent reaction with irregular fragmented hyphae. Variable aspect. Fungi are
pigmented or not in lesions.
Definitive diagnosis only by fungal culture (specialized
Lab.)(multiple culture, on different medias may be necessary). Interest of immunochemistry controversial (specificity ?).
Treatment :
Surgical excision can be curative ?
Variable efficacy of antifungals (no rule). Modern azoles
(Ketoconazole, Itraconazole) or (and) Amphotericin B (IV
slowly ex 0,2 mg/kg alternate day).
- Histopathology : Suggestive but not diagnostic. Abundant yeasts, surrounded by an empty halo (capsule). Capsule can be stained by alcian blue.
Prognosis guarded to poor (unresponsiveness to antifungals or relapses not rare).
- Serology :
V Mycetoma
Very useful by detection of circulating capsular antigens
(agglutination). Positive at titers > 8 (frequently 16000).
Occasionally false negative. Response to therapy is associated to decrease at least by 2 or 4 of the titer.
- Fungal mycetomas = Eumycetomas
IV Phaeohyphomycosis
- Subcutanous mycoses. Generally necrotic and ulcerative with cavities containing pus. Pus contains grains =
microcolonies of hyphae.
- Grains may be dark (black fungi) or light (Acremonium,
Pseudallescheria…dermatophytes).
- Mycoses due to Brown fungi (Dematiaceous), generally
subcutaneous, secondarily ulcerative.
- To differenciate from actinomycotic mycetomas.
- Unfrequent but certainly underdiagnosed. (Confusions
with abcesses, neoplasms..).
- At least 15 fungi involved in humans. In animals mainly: Curvularia (C. geniculata), Drechslera, Pseudallescheria, Altenaria…
- Frequent in tropical areas. In veterinary medicine mainly on cats (dogs, equine, birds, amphibians…) .
Most of agents are saprophytic on plants and opportunistics: At least 60 species involved. These fungi contain
melanin and are pigmented ; olivaceous to dark brown in
culture. Identification difficult : Nomenclature changing
(many names in papers are obsolete): i.e. Drechslera
(Bipolaris) spicifera, Alternaria, Exophiala jeanselmi, Phialemonium sp. Phialophora verrucosa, Scoleobasidium
humicola, Pseudomicrodochium suttonii.
- Sporadic
- In general infection by traumatic inoculation rarely inhalation (human).
- Contamination probably by inoculation.
- Worldwide or localized distribution according to species. Most of these fungi are saprophytic on plants.
Clinical presentation :
- Cats the most frequently species concerned
- Dermatophytic mycetomas (improperly called: pseudomycetomas). Essentially Microsporum canis in persian
cats.
- Lesions mainly on extremities, face, dorsum.
- Plaques or nodule(s) with pus that contains visible grains
(0,1 to 3 mm).
- Favourized by intercurrent diseases or immunosuppressive therapies.
Diagnosis : Direct observation of grains in lactic blue or
KOH 10%. Differenciate from actinomycetes.
- May occur years after infection. Chronic evolution.
Histopathology = may also differenciate the 2 types of
mycetomas.
- Unique or multiple lesions : nodules, plaques, occasionally ulcers
Fungal culture necessary for definitive diagnosis.
- Other localisations (± associated) (joints, bones, ocular, CNS). Pure neurologic forms may exist.
Treatment : Difficult ; careful surgical excision + long
and massive antifungal therapy (azoles, amphotericin B).
55
53
ZBORNIK REFERA
TOV
REFERATOV
IV Hyalohyphomycosis
Complication : dissemination, rarely respiratory .
- Subcutaneous mycoses due to colourless ( non melanized) fungi.
Diagnosis
- Many species of opportunistic fungi involved.
- Pyogranulomatous lesions on inoculation sites.
- Frequent diffuse panniculitis and extension.
Diagnosis :
Direct observation of hyphae in the pus (possible staining)
Careful samping and culture in a specialized laboratory.
Histopathology (not very specific)
Prognosis poor.
Treatment include surgical excision and drainage, systemic antifungals, correction of intercurrent diseases.
Yeasts abundant in pus (if present). In most animal species (except cat ?) fungi are rarely seen in biopsies. Special stains ( silver) mandatory.
Culture.
Immunology (immunofluorescence, immunodiffusion)
possible in humans.
Treatment
Modern systemic antifungals.
Classical with NaI (solution 20% IV : 20g ou 40 mg/kg 25 days) then orally.
Problem of tolerance.
Risk of transmission to humans ; bite or even licking
from cats.
V Sporotrichosis
Infection due to the dimorphic fungus Sporothrix
schenckii. (Previously Sporotrichum schenckii).
Worldwide mainly tropics
VI Histoplamosis
Mycosis due to systemic infection by the dimorphic Histoplasma capsulatum. « Darling disease ».
Cat but also pig, rodents/rabbits, birds ( parrots), horse,
dog and mainly Human being.
Wide distribution in warm and temperate countries. North
America, South and central America (sporadic) Africa an
Asia. In Europe : Italy, Rumania, Denmark.
Pathogenic form = yeast
Many species are concerned : Human, dog and cat …
(37°C in blood agar + thiamin) non inhibited by cycloheximide.
- Pathogenic form (generally intracellular)
Globose to elongated (« cigar » like) yeasts (3-6 µm).
Histopathology : typical when surrounded by star shape
Splendore-Hoeppli reaction (= asteroid bodies)
Filamentous form ( environment on soil and plants)
Culture 25°C. on usual medias 7 - 20 days. Mycelium
very thin (1-2 µm), sympodial ovoid to trinagular conidias.,
Slow development in culture at 37°C. (3-4 wks on blood
agar +CO2). Very small yeasts (2-3 X 3 -4 µm) thickwalled, lemon shape, terminal budding on narrow basis.
- Filamentous form produced in environnement (humid
and rich in organic debris) like birds nests (caves of bats…)
or culture in usual media inf 30°C. Thin filaments with
echinulated microconidias (2-6µm) and globose conidias
with tubercles (6 - 25µm)
Infection :
Sporadic disease, mainly rural. Telluric origin
Inoculation (rarely ingestion). Incubation variable 2-3
weeks.
- Inhalation of conidias.( ingestion ( ?) pure digestive forms
in dogs).
- Conidias transform to yeast in lungs then are phagocytised and disseminate (lymphatic , blood).
Cutaneo-lymphatic form
Favourized by any immunodeficiency inclusion iatrogenic.
Mainly on extremities, face (indurated plaques, nodules)
frequent ulceration with brownish pus ?
In cats also nummular crusts.
Lesions may spontaneously heal whereas other appear.
Lymphatic vessels and lymph node reaction
Many latent forms; Respiratory forms ; Digestive forms
(diarrhoea bloody or liquid) occasional vomiting.
Cutaneous forms (occasional): Nodules, plaques, fistulae; oral ulcers,
56
54
ZBORNIK REFERA
TOV
REFERATOV
Others: ocular, neurologic, joints
Lymph nodes en,largement.
Anemia with neutrophilia and monocytosis.
Hyerbilirubinemia, increase of alkaline phosphatases and
ALT.
Diagnosis
Difficult
Radiography (thorax, abdomen : enlargement of liver and
spleen)
Observation of yeasts from stained smears (special stain)
of pus (broncho alveolar liquid, punctions…) very small,
intracellular.
Histopathology
(APS, Gomori-Grocott) very small intracytoplasmic yeasts
( possible confusion with Leishmania)
IDST histoplasmin : little interest in companion animals.
Serology (immunodiffusion, IDGA, agglutination...) in
humans. Some cross reactions remain with Blastomycosis, Coccidioidomycosis).
57
55
ZBORNIK REFERA
TOV
REFERATOV
Skin conditions in cats: parasitic or not?
Patrick Bourdeau
Dermatologic conditions in cats are particularly difficult
to diagnose. In this species the clinical presentation is
frequently common to very different disease conducing
to “syndromes”.
Amongst these syndromes
Alopecia, Pruritus and scales, Nodules and plaques are
the most common
I Alopecia and parasites
In cats alopecia appears usually in large, sometimes confluent patches.
It can be self inflicted or due to abnormally easy epilation
or shedding.
The underlying cause is often difficult to precise.
Ia Self inflicted alopecia
Fleas
Fleas are a common cause for alopecia in sensitized cats.
The parasitism due to fleas is extremely common and, in
France, there is little seasonal variation during the year. It
means that the monthly percentage of infested cats is
more or less stable (± 30% on dermatological cases) due
to infestations from indoor environment.
Clinical presentation:
Licking occurs mainly on the lateral parts of the body
symmetrically to the dorsal line. In general a certain degree of pruritus is also present and lesion extend on the
body surface. The lesions can be complicated by excoriations crusts and papules.
Diagnosis:
Fleas can be easily observed in light coloured animals or
collected with a flea comb. Flea faeces are also easy to
see and sometimes larvae are observed by owners in the
bedding.
Control
Flea control in cats is not easy although mainly active
products are available. One of the main key points is the
action on fleas present in the environment of animals and
the prevention of contamination of this environment (indoors and outdoors). This is of importance in cat that
goes outside.
Most commonly used insecticides are fipronil and imidacloprid as spot on. Nitempyram is also very efficient but
short acting. Once fleas have been seen the treatment
has to be done for months in order to control the already
present generation of fleas from the environment. Arthropod growth regulators have been developed for cat:
lufenuron is given once a month and control the development of flea larvae that ingest the AGR in their food (adult
flea faeces) this prevent the development of cocoon and
further generation of fleas. Pyriproxyfen can be used as a
spot on and blocks the larval stages and even the egg
laying, with a very long residual effect.
S methopren is combined to fipronil to extend the action
of the insecticide.
To be effective the flea control has to be maintained on a
long period (several and AGR combined to insecticides
to break the life cycle.
Other causes of self inflicted alopecia (non
parasitic)
Food allergy
Probably the second major allergic condition in cats associated to alopecia (not detailed here).
Prof. Patrick Bourdeau, DVM, Dipl. ECVD, EVCP
Dermatology /Parasitology / Mycology
Oniris: Ecole Nationale Vétérinaire de Nantes, France
[email protected]
Comments on Psychogenic alopecia
This disease is diagnosed when all allergic/parasitic causes
have been excluded and if the cat has some behavioural troubles.
58
56
ZBORNIK REFERA
TOV
REFERATOV
Stereotypies are obsessive-compulsive disorders (OCD). They
derive from modified behaviours ex sudden running or jumping, circling (tail chasing), head shaking, etc. Behaviours derived from grooming include self-licking and hair chewing/
pulling in the cat.
This may result of an underlying abnormality (i.e: physical
trauma of the CNS, epilepsy) or an abnormal behaviour, in
reaction to a conflict due to inappropriate environment or
management. If the conflict persists the behaviour might become repetitive and develop into a stereotypy to any unfavourable situation. Endorphins (opioid peptides) might be important in the onset of the behaviour and, dopamine involved
with the maintenance of the behaviour. As the dopamine turnover is increased, stereotypies can be induced by drugs that
activate the dopamine system, such as amphetamine and apomorphine. Also a serotonin subsystem in cats could selectively activated by chewing or grooming.
Clinical presentation:
Siamese, Burmese, Himalayan and Abyssinian cats could be
predisposed. The lesions are the result of chewing, licking and
hair pulling
Alopecia: middle of the back, perineal, genital areas, medial
thighs, ventral abdomen, front legs, shoulder and feet.
Initially the skin surface is normal until traumatized by the
tongue (development of a plaque).
Diagnosis:
Trichoscopy shows broken hair and licking restriction by the
application of an Elizabethan collar is temporarily curative. All
other pruritic causes of self-licking (allergies, parasites) have
to be ruled out.
Control
Behavioural Identification and removal of the stress cause is
the ideal therapy.
Drugs like: amitriptyline (5 mg PO BID), diazepam (1-2 mg PO
BID or SID); Opiate-receptor blockers for short-term stereotypies: naloxone (1 mg/kg SC once) (naltrexone, nalmefene,
diprenorphine) or dopamine antagonist haloperidol (1 mg/kg
PO SID initially, then taper), for a longer period (> 1 year).
Drugs that - inhibit the serotonin re-uptake: fluoxetine (1
mg/kg SID), clomipramine (1,25 – 2,5 mg PO SID), imipramine.
Sedatives and tranquilizers are generally ineffective.
- Observed in groups or catteries or rescue facilities but
also many individuals without any apparent contamination. Contagious?- Not necessarily underlying disease but
often FIV positive, diabetes, renal disease, neoplasia, Iatrogenic due to steroids, - Age variable: often aged catsInfection combined to Demodex cati not rare - Biology of
this form: unknown. Superficial?
Clinical presentation:Pruritus often present, occasionally absentAlopecia, erythema, scaly and crusty dermatitis
on the face, neck and ears. In some cases rather on ventrum and limbs; rarely generalized or otoacariosis like
with Demodex cati. DiagnosisSkin scrapings: on a large
surface (eventually apply mineral oil on skin). Examine
other cats of the household. Variable abundance: In some
cases More than half of the D. gatoi population sampled
is made of ova, indicating rapid population growthTrichoscopy, Histopathology Microscopic observation
Adults of Demodex cati are quite long 180 to 220 microm. and Demodex gatoi is only 110 – 140 microm
.Mixed infection with D. cati not uncommonControl
Treatment of demodicosis in cats is not as well established as it is in dogs. The most regularly active drug on
D. gatoi should be Lime Sulfur dips (6 times at 5 to 7
days interval)Macrocyclic lactones: Very controversial.
Ivermectin orally. Start with 200 ug/kg daily for one week,
if no side-effects increase dose to 0,4 mg/kg? Or 0.3 mg/
kg for months Lower or stop treatment if showing neurological signs of in coordination or lethargy. Milbemycin 1 mg/kg orally e” 2 months or higher dosages ( problems of tolerance)Amitraz (0,02% once/twice a week): ±
tolerated by cats (concentration of active ingredients?)
contraindicated in diabetic catsTreatment of environment
sometimes mentioned (never done).
Other causes for alopecia in cats
Immune-mediated
Sebaceous adenitis, mural lymphocytic folliculitis, alopecia areata
Associated with trauma/injections/topical treatments:
Ib Alopecia with broken hairs
Injection site cicatricial alopecia, topical steroid treatment,
post-traumatic alopecia (fracture of pelvis, sacrum)
Endocrine/Metabolic
Broken hair due to infection or parasites; Dermatophytosis (see other lecture), Demodicosis
Diabetes, Cushings, iatrogenic/spontaneous – (± skin
hyperfragility syndrome)
Neoplastic
Demodex
Paraneoplastic alopecia, epitheliotropic lymphoma.
Two forms of Demodex have been described in cats and
received different names. Demodex cati (the “regular”Demodex) and short demodex: D. gatoi.
Demodex gatoi
- Almost no publication is available. Mainly described and
observed in North America (sunny, hot humid) In Europe
very rare
59
57
ZBORNIK REFERA
TOV
REFERATOV
II Pruritus
If pruritus is observed in cats it is necessary to initially
evaluate a parasitic disease (not all detailed here)
Parasites causing pruritus in cats
Mites
Mange : Notoedres cati
Eosinophilic plaque :
Well defined, surelevated, rounded to oval lesions.
Erythematous and highly pruritic. Sometimes ulcerated.
Mainly located on ventral abdomen and thighs. Occasionally in other places.
May occur on every cat: classically associated to Flea
allergy, atopy or food allergy.
Can be combined to Feline miliary dermatitis.
Ear mite : Otodectes cynotis
As licking is important secondary bacterial dermatitis is
common.
Fur mite : Cheyletiella blakei, Lynxacarus radovskyi
Histopathology :
Chiggers : Trombicula autumnalis
Eosinophilic dermatitis with hyperplasia, mastocytes abundant and epidermis frequently ulcerated.
Insects
Fleas
Cat flea : Ctenocephalides felis
Feline miliary dermatitis
Rabbit flea : Spilopsyllus cuniculi
Small yellowish crusts and papules with diffuse distribution. Prurit present, generally moderate. Dorsum, neck,
generalized.
…
Lice
Felicola subrostrata
Diptera
Mosquitoes :
Non-parasitic causes of primary pruritic skin disease in
cats are mainly related to allergies (Food intolerance allergy), infections (superficial pyodermas), neurologic defects (i.e: cervical pruritus) or even neoplasia.
Most often the clinical presentation and skin lesions accompanying these diseases are not specific and include
syndrome like: Feline miliary dermatitis, eosinophilic granuloma complex, and indolent ulcer.
Histopathology similar to eosinophilic plaque bust less
severe. FMD could be a relatively initial step before other
clinical manifestations. Observed with allergies, ectoparasites, bacterias, dermatophytes, drug reactions, pemphigus foliaceus….
Indolent ulcer
A necrotic, ulcer, generally localized to the upper lip (uni
–bilateral). Not painful. Has been associated to allergies
or infections
Histopathology variable: frequent neutrophilic infiltrate,
fibrosis, occasional “eosinophilic mush”.
Occasionally could evoluate in epidermoïd carcinoma? (Or
rather carcinoma from the beginning).
Mosquito bite hypersensitivity.
Eosinophilc granuloma, linear granuloma
Eosinophilic granuloma is composed of surelevated well
delimited lesion (papules, nodules), firm, yellow to pink
in colour, linear, frequently on the posterior aspect of
Thighs (also chin, digits, oral cavity).
It is asymptomatic and rarely the lesion may become ulcerate with white points (collagen).
Repeated mosquito bites on cats may result in papular to
ulcerative lesions (nose, pinnae …).
It is a seasonal condition, more frequent in cats living
outside during night.
Histopathology reveals an inflammation rich in eosinophils.
Initial pruritus is minimal but may increase
Differential includes allergies, viral (herpes, pox) dermatoses and dermatophytes.
There is no breed predisposition but young animals and
females seem predisposed.
Comments on Exotic fur mite
This condition may spontaneously resolve or associated
to eosinophilic plaques or indolent ulcer.
It has been associated to flea hypersensitivity, food allergies, atopy, mosquito bites, genetic predisposition, bacterial or viral (calicivirus) infection.
Histopathology: a granulomatous nodular infiltrate multifocal (eosinophilic mush).
Lynxacarus radovskyi (= Felistrophorus radovskyi) is a parasite in cat, another species is found on Lynx in America: Lynxacarus morhani slightly different. - It is a permanent parasite,
eggs; larvae nymphs and adults are found onto the host. Known distribution is warm and humid areas: Pacific, west
tropical Atlantic, south and central America USA (Texas).
This parasite could easily extend (cf worldwide extension of
60
58
ZBORNIK REFERA
TOV
REFERATOV
Cheyletiella in cats and dogs).The condition is contagious and
sometimes epizootic. Transmission probably by direct contact.
Nothing is known about the resistance in environment. More
prevalent in adults (6 – 12 years)- Pruritus is occasional. Feline Miliary dermatitis has been observed. Occasional gastrointestinal signs and gingivitis (licking?) Clinical signs are not
specific. Haircoat matted, scaling, a « pepper and salt » aspect
(scales + mites). Epilation is easy and tegument itself not
concerned. - Lesions are more pronounced on dorsal and lumbar area, head and neck.- Differential includes causes of scaling in cats: ectoparasites (Cheyletiella, fleas an lice), causes of
seborrhoea. - Final diagnosis is based on trichoscopy with parasites and eggs.
The control is not difficult and similar to lice. Carbamates,
lime sulfur, pyrethrins have shown to be effective. Macrocyclic lactones are also effective (i.e. ivermectin 0.3 mg/kg once).
Probably all other acaricidal (phenylpyrazoles) are also effective.- There is no risk of human contamination.
Nodules and plaques
Causes for nodules and plaques in cats include:
Infection:
Abscesses (very common), bacterial granulomas (including actinomycetes and mycobacterias), fungal granulomas (phaehyphomycosis, cryptococcosis, mycetoma).
Neoplasia
A variety of skin tumours develop in cats like in other
species.
Parasites
Various ectoparasites may induce the eosinophili granuloma complex (see above)
Parasite granulomas: myiasis, aberrant migration of nematodes, and rare cases of Dirofilaria repens.
Feline leishmaniosis.
Leishmaniosis in cats a new reality ?
- General leishmaniosis (leishmania infantum) is described
in cats in some foci (particularly in Italy). - During a long
time this disease was considered as non existing (failure
of inoculations. and negative surveys). However arguments “pro” also existed, and infections were observed
in a number of countries in new and old world, half of
them asymptomatic.
Leishmania infantum is involved in Mediterranean countries however other species may develop in cats.
Clinical signs
- General symptoms (50%), Loss weight, anorexia, occasion anal fever.- Haematology:
Anaemia frequent (pale mucosae) (non regenerative), (±
leucopoenia, leucocytosis, monocytosis) Hyperproteinemia, less marked/dog: gamma-beta Glob.± incr. Creatinin, urea.
- Skin
Ulcers = the most frequent (> 50%) on face, ears, lips,
tongue, ± disseminated.Nodules = Suggestive (± 50%)
« Oriental sore » like? Inoculation sore?
Unique or multiple Simultaneous or progressiveGenerally small (± 0.5 cm) occasionally large > 3 cm. Ears,
nose, lips, eyelids, extremitiesAlopecia: Head, ventral
…Scales, crustsEosinophilic granuloma complex: one
case ( Hubert)
Lymphadenopathy (30%)
- Also mentioned: Bronchopneumonia, digestive, stomatitis, renal failure, - Ocular signs- Asymptomatic carriage
(isolation of Leishmania or serology)
- Diagnosis:
Blood: Anaemia frequent (± leucopoenia, monocytosis),
Hyperproteinemia, ± incr. Creatinin, urea. Less marked/
dogDetection of FIV ± FeLV ± IFPSerology Antibodies:
IFA: positive generally low titers: 80 to 160 (-> 2560);
ELISA, pos. > 0.5?Others: Circulating antigens? PCR
Passos et al (1996): Positive on isolated confirmed cases
(Laruelle, Pennisi) Positive on 61% of a group of suspected cases (Pennisi)
IFA + PCR to recommend? Smears (cf dog): Ulcers, lymph
nodes, bone marrow ++ (necropsy: liver, spleen)
Histopathology (cf dog)
Direct observation routine stains or Immunochemistry
(when not visible).
-Treatment: Medical: very few data on series and nor real
reference treatment
Treatment similar to those used in dogs.
Epidemiology :
The age is often not indicatedThere is no role of sex or
breed although facial lesions are common in longhaired
breed.It may occur on domestic or feral cats.
The role of an underlying disease, like in humans, remains unclear and a variety of associated conditions have
been described (ectoparasites, fungal infections, allergic
or auto-immune diseases).
61
59
ZBORNIK REFERA
TOV
REFERATOV
PRISTOP K DIAGNOSTIKI BOLEZNI
SPODNJIH SEÎL PRI MA^KI
Maja Brlo`nik1, Pavo Zaninovi}1, Irena Zdovc2
Prevalenca bolezni spodnjih se~il pri ma~ki (BSSM) je okrog 7%. Pri ma~kah do 10 let, so najpogostejši idiopatsko vnetje, urolitiaza in uretralni plaki. Bakterijske oku`be
najdemo ve~inoma le pri ma~kah nad 10 let.
V prispevku je podan problemski pristop k diagnostiki
obolenj s prikazom zna~ilnih klini~nih skupin (obstrukcija
se~nice, bakterijska oku`ba in idiopatski cistitis). Podane
so zna~ilnosti anamnesti~nih podatkov, opaànja ob
klini~nem pregledu in razlike v urinskih sedimentih pri
skupini sedemdesetih ma~k - klini~nih pacientov z znaki
BSSM.
Na osnovi anamnesti~nih podatkov, temeljitega klini~nega
pregleda in analize urina lahko v ve~ini primerov postavimo zanesljivo diagnozo
Maja Brlo`nik, dr.vet.med., dr. Pavo Zaninovi}, dr.vet.med., doc.dr. Irena Zdovc, dr.vet.med.
1
PRVA-K, Klinika za male ìvali, Gorki~eva 6, SI-1000 Ljubljana
2
Univerza v Ljubljani, Veterinarska fakulteta, Inštitut za mikrobiologijo in parazitologijo,
Gerbi~eva 60, SI-1000 Ljubljana
[email protected]; [email protected]; [email protected]
62
60
ZBORNIK REFERA
TOV
REFERATOV
POSPEŠENI PROTOKOL OBSEVANJA PRI ZDRAVLJENJU
PLOŠÂTOCELI^NEGA KARCINOMA SMR^KA IN
USTNE VOTLINE PRI MA^KAH
Ana Rejec1, Matja` Jeraj2, Janoš Butinar1, Janean L Fidel3
Ploš~ato celi~ni karcinom (PCK) smr~ka pri ma~kah je
tumor belih ali svetlejših ma~k, nastanek pripisujemo
ultravijoli~nim àrkom. PCK ustne votline je najpogostejši tumor ustne votline pri ma~kah, povezujemo ga z okoljskimi dejavniki in mutacijami. PCK smr~ka je lokalno agresiven tumor, ki redko metastazira. PCK ustne votline je
lokalno agresiven tumor z napredujo~o destrukcijo kosti
in visokim metastatskim potencialom. Incidenca
metastaziranja je razmeroma neraziskana zaradi te`ke
lokalne kontrole in umiranja preden se razvije metastatska bolezen. Prognoza PCK smr~ka je dobra, posebej pri
zdravljenju v zgodnjih fazah, pri ustnem PCK je prognoza slaba, problem je uspešna in trajna lokalna kontrola,
boljša je v zgodnjih fazah bolezni.
brez napredovanja) je trenutno 4,5 mesece. PCK ustne
votline, zdravljen s 14 frakcijami v 9 dneh pa je ravnokar
kon~an. Vidni del tumorja je v regresiji.
Zdravljenje PCK smr~ka je kirurško, resekcija ulcerativne
lezije z ustreznimi zdravimi robovi, vendar povzro~i iznakaènost obraza; v poštev pride še krioterapija, fototerapija, intralezijska kemoterapija z derivati platine, sama in v
kombinaciji z radioterapijo in radioterapija sama. PCK
ustne votline pri ma~kah lahko zdravimo kirurško, uspešnost je mo~no odvisna od lokacije. Znano je, da ma~ke
prenašajo velike ustne resekcije slabše od psov. Empiri~no
vemo, da so ustni PCK locirani bolj rostralno manj maligni, novejši podatki pa govorijo o korelaciji volumna tumorja in malignosti, kar govori v prid manjše malignosti
bolj rostralnih tumorjev, saj jih odkrijemo la`je, ko so še
manjši in najverjetneje manj maligni. Radioterapija PCK
smr~ka je znana kot uspešna, manj pa je uspešna pri PCK
ustne votline. Znano je, da ima PCK kratek podvojitveni
~as, kar govori v prid radioterapiji s kratkimi ~asovnimi
intervali (hiperfrakcioniranje) z majhnimi dozami. Avtorica (JF) je razvila pospešene protokole, ki smo jih uporabili pri dveh ma~kah z obema vrstama PCK. PCK smr~ka
smo uspešno zdravili (10 frakcij v 5 dneh), PFI (interval
Ana Rejec, dr.vet.med., Matja` Jeraj, dipl.ing.radiol., prof.dr. Janoš Butinar, dr.vet.med., Janean
Fidel DVM MS DACVR (radiation oncology) DACVIM (oncology), Dept.of Veterinary Clinical
Sciences, Washington State University, USA
1
Bolnica za ìvali Postojna, Cesta v Staro vas 20, SI-6230 Postojna
2
Onkološki Inštitut Ljubljana, Zaloška c. 2, SI-1000 Ljubljana
3
Dept.of Veterinary Clinical Sciences, Washington State University, College of Veterinary
Medicine, ZDA
[email protected]; [email protected]; [email protected]; [email protected]
63
61
ZBORNIK REFERA
TOV
REFERATOV
SINDROM »OKNA NA KIP« IN AKUTNE LEDVI^NE ODPOVEDI
PRI DOMAÎ MA^KI
Igor Firm1, Ana Rejec2, Janoš Butinar2
Sindrom “okna na kip” je zaradi pogostosti takšnega tipa
oken v Evropi pogost vzrok travmatske ishemi~ne nevromiopatije. Predstavljamo primer doma~e ma~ke, ki je bila
pripeljana v Bolnico za ìvali Postojna dva dni po tem, ko
je obvisela na doma~em oknu. Tipi~ni simptomi, zna~ilni
za ta tip poškodbe, so: hipotermija; bole~ine v zadnjih
okon~inah, ledvenem podro~ju in trebuhu; otekline mišic
zadnjih nog; hladne zadnje okon~ine; slaboten do odsoten femoralni pulz; parapareza ali paraplegija, pogosto v
povezavi z zmanjšanimi spinalnimi refleksi zadnjih okon~in;
odsotnost globinske bole~ine. V opisanem primeru je prišlo
še do dodatnih zapletov v zdravljenju (ventrikularna tahikardija, hiperkalemija), ki smo jih pripisali reperfuzijski
poškodbi, in do akutne ledvi~ne odpovedi (v nadaljevanju
ALO), ki je bila najverjetneje posledica ledvi~ne ishemije
in hipoperfuzije v ~asu vkleš~enja v okno. Zaradi ALO
smo se znašli pred resno dilemo, kakšno prognozo dati v
tem primeru in kaj svetovati skrbnici ìvali glede na omejene fina~ne zmo`nosti in negotovo prognozo, ki je brez
ALO kar dobra, saj si kar 80% ìvali po enem mesecu
opomore (~as trajanja hospitalnega zdravljenja je od 1 do
12 dni). Kljub negotovi prognozi smo se skupaj s skrbnico odlo~ili za nadaljevanje zdravljenja, ki je bilo v prvih
dneh usmerjeno predvsem v protibole~insko terapijo,
zdravljenje šoka, zdravljenje motenj v sr~nem ritmu in
antibioti~no profilakso zaradi nevarnosti bakterijske translokacije iz ~revesja. V nadaljevanju pa se je terapija
osredoto~ila predvsem na lajšanje simptomov ALO in
zadostno energijsko oskrbo anoreksi~ne ìvali. Zato smo
ma~ki vstavili ezofagealno sondo, ki se je pokazala kot
klju~ni del terapije. Slednje izpostavljamo, ker je bilo glede na etiologijo in akutnost procesa ledvi~ne odpovedi
predvsem pomembno dati ma~ki dovolj ~asa za vzpostavitev normalne ledvi~ne funkcije, k ~emer bi seveda pripomogla tudi hemodializa, ki pa àl v Sloveniji in bli`nji okolici
ni dostopna. Po desetih dneh smo ma~ko odpustili v
doma~o oskrbo.
Igor Firm, dr.vet.med., Ana Rejec, dr.vet.med., prof.dr. Janoš Butinar, dr.vet.med.
1
FIRM, Veterinarska interna medicina, Igor Firm s.p., Nove Loke 35, SI-3330 Mozirje
2
Bolnica za ìvali Postojna, Cesta v Staro vas 20, SI-6230 Postojna
[email protected]; [email protected]; [email protected];
64
62
ZBORNIK REFERA
TOV
REFERATOV
DIAGNOSTIKA PANKREATITISA PRI MA^KAH
Estera Pogorevc, Barbara Celinšek
UVOD
KLINI^NI ZNAKI
Bolezni eksokrinega pankreasa so relativno pogoste, vendar pri ma~kah àl mnogokrat napa~no diagnosticirane
zaradi nespecifi~nih klini~nih znakov ter pomanjkanja
ob~utljivih in specifi~nih laboratorijskih testov. Napredek
na podro~ju razumevanja patofiziologije, prevalence in
potencialnih vzrokov pankreatitisa je lahko klju~nega pomena na poti do pravilne in uspešne terapije.
Klini~ni znaki pri ma~kah s pankreatitisom so nespecifi~ni.
Ma~ke so letargi~ne in neješ~e; izguba teè, bruhanje in
driska se pojavijo redkeje (1-4).
ETIOPATOGENEZA PANKREATITISA
Ne glede na vzrok je pri vseh pacientih problem nepravilna zgodnja aktivacija tripsinogena znotraj pankreasa kot
posledica avtoaktivacije in/ali zmanjšane avtolize. Tripsin
je glavna proteaza, ki jo izlo~a pankreas. Njegova prezgodnja aktivacija znotraj acinarnih celic vodi do avtodigestije in hudega vnetja, zato je zaš~itni mehanizem ta,
da je tripsin shranjen v zimogenih granulah v acinusih v
obliki inaktivnega prekurzorja tripsinogena. Kadar se avtoaktivira prevelika koli~ina tripsina, zaš~itni mehanizem
popusti in pride do veri`ne reakcije, kar vodi v avtodigestijo pankreasa, vnetje in nekrozo peripankreati~ne
maš~obe ter lokalnega ali bolj generaliziranega sterilnega
peritonitisa (1).
Dejavniki tveganja za pojav pankreatitisa so holangitis,
vnetno obolenje ~revesja (IBD), infekcije (FIP, herpesvirus, calicivirus, panleukopenija, toksoplazmoza), travma,
ishemija, hiperkalcemija, hipertrigliceridemija, zastrupitev z organofosfati, mastna hrana.
Pri ma~ki se izvodilo trebušne slinavke in òl~no izvodilo
stekata v duodenum preko skupnega voda. Ob mehanski
ali funkcionalni obstrukciji tega voda pride do vdora òl~nih
kislin v izvodilo trebušne slinavke. IBD lahko povzro~i
pankreatitis zaradi bruhanja (zviša se intraduodenalni
pritisk, kar lahko povzro~i pankreati~nobiliarni refluks),
refluksa duodenalne vsebine in vdora bakterij skozi skupno papilo (2).
asist. Estera Pogorevc, dr.vet.med., Barbara Celinšek, dr.vet.med.
SI-1000 Ljubljana
[email protected], barbara.celinš[email protected]
Pri pregledu lahko ugotovimo dehidracijo (54%), hipotermijo (46%), ikterus (37%), povišano temperaturo (25 %),
bole~ trebuh (19%) ali maso v trebuhu (11%) (2).
Pri ma~kah s hujšo obliko pankreatitisa se lahko pojavijo
resni sistemski zapleti kot so diseminirana intravaskularna koagulacija (DIC), plju~na tromboembolija, kardiovaskularni šok in multiorganska odpoved (4).
LABORATORIJSKE UGOTOVITVE
Hematološke preiskave lahko pokaèjo normocitno, normohromno, regenerativno ali neregenerativno anemijo,
hemokoncentracijo, levkocitozo ali levkopenijo.
Biokemijske preiskave: hiperbilirubinemija, povišana vrednost alanin aminotransferaze in alkalne fosfataze, hiperholesterolemija, hiperglikemija, hipokalcemija in hipoalbuminemija (2). Zniàne vrednosti kobalamina se lahko
pojavijo pri nekaterih ma~kah, najverjetneje v povezavi s
spremljajo~im ~revesnim obolenjem (motena absorbcija
v ileumu) (1, 4).
SPECIFI^NI TESTI
Aktivnost amilaze in lipaze
Nimata klini~nega pomena pri diagnostiki pankreatitisa
ma~k (4).
Tripsin-like immunoreactivity (TLI)
Ma~ji TLI (fTLI) meri tripsinogen in tripsin v serumu.
Kljub temu, da imata tripsinogen in tripsin izklju~no
pankreati~ni izvor, je ob~utljivost tega testa pri diagnostiki pankreatitisa ma~k nizka.
Pancreatic lipaze immunoreactivity (PLI)
Specifi~no dolo~a koncentracijo ma~je pankreasne lipaze
v serumu in je trenutno najbolj ob~utljiv in uporaben test
za diagnostiko pankreatitisa pri ma~ki (2, 3, 4).
Diagnosti~na ob~utljivost fPLI pri kroni~nem pankreatitisu ni znana (1). Trenutno se test izvaja le v Idexx-ovih
referen~nih laboratorijih.
65
63
ZBORNIK REFERA
TOV
REFERATOV
RENTGENSKA DIAGNOSTIKA
Na rentgenski sliki trebuha so lahko le blage spremembe
ali pa jih ni, vendar je slikanje zelo pomembno za izklju~itev
morebitne akutne popolne obstrukcije ~revesja.
ULTRAZVO^NA DIAGNOSTIKA
Najbolj ob~utljiva in neinvazivna slikovna metoda je ultrazvok, ki je zelo specifi~en, ob~utljivost same preiskave
pa je v veliki meri odvisna od izkušenosti operaterja in
resnosti bolezni. Še ve~jo ob~utljivost se ugotavlja pri
akutnem pankreatitisu, saj je takrat dobro vidna meja med
edemom pankreasa in nekrotizirajo~o peripankreati~no
maš~obo.
CITOLOGIJA
Pri citološkem pregledu vzorca tankoigelne biopsije, lo~imo
lahko med vnetjem in novotvorbo. Negativni izvid ne
izklju~i pankreatitisa, saj gre lahko za fokalne spremembe
(4).
PATOHISTOLOGIJA
Na podlagi ugotovitev klini~nega pregleda, laboratorijske
in slikovne diagnostike za ~asa ìvljenja ma~ke ne moremo lo~iti med kroni~nim in akutnim pankreatitisom –
potrebna je patohistološka preiskava post mortem.
Akutni nekrotizirajo~i pankreatitis (ANP-Acute Necrotizing Pancreatitis) se kaè kot nekroza acinarnih celic
pankreasa in peripankreati~ne maš~obe z razli~nim obsegom vnetja, krvavitev, mineralizacije in fibroze. Vnetje je
lahko prisotno, vendar prevladuje nekroza.
Akutni gnojni pankreatitis (ASP-Acute Suppurative Pancreatitis) se razlikuje od ANP po tem, da je prisotno vnetje
(lahko tudi nekroza), vendar prevladujejo nevtrofilci. Pojavlja se redkeje kot ANP in ve~krat prizadene mlajše ìvali.
Kroni~ni negnojni pankreatitis (CP-Chronic Nonsuppurative Pancreatitis) se kaè kot vnetje, kjer prevladujejo limfociti, fibroza in atrofija acinusov, prisotna je lahko tudi
nekroza.
Ostala obolenja pankreasa, ki jih lahko natan~no razlikujemo le na podlagi patohistološke preiskave, so še
nodularna hiperplazija pankreasa, novotvorbe, pseudociste
in absces pankreasa. Atrofija pankreasa je pogosto rezultat degeneracije, involucije, nekroze in apoptoze eksokrinega dela `leze. Pri ma~kah to najve~krat kaè na zadnjo
fazo kroni~nega pankreatitisa.
LITERATURA
1. Watson PJ, Bunch SE. The Exocrine Pancreas. In: Nelson RW, Guillermo Couto C. Small Animal Internal Medicine. 4th Ed., Missouri,
Mosby Elsevier, 2009: 579-606.
2. Washabau RJ. Acute necrotizing pancreatitis. In: August JR. Consultations in feline internal medicine. Vol. 5, Missouri: Elsevier
Saunders, 2006: 109 – 119.
3. Stinehewer J. The liver and pancreas. In: Chandler EA, Gaskell CJ, Gaskell RM. Feline Medicine and Therapeutics. 3rd Ed., Gloucester:
BSAVA, 2007: 435 – 453.
4. Xenoulis P, Steiner J. Feline pancreatitis. Veterinary Focus. Vol. 19, No. 2, 2009: 11 – 19.
66
64
ZBORNIK REFERA
TOV
REFERATOV
DIHALNA STISKA PRI MA^KI – STABILIZACIJA,
DIAGNOSTIKA IN POGOSTI VZROKI
Radovan Zajc
Uvod
Zdravljenje dihalne stiske (DS) pri ma~ki je lahko zelo stresno za veterinarja. Njihova ob~utljiva narava nam oteùje
delo. Slabo se odzivajo na diagnosti~ne in terapevtske
ukrepe, saj jih prestrašijo, s tem pa se njihova DS še
poglobi. Zato nam primanjkuje ~asa za poglobljeno diagnostiko in vzro~no terapijo. Odzivati se moramo hitro,
vzporedno morata potekati diagnostika in terapija. Koristne informacije dobimo s hitro, a iz~rpno anamnezo.
Zelo pomembno je, da si vzamemo ~as in natan~no opazujemo dispnoi~no ma~ko. Na koncu opravimo še hiter
klini~ni pregled.
Anamneza
Anamnesti~ne ugotovitve nam lahko mo~no pomagajo
pri diagnostiki in terapiji. Nekaj uporabnih vprašanj, ki jih
zastavimo lastniku: Koliko ~asa te`ko diha? Kje ìvi ma~ek?
Ali kašlja? Ali hujša in nima apetita?
Klini~ni znaki
Pomembno je prepoznati klini~ne znake DS pri ma~ki.
Lahko se pove~a frekvenca dihanja, pove~a se napor pri
vdihu in izdihu, diha z odprtimi usti, lahko je zaspana in
depresivna. Ma~ka sedi ali leì v sternalni poziciji (ortopnea). Za DS ma~ke sta zna~ilna dva dihalna vzorca: restriktivni in obstruktivni. Pri restriktivnih motnjah se plju~a
te`ko razširijo ob vdihu. Zato je dihanje hitro, kratko in
plitvo. Sem prištevamo bolezni plju~nega parenhima, kot
so plju~nica, edem in novotvorbe ter bolezni plevralnega
prostora, kot so pnevmotoraks in plevralni izliv.
Pri obstruktivnih motnjah prihaja do mehani~nega oènja
dihalnih poti, kar povzro~i, da je dihanje po~asnejše in
globoko. Oènje zgornjih dihalnih poti sproì napor pri
vdihu, medtem ko pri boleznih spodnjih dihalnih poti (astma) opazimo napor ob izdihu.
Pri hudi in dolgi DS se dihalne mišice utrudijo. Nastopi
paradoksalni vzorec dihanja. Zanj je zna~ilno, da se ob
vdihu medrebrne in trebušne mišice skr~ijo. Zato se meRadovan Zajc, dr.vet.med.
Veterinarstvo Trstenjak – Zajc, d.o.o., Klinika za male ìvali, Ul. padlih borcev 23,
SI-1000 Ljubljana, www.klinika-vtz.si
[email protected]
drebrni prostori vbo~ijo, prav tako trebušna stena. Ob
izdihu pa se trebuh izbo~i.
Klini~ni pregled
Pri klini~nem pregledu opazujemo barvo vidnih sluznic.
Blede sluznice kaèjo na hipoksemijo, anemijo ali periferno vazokonstrikcijo, cianoti~ne ali modre sluznice pa
na hudo hipoksemijo.
Pri avskultaciji plju~ lahko slišimo piske, poke in pove~ano
ali pridušeno plju~no dihanje. Piski so nepretrgani zvoki
razli~nih višin in glasnosti, ki jih slišimo obi~ajno le med
izdihom. Ko sta steni bronhija dovolj blizu, nastane pisk
zaradi vibriranja sten. Slišimo jih pri obstruktivnih boleznih
dihal (astma). Poki nastanejo zaradi nenadnega odprtja
prej stisnjene dihalne poti. Slišimo jih lahko med vdihom
(bronhitis) in izdihom (bronhitis, plju~ni edem). Kadar
so dihalni zvoki tihi, govorimo o pridušenem plju~nem
zvoku. Nastane takrat, ko se plevralni prostor napolni z
zrakom, teko~ino ali tkivom (pnevmotoraks, plevralni izliv).
Sr~no avskultacijo in palpacijo pulza delamo so~asno, da
zaznamo sr~ne šume ali aritmije. Izvid sr~ne avskultacije
pri ma~ki pogosto ni v sorazmerju s sr~no disfunkcijo.
Zato odsotnost sr~nih šumov in galopnega ritma ne
izklju~uje bolezni srca.
Stabilizacija
Vzporedno z iskanjem vzrokov DS za~nemo tudi z zdravljenjem. Na prvem mestu je to dovajanje kisika.
Na naši kliniki v ta namen uporabljamo kisikovo kletko in
kisikov ovratnik. Kisikova kletka je optimalna metoda za
zagotavljanje dobre oksigenacije. Prednosti te metode so:
minimalni stres za ma~ke, dobra kontrola koncentracije
kisika, ogljikovega dioksida, temperature in vla`nosti zraka. Edina slabost je izolacija pacienta.
Zelo priro~en in u~inkovit za kratkotrajno dajanje kisika je
kisikov ovratnik. Za dolgotrajno terapijo ni primeren, ker
lahko nekontrolirano naraste koncentracija ogljikovega
dioksida, hkrati pa se zrak v ovratniku preve~ segreje.
Zelo dispnoi~ne ma~ke pogosto niso dovolj stabilne za
diagnostiko. Hkrati nam klini~ni znaki in hitri klini~ni pregled ne povesta dovolj. V takšnih primerih uporabljamo
empiri~no zdravljenje, dokler ma~ka ni dovolj stabilna za
nadaljevanje diagnostike.
67
65
ZBORNIK REFERA
TOV
REFERATOV
anamneze te`kega dihanja in drugih klini~nih znakov. V
nasprotju z psi ma~ke ne kašljajo, obi~ajno nimajo šuma,
niti galopnega ritma. Vzorec dihanja je restriktiven, pri
avskultaciji plju~ slišimo glasnejše dihalne zvoke ali poke.
Rentgenska slika plju~ nam kaè klasi~ni perihilarni alveolarni vzorec ali so alveolarni vzorci kjerkoli po plju~ih.
Ker je plevralni izliv zelo pogost vzrok DS pri ma~ki, naredimo plevralno punkcijo, posebno pri ma~ki, ki ima tihe
dihalne zvoke. Plevralno punkcijo naredimo pred RTG slikanjem . V primeru pozitivnega rezultata diagnosti~na
plevralna punkcija preide v terapevtsko.
ê je plevralna punkcija negativna, posumimo na dva najpogostejša vzroka DS: kardiogeni plju~ni edem in astmo.
Zato je empiri~na terapija sestavljena iz enega odmerka
furosemida
Bolezni plevralnega prostora
V našem okolju so bolezni plevralnega prostora med
najpogostejšimi vzroki DS pri ma~ki. Sem spadata plevralni izliv in pnevmotoraks.
(1 – 2 mg/kg, IM, IV) in enega odmerka kortikosteroida
(deksametazon 0,25 – 0,5 mg/ kg, IM, IV ). Nizka doza
furosemida ni škodljiva za astmo, prav tako tudi nizka
doza steroida ne bo škodila ma~ki z boleznijo srca.
Restriktivni dihalni vzorec in pridušen dihalni zvok ob
avskultaciji sta klasi~na znaka bolezni plevralnega prostora. Z rentgenskim slikanjem prsnega koša potrdimo prisotnost teko~ine. Ob hudi DS in sumu na plevralni izliv se
zgodaj odlo~imo za plevralno punkcijo.
Pogosti vzroki DS pri ma~ki
Najpogostejši vzroki DS pri ma~ki so: bolezni srca, bolezni
plevralnega prostora in astma. Manj pogosti vzroki pa
so: bolezni zgornjih dihal, bakterijska plju~nica in plju~na
tromboembolija.
Diagnosti~na punkcija preide v terapevtsko. Analiza plevralne teko~ine (celokupni proteini, število celic, citologija)
nam pomaga zdraviti osnovno bolezen.
Bolezni srca
Astma
K boleznim srca pri ma~ki spadajo: hipertrofna, restriktivna in dilatativna kardiomiopatija. Hipertrofna in restriktivna kardiomiopatija vodita v diastoli~no disfunkcijo in
posledi~no pomanjkljivo polnjenje levega prekata. Dilatativna kardiomiopatija pa vodi v sistoli~no disfunkcijo in
zmanjšano kr~ljivost levega prekata. Vsem pa je skupno
levostransko sr~no popuš~anje, ki se klini~no kaè z
plju~nim edemom. Obi~ajno ma~ke preidejo v DS brez
Pomemben vzrok DS pri ma~ki je astma. Pri njej gre za
so~asno stiskanje bronhijev, pove~ano produkcijo sluzi
in hipertrofijo gladkih mišic bronhijev. Pomemben je
anamnesti~ni podatek o dolgotrajnem kašlju. Dihalni
vzorec je obstruktivni z pove~anim naporom pri izdihu.
Pri avskultaciji slišimo ekspiratorne polifone piske. Rentgenska slika pokaè bronhialen vzorec z »krofi« in
»tra~nicami«, hiperinflacijo in ravno trebušno prepono.
Astma
Bolezni srca
Bolezni plevralnega prostora
Piski
Poki
Pridušen dihalni zvok
Poki
Sr~ni šumi
Pove~an ekspiratorni napor
Galopni ritem
Kašelj
Obstruktivni vzorec
Restriktivni vzorec
Restriktivni vzorec
Kisik
Kisik
Kisik
Bronhodilatatorji
Diuretki
Plevralna punkcija
Zdravljenje osnovne bolezni
Glukokortikoidi
Slika1: Algoritem diagnostike in zdravljenja DS pri ma~ki
Literatura
1. King LG. Respiratory Disease in Dogs and Cats: Elsevier, Saunders, 2004
2. Smith FWK, Jr., Keene BW, Tilley LP. Rapid Interpretation of Heart and Lung Sounds: Elsevier, Saunders, 2006
3. Schwarz T, Johnson V. BSAVA Manual of Canine and Feline Thoracic Imaging: BSAVA, 2008
68
66
ZBORNIK REFERA
TOV
REFERATOV
REHABILITACIJA IN FIZIOTERAPIJA PSA PO
OPERACIJI KOLKA - klini~na primera
Kristina Porenta
zadnejga dela telesa, predvsem zadnje desne noge,
miši~ast prednji del telesa, izrazit prenos teè na prednje
noge, razbremenjevanje zadnjih nog. Omejena in bole~a
ekstenzija (110°/B) in abdukcija operiranega kolka,
propriocepcija zadnje desne noge odsotna. Gibljivost
ostalih sklepov ohranjena. Trias znotraj referen~nih
vrednosti.
1. UVOD
Med pogostejše operativne posege na kol~nem sklepu
štejemo trojno osteotomijo medenice, totalno endoprotezo kolka, stabilizacijo po luksaciji in zlomih kolka ter
odstranitev glavice stegnenice. Najpogostejši problem po
operaciji kolka so bole~ina, atrofija mišic operirane noge
in zmanjšana gibljivost prizadetih sklepov, še posebno,
~e so bile te teàve prisotne è pred operacijo. Zaradi
bole~ine in oslabelih mišic ìval noge ne uporablja primerno, kar pogosto vodi v dodatne komplikacije, ki okrevanje podaljšujejo. Program rehabilitacije in fizioterapije
se sestavi na podlagi vrste operativnega posega, klini~nega
stanja pacienta in mo`nosti lastnika za sodelovanje. V
prispevku sta predstavljena program rehabilitacije po
odstranitvi glavice stegnenice in program rehabilitacije po
trojni osteotomiji medenice. Bistvena razlika med njima
je, da se obremenjevanje operiranega uda po osteotomiji
glavice stegenice spodbuja ~imprej, po osteotomiji medenice pa bolj postopno in previdno (1).
b) Klini~ni primer 2 - po osteotomiji medenice
V fizioterapevtski ambulanti je bil sprejet 1 leto star,
nekastriran, 40 kg teàk nemški ov~ar Thor, 3 tedne
po operaciji desnega kolka (trojna osteotomija medenice) zaradi kol~ne displazije. Pri klini~nem pregledu je
ugotovljeno šepanje na zadnjo desno nogo med stojo
1/5, hojo 2/5 in tekom 3-4/5. Pri sedanju spodvije zadnji
nogi v desno stran, pri vstajanju izrazito razbremeni
operirano nogo, pri hoji jo postavlja preve~ vstran in
obra~a navzven. Pri uriniranju ne dvigne nobene noge.
Prisotna atrofija in zmanjšan tonus mišic operirane
noge, napete in bole~e mišice hrbta, predvsem lumbosakralno in interskapularno, bole~e tudi mišice ramenskega obro~a. Ob brazgotini tipne trdoelasti~ne
bulice. Gibljivost operiranega kolka rahlo zmanjšana fleksija (60°/B), extenzija (155°/B), bole~ina (B) prisotna tudi pri kon~nih obsegih gibov abdukcije ter notranje
in zunanje rotacije. Gibljivost ostalih sklepov ohranjena in nebole~a, propriocepcija ohranjena. Trias znotraj
referen~nih vrednosti.
2. MATERIALI IN METODE
Anamneza:
a) Klini~ni primer 1 - po osteotomiji glavice stegnenice
V fizioterapevtski ambulanti je bila sprejeta 15 mesecev
stara, sterilizirana, 48 kg te`ka psica Lia, pasme veliki
švicarski planšarski pes. Pri 6-ih mesecih starosti je prišlo do epifiziolize glavice femorja in opravljena je bila fiksacija s 3 iglami. êz ~as psica noge ni ve~ obremenjevala,
ugotovljena je bila asepti~na nekroza glavice stegnenice
in migracija ene igle, zaradi hudih bole~in na nogo ni ve~
stopila, zato je bila opravljena osteotomija glavice. Pri
klini~nem pregledu 10 dni po odstranitvi desne glavice
stegnenice je ugotovljeno šepanje na zadnjo desno nogo
med stojo 2/5, hojo 3/5, teka ne zmore. Strma stoja zadnjih nog. Pri sedanju se vrè na levi bok, vstane s teàvo.
Med hojo zelo zvija telo. Opazna je huda atrofija mišic
Lestvica šepanja:
OBREMENJEVANJE UDA MED STOJO: 0 - normalno; 1 - delno obremenjuje;, 2 - rahlo se dotika tal; 3 drì ud v zrak; 4 - ne more stati MED HOJO in MED
TEKOM: 0 - ne šepa (vse ude obremenjuje enakomerno); 1 - komaj opazno šepa (z razbremenjevanjem uda;,
2 - o~itno šepa (z razbremenjevanjem;, 3 - o~itno šepa
(z intermitentnim obremenjevanjem); 4 - sploh ne stopi
(drì ud v zrak ves ~as)
Kristina Porenta, dr.vet.med., dipl.fiziot., CCRP
Univerzitetni rehabilitacijski inštitut Republike Slovenije – So~a, Linhartova 51,
SI-1000 Ljubljana
[email protected]
69
67
ZBORNIK REFERA
TOV
REFERATOV
Program fizioterapije:
4. DISKUSIJA
-
Hlajenje operiranega kolka v akutni fazi.
-
Segrevanje operiranega kolka pred razgibavanjem.
-
Masaà zadnjih nog, hrbta, mišic ramenskega
obro~a.
-
Pasivno razgibavanje in raztezanje sklepov operirane
noge.
-
Stimulacija refleksov.
-
Vaje za propriocepcijo, koordinacijo in ravnote`je.
-
Vaje za krepitev atrofiranih mišic.
-
Hoja v vodi.
-
Krajši po~asni sprehodi na vrvici ve~krat na dan,
kasneje postopna uvedba teka.
-
2 dni v tednu po~itek, od aktivnosti samo sprehodi.
-
Uporaba pripomo~ka za la`jo hojo za zadnje noge.
Vrnitev ìvali v normalno funkcijo se po osteotomiji glavice stegnenice pri~akuje po treh mesecih, pri osteotomiji
medenice pa po štirih mesecih po operaciji (2), ~e je bila
ìval pred posegom v dobri fizi~ni kondiciji. Lia noge
pred operacijo è ve~ tednov ni uporabljala. Prišlo je do
hude atrofije in skrajšave mišic zadnje desne noge ter
posledi~ne omejene gibljivosti sklepov, predvsem kol~nega,
kar je zahtevalo daljšo in zahtevnejšo rehabilitacijo. Zaradi velikosti in teè pasme bo šepanje verjetno stalno prisotno, saj bi bila optimalna rešitev le kol~na endoproteza,
za kar pa se lastniki niso odlo~ili. Nasprotno je Thor okreval hitreje od pri~akovanj, kar morda lahko pripišemo
zgodnjemu pri~etku intenzivne in strogo nadzorovane
rehabilitacije in fizioterapevtskih postopkov. K uspehu terapije so v obeh primerih veliko pripomogli tudi lastniki, ki
so upoštevali navodila in redno izvajali del terapije tudi
doma.
-
NSAID in hondroprotektivna terapija.
-
Ambulantna terapija 2 – krat na teden, druge dneve
lastniki v omejenem obsegu izvajajo sami.
-
Prepre~evaje skokov, zdrsov, padcev in nenadnih
ekstremnih gibov.
3. REZULTATI
a) Po 16-ih tednih rehabilitacije Lia hodi lepo, vsede se,
uleè in vstane pravilno. Zmore enouren sprehod in hojo
v klanec. Nogo med stojo obremeni normalno, šepa med
hojo (1/5) in tekom (1-2/5), sicer je ìvahna in razigrana.
Razlika v miši~ni masi zadnjih nog ni ve~ opazna, okrepljen cel zadnji del telesa. Boljša gibljivost operiranega kolka - ekstenzija 145°. Propriocepcija prisotna.
5. ZAKLJUÊK
Program rehabilitacije po osteotomiji medenice se uporablja tudi pri okrevanju po vstavitvi kol~ne endoproteze in
stabilizaciji kolka po poškodbi. Zgodnje vklju~evanje pooperativne rehabilitacije omogo~a hitrejše in boljše okrevanje, in tako lahko pripomore k optimalnemu rezultatu
operacije, ne glede na vrsto operativnega posega na kolku.
b) Po devetih tednih rehabilitacije (12 tednov po operaciji)
je Thor zelo ìvahen in razigran, vsede se, uleè in vstane
pravilno, poskuša skakati, kar se mu še ne dovoli, pri
uriniranju pa dviguje obe nogi. Pri stoji in hoji operirano
nogo normalno obremenjuje, pri teku in po intenzivnejši
aktivnosti pa ob~asno še šepa (1/5), Ohranjena polna gibljivost operiranega kolka, rahlo bole~a le v kon~nih stopinjah
obsegov gibov. Obseg miši~ne mase na zadnjih nogah
simetri~en.
6. LITERATURA
1. Schulz K. Diseases of the Joints. In: Fossum TW. Small animal surgery. 3rd ed. St. Louis: Saunders, 2007: 1143-315.
2. Bockstahler B. Postoperative Joint Rehabilitation. In: Bockstahler B, Levine D, Millis D. Essential facts of physiotherapy in dogs and
cats. Im Schloss: BE Vet Verlag 2004, 128-72.
70
68
ZBORNIK REFERA
TOV
REFERATOV
Osnove elektrokardiografije
za veterinarske tehnike
Igor Firm
Uvod
Elektri~na aktivnost srca
Elektrokardiograf (EKG) ni v svoji najbolj osnovni obliki
ni~ drugega kot voltmeter (galvanometer), ki meri spremembe v elektri~ni aktivnosti srca med dvema elektrodama. Elektrokardiografija je postopek zapisovanja teh
sprememb na papir oziroma monitor. Prvi, ki se je resneje ukvarjal z beleènjem elektri~ne aktivnosti srca, je bil
Nizozemec Willem Einthoven, ki je tudi uvedel poimenovanje valov, uporabljano še danes (P-QRS-T), ter leta 1924
prejel za svoje izsledke tudi Nobelovo nagrado za medicino.
Da bi lahko srce u~inkovito opravljalo svojo funkcijo
~rpalke, mora delovati usklajeno. Kr~enju obeh preddvorov,
ki kri iztisneta v prekata, sledi kr~enje le-teh in iztisk krvi
v aorto in plju~no arterijo. Govorimo o usklajeni atrioventrikularni kontrakciji. Miši~ne celice srca se skr~ijo le v
primeru sprejema elektri~nega stimulusa, kar strokovno
imenujemo depolarizacija. V fizioloških okoliš~inah se
najprej depolarizirata oba atrija in nato z ustreznim
zamikom še oba prekata. Temu sledi obdobje repolarizacije, ki omogo~i ponovitev celotnega procesa.
Pozitivno in negativno elektrodo lahko postavimo kamor
koli na ali v telo. Najpogosteje uporabljana in najenostavnejša postavitev je namestitev elektrod na koò
okon~in. Tako pridobljen posnetek elektri~ne aktivnosti
imenujemo površinski EKG s postavitvijo elektrod na
okon~ine (za razliko od prekordialnega, ezofagealnega
oziroma intrakardialnega na~ina, pri katerih postavimo
elektrode na prsni koš, v poìralnik oziroma neposredno
v sr~ne votline).
Vse sr~ne celice imajo sposobnost lastne elektri~ne aktivnosti, vendar je v desnem atriju podro~je, ki ga imenujemo sinoatrijski vozel (SA vozel), v katerem prihaja do
pospešenga nastanka elektri~nih dra`ljajev. Zaradi te lastnosti imenujemo ta del srca tudi sr~ni ritmovnik (’pacemaker’), ki lahko pod vplivom simpati~nega ìv~nega sistema sr~no frekvenco zviša, pod vplivom parasimpatikusa
pa znià.
Uporabnost EKG v veterinarski medicini se kaè danes
predvsem pri diagnosticiranju in monitoriranju aritmij in
motenj v prevajanju dra`ljajev, spremljanju u~inkov zdravil
z vplivom na srce, monitoriranju sr~ne funkcije pred, med
in po anesteziji ter oceni sr~ne frekvence v primerih, ko
zaradi slabo tipljivega femoralnega pulza ali zelo neenakomernega in hitrega ritma to ni mogo~e.
Za~etek vsakega sr~nega cikla je torej v SA vozlu, od koder se elektri~ni dra`ljaj najprej širi skozi mišice preddvora in naprej skozi atrioventrikularni vozel, v katerem pride
do kratkega zamika oziroma upo~asnitve prenosa. Prehod elektri~nega dra`ljaja iz preddvorov v prekata poteka
skozi Hisov snop, ki se nato razcepi na levo in desno vejo
ter kon~uje v sr~ni mišici kot Purkinjejeva vlakna.
Snemanje elektrokardiograma
Za pogled na elektri~no aktivnost srca iz šestih smeri (standardni površinski EKG s šestimi odvodi – I, II, III, aVL, aVF,
aVR) moramo na pacienta pritrditi vsaj tri ìce, ki glede na nastavitev na aparatu predstavljajo pozitivno ali negativno
elektrodo. Lahko pa pritrdimo še ~etrto, ki jo pritrdimo samo zaradi zmanjšanja motenj (ozemljitev).
Okon~ina
Standardni
Ameriški
Oznake na medicinskih EKG napravah
Rde~a
Bela
RA (right arm – desna roka)
Prednja leva
Rumena
^rna
LA (left arm – leva roka)
Zadnja leva
Zelena
Rde~a
LL (left leg – leva noga)
^rna
Zelena
RL (right leg – desna noga)
Prednja desna
Zadnja desna
Igor Firm dr. vet. med. - FIRM, Veterinarska interna medicina, Igor Firm s.p., Nove Loke 35,
3330 Mozirje, [email protected]
71
69
ZBORNIK REFERA
TOV
REFERATOV
Standardni površinski EKG idealno snemamo v desnem
stranskem poloàju, na podlagi, ki izolira pacienta od
okolice (plastificirana pena, debela brisa~a). Pri zelo nemirnih pacientih, ki no~ejo leàti na boku, pa ga lahko
posnamemo tudi v stoje~em poloàju. Pri snemanju v
stoje~em poloàju moramo biti še toliko bolj pozorni na
mo`nost motenj, ki nastanejo kot posledica premikanja
okon~in, nekoliko pa se lahko tudi spremeni velikost
posameznih kompleksov. Elektrode v veterinarski medicini pritrdimo na okon~ine ìvali s pomo~jo ’krokodil~kov’
(na prednjih tacah na ko`no gubo nad komol~nim sklepom, na zadnjih tacah na ko`no gubo nad kolenskim sklepom), ki jim nekoliko pobrusimo zobe ali pa uporabimo
samolepilne elektrode za enkratno uporabo, ki jih prilepimo na blazinice stopal. Stik elektrod s koò izboljšamo z
uporabo ultrazvo~nega gela (nekaj ve~ dela s ~iš~enjem)
ali pa kar z raztopino za razkuèvanje koè, ki vsebuje
alkohol.
Najprej obi~ajno posnamemo kratke odseke vseh šestih
odvodov pri standardni kalibraciji (hitrost papirja 25 mm/
s in ob~utljivosti 10 mm/mV). Temu sledi še snemanje
daljšega odseka v II odvodu za interpretacijo ritma. Novejše ve~kanalne EKG naprave naredijo to avtomatsko. Pri
snemanju bodimo pozorni na mo`nost nastanka artefaktov. Najpogostejši artefakti so motnje zaradi elektri~ne
interference, miši~nih kr~ev (tremorji) in gibanja ìvali.
Ve~ini se lahko izognemo z ustreznimi filtri, premike ìvali
pa lahko na EKG izpisu ustrezno ozna~imo.
Po izpisu zadovoljivega EKGja ne pozabimo na ustrezno
ozna~itev, ki naj vsebuje datum, podatke o kalibraciji, oznako odvodov, podatke o pacientu in uporabljenih zdravilih.
Interpretacija EKG zapisa
Pri interpretaciji EKGja je najbolje slediti naslednjim korakom:
1. ocenimo kakovost in kalibracijo zapisa
2. dolo~imo frekvenco in ritem
3. ocenimo morfologijo P-QRS-T valov
4. dolo~imo srednjo elektri~no os srca
5. posvetimo se interpretaciji motenj v ritmu.
Najenostavneje dolo~imo frekvenco iz EKG posnetka tako,
da ozna~imo na posnetku šest sekundni odsek (pri hitrosti
snemanja 25 mm/s je to 15 cm in pri hitrosti 50 mm/s 30
cm), v katerem preštejemo komplekse in njihovo število
pomnoìmo z deset. V primeru, da število P valov ni enako številu QRS-T kompleksov, si njihovo število zabeleìmo
lo~eno. Preverimo tudi, ~e so kompleksi kompletni, t.j.
ali ima vsak QRS-T kompleks pripadajo~ P val in vsak P
val svoj QRS-T kompleks.
Izmerimo amplitude in trajanje intervalov reprezentativnega
P-QRS-T kompleksa v II odvodu, obi~ajno pri hitrosti
snemanja 50 mm/s (1 mm = 0,02 s) in ob~utljivosti 1
mm = 0,1 mV.
Parameter
Enota
PES
MA^KA
Frekvenca
Udarci na minut
60-180 (mladi~i <220)
120-240
Trajanje P vala
Sekunda
0,04
0,04
Amplituda P vala
mV
0,4
0,2
P-Q interval
Sekunda
0,06 – 0,13
0,05 – 0,09
Trajanje QRS
Sekunda
0,06
0,04
Amplituda R vala
mV
<2,5-3,0
<0,9
Trajanje Q-T intervala
Sekunda
0,15-0,25
0,12-0,18
Srednja elektri~na os
Kotne stopinje
40-100
0-160
72
70
ZBORNIK REFERA
TOV
REFERATOV
POOPERACIJSKA OSKRBA MA^KE
Barbara Lukanc
Nadzor in pomo~ pri zbujanju ma~k iz anestezije moramo zagotavljati tako dolgo, dokler ni ma~ka popolnoma
pri zavesti. Bolne ìvali lahko po~asneje okrevajo po anesteziji in pri teh je potreben daljši nadzor. Najve~ nenadnih
in nepri~akovanih anestezijskih smrti se zgodi ravno med
prebujanjem in to najpogosteje zaradi neèlenih u~inkov
anestetikov (zavor kardiovaskularnega in respiratornega
sistema) in pomanjkljivega spremljanja ter pomo~i med
prebujanjem (1).
Ekstubacija
Preden ìval ekstubiramo, pogledamo ustno votlino, jo
o~istimo in s prijemalkami ali s sukcijo, odstranimo krvne
strdke, slino, zloènce, zlasti po posegih v ustni votlini
(2) in po potrebi s sukcijo skozi traheotubus o~istimo kri,
sluz in slino iz dihalne poti (3, 4). Odpihnemo meši~ek in
odveèmo tubus (5). Pri prebujanju moramo biti pozorni
tudi na bruhanje, da ma~ka ne bi aspirirala vsebine zlasti,
ko je è ekstubirana. ê ma~ka bruha po ekstubaciji, ji
nagnemo glavo navzdol, da je ni`je od prsnega koša in s
tem prepre~imo aspiracijo. Nato pregledamo ustno votlino in odstranimo izbruhano vsebino. Ma~ke ekstubiramo
zelo zgodaj, ko se jim povrne palpebralni refleks in refleks poìranja. Pri ma~kah ne odlašamo z ekstubacijo, saj s
tem lahko sproìmo laringospazem (2, 5). Pri laringospazmu so grlni hrustanci tesno skupaj, da zrak ne
more prehajati v sapnik. Pri nekaterih ma~kah lahko pride
do refleksnega zaprtja dihalnih poti ob ekstubaciji in ~e
so nezavestne lahko pride do popolne zapore dihalnih
poti (4). Klini~no izgleda zelo podobno laringealni edem,
ki lahko nastane po ponavljajo~i intubaciji v plitvi anesteziji, po poškodb pri intubaciji, zaradi prevelikega tubusa
ali zaradi alergije (2, 4). Pri laringospazmu in laringealnem edemu ma~ke dihajo glasno, hropejo ali te`ko dihajo, poudarjeno je gibanje prsnega koša, lovijo sapo in
pri vdihu vzdigujejo glavo. Preverimo barvo sluznic,
pomerimo saturacijo s pulznim oksimetrom in ~e je nad
asist.dr. Barbara Lukanc, dr.vet.med.
SI-1000 Ljubljana
[email protected]
90 %, je obstrukcija najverjetneje le delna in ne popolna.
V tem primeru ma~ke oksigeniramo, ~e jim s tem ne
povzro~amo preve~ stresa in jim iztegnemo vrat. ê je
ma~ka cianoti~na, izgublja zavest ali je saturacija pod 90
%, jo moramo intubirat, ~e je mogo~e, sicer napravimo
tra-heotomijo (4). Po ekstubaciji ìvali namestimo sternalno z iztegnjenim vratom in jezikom, da omogo~imo
prosto dihalno pot (2, 5).
Podporna terapija pri prebujanju pri skoraj vseh ìvalih
zajema teko~insko in protibole~insko terapijo (1) ter ogrevanje (3).
Ogrevanje
Po operaciji so ìvali pogosto hipotermi~ne, ker anestetiki
zavirajo proces termoregulacije. Hipotermija je najve~krat
razlog za podaljšano zbujanje (1), ker je zmanjšana presnova in podaljšano izlo~anje anestetikov. Za hipotermijo
so dovzetnejše manjše ìvali, zato je najbolje, ~e hipotermijo lahko prepre~imo. Dodatno se ìvali ohlajajo pri operacijah, kjer je odprt prsni koš ali trebušna votlina. Blago
hipotermijo ìvali dobro prenašajo, hujša hipotermija pa
lahko povzro~i ve~ komplikacij (3). Zaradi hipotermije lahko
pride do motenj v koagualciji (slabša funkcija trombocitov, po~asnejša aktivacija kaskadnega sistema koagulacije),
pove~a se mo`nost infekcije, upo~asnjena je presnova
zdravil, nastane tkivna hipoksija (sekundarno zaradi vazokonstrikcije (1), ker se pove~a periferni ìlni upor in
zmanjša poraba kisika), acidoza in motena je elektri~na
prevodnost srca. Z drgetanjem ìvali pove~ajo telesno
temperaturo, zaradi pove~anega miši~nega dela se pove~a
poraba kisika, lahko za ve~ kot za 200 %. Hipotermi~ne
ma~ke lahko ogrevamo z ogretimi odejami, vodno grelno
blazino, masaò (3), grelnimi telesi, ki so lahko polnjeni s
suhim rièm in jih pogrejemo v mikrovalovni pe~ici. Preden jih poloìmo ob ìvali, preverimo temperaturo grelnih
teles in jih zavijemo v brisa~o. Kadar ogrevamo
hipovolemi~ne ìvali, damo grelna telesa na prsni koš in
abdomen, ekstremitete pa pustimo hladne, da prepre~imo
periferno vazodilatacijo in da z ogrevanjem periferije ne
zmanjšamo povratne informacije nevronov do termoregulacijskega centra. Manjše ma~ke lahko ogrevamo v inkubatorju. Pomembno je, da ma~ke med ogrevanjem oskrbimo tudi s teko~insko terapijo in smo pozorni na hipo-
73
71
ZBORNIK REFERA
TOV
REFERATOV
tenzijo, aritmije, odstopanja v elektrolitih, prizadetost centralnega ìv~nega sistema in plju~ne zaplete (6). S preve~
intenzivnim ogrevanjem ìvali z elektri~nimi grelnimi blazinami in s toplimi plastenkami lahko ìvalim povzro~imo
opekline, ki so zelo bole~e in jih lahko opazimo šele ~ez
nekaj dni (3). Ko telesna temperatura ma~ka doseè 37°C,
ponovno preverimo krvni tlak, ki ga po potrebi lahko zvišamo z infuzijo hetaškroba (6). Sistoli~ni krvni tlak pri
ma~kah lahko merimo neinvazivno s pomo~jo doplerskega
merilca tlaka (3).
Teko~inska terapija
Nezadostno nadomeš~anje in vzdrèvanje intravaskularnega in intersticialnega volumna je najpogostejši razlog za
dekompenzacijo in smrt ma~k. Za oìvljanje ma~ka s
hipovolemi~nim šokom uporabimo kombinacijo kristaloidov in koloidov ter ma~ka ogrevamo. Z oìvljanjem s
samimi kristaloidi pogosto povzro~imo nabiranje teko~ine
v plju~ih in plevralno (6). Koloide uporabljamo pri ma~kah
v odmerku 10 do 15 ml/kg/dan intravensko (i.v.), kadar
pa je potrebno hitro pove~anje volumna, jih lahko damo
nekoliko hitreje in sicer 1 do 3 ml/kg i.v. v 15 do 30
minutah (1), oziroma 5 ml/kg v 10 do 15 minutah, dokler
ni sistoli~ni tlak nad 90 mmHg. Hitra intravenska infuzija
hetaškroba lahko povzro~i bruhanje in hipotenzijo. ê se
krvni tlak ni zvišal odmerek hetaškroba ponovimo in nadaljujemo s kontinuirano infuzijo hetaškroba in sicer 0,2 do
1 ml/kg/uro. Pri tem skrbno spremljamo ma~ka, da mu
ne damo prevelike koli~ine teko~in, s ~imer bi povzro~ili
edem plju~. ê se nam to zgodi, zmanjšamo koli~ino kristaloidov, koloide prenehamo dajati in damo furosemid
(6).
Intravenski katetri
Ve~krat na dan preverimo poloàj intravenskega katetra
in morebitno ote~enost ta~ke distalno od venskega katetra. Za zaš~ito pred grizenjem venskega katetra lahko uporabimo ovratnik (6).
Transfuzija
Pri podaljšani koagulaciji ìvali potrebujejo koagulacijske
faktorje, ki jih lahko nadomestimo s transfuzijo sveè krvi,
ki je prav tako potrebna pri hipoproteinemiji in hematokritu ni`jem od 18 % (1).
Oksigenacija
@ivali lahko oteèno dihajo pri: poškodbah glave (oslabljena odzivnost na hiperkarbijo), po operacijah v prsnem
košu, ìvali s plju~nim edemom, ascitesom (zaradi pritiska na diafragmo), anemijo, hipermetabolnimi stanji (hipertiroidizem), bronhospazmom (astma, bronhitis) (2),
kriti~no bolne in resno poškodovane ìvali, ìvali v stresu
(zaradi hospitalizacije, bole~ine) (1). Tem ìvalim poleg
ostalega potrebnega zdravljenja (analgetiki, diuretiki) zagotovimo še oskrbo s kisikom (1, 2). Nasi~enost hemoglobina s kisikom (preskrbljenost tkiv s kisikom) lahko ugotavljamo s pulznim oksimetrom (3). Kisik jim lahko dovajamo prek maske, nosnega katetra, kisikovega ovratnika
ali s pihanjem kisika s pomo~jo anestezijskih cevi. Na ta
na~in pove~amo vdihano koncentracijo kisika na pribli`no
40 % (1).
Tabela 1: Dele` vdihanega kisika (FiO2) glede na na~in
dovajanja (7).
Šokovna triada pri ma~kah
Šokovno triado pri ma~ku predstavljajo hipotenzija bradikardija - hipotermija. Ko baroreceptorji zaznajo nezadostno napetost arterij, se simultano s simpati~nimi vlakni
stimulirajo tudi vagusova vlakna. Zaradi tega ma~ki v šoku
ne odgovorijo s tahikardijo. Tkivna prekrvitev na periferiji
je poslabšana, kar prispeva k hipotermiji. Ko pade telesna
temperatura, se znià tudi sr~ni utrip. Kratko obdobje
hipotermije je koristno pri krvavitvi, da se mo`gani in
srce zaš~itijo pred ishemijo, dokler ne nadomestimo volumna krvi. Kadar pa telesna temperatura pade pod 34°C
je termoregulacija oslabljena. @ivali se pri tej temperaturi
niso sposobne same ogreti, ker jim preneha sposobnost
drgetanja. Ko telesna temperatura pade pod 31°C termoregulacija popolnoma odpove. Pove~ana viskoznost
krvi in metabolna acidoza, ki spremljata hipotermijo lahko še zmanjšata funkcijo miokarda. Pri ni`ji temperaturi
se tudi izgubi termoregulacijski mehanizem vazokonstrikcije in pojavi se vazodilatacija z bradikardijo, ki ima
za posledico hipotenzijo (6).
Na~in dovajanja kisika
FiO2
Pretok kisika (l/min)
»flow-by« - z anestezijsko cevjo
0,24 – 0,45
6–8
Obrazna maska
0,35 – 0,55
6 – 10
Nosni kateter
0,3 – 0,5
1–6
Kisikova kletka
0,4 – 0,5
Kisikov ovratnik
0,3 – 0,4
0,2 – 0,5
Predihavanje
0,21 – 1,0
10 – 15
Intratrahealni kateter
0,4 – 0,6
50 ml/kg/min
Pretok kisika pri nosnem katetru uporabljamo 100 do 200
ml/kg/min, kar nam zagotavlja 30 do 50 % kisika (2, 5).
Kadar pa uporabljamo kisikov ovratnik pa za dosego 30
do 40 % kisika uporabljamo pretok kisika 1 l/min. (5). Za
zelo hipoksi~ne ìvali uporabljamo kisikovo kletko ali inkubator (2). Zaplete pri zbujanju lahko pri~akujemo tudi po
operaciji diafragmalne kile in sicer reekspanzijski plju~ni
edem, ki nastane zaradi hitre ponovne razširitve
atelektati~nih plju~. Ve~krat se ti zapleti pojavijo po operaciji kroni~ne diafragmalne kile. To lahko prepre~imo med
anestezijo, da se izognemo agresivnemu predihavanju
74
72
ZBORNIK REFERA
TOV
REFERATOV
plju~ s pozitivnim pritiskom in agresivnemu odstranjevanju zraka iz prsne votline prek torakalnega drena (8).
Analgezija
Ustrezna in zadostna protibole~inska terapija omogo~i
hitrejše zbujanje in manj neèlenih u~inkov, kot so: tahikardija, vazokonstrikcija, aritmije, tahipnoa in nezadostno
dihanje, slabše celjenje ran zaradi sproš~anja kortizola in
imunosupresivnega delovanja. Prav tako nam bole~ina
lahko npr. pri poškodovanih ìvalih zakrije druge znake
(tahikardija, blede sluznice, podaljšan ~as polnjenja kapilar),
ki so prav tako lahko znak hipovolemi~nega (hemoragi~nega) šoka (1). Za analgezijo in kemi~no imobilizacijo ma~k poskrbimo še pred bole~im posegom. Ma~ke
bole~ino pokaèjo z nemirom, depimiranostjo in razdra`ljivostjo, agresivnostjo, redko pa s tahikardijo (6). Opioidni analgetiki in lokalni anestetiki so primerni skoraj pri
vseh prizadetih ìvalih, medtem, ko nesteroidne analgetike smemo uporabljati le pri zdravih ìvalih, prizadetim
ìvalim pa jih smemo dati le po rehidraciji in po ustreznih
laboratorijskih izvidih seruma (ledvica, jetra) (1). Hudo
bolnim ma~kam sedative in analgetike titriramo do u~inka,
ker je lahko odgovor organizma razli~en (disfunkcija ledvic in jeter). Za blago sedacijo in protibole~insko terapijo
lahko uporabimo butorfanol (0,4 do 0,8 mg/kg intravenozno), na 2 do 6 ur na za~etku. Pri hudi bole~ini pa
uporabimo morfij (0,1 mg/kg intramuskularno) skupaj z
diazepamom (0,2 mg/kg intravenozno). Uporabimo lahko fentanilske obliè z odmerkom 12 ali 25 µg/h na ma~ka
(6). Terapevtski odmerek v krvi doseè po pribli`no 12
urah in traja do 6 dni. Pri ma~kah moramo paziti, da jim
ne damo prevelikih odmerkov opioidov, saj lahko
povzro~ijo vznemirjenost in zmedenost, zlasti pri tistih
ma~kah, ki niso dobile sedativa. Pri mo~ni bole~ini bomo
to razburjenje zaradi opioidov redko opazili (5).
Kletka
Poskrbimo, da so ìvali na mehkem in ~istem, da jim sproti
odstranimo blato, urin, bruhanje in jih o~istimo oziroma
umijemo. V kletkah za prebujanje pa naj ne bo hrane in
vode (3).
Literatura
1. Grubb TL. Anesthesia for patients with special concerns. In: GL Carroll ed. Small animal anesthesia and analgesia. Ames: Blackwell,
2008:193 – 238.
2. Holden D. Postoperative care: general principles. In: Seymour C, Duke-Novakovski T eds. BSAVA Manual of canine and feline
anaesthesia and analgesia. 2nd ed. Gloucester: BSAVA, 2007: 265-73.
3. Taylor R, McGehee R. Postoperative management. In: Manual of small animal postoperative care. Williams & Wilkins, USA,
1995:5 -23.
4. McKelvey D, Hollingshead KW. Anesthetic problems and emergencies. In: Veterinary anesthesia and analgesia. 3rd ed. St. Louis:
Mosby, 2003: 238-85.
5. McKelvey D, Hollingshead KW. General anesthesia. In: Veterinary anesthesia and analgesia. 3rd ed.St. Louis: Mosby, 2003: 51-118.
6. Kirby R. The cat is not a small dog in ICU: Parts I and II. In: Proceedings of WSAVA, Rhodes, 2004.
7. Cave C. High Dependency Nursing. In: Aspinall V. The complete textbook of veterinary nursing. Elsevier, 2006:533 – 554.
8. MacPhail CM. Diaphragmatic hernias. Proceedings of the European Veterinary Conference - Voorjaarsdagen, Amsterdam,
Netherlands 2009.
75
73
ZBORNIK REFERA
TOV
REFERATOV
MA^KA IN ANALGETIKI
Alenka Seliškar
Prepoznavanje bole~ine
Ankete, ki so jih izvedli med veterinarji in veterinarskimi
tehniki v razli~nih dràvah (1, 2, 3, 4), so pokazale, da pri
ma~kah uporabljajo bistveno manj analgetikov kot pri psih.
Razlog naj bi bila bojazen pred neèlenimi u~inki analgetikov in nepoznavanje vzorcev obnašanja, s katerimi ma~ke
izraàjo bole~ino.
Znaki akutne bole~ine so bolj izraziti kot pri kroni~ni
bole~ini in jih je zato la`je prepoznati. Ma~ke se le redko
oglašajo v primerjavi s psi, ki pogosto cvilijo ali stokajo.
ê se poskusimo dotakniti bole~ega dela telesa, nekatere
ma~ke pihajo ali ren~ijo, druge pa se poskušajo skriti ali
pobegniti. Pri bole~ini v trebušni votlini se drìjo zgrbljeno. Manj se gibljejo in ne kaèjo zanimanja za okolico,
se ne ~istijo in imajo zanemarjen koùh, odklanjajo hrano
in stike s ~lovekom (prostoìve~e ma~ke se zavle~ejo na
nedostopno mesto ali se sploh ne vrnejo domov). Pri
mo~ni bole~ini pospešeno dihajo, pri prebujanju iz anestezije po bole~ih posegih brez ustrezne analgezije pa lahko
pride celo do mani~ne reakcije. Ma~ke se me~ejo po kletki, grizejo obvezo, nas poskušajo napasti, ren~ijo in zavijajo (5, 6).
Znaki kroni~ne bole~ine so bolj subtilni in nemalokrat jih
spregledamo. Ma~ke so manj aktivne, ne zanimajo se za
okolico, telesna teà se zmanjša na ra~un neješ~nosti. Pri
lokalizirani bole~ini so znaki bolj specifi~ni; npr. pri bole~ini
v ustni votlini grizejo z manj prizadeto stranjo gobca,
šepajo na prizadeto okon~ino, mišice okon~ine, ki je ne
obremenjujejo, so atrofi~ne. Kadar je prizadetih ve~ sklepov, hodijo zvezano (5).
Za uspešno zdravljenje bole~ine je klju~nega pomena
poznavanje obnašanja ma~k in zdravil, s katerimi odpravljamo bole~ino. Pomembno je tudi, da pristopimo k odkrivanju in zdravljenju bole~ine antropomorfno, kar pomeni, da predvidevamo, da ma~ka ~uti bole~ino vselej, kadar bi jo ~util ~lovek v podobni situaciji oziroma pri enakem
doc.dr. Alenka Seliškar, dr.vet.med.
SI-1000 Ljubljana
[email protected]
bolezenskem procesu. Uporabimo multimodalni na~in
zdravljenja, kar pomeni, da hkrati zdravimo z razli~nimi
analgetiki, kar nam omogo~i boljši izid zdravljenja.
Opioidi
Opioidi se uporabljajo za zdravljenje bole~ine è ve~ kot
2000 let in še vedno ostajajo zdravilo izbora za zdravljenje zmerne do mo~ne bole~ine. Spadajo med mamila, katerih proizvodnjo in promet ureja Zakon o proizvodnji in
prometu s prepovedanimi drogami. Veterinarski tehnik
jih lahko aplicira ìvali le pod nadzorom dr.vet.med. z
licenco za opravljanje veterinarske dejavnosti, ki odredi
koli~ino in na~in aplikacije mamila. O nabavi in izdajanju
opioidov mora dr.vet.med. voditi ustrezno evidenco,
mamila pa shranjevati na predpisan na~in.
Opioidi lahko pri ljudeh in nekaterih ìvalskih vrstah
povzro~ijo spanje, zato jih imenujemo tudi narkoti~ni analgetiki. Ve~ji odmerki (npr. morfij ali metadon nad 0,3 mg/
kg) lahko povzro~ijo ekscitacije ali mani~no reakcijo pri
ma~ki. V Tabeli 1 so našteti le opioidi, ki so dostopni v
Republiki Sloveniji. Za uporabo pri ìvalih je registriran
butorfanol (Torbugesic, Fort Dodge Animal Health), zanj
velja tudi manj oster reìm uporabe (ni potrebno voditi
evidence izdajanja zdravila, ni potrebno shranjevanje na
na~in, ki je predpisan za npr. morfij). Vsi ostali našteti
opioidi so registrirani za uporabo pri ljudeh. Te lahko ob
upoštevanju kaskadnega sistema uporabljamo tudi pri ljubiteljskih vrstah ìvali, ki niso namenjene za prehrano ljudi.
Opioidi zavirajo dihanje, minutni dihalni volumen se zmanjša predvsem na ra~un frekvence dihanja. Zavor dihanja
obi~ajno ni izrazit, razen kadar uporabimo visoke odmerke
opioidov v kombinaciji s sedativi ali anestetiki. Ve~ina
opioidov minimalno vpliva na sr~no-ìlni sistem. îsti
agonisti povzro~ijo bradikardijo in hipotenzijo pri hitrem
intravenskem injiciranju. Bradikardijo lahko zdravimo z
dajanjem antiholinergikov, hipotenziji (posledica sproš~anja
histamina in zavora vazomotornega centra) pa se poskušamo izogniti s po~asnim intravenskim ali intramuskularnim dajanjem. Petidin lahko injiciramo samo intramuskularno.
76
74
ZBORNIK REFERA
TOV
REFERATOV
Opioidi u~inkujejo tudi kot antitusiki, pri psih in ma~kah
je v te namen registriran butorfanol. Zmanjšanje venskega
tonusa in s tem zmanjšanje venskega priliva po dajanju
opioidov (morfij) s pridom izkoriš~amo tudi pri zdravljenju kongestivnega sr~nega popuš~anja.
dola z opioidnim antagonistom naloksonom. Zaradi mešanega mehanizma delovanja tramadol spada med zdravila
z manj ostrim reìmom uporabe, podobno kot butorfanol. Injekcijska oblika tramadola se lahko uporablja le v
veterinarskih klinikah, medtem, ko lahko peroralno obliko (tablete s podaljšanim delovanjem, kapsule, kapljice)
in rektalne sve~ke predpišemo tudi za doma~o uporabo.
Opioidi zmanjšajo propulzivno aktivnost prebavil. Tonus
gladke miši~nine in sfinkterjev se zve~a, peristaltika pa
upo~asni. Bruhanje je posledica draènja centra za bruhanje (morfij) (7, 8).
Tramadol lahko povzro~i zavor dihanja v kombinaciji z
anestetiki. Kratkotrajno dajanje lahko izzove slabost in
bruhanje (zelo redko pri ma~kah), dolgotrajno pa zaprtje
ali drisko.
Tramadol je sinteti~ni centralno delujo~i analgetik, ki se
veè na m opioidne receptorje, obenem pa inhibira
sproš~anje noradrenalina in serotonina, zato ga razvrš~ajo
med druge opioide. Mešani mehanizem delovanja lahko
pojasnimo z le delnim antagoniziranjem u~inkov trama-
Tramadol se uporablja za zdravljenje zmerne do mo~ne
akutne in kroni~ne bole~ine. Po oralnem dajanju se dobro
absorbira (75% biorazpolo`ljivost).
Tabela 1: Priporo~eni odmerki opioidov pri ma~ki
generi~no ime
lastniško ime, proizvajalec
odmerek, ~as delovanja
morfij
Morphini chl., Alkaloid Skopje
0,1 – 0,2 mg/kg i.m., s.c 6 – 8 h
metadon
Heptanon, Pliva
0,1 – 0,2 mg/kg i.m., s.c 6 – 8 h
petidin
Dolantin, Hoechst
5 – 10 mg/kg s.c., i.m.2 h, u~inkuje v 30 min po s.c. aplikaciji
fentanil – injekcijska oblika
Fentanyl Torrex 50 mcg/ml, Torrex Pharma
1 – 4 mcg/kg i.v.medoperacijsko, 15 – 20 min, u~inkuje v 2 – 5 min
fentanil – transdermalni obli`
Durogesic, Janssen Pharmaceutica NV
2 – 5 mcg/kg/h, 6 dni, u~inkovina doseè terapevtsko plazemsko
koncentracijo v 12 h po namestitvi oblià, 12 in 25 mcg/h
butorfanol
Torbugesic, Fort Dodge Animal Health
0,2 – 0,4 mg/kg, iv., i.m., s.c., 1 – 2,5 h
tramadol
Tramal, Grunenthal GmbH; Tadol, Krka
maks. do 3 mg/kg s.c. ali im. ali p.o., 8 – 12 h
(do maks. 15 mg/ma~ko)
Nesteroidni analgetiki
Nesteroidni analgetiki (NSAID iz angl. non-steroidal antiinflammatory drugs) u~inkujejo protivnetno, analgeti~no
in antipireti~no. NSAID inhibirajo ciklooksigenaze (COX),
s ~imer zmanjšajo sproš~anje prostaglandinov in tromboksana A2 (7).
Znani sta dve obliki COX, t.j. COX-1 ali osnovni encim ter
COX-2 ali induktivni encim. COX-2 sodeluje pri nastanku
prostaglandinov odgovornih za vnetje, povišano telesno
temepraturo in bole~ino, COX-1 pa pri nastanku prostaglandinov, ki imajo pomembno vlogo pri vzdrèvanju normalne funkcije ledvic in prebavil. Terapevtski u~inki NSAID
naj bi bili vezani na inhibicijo COX-2, medtem ko naj bi
bila inhibicija COX-1 odgovorna za nekatere toksi~ne u~inke
NSAID (razjeda èlodca, odpoved ledvic).
Ve~ina NSAID v terapevtskih odmerkih ne vpliva na strjevanje krvi. Izjema je acetilsalicilna kislina (Aspirin, Bayer
Pharma), ki se ireverzibilno veè na COX trombocitov in
inhibira tvorbo tromboksana A2, vse dokler se trombociti
ne obnovijo (5 do 8 dni do nastanka novih trombocitov)
(1).
Do nefrotoksi~nosti NSAID lahko pride, kadar je zmanjšana prekrvitev ledvic, npr. pri hipovolemi~nih ìvalih ali
pri hipotenziji med anestezijo. Pri zmanjšani prekrvitvi
ledvic se v ledvi~no ìlje sproš~ata PGE2 (ledvi~na sredica) in PGI2 (glomeruli), ki povzro~ita vazodilatacijo, s ~imer
vzdrùjeta prekrvitev ledvic. Kadar je produkcija prostaglandinov znatno zmanjšana zaradi uporabe NSAID, ledvice ne morejo vzdrèvati normalnega pretoka krvi, kar
vodi v odpoved ledvic. Ni povsem jasno ali je ta u~inek
odvisen samo od COX-1 ali tudi od COX-2 inhibitorjev. Z
vzdrèvanjem zadostne prekrvitve ledvic z uporabo minimalnih odmerkov zdravil, ki zavirajo sr~no-ìlni sistem
med anestezijo ter uporabo primerne teko~inske terapije,
lahko zmanjšamo tveganje za nefrotoksi~nost. Prav tako
naj ne bi uporabljali NSAID hkrati z drugimi potencialno
nefrotoksi~nimi zdravili ter izredno previdno pri ìvalih z
boleznimi ledvic.
Uporabo NSAID med brejostjo odsvetujejo, prav tako pa
naj jih ìvali ne bi jemale vsaj pet dni pred uporabo prostaglandinov za reprodukcijske namene.
Hkratna uporaba NSAID in kortikosteroidov je kontraindicirana, saj kortikosteroidi inhibirajo fosfolipazo A2, ki
sodeluje pri sproš~anju arahidonske kisline iz fosfolipidne celi~ne membrane. Ker NSAID inhibirajo COX, ki
katalizirajo konverzijo arahidonske kisline v prostaglandine in tromboksan, se zve~a tveganje za neèlene u~inke
(7, 8).
77
75
ZBORNIK REFERA
TOV
REFERATOV
Tabela 2: Priporo~eni odmerki nesteroidnih analgetikov pri ma~ki
generi~no ime
lastniško ime, proizvajalec
odmerek, ~as delovanja
karprofen
Rimadyl, Pfizer
do 4 mg/kg s.c., i.v. enkratni odmerek (lahko ponovimo najve~ enkrat ~ez 3 dni
s.c.), p.o. dajanje ni priporo~eno
meloksikam
Metacam, Boehringer Ingelheim
0,2 mg/kg p.o., s.c. ali i.v. prvi dan, naslednji dan nadaljujemo z 0,1 mg/kg
p.o./24 h do najve~ 4 dni, nato 0,05 do 0,1 mg/kg p.o. vsak drugi ali tretji dan
robenakoksib
Onsior, Novartis
1 mg/kg p.o. (s.c. perioperacijsko), do najve~ 6 dni
Gabapentin
Gabapentin (Neurontin, Pfizer) je strukturno analog gamaaminomaslene kisline, registriran za zdravljenje nevropatske bole~ine pri ljudeh. Dnevni odmerek pri ma~ki je
5 – 10 mg/kg p.o., razdeljeno v dva odmerka. Neèleni
u~inki se pojavijo pri do 25% ìvali in sicer zaspanost,
utrujenost in pridobivanje telesne teè pri dolgotrajnem
dajanju (1).
Katerih analgetikov ne smemo uporabiti pri
ma~ki?
Pri nesteroidnih analgetikih se drìmo pravila, da uporabljamo le zdravila, ki so registrirana za uporabo pri
ma~kah, saj ma~ke zaradi druga~ne jetrne presnove kot
jo imajo psi in ljudje (imajo omejeno koli~ino encima glukuronil transferaza, ki omogo~a presnovo NSAID prek glukuronske konjugacije), niso sposobne presnoviti NSAID.
Posledica je mo~no podaljšan razpolovni ~as zdravila in
kopi~enje zdravila do toksi~nega odmerka, ~e zdravilo
odmerjamo na enak na~in kot pri psu ali ~loveku. Torej,
ne uporabljamo NSAID registriranih za ljudi, saj jih ima
ve~ina zelo ozek varnostni profil ali pa so celo toksi~na za
ma~ko!
hemoglobinurijo, intravaskularno hemolizo, zlatenico in
znake okvare jeter (zve~anje aktivnosti jetrnega encima
alanin transaminaza ali ALT). Koma, kr~i, plju~ni edem,
jetrna nekroza in akutna odpoved ledvic so slabi
prognosti~ni znaki. Smrt nastopi obi~ajno 2 do 6 dni po
zauìtju paracetamola.
Zdravljenje do 2 uri po zauìtju paracetamola vklju~uje
gastri~no lavaò (ali pa izzovemo bruhanje). Ma~ki apliciramo protistrup (N-acetilcistein, Fluimikan, Lek) v kombinaciji s C vitaminom, jo oksigeniramo in nudimo podporno teko~insko terapijo (2).
Nesteroidni analgetik fenilbutazon (ena od u~inkovin v
preparatih Tomanol, Dexa-Tomanol, Byk Gulden Konstanz), ki se ponekod še uporablja pri zdravljenju vnetij
lomotornega aparata pri psih in konjih, je izredno toksi~en
za ma~ke in sicer povzro~a hepatopatije, nefropatije, krvavitve iz prebavil in ob~asno tudi ireverzibilno supresijo
kostnega mozga (7, 8).
Paracetamol ali acetaminofen je analgetik-antipiretik. Ne
u~inkuje protivnetno. Pri ljudeh ima dober varnostni profil, ~e ga uporabljamo v predpisanih odmerkih. U~inkovino
najdemo v številnih preparatih (npr. Lekadol, Lek; Daleron, Krka; Panadol, Glaxo Smith Kline; Calpol, Mc Neil
Products), ki so naprodaj v lekarnah brez recepta. @e najmanjši odmerek za npr. otroka je toksi~en za ma~ko. Zaradi omejene glukuronske konjugacije pri ma~ki se paracetamol presnavlja na druge na~ine (sulfacija, oksidacija),
pri ~emer nastajajo toksi~ni presnovki, ki povzro~ijo methemoglobinemijo, nastanek Heinzovih telesc in denaturacijo eritrocitne membrane.
Klini~ni znaki zastrupitve v prvih 4 urah po zauìtju paracetamola so: progresivna cianoza (blede sivomodre
sluznice), tahikardija, tahipnoa, dispnoa, apati~nost, bruhanje, neješ~nost, obrazni edem in edem šap, srbe` in
hipotermija. Ma~ke so redkeje hipertermi~ne. S preiskavo
krvi in urina ugotovimo hematurijo, anemijo in hemolizo.
Redkeje prisotni klini~ni znaki so: ataksija, letargija, razširjene in neodzivne zenice, nistagmus, fotofobija, slinjenje, solzenje, napet trebuh, hiperestezija in trzanje. Kasneje (2. do 7. dan po zauìtju paracetamola) ugotovimo
78
76
ZBORNIK REFERA
TOV
REFERATOV
Literatura
1
Dohoo SE, Dohoo IR. Attitudes and concerns of Canadian animal health technologists toward postoperative pain management in
dogs and cats. Can Vet J 1998; 39: 491-6.
2 Dohoo SE, Dohoo IR. Factors influencing the postoperative use of analgesics in dogs and cats by Canadian veterinarians. Can Vet J
1996; 37: 552-6.
3 Lascelles VBX, Waterman A. Analgesia in cats. In Practice 1997; 19(4): 203-13.
4 Watson ADJ, Nicholson A, Church DB, Pearson MRB. Use of antiinflammatory and analgesic drugs in dogs and cats. Aust Vet J
1996; 74: 203-10.
5 Mathews KA. Management of pain in cats. In: Hellebrekers LJ, editor: Animal pain. Utrecht: Van der Wees, 2000: 131-44.
6 Dobromylskyj P, Flecknell PA, Lascelles BD, Livingston A, Taylor P, Waterman-Pearson A. Pain assesment. In: Flecknell P, WatermanPearson A, editors: Pain management in animals. London: W.B. Saunders Company, 2000: 53-79.
7 Nolan AM. Pharmacology of analgesic drugs. In: Flecknell PA, Waterman-Pearson A, editors. Pain management in animals. London:
WB Saunders, 2000: 21-52.
8 Lascalles BDX. Clinical pharmacology of analgesic agents. In: Hellebrekers LJ, editor. Animal pain. Utrecht: Van der Wees Uitgeverij,
2000: 85-116.
9 Pascoe PJ. Problems of pain management. In: Flecknell PA, Waterman-Pearson A, editors. Pain management in animals. London: WB
Saunders, 2000: 161-77.
10 Gaynor JS. Other drugs used to treat pain. In: Gaynor JS, Muir WW III., editors. Handbook of veterinary pain management. St.
Louis: Mosby, 2002: 251-60.
11 Campbell A. Paracetamol. In: Campbell A, Chapman M, editors. Handbook of
poisoning in dogs and cats. Oxford: Blackwell Science, 2000: 31-8.
79
77
ZBORNIK REFERA
TOV
REFERATOV
ODVZEM BIOLOŠKEGA MATERIALA PRI MA^KI
Barbara Celinšek
UVOD
ODVZEM VENSKE KRVI
Jemanje vzorcev pri ma~ki lahko predstavlja pravi izziv.
Praskala bo in se upirala, poleg tega je tudi izredno gib~na,
zato moramo izbrati najmanj stresen na~in zanjo in hkrati ne pozabiti tudi na svojo varnost.
Epruvete
Pred jemanjem krvi si pripravimo ustrezne epruvete:
-
* epruveta z EDTA za hematološke preiskave
(vijoli~en zamašek)
Pri naro~ilu preiskave, odvzemu in ravnanju z vzorcem
se moramo izogniti napakam, ki lahko klju~no vplivajo na
kon~ni rezultat laboratorijske analize in s tem na interpretacijo laboratorijskega rezultata.
* epruveta z litijevo soljo heparina za npr.
amoniak (zeleni zamašek)
* epruveta s soljo heparina in litijevega
jodacetata za dolo~anje glukoze in laktata
(sivi zamašek)
PREDPRIPRAVA NA ODVZEM
Pred vsakim jemanjem vzorcev izpolnimo spremni dopis
s podatki o vrsti analize, katero èlimo, da naj laboratorij
opravi, vrsti ìvali, priimku lastnika, imenu napotnega
veterinarja, datumom in ~asom odvzema ter ostalimi podatki, ki bi lahko vplivali na rezultat analize (1). Vzorce po
odvzemu tudi ustrezno ozna~imo.
Pripravimo si tudi material za odvzem (igle, brizge,
katetri,...) in material za hranjenje vzorca (epruvete,
sto`~aste epruvete za urin,…).
Roke si umijemo in razkuìmo, pri jemanju urina obvezno
uporabimo rokavice.
epruvete z antikoagulanti :
-
epruveta za odvzem krvi z natrijevim citratom za
teste hemostaze (modri zamašek)
-
epruveta za odvzem krvi brez dodatkov – serum (rde~i
zamašek) (1).
Mesta odvzema
Vzorec venske krvi lahko pri ma~ki odvzamemo iz jugularne vene, v. cephalice in redkeje, iz v. saphene med.
Odlo~itev, iz katere vene bomo jemali kri, je odvisna od
koli~ine krvi, ki jo potrebujemo, klini~nega stanja in kooperativnosti ma~jega pacienta.
Jugularni veni potekata po obeh straneh vratu od baze
uhlja do vhoda v prsno votlino. Asistent prime ma~ko v
sternalnem poloàju z eno roko za glavo in jo rahlo povle~e
navzgor, z drugo pa jo prime za sprednje ta~ke in jo raztegne preko roba mize. Na ta na~in si zagotovimo dovolj
maneverskega prostora in varen odvzem.
Prednost jemanja iz jugularne vene je hitrost odvzema in
zadostna koli~ina krvi, kar zagotavlja kakovostno odvzet
vzorec.
Previdnost pri takem odvzemu velja pri ma~kah v dihalni
stiski, ma~kah z izcedkom iz nosnic in ma~kah s hujšimi
stomatološkimi teàvami.
Barbara Celinšek, dr.vet.med.
SI-1000 Ljubljana
[email protected]
Vena cephalica antebrachii poteka od medialne strani karpusa preko dorzomedialnega dela sprednje tace do
komol~nega pregiba.
Ma~ko fiksiramo s prijemom za vratno gubo in ji glavo
usmerimo v nasprotno stran od mesta odvzema. S pal-
80
78
ZBORNIK REFERA
TOV
REFERATOV
cem druge roke komprimiramo veno v komol~nem pregibu in jo malce potegnemo lateralno, da jo zravnamo. Z
ostalimi prsti ~vrsto drìmo za komolcem, s ~imer
prepre~imo, da bi ma~ka potegnila taco k sebi (2).
Vpliv odvzema
Pri po~asnejšem odvzemu lahko pride do strdkov v vzorcu. Tak vzorec ni primeren za hematološke preiskave.
Sprostitev hemoglobina iz eritrocitov (hemoliza) je
najve~krat posledica nepravilnega odvzema in lahko vpliva na laboratorijske analize. Vzroki za hemolizo so lahko:
-
mesto vboda nismo posušili po uporabi dezin
fekcijskega sredstva
-
predolga uporaba ìlne preveze
-
dolgotrajni odvzemi s tanko iglo
-
premajhen volumen krvi odvzet v epruveto s
prevelikim volumnom, v kateri je vakuum
-
pregrobo stresanje epruvete (1).
ODVZEM URINA
Faktorji, ki vplivajo na odlo~itev, s katero metodo bomo
pridobili urinski vzorec, vklju~ujejo klini~no stanje pacienta,
logistiko jemanja in vrsto preiskave, ki jo èlimo opraviti.
Ker na~in odvzema vzorca lahko vpliva na interpretacijo
urinske analize, je pomembno, da na spremni dopis
zabeleìmo, s katero metodo je bil urin odvzet.
Prosto ujet urin, ki ga prinesejo lastniki ali ki ga dobimo
s stiskanjem mehurja, je preprosto, neinvazivno pridobljen vzorec, primeren za splošne urinske preiskave. Slabost takega odvzema je mo`na kontaminacija preko
se~nice ali posode za lovljenje urina.
Cistocenteza je najprimernejša metoda, kadar èlimo pridobiti vzorec za bakterijske kulture, saj se izognemo kontaminaciji preko spodnjega genitourinarnega trakta. Potreben pa je zadostno poln mehur, kar pa je pri pacientih
s cistitisom v~asih nemogo~e. V vzorcu se lahko pojavi
tudi iatrogena hematurija, ki se je ne da lo~iti od patološke, bolezensko povzro~ene, zato je ta metoda manj
primerna za monitoriranje pacientov s patološko hematurijo (3, 4).
ODVZEM DLAKE ZA MIKOLOŠKE
PREISKAVE
Kadar dlake pri preiskavi z Woodovo svetilko fluorescirajo, s pomo~jo forcepsa populimo predvsem te dlake ter
jih shranimo v primerno embalaò (npr. petrijevka).
V primeru, da dlake ne fluorescirajo, populimo ~im ve~
dlak z roba sprememb, po mo`nosti take, ki so polomljene in nezdravega videza.
ê klini~nih sprememb ni in sumimo, da gre za asimptomatskega nosilca oku`be, dlako odvzamemo tako, da s
primerno sterilno krta~ko pre~ešemo ìval.
KLAMIDIOZA
S sterilno vatenko naredimo konjunktivalni, `relni ali nosni bris. Poleg vzorca epitelija je primeren tudi bris izlo~ka.
VZOREC BLATA
Za parazitološke preiskave je potrebno nekajdnevno zbiranje blata, ki ga v tem ~asu hranimo v hladilniku.
Kateterizacije se posluùjemo pri samcih in je relativno
sterilen postopek, ki pa najve~krat zahteva sedacijo pacienta. S ~im bolj sterilnim odvzemom moramo prepre~iti
iatrogene infekcije. Urinski vzorec, odvzet s kateterizacijo, lahko vsebuje ve~ eritrocitov kot prosto ujet urin, primeren je za dolo~anje bakterijskih kultur in diferencialno diagnostiko vnetja mehurja in ledvic.
LITERATURA
1. Nemec A. Vzor~enje in faktorji vpliva na interpretacijo laboratorijskih rezultatov. In: Zbornik referatov XVI. simpozija o aktualnih
boleznih malih ìvali. Polj~e: Slovensko zdruènje veterinarjev za male ìvali, 2003: 26 – 31.
2. Robben JH, Dongen AM. Collection of material for laboratory examinatin. In: Rijnberk A, van Sluijs FJ. History and Physical
Examination in Companion Animals. 2nd ed., Elsevier Limited, 2009: 232 – 242.
3. Foster D, Matthewman L. Laboratory techniques. In. Simpson G. Practical Veterinary Nursing. 3rd ed. Glouchester: British Small
Animal Veterinary Association, 1994: 115 – 169.
4. Wamsley H, Alleman R. Complete urinalysis. In: Elliot J, Grauer Gf. BSAVA Manual of Canine and Feline Nefrology and Urology.
2nd ed. Gloucester: British Small Animal Veterinary Association, 2007: 87 - 116.
81
79
ZBORNIK REFERA
TOV
REFERATOV
RAVNANJE Z VZORCI ZA IZVAJANJE TESTOV ZA
UGOTAVLJANJE KU@NIH BOLEZNI MA^K
Alenka Nemec Svete, Nataša Tozon
Izvle~ek
1. Uvod
Hitri testi, s katerimi ugotavljamo oku`bo ma~k s parvovirusom (ma~ji panleukopenia virus), z ma~jim virusom imunske pomanjkljivosti (FIV), virusom ma~je levkoze
(FeLV) in corona virusom (FECV), temeljijo na uporabi
imunokemijskih metod s katerimi dolo~imo prisotnost
protiteles ali antigena v vzorcih blata ali krvi (polna kri,
serum ali plazma). Za zagotavljanje pravilnosti rezultatov
z odvzetimi vzorci krvi oziroma fecesa ravnamo v skladu
s priporo~ili za ravnanje z biološkimi vzorci. Pri izvajanju
hitrega testa upoštevamo navodila proizvajalca tako za
samo izvajanje testa kot tudi glede ~asovne stabilnosti
vzorcev.
Laboratorijsko medicino lahko opredelimo kot dejavnost
v okviru katere izvajamo razli~ne preiskave biološkega materiala, ki izhajajo iz ~loveškega ali ìvalskega telesa. To
so na primer kri, urin, blato, znoj, likvor, kostni mozeg,
punktati telesnih votlin, solze, plodovnica in tkiva. V sodobni medicini je vloga medicinskega (=klini~nega=diagnosti~nega) laboratorija zelo pomembna pri
postavljanju ali potrditvi diagnoze, pri spremljanju zdravljenja bolezni in tudi pri oceni splošnega zdravstvenega
stanja. Za kakovost rezultatov, ki jih posreduje medicinski
laboratorij, pa so pomembne vse tri faze dela: predanalitska, analitska in poanalitska faza. Laboratorijsko osebje
zagotavlja natan~nost in pravilnost laboratorijskih rezultatov preko procesa zagotavljanja kakovosti v skladu s
trenutno veljavnimi predpisi in standardi (ISO 15189) v
vseh treh fazah dela (1). V veterinarski medicini, pa tudi v
humani (bolnišnice), se predanalitska faza, ki zajema
naro~ilo preiskave, odvzem vzorca in ravnanje z vzorcem
do analize, ne odvija v celoti v laboratoriju. V tej fazi velikokrat sodeluje ve~ oseb razli~nih profilov, kar je nemalokrat vzrok številnih napak. V nedavno objavljenem
~lanku P. Boninija in sodelavcev je prikazano, da 44-75 %
napak izvira iz predanalitske faze (2).
Abstract
Rapid tests for the determination of infection of cats with
parvovirus (feline panleukopenia virus), feline immunodeficiency virus (FIV), feline leukemia virus (FeLV) and
feline enteritic coronavirus (FECV) are based on the immunochemical methods that detect antibodies or antigen
in blood (whole blood, serum, plasma) or faeces. In order to assure the accuracy and correctness of laboratory
results collected samples of blood or faeces must be handled with the recommendations for handling with biological samples.
doc.dr. Alenka Nemec Svete, univ.dipl.in`.kem.in`., prof.dr. Nataša Tozon, dr.vet.med.
SI-1000 Ljubljana
Hitri testi, s katerimi ugotavljamo morebitno oku`bo ma~k
s parvovirusom, s FIV-om, FeLV in corona virusom, temeljijo na uporabi imunokemijskih metod s katerimi
dolo~imo prisotnost protiteles ali antigena v vzorcih blata
ali krvi. Najpogosteje uporabljene imunokemijske metode
so ELISA in imunokromatografske metode. Protitelesa
ali imunoglobulini so proteini, ki jih organizem proizvede
kot odziv na telesu tujo molekulo, imenovano antigen.
Antigeni pa so po svoji naravi lahko proteini, polisaharidi, nukleinske kisline, pa tudi manjše molekule. Imunokemijske so torej metode, pri katerih izkoriš~amo za identifikacijo dolo~enih protiteles ali antigenov v bioloških vzorcih, interakcijo protiteles z antigeni, ki so povzro~ili njihov nastanek. Lastnost imunokemijskih metod je visoka
specifi~nost in ob~utljivost (3).
Hitri testi za ugotavljanje omenjenih oku`b pri ma~kah so
enostavni za uporabo in, kot è samo ime pove, ne
zahtevajo veliko ~asa za izvedbo. Kot vzorec uporabljamo
[email protected]; [email protected]
82
80
ZBORNIK REFERA
TOV
REFERATOV
razli~ne vrste biološkega materiala, to je lahko polna kri,
serum ali plazma ter feces. Z odvzetimi vzorci ravnamo v
skladu s priporo~ili za ravnanje s krvnimi in drugimi vzorci,
saj omenjene vzorce velikokrat uporabimo za nadaljnje
analize (4). Pri izvajanju hitrega testa upoštevamo navodila
proizvajalca tako za izvajanje testa kot tudi glede ~asovne
stabilnosti vzorcev.
2. Ravnanje z vzorcem venske krvi
Potem, ko smo odvzeli kri po priporo~enih navodilih za
odvzem venske krvi, moramo s takimi vzorci ravnati skrbno in v skladu s spodaj navedenimi navodili (4).
2.1 Polna kri, plazma, serum
Polna kri imenujemo vzorec krvi, katerega smo odvzeli v
epruveto z antikoagulantom. Antikoagulanti (EDTA, litijev
heparin, natrijev citrat, natrijev flurid z litijevim heparinom) na razli~ne na~ine prepre~ijo nastanek strdka. Vse
epruvete z antikoagulanti, razen epruvete z natrijevim citratom, moramo po odvzemu rahlo premešati. Epruvete
z antikoagulantom vedno napolnimo s predpisanim volumnom, saj premajhen volumen vzorca, glede na koli~ino
antikoagulanta, lahko povzro~i nastanek mikro strdkov in
vpliva na rezultate hematoloških analiz (5). Pred izvajanjem hitrih testov preverimo morebitno prisotnost strdkov v odvzetem vzorcu polne krvi. Znano je, da so ma~ji
trombociti podvrèni in vitro agregaciji (6,7). Agregacija
trombocitov v ve~je skupke, lahko tudi manjše strdke,
vpliva ne le na rezultate hematološke analize, temve~ tudi
na rezultate hitrih testov, kjer lahko ugotovimo razli~ne
nespecifi~ne reakcije.
vzorec centrifugiramo po pribli`no 2 do 5 minutah. ê
pa vzamemo epruvete, ki vsebujejo delce stekla, lahko
vzorec centrifugiramo po 15 do 30 minutah po odvzemu. Za pridobitev seruma zadostuje centrifugiranje
vzorcev na 1300g, 10 minut. Tako pridobljeni serum
odlo~imo iz istih razlogov kot plazmo. Serum ni potrebno odlo~iti v primeru uporabe epruvet z dodano inertno
gelsko snovjo, ki zaradi centrifugiranja ustvari neprepustno
pregrdo med serumom in strdkom.
2.2 Dejavniki, ki vplivajo na rezultate
Najpomembnejši in najpogostejši dejavniki, ki lahko med
ravnanjem s krvnim vzorcem in njegovim transportom
vplivajo na rezultat analize, so izbira antikoagulanta, ~as,
lega epruvete, temperatura in pretresanje vzorcev (4).
Antikoagulant
Za nekatere analize je zelo pomembno, da je kri odvzeta v
epruveto z antikoagulantom, za druge analize pa brez njega. Za izvajanje hitrih testov je najpogosteje uporabljeni
antikoagulant EDTA, to je vzorec, ki se uporablja za izvajanje hematoloških preiskav.
âs
Priporo~a se, da serum ali plazmo takoj lo~imo od krvnih
celic oziroma najkasneje v dveh urah po odvzemu krvi
(8). Po kon~anem izvajanju hitrega testa preostanek vzorca seruma oziroma plazme shranimo v hladilniku ali zamrzovalniku za morebitne nadaljnje preiskave.
Lega epruvete
Plazma je supernatant, ki ga dobimo po centrifugiranju
vzorca polne krvi, odvzete v epruveto z antikoagulantom.
Tak vzorec lahko centrifugiramo takoj. Za pridobitev
plazme, vzorce, z izjemo vzorcev odvzetih v natrijev citrat (koagulacijske preiskave), obi~ajno centrifugiramo na
1500g 15 minut. Po kon~anem centrifugiranju vzorec
plazme takoj odlo~imo od celic. Podaljšani stik plazme s
celicami vpliva na koncentracijo analitov v plazmi zaradi
metabolizma, ki poteka v celicah ter aktivnega in pasivnega prehoda analitov med celicami in plazmo (8). Plazme
ni potrebno takoj odlo~iti v primeru uporabe epruvet z
dodano inertno gelsko snovjo, ki zaradi centrifugiranja
ustvari neprepustno pregrado med serumom in celicami.
Serum je supernatant, ki ga dobimo po centrifugiranju
vzorca polne krvi, odvzete v epruveto brez antikoagulantov. Vzorec centrifugiramo po kon~ani popolni koagulaciji, ki obi~ajno pote~e v 45 do 60 minutah pri sobni
temperaturi. ê ~as koagulacije ni zadosti dolg, lahko latentni fibrin povzro~a teàve tako pri izvajanju hitrih testov, kot tudi pri uporabi v analizatorjih. Koagulacijo lahko
pospešimo z aktivatorjem. ê uporabimo trombin lahko
Po odvzemu krvi postavimo epruvete v stojalo pokonci, z
zamaškom navzgor. Tak poloàj omogo~a popolno koagulacijo, manj se pretresa vsebina epruvete in manjše je
tveganje za nastanek hemolize, ki klju~no vpliva na številne biokemijske parametre, ki bi jih morebiti dolo~ali po
kon~anem izvajanju hitrega testa.
Temperatura
V primeru, da bomo vzorec plazme ali seruma uporabili,
ne le za izvajanje hitrega testa, temve~ tudi za dolo~anje
analitov, ki zahtevajo hlajenje vzorcev (koagulacijske
prekave, laktat, amonijev ion, kateholamini), vzorce
odvzete krvi postavimo v ledeno kopel in centrifugiramo
v hladilni centrifugi. Pri ravnanju s krvnimi vzorci se moramo izogibati temperaturam nad 35°C, saj se pri tako visoki temperaturi pospeši spreminjanje sestavin, tudi protiteles in antigenov, ki jih dolo~amo s hitrimi testi. Za
nekatere parametre è temperatura nad 22°C ni primerna. V strokovni literaturi se priporo~a, da odlo~eni serum
ali plazma ne ostane pri temperaturi 22°C dlje od 8 ur (9).
Zato v primeru, da bomo z odvzetim vzorcem seruma ali
83
81
ZBORNIK REFERA
TOV
REFERATOV
plazme izvajali dodatne biokemijske preiskave, serum ali
plazmo shranimo v hladilniku. Serum ali plazmo na gelu
praviloma shranjujemo pri 4°C do 24 ur. Po tem ~asu
vzorec seruma ali plazme odlo~imo v plasti~no epruvetko
in, odvisno od namena, vzorec shranimo v hladilniku ali
zamrzovalniku (4).
V nasprotju s serumom ali plazmo, polno kri hranimo na
sobni temperaturi do 24 ur po odvzemu za morebitne
hematološke preiskave (10).
(13). V primeru odloène analize lahko vzorce seruma ali
plazme, shranjene v hladilniku na temperaturi 2 - 7°C,
uporabimo do 7 dni po odvzemu. Uporabimo lahko tudi
predhodno zamrznjene vzorce, katere pred analizo centrifugiramo. Hemoliti~ni ali lipemi~ni vzorci ne vplivajo
na rezultate analiz. V primeru uporabe vzorcev polne krvi,
kri odvzamemo v EDTA ali litijev heparin. Vzorce polne
krvi uporabimo sveè ali shranjene v hladilniku na temperaturi 2 - 7°C v sedmih dneh po odvzemu. Pred izvajanjem testa preverimo morebitno prisotnost strdkov, saj
le-ti vplivajo na rezultat.
Pretresanje vzorcev
Z odvzetim vzorcem ravnamo skrbno, še posebej, ~e èlimo odvzeti vzorec uporabiti za nadaljnje biokemijske preiskave. Pretirano pretresanje vzorcev lahko poškoduje
eritrocite, kar povzro~i nastanek hemolize. Hemoglobin
v hemoliziranem vzorcu ne vliva na rezultate hitrih testov, zato pa vpliva na vrednosti številnih biokemijskih
parametrov (pove~a aktivnost alanin aminotransferaze,
aspartat aminotransferaze, laktat dehidogenaze, koncentracijo T4 in èleza, rahlo pove~a koncentracijo hemoglobina, fosfata, magnezija, kalcija, serumskih beljakovin in
albumnov ter zelo znià aktivnost alkalne fosfataze).
3. Ravnanje z vzorcem fecesa
Vzorec fecesa, v primeru odloène analize, lahko shranimo v hladilniku (do 2 dni) ali za dlje ~asa v zamrzovalniku.
4. Hitri testi za ugotavljanje oku`b s panleukopenia
virusom, FeLV, FIV in FECV
4.1 ’Parvo’ test
S hitrim ‘parvo’ testom, ELISA ali imunokromatografskim, ugotavljamo prisotnost antigena, panleukopenia
(parvo) virusa, v vzorcih fecesa ma~k. Test lahko uporabimo tudi ugotavljanje parvovirusa v fecesu psov in virusa enteritisa v fecesu kun, lisic in rakunov, saj imajo vsi
trije virusi zelo podobno strukturo (11). Hitri test izvajamo s sveìm vzorcem fecesa. V primeru, da testa ne bomo
izvajali na dan odvzema vzorca, lahko vzorec shranimo
do 48 ur na temperaturi 2 - 7°C ali zamrznemo za daljše
~asovno obdobje.
4.3 ’FIP’ test
S FIP hitrim testom, ELISA ali imunokromatografskim,
ugotavljamo prisotnost protiteles proti FECV virusu v polni
krvi, plazmi ali serumu. Kot vzorec lahko uporabimo polno kri odvzeto v epruvete z EDTA, litijevim heparinom ali
natrijevim citratom, pri ~emer preverimo morebitno prisotnost strdkov, saj le-ti vplivajo na rezultat. V primeru
odloène analize lahko vzorce seruma ali plazme, shranjene na sobni temperaturi, uporabimo do 4 ure po odvzemu, oziroma do 4 dni, v primeru shranjevanja vzorcev v
hladilniku, na temperaturi 2 - 7°C.
5. Zaklju~ek
Rezultate testov je potrebno ustrezno interpretirat, saj
prisotnost specifi~nih protiteles ne pomeni nujno bolezni, in nasprotno, njihova odsotnost ne nujno izklju~uje
oku`be.
Kljub visoki ob~utljivosti in specifi~nosti testov in predhodnemu ravnanju z vzorci ter strokovni izvedbi testov,
so mogo~i tako la`no negativni, kot tudi pozitivni rezultati. Poleg tega je mo`na navzkri`na reaktivnost pri oku`bi
z medsebojno sorodnimi vrstami virusov. Presoja mora
vedno sloneti na celostni obravnavi pacienta.
4.2 FeLV/FIV testi
S hitrimi FeLV/FIV ELISA testi ugotavljamo prisotnost
antigena virusa FeLV (p27 protein) in protiteles proti virusu FIV v krvi. Na trìš~u so na voljo številni hitri testi,
kombinirani in posamezni, katerih rezultati so primerljivi
s klasi~nim ELISA testom (12). Kot vzorec lahko, v skladu
z navodili proizvajalcev uporabimo serum, plazmo ali polno
kri. V primeru dolo~anja FeLV antigena je prioritetni vzorec
serum ali plazma, nekoliko manj zanesljiva je polna kri
84
82
ZBORNIK REFERA
TOV
REFERATOV
Reference
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Tietz NW. Quality assurance. In: Tietz NW, ed. Textbook of clinical chemistry. Philadelphia: W.B. Saunders Company, 1986; 548-592.
Bonini P, Plebani M, Ceriotti F, Rubboli F. Errors in laboratory medicine. Clin Chem 2002; 48(5):691-698.
Crowther JR. Basic immunology. In: Walker Jm, ed. ELISA. Theory and practice. Totowa: Humana Press, 1995: 1-34.
Prezelj M. Priporo~ila za ravnanje s krvnimi vzorci. Ljubljana: Slovensko zdruènje za klini~no kemijo 2006: 1-18.
Piskar M. Priporo~eni postopek za odvzem venske krvi. Ljubljana: Slovensko zdruènje za klini~no kemijo 1999: 1-18.
Zelmanovic D, Hetherington EJ. Automated analysis of feline platelets in whole blood, including platelet count, mean platelet
volume, and activation state. Vet Clin Pathol 1998; 27: 2-9.
Thrall MA, Weiser MG. Hematology. In: Kantrowitz B, ed. Laboratory Procedures for veterinary tehnicians. 2nd ed. Goleta, Calif:
American Veterinary Publications; 1992: 35-98.
Boyanton BL, Blick KE. Stability studies of twenty-four analytes in human plasma and serum. Clin Chem 2002; 48: 2242-2247.
Rehak NN, Chiang BT, Storage of whole blood: effect of temperature on the measured concentration of analytes in serum. Clin Chem
1988; 34: 2111-2114.
Gulati GL, Hyland LJ, Kocher W, Schwarting R. Changes in automated complete blood cell count and differential leukocyte count
results induced by storage of blood at room temperature. Arch Pathol Lab Med 2002; 126: 336-342.
Esfandiari J, Klingeborn B. A comparative study of a new rapid and one-step test for the detection of parvovirus in faeces from dogs,
cats and mink. J Vet Med B 2000; 47: 145-153.
Hartmann K, Griessmayr P, Schulz B, et al. Quality of different in-clinic test systems for feline immunodeficiency virus and feline
leukemia virus infection. J Feline Med Surg 2007; 9: 439-445.
Panel report on the colloquium on feline leukemia virus/feline immunodeficiency virus: tests and vaccination.
JAVMA 1991; 199: 1273-1277.
85
83
ZBORNIK REFERA
TOV
REFERATOV
KRVNE SKUPINE MA^K
Vanja Knez
Poznavanje krvnih skupin je v praksi pomembno zaradi
transfuzije, pri pasemskih ma~kah pa zaradi neonatalne
izoeritrolize.
Krvne skupine so genetsko zapisane na eritrocitih in so
za vsako vrsto specifi~ne. Set alelov za krvno skupino
(dva ali ve~ alelov) tvori skupaj sistem krvne skupine. @ivali
lahko proti drugi krvni skupini razvijejo protitelesa, imenovana izoprotitelesa ali aloprotitelesa. Zaradi teh protiteles nastanejo hemoliti~ne transfuzijske reakcije in pri
mladi~ih po porodu neonatalna izoeritroliza.
Ma~ji sistem krvnih skupin ima tri alele: A, B in izredno
redko AB. Krvna skupina A je dominantna nad B. Ma~ke
krvne skupine A imajo genotip AA, Ab, AAB in samo
homozigotna bb.
Zelo redka ma~ka s krvno skupino AB ima tretji alel recesiven na A in dominanten nad B, kar privede do izraza
obeh substanc. Parjenje ma~ke s krvno skupino A z ma~ko
s krvno skupino B ne privede do krvne skupine AB, razen
~e ni A nosilec recesivne AB.
Poznavanje krvnih skupin je pomembno zaradi transfuzij,
saj imajo ma~ke naravna protitelesa, razen redke krvne
skupine AB. Krvna skupina B ima mo~na protitelesa antiA. Ma~ke s krvno skupino A imajo malo protiteles anti-B.
Pri transfuziji dajalca B in prejemnika A zasledimo hiter
razpad eritrocitov, ni pa takšne hude reakcije kot pri neonatalni eritrolizi, kjer pride posledi~no do pogina mladi~ev
krvne skupine A od matere krvne skupine B. (1-2)
Vanja Knez, dr. vet. med.
Klinika Tristokosmatih, velika klinika za male ìvali, Kajuhova 5a, SI-1000 Ljubljana
Neonatalna izoeritroliza
V ma~ji pediatriji se pogosto sre~ujemo s pojavom
nenadne smrti na videz popolnoma zdravih mladi~ev in
eden od vzrokov je lahko tudi neonatalna izoeritroliza. To
je poškodba neonatalnih eritrocitov zaradi maternalnih
protiteles, ki jih mladi~ zauìje s kolostrumom v prvih
urah ìvljenja, ko je gastrointestinalna bariera prehodna.
Pojavlja se samo pri mladi~ih krvne skupine A, rojenih
materi krvne skupine B po porodu.
Prebavni trakt je prvih 16 ur ìvljenja prehoden za maternalna protitelesa. Pri materi s krvno skupino B se razvijejo mo~na protitelesa proti antigenom krvne skupine A v
obdobju od 1. do 3. meseca po rojstvu. Ta protitelesa
lahko pri mladi~ih povzro~ijo akutno hemoliti~no reakcijo. Mladi~i krvne skupine A in AB se rodijo zdravi, vendar
po zauìtju kolostruma razvijejo klini~ne znake neonatalne izoeritrolize. Prenehajo jesti, postanejo letargi~ni, pojavi se hematurija in poginejo v nekaj minutah ali urah.
Vsi mladi~i iz rizi~ne skupine ne odreagirajo vedno tako,
ampak lahko razvijejo milejšo obliko: sprva postanejo
anemi~ni, v prvem tednu ikteri~ni, v drugem tednu pa se
pokaè še nekroza konice repka, ki kasneje odpade.
Zaradi visoke rizi~nosti pri reprodukciji pasemskih ma~k
odgovoren vzreditelj pred paritvijo testira svoje vzrejne
ma~ke. V primeru, da ima samica s krvno skupino B samca
s krvno skupino A, bo vzreditelj mladi~e po porodu odstranil od samice za 16-24 ur in jih hranil z nadomestnim
mlekom. Lahko pa jih po porodu tudi testira s komercialnimi testi, pri ~emer uporabi popkovno kri po porodu.
Mladi~i s krvno skupino B lahko ostanejo pri mami, mladi~e
s krvno skupino A pa se odstrani za 16-24 ur.
Posamezni vzreditelji si pomagajo tudi tako, da isto~asno
parijo še samico s krvno skupino A in mladi~e s krvno
skupino A prestavijo k njej, da dobijo kolostrum. Mladi~em,
ki ga niso dobili, pa je za zaš~ito priporo~ljivo aplicirati
pod koò serum ma~ke s krvno skupino A. Mladi~e je
mogo~e prvih 24 ur tudi pustiti pri materi, da jih neguje,
seske pa se prekrije, da ne morejo sesati. To pa je v~asih
lahko neu~inkovito, saj so mladi~i izredno iznajdljivi in se
nekako prerinejo do seskov, posledica pa je seveda pogin.
[email protected]
86
84
ZBORNIK REFERA
TOV
REFERATOV
Zastopanost krvnih skupin
Zastopanost krvnih skupin v posameznih pasmah v Sloveniji je slede~a (testiranje krvnih skupin pri pasemskih
ma~kah v Sloveniji 2005):
pasma
št. ma~k krvna skupina A
PERZIJSKA
9
krvna skupina B
8
1
EKSOT
8
6
2
ORIENTALKA
12
12
0
SIAMKA
9
9
0
NORVEŠKA GOZDNA
3
3
0
ABESINKA
5
5
0
BRITANKA
14
13
2
BIRMANKA
3
3
0
DEVON REKS
17
15
2
AMERIŠKA GOZDNA
17
15
2
TURŠKA ANGORA
2
2
0
DOMAÂ MA^KA
70
70
0
OCICAT
7
7
0
skupaj
176
94,9%
5,1%
Dolo~ene pasme, kot so siamska, ruska modra, ocicat in
orientalska, so zastopane le pri krvni skupini A. Krvna
skupina B pa je pogosto prisotna pri devonih, korniš
rexih, britancih, perzijcih, eksotih ipd. V tujini je stanje
podobno, pozorni pa moramo biti na imena pasem, saj
razli~ne organizacije pasme razli~no poimenujejo (npr. himalajka – colorpoint perzijka).(1-2,4)
Samo skupina A
Nizka zastopanost skupine B(1-10 %)
Srednja zastopanost skupine B(10-25 %)
Visoka zastopanost skupine B (>25 %)
Siamka
Ameriška kratkodlaka ma~ka
Abesinka
Britanka1 2
1
1
1
Tonkineska1
Ameriška gozdna ma~ka1
Birmanka1 2 3
Korniš reks1
Orientalka1
Manx1
Burmanka2
Devon reks1 3
Norveška gozdna ma~ka1
Himalajka1
Eksot1
Perzijka
Ragdolka1
Škotska klapouška1
Turška van ma~ka1
Somalijka1
Turška angora ma~ka1
12
Sfinga1 3
1
2
3
vir: Dr. Giger, University of Pennsylvania
rezultati raziskave opravljene na ma~kah v Veliki Britaniji, vir: C. Knottenbelt, University of Glasgow“
vir: Dr Addie, University of Glasgow
87
85
ZBORNIK REFERA
TOV
REFERATOV
Testi
Povzetek
Testi, ki se uporabljajo za dolo~anje krvnih skupin, so
komercialni in enostavni za uporabo. Testira se lahko v
ambulanti, rezultat pa je na voljo è v pol ure. Najpogosteje je v uporabi test Rapidvet-H Dms laboratories,
Agrolabo S. p. A, v zadnjem ~asu pa tudi Alvedia, Quick
Test A+B. Slednjega je la`je shranjevati, saj ga ni potrebno hraniti v hladilniku.
Poznavanje krvnih skupin pri ma~kah torej ni pomembno
samo pri transfuziji, ampak tudi pri vzreji, da bi prepre~ili
neonatalno izoeritrolizo.
V primeru genetskih testov za ma~ke se lahko hkrati ugotavlja še krvna skupina. Laboratoriji ponujajo razli~ne pakete testov. Odvzem krvi je po navodilu laboratorija. Najpogosteje jemljemo kri z EDTA ali pa tudi vzorec sline.
Rezultati testa
Krvna skupina
N/N
tip A ali AB
N/b
nosilec B; lahko tip A ali AB
b/b
tip B
Pred paritvijo dolo~enih pasem je potrebno narediti test
krvne skupine ma~ke.
Kljub znani krvni skupini ma~ke je potrebno pred vsako
transfuzijo narediti navzkri`no reakcijo zaradi kompatibilnosti, ker ni univerzalnega dajalca.
Genetski test ne lo~i med krvno skupino A in redko skupino AB, zato ga ozna~ijo z N. To pomeni: ~e ima ma~ka
genotip N/b, je nosilec krvne skupine B, ~e pa je rezultat
b/b, ima ma~ka krvno skupino B.
S pomo~jo genetskega testa lahko izlo~imo nosilce krvne
skupine, da bi prepre~ili neonatalno izoeritrolizo. Dogaja
se tudi, da vzreditelji, ki imajo samico krvne skupine B,
iš~ejo le samce krvne skupine B. To pa ni priporo~ljivo,
saj se tako oà è tako ozek genetski krog pasemskih
ma~k.
Kljub temu, da ima ma~ka znano krvno skupino, je pred
transfuzijo vedno potrebno narediti navzkri`no reakcijo
pred posegom zaradi nevarnosti hemolize. V zadnjem
~asu so odkrili krvno skupino anti Mik. Nekompatibilnost
le-te lahko povzro~i transfuzijsko reakcijo kljub temu, da
se ma~ke ujemajo po krvni skupini.
Navzkri`na reakcija
Major; 1gtt krvi dajalca + 2 gtt plazme prejemnika
Minor; 2 gtt plazme dajalca + 1 gtt krvi prejemnika
Kontrola; 1 gtt krvi dajalca + 2 gtt plazme prejmnika
S pipeto nanesemo na predmetnico in zmešamo. Reakcija se pokaè v 15-ih sekundah.V primeru aglutinacije dajalec ni primeren za transfuzijo.(3)
Viri:
1. Urs Giger et al., Feline Blood Typing and Crossmatching to Ensure Blood Compatibility: How to Avoid Hemolytic Transfusion
Reactions and Neonatal Isoerythrolysis, ACVIM 2007, DACVIM, ECVIM, ECVCP; Karen V. Jackson; Nicole M. Weinstein; Elanor
Withnall. Philadelphia, PA, USA.
2. Susan Little. The Winn Feline Foundation, Feline blood types and Neonatal Isoerythrolysis. DVM, DABVP (Feline).
3. ESAVS, Feline Medicine & Surgery III, Zurich 1998.
4. Vanja Knez. Zbornik 6. podiplomskega izobraèvanja veterinarske zbornice, Neonatalna izoeritroliza, Ljubljana 2010.
88
86
ZBORNIK REFERA
TOV
REFERATOV
ROKOVANJE S KATETRI IN SONDAMI
Darja Pavlin
Venske kanile
Indikacije: intravenozna aplikacija zdravil, aplikacija anestetikov, infuzje kristaloidov in koloidov, transfuzija, merjenje centralnega venskega tlaka
Kontraindikacije: kanile ne vstavljamo preko koè, ki kaè
kakršnekoli znake vnetja oz. infekcije (pordela, gnojna koà,
izpuš~aji), centralne kanile (v v. jugularis) ne vstavljamo
ìvalim z motnjami v strjevanju krvi.
Za intravenski dostop pri ma~kah najpogosteje uporabljamo periferne venske kanile, saj je njihovo vstavljanje
preprosto in vzdrèvanje nezahtevno. Kanilo najpogosteje vstavljamo v v. cephalico antebrachii na prednji nogi,
lahko pa tudi v lateralno ali medialno v. sapheno na zadnji
nogi. Pri ma~kah za periferni venski dostop ponavadi
uporabljamo 20 - 22 GA kanile. Skozi periferno kanilo
nikoli ne apliciramo hipertoni~nih infuzijskih raztopin (npr.
ve~ kot 0,9-odstotni NaCl, 40-odstotna glukoza, ...).
Vensko kanilo pri ma~kah zlahka vstavimo tudi v v. jugularis, saj je lahko dostopna in bistveno ve~jega premera
kot periferne vene, kar je še posebej pripravno pri manjših ìvalih in mladi~ih. V jugularno veno pri ma~ki ponavadi vstavimo 18 - 20 GA kanilo, pri mladi~ih 22 GA.
Posebej je primerna za hitro aplikacijo ve~jih volumnov
infuzije, kontinuirano aplikacijo zdravil (s perfuzorjem),
parenteralno hranjenje in aplikacijo hipertoni~nih raztopin.
Skozi centalno vensko kanilo ne apliciramo anestetikov in
infuzijskih raztopin z dodanim kalijem.
Kanilo vedno vstavljamo preko koè, nad katero smo prej
natan~no pobrili dlako in jo asepti~no pripravili. Pri starejših ma~kah, ki imajo debelejšo oz. bolj trdo koò ter pri
mo~no dehidriranih ìvalih si pri vstavljanju lahko pomagamo tako, da najprej z debelejšo iglo naredimo majhno
zarezo v koì, s ~imer si olajšamo dostop do ìle. Vstavljeno kanilo preperemo s heparinizirano fiziološko raztopino (2 IE heparina/ml fiziološke raztopine). Na ta na~in
asist. Darja Pavlin, dr.vet.med.
SI-1000 Ljubljana
[email protected]
preverimo, da smo kanilo dejansko vstavili intra- in ne
paravenozno in prepre~imo nastanek krvnih strdkov v
kanili. Kanilo pritrdimo z lepljivimi trakovi ter povijemo z
obvezo (vata in elasti~ni povoj), pri ~emer pazimo, da
nobena od obvez ni pri~rvrš~ena pretesno, saj bi to
oteèvalo pretok teko~ine skozi kanilo. Pri jugularni kanili
bi pretesna obveza povzro~ila dodatno neugodje ìvali in
v skrajnih primerih celo teàve z zauìvanjem hrane in
dihanjem, pri perferni kanili pa otekanje šape. Pri ma~kah
se je izkazalo najbolje, da nogo z vstavljeno kanilo povijemo celo (vklju~no s šapo), zaš~itnega ovratnika pa ponavadi ne potrebujejo. Obvezo nad kanilo vsaj enkrat dnevno
odvijemo, kanilo preperemo s heparinizirano fiziološko
raztopino, da preverimo lokacijo kanile in preverimo, da
se niso pojavili znaki tromboflebitisa, da ni prišlo do iztekanja teko~ine paravenozno in zatekanja okon~ine. Pri
ma~kah, ki potrebujejo dolgotrajni venski dostop, eno
kanilo uporabljamo najve~ 4 dni, nato vstavimo novo v
drugo ìlo/okon~ino. ê se pojavijo znaki vnetja na mestu
vstavitve kanile, jo takoj odstranimo.
Urinski katetri
Indikacije: reševanje zapore se~nice, sterilni odvzem vzorca
urina, merjenje proizvodnje urina.
Kontraindikacije: ne vstavljamo ga ìvalim brez zapore
se~nice, pri katerih ne potrebujemo vzorca urina in so
sposobne samostojnega odvajanja in higiene (se lahko
premikajo in postavijo v poloàj za uriniranje).
Ma~ji samci poosto potrebujejo vstavitev urinskega katetra. Pri ve~ini, še zlasti pa pri tistih z zaporo se~nice, je za
vstavitev katetra potrebna sedacija. Kateter lahko samcu
vstavljamo tako, da ìval leì bodisi na boku ali na hrbtu.
Pomo~nik z eno roko zagrabi bazo repa ìvali in ga nekoliko potegne navzor in proti glavi, s ~imer olajša prolabiranje penisa iz prepucija. Prepucij pred kateterizacijo dobro o~istimo in asepti~no pripravimo in pri vstavljanju
uporabljamo sterilne rokavice. Urinski kateter namaèmo
z lubrikantom in ga vstavimo v se~nico. Pri ma~kih z zaporo
se~nice si pri odpravljanju zapore pogosto pomagamo s
prepiranjem se~nice s toplo sterilno fiziološko raztopino.
@ivalim, ki bodo kateter imele vstavljen ve~ dni, tega
prišijemo na prepucij z dvema šivoma. Kateter poveèmo
89
87
ZBORNIK REFERA
TOV
REFERATOV
z zaprtim sterilnim sistemom zbiranja urina (vre~ka za
zbiranje urina ali ve~ja brizga) preko podaljška za infuzijo, ki ga je priporo~ljivo na enem mestu z lepilnim trakom pritrditi na rep ìvali, s ~imer še dodatno onemogo~imo, da bi si ìval kateter odstranila. @ivali obvezno
namestimo zaš~itni ovratnik.
Kateterizacija ma~je samice je mogo~a, vendar se je
posluùjemo redkeje. Pri ma~kah urinski kateter vstavljamo v enakem poloàju, kot pri samcih, s tem da pri samicah kateter v se~nico vstavimo na slepo preko vhoda v
se~nico, ki se nahaja na dnu vagine. To izvedemo tako,
da konico katetra vstavimo v vulvo vzdol` ventralne stene
in jo potisnemo kranialno, medtem ko z drugo roko robove
vulve povle~emo narahlo kavdalno. Na ta na~in kateter
zdrsne skozi uretralno papilo v se~nico.
Hranilne sonde
Indikacije: prehranska podpora za ìvali, ki ne morejo oz.
no~ejo jesti.
Kontraindikacije: razli~ne, odvisno od vrste sonde: bruhanje, regurgitacija, nezmo`nost poìranja, funkcionalne
ali anatomske bolezni poìralnika, nezavest, poškodbe
obraza, nosnih votlin in `rela, ...
Hranilne sonde se uporablja za asistirano hranjenje ìvali, ki same niso zmo`ne zauìvanja hrane ali hrano dolgotrajno zavra~ajo. Pri ma~kah najpoosteje uporabljamo dve
vrsti sond: nazogastri~no (oz. nazoezofagialno), ki jo skozi
nos vstavimo v poìralnik ali èlodec in ezofagostomo, ki
jo vstavimo v poìralnik skozi kirurško rano na vratu.
komplikacija uporabe ezofaostome. Pri previjaju kirurško
rano okoli sonde vsaki~ namaèmo z antibioti~nim mazilom.
Pri vseh hranilnih sondah je izrednega pomena, da se ne
zamašijo z ostanki hrane. Nazogastri~na sonda zelo majhen premer, zato moramo biti pri pripravi hrane izredno
previdni, da jo pripravimo dovolj teko~o in brez kakršnihkoli grudic ali koš~kov, ki bi lahko zamašile sondo (npr. a/
d dodatno razred~imo z vodo ali uporabljamo hrano v
prahu, ki se zmeša z vodo, odsvetuje se uporaba katerekoli zrnate hrane, tudi ~e jo dodatno spasiramo). Ezofaostoma ima ponavadi nekoliko ve~ji premer, vseeno pa
hrano pripravimo ustrezno teko~e konsistence, da si olajšamo aplikacijoz brizgo. Sondo pred za~etkom hranjenja
najprej preperemo s toplo vodo, da se prepri~amo, da je
normalno prehodna. Hrano pred aplikacijo pogrejemo
malo nad sobno temperaturo in apliciramo po~asi ter ves
~as opazujemo, ali ìval kaè znake nelagodja (slabost,
bruhanje). Sondo po vsakem hranjenju obvezno preperemo z vodo, da iz nje odstranimo vse ostanke hrane in
zapremo s pokrov~kom. Kljub hranilni sondi naj imajo
ìvali vedno na voljo tudi hrano in vodo v posodici, da
lahko za~nejo jesti samostojno, ~e to èlijo, saj obe omenjeni sondi ne onemogo~ata prostovoljnea jemanja in
poìranja hrane.
Nazogastri~na je preprosta za vstavljanje (ne potrebujemo
posebne opreme in pri kooperativnih ìvalih lahko vstavimo brez anestezije), vendar lahko preko nje hranimo le
manjše koli~ine zelo teko~e hrane, saj je sonda zelo tanka. Za hranjenje jo lahko uporabljamo do najve~ dva tedna. Sondo po vstavitvi ponavadi prišijemo z nekaj šivi na
koò na ~elu in ìvalim namestimo zaš~itni ovratnik.
Posebne nege ne potrebuje. Hrano lahko po njej apliciramo kontinuirano (s pomo~jo perfuzorja), ali pa dnevno
koli~ino hrane razdelimo v ve~ manjših obrokov.
Ezofagostomo vstavimo kirurško pri anestezirani ìvali.
Po vstavitvi ìvali obvezno namestimo zaš~itni ovratnik in
vrat na rahlo povijemo, da zaš~itimo kirurško rano. Obvezo vsaj enkrat dnevno odstranimo in preverimo izgled
kirurške rane, saj je infekcija ne tem mestu glavna resna
Literatura
Vascular access techniques. In: Hackett TB, Mazzaferro EM. Veterinary emergency & critical care procedures. Ames: Blackwell Publishing
Professional, 2006: 29-34.
Urethral catheterization in male cats. In: Hackett TB, Mazzaferro EM. Veterinary emergency & critical care procedures. Ames: Blackwell
Publishing Professional, 2006: 126-137.
White RN. Emerency techniques. In: King L, Hammond R, eds. Manual of Canine and Feline Emergency and Critical Care. Cheltenham:
BSAVA, 1999:307-341.
Eirmann L, Michel KE. Enteral nutrition. In: Silverstein DC, Hopper K, eds. Small animal critical care medicine. St. Louis: SaundersElsevier, 2009: 53-8.
Jackson MW. Nutritional support of the critically ill cat: theoretical and practical concerns. Congress Proceedings of the 18th ECVIM-CA
Congress, 2008: 134-6.
90
88
ZBORNIK REFERA
TOV
REFERATOV
RAZLIKA MED MA^JO IN PASJO USTNO VOTLINO
Vladimira Erjavec
Ma~ke so kot ljubiteljske ìvali v ZDA in VB številnejše od
psov. Od psov se razlikujejo po številnih zna~ilnostih. Zelo
pogosto se ma~ke obravnava kot majhne pse, zato prihaja tako pri postavljanju diagnoze kot pri samem zdravljenju do številnih nepravilnosti. Zaradi tega bodimo pozorni in imejmo za relevantne informacije samo tiste, ki
so rezultat prou~evanja ma~k.
Razlika med usti in ustno votlino
Usta so odprtina v obrazu, s katero se pri~enjajo prebavila. To je prostor med zgornjo in spodnjo ustnico. Ustna
votlina (cavum oris) pa je del prebavil, ki jo omejujejo
spredaj ustnici, lica od strani, svod oblikuje trdo nebo,
spodaj pa podjezi~no dno in jezik. Zobni lok jo razdeli na
ustni preddvor (vestibulum oris) in pravo ustno votlino
(cavum oris proprium).
K strukturam ustne votline sodijo poleg zob, jezika, sten
(lica, trdo nebo, podjezi~no dno) še ustnice in slinske
`leze.
Pri ma~ki je ustna votlina kratka in široka, zato je pregled
pri ìvalih, ki so kooperativne, razmeroma enostaven.
Divji psi, ki sami lovijo, plen najprej zgrabijo z zobmi in
ga usmrtijo z grabilci (kaninusi). Medtem ko ~vrsto drìjo
plen, s sekalci in grabilci trgajo kose mesa. Pri tem si
pomagajo s prednjima nogama. Hrana se tare med griznimi ploskvami zob v zgornji in spodnji ~eljusti. Psi hrano bolj malo `ve~ijo. Pogoltnejo lahko namre~ razmeroma velike kose mesa, ne da bi jih pre`ve~ili, temeljiteje pa
drobijo kosti ali druge trde dele hrane.
Ma~ke z zobmi odreèjo manjše kose mesa, ki jih oblikujejo v gri`ljaj in ga pogoltnejo.
asist.dr. Vladimira Erjavec, dr.vet.med.
SI-1000 Ljubljana
Klinika za kirurgijo in male ìvali, Veterinarska fakulteta – UL, Cesta v Mestni log 47,
1115 Ljubljana
[email protected]
Ustna sluznica
Celotno ustno votlino z izjemo zob pokriva ustna sluznica, ki ima številne naloge; s svojo strukturo š~iti spodaj
leè~a tkiva in vsebuje receptorje za temperaturo, dotik in
bole~ino ter okušalne brbon~ice. Slina, ki je produkt slinskih `lez, sodeluje pri zaš~itni vlogi ustne sluznice. Pri
psu ima ustna sluznica klju~no vlogo pri uravnavanju
telesne temperature.
Glede na poloàj, funkcijo in sestavo delimo ustno sluznico
na `ve~no, oblo`no in specializirano ustno sluznico.
@ve~na sluznica pokriva mesta, ki so izpostavljena `ve~nim
silam, primer sta dlesen in trdo nebo. @ve~na sluznica je
~vrsta in poroèneva, trdno je pripeta na periost (vezivno
ovojnico na površju kosti). Ker ima veliko manj ìv~nih
kon~i~ev kot oblo`na sluznica, je veliko manj ob~utljiva.
Oblo`no sluznico najdemo na spodnji strani jezika, ustnem dnu, licih, zobiš~nem nastavku in mehkem nebu. Ta
sluznica je zelo ob~utljiva, mehka in premi~na, na spodaj
leè~a tkiva je rahlo pritrjena. K specializirani ustni sluznici
štejemo sluznico zgornje površine jezika z jezi~nimi papilami, ki vsebujejo okušalne brbon~ice. Jezi~ne papile imajo
zaš~itno in ~utilno vlogo, saj vsebujejo receptorje za dotik, vro~ino, bole~ino in okus.
Ustnice
Pri nekaterih vrstah ìvali (konj) sodelujejo ustnice pri razbiranju in preskušanju hrane, ki jo posredujejo v ustno
votlino, zato so zelo ob~utljive in premi~ne. Pri ma~kah
ustnice nimajo tako pomembne vloge pri hranjenju, zato
so manj premi~ne in tanjše. Pes ima obse`ne in ohlapne
ustnice, ki so zelo gibljive, a jih hotno lahko zelo omejeno
premika. Zgornja in spodnja ustnica sta poraš~eni in nosita
številne dolge tipalne (sinusne) dlake, zlasti na zgornji
ustnici pri ma~ki. Imenujejo se brki. Na notranji strani
zgornje ustnice se pri ma~ki nahajajo labialne papile Kakšno funkcijo imajo labialne papile (zaradi njih so ustnice
nazob~ane), ni znano.
Zgornja ustnica ima v sredinski ~rti zarezo, ki se imenuje
filtrum ali `lebi~, pri nekaterih pasmah psov je zelo globoka.
To je ozko podro~je modificirane koè. Maksilarni labialni
frenulum je pri ma~ki zelo kratek in tesno pripenja zgornjo ustnico na dlesni~no sluznico.
91
89
ZBORNIK REFERA
TOV
REFERATOV
Spodnja ustnica je krajša in jo zgornja presega predvsem
spredaj, delno pa tudi na straneh. Pri ma~ki so v njej
lojnice, t.i. cirkumoralne `leze (snaìlne `leze), ki so številnejše kot v zgornji ustnici. Ustni~ne ko`ne `leze izlo~ajo
snov, ki se med umivanjem nanaša na dlako in jo na ta
na~in neguje, igra pa tudi pomembno socialno vlogo. V
negovanju koùha ma~ke izjemno uìvajo. Pri hujših obolenjih ustne votline ma~ke prenehajo z negovanjem koùha.
Pri psu je spodnja ustnica ohlapna in tanka, njen rob je
nazob~an. Na spodnjo ~eljust je pripeta s frenulumom
(vezico) v podro~ju grabilca ter s slabo nakazanimi gubami
sluznice mediano, ki onemogo~ajo ve~je premike ustnic.
Jezik
Jezik je zelo gibljiva miši~na struktura, ki leì na dnu ustne votline med mandibulama in se nadaljuje v orofarinks.
Kadar je gobec zaprt, zapolnjuje celotno ustno votlino.
Jezi~na konica (apex linguae) prehaja nazaj v telo (corpus
linguae), to pa se nadaljuje v koren jezika (radix linguae).
Pri psu igra jezik veliko vlogo pri hlajenju. V miši~ju blizu
spodnje ploskve jezika je mediana vretenasta tvorba, t.i.
steklinski ~rv, lyssa, ki jo pri palpaciji jezika zlahka zatipamo. Lyssa je vezivna cevka, napolnjena z maš~obnim
tkivom, pri psu so v srednjem delu cevke pre~noprogasta
miši~na vlakna in hrustan~ni oto~ki. Pri ma~ki se pojavlja
muskulatura le redko, hrustanec pa nikoli. Od steklinskega ~rva poteka fibrozni septum do dorzalne površine
jezika in po sredini jezika in pri psu oblikuje `leb, ki poteka kavdalno skozi celotno telo jezika. Pri ma~ki `leba ni.
Posebno pri psu ima jezik spredaj ostra stranska robova,
tu je jezik širok in plosk, izoblikuje pa se lahko v nekakšno
`lico za zajemanje teko~in.
Slinske `leze
Pri psu in ma~ki je tkivo slinskih `lez v ustni votlini bogato in razporejeno po prete`nem delu ustne sluznice.
•
številne male slinske `leze, ki imajo številna kratka izvodila, so razporejene po zadnji tretjini jezika, li~ni sluznici
ter sluznici ustnic in mehkega neba, poìralnika in `rela.
êprav so majhne, pa je njihovo število veliko, zato je
njihova sekrecija sline pomembna in veliko doprinese k
skupni koli~ini izlo~ene sline.
•
Trdo nebo
Sluznica trdega neba tvori parne, poroènele, proti `relu
rahlo konkavno uslo~ene pre~ne sluzni~ne gube, nebne
gube, rugae palatinae, ki jih je pri psu 8 – 12, pri ma~ki
pa 7 -8.
Papile na trdem nebu so zna~ilne le za ma~ke. Usmerjene
so kavdalno in sodelujejo pri prijemanju.
velike slinske `leze:
ma~ke in psi imajo nekaj parnih velikih slinskih `lez. Zanje je zna~ilno eno dolgo izvodilo, ki se izteka v ustno votlino razmeroma dale~ stran od same slinske `leze.
Nitkaste bradavice so mehke, roène nitke na jezi~nem
hrbtu, ki dajejo jeziku barùnast videz. Te nitke so majhne, zakrivljene in obrnjene proti `relu. Pri ma~ki so, za
razliko od psa, mo~no poroènele, ve~je, a manj številne.
Zato daje njihov jezik videz fine ì~ne š~etke, nitkaste bradavice sluìjo predvsem za jemanje teko~in, za „ostrganje“ hrane (npr. ostankov mesa s kosti).
S pomo~jo bradavic si ma~ke negujejo koùh, po drugi
strani pa bradavice ma~kam onemogo~ajo, da bi izvrgle
linearne tujke, ki jih vzamejo v ustno votlino (npr. sukanec). Dlake, ki izpadejo med negovanjem koùha, se
zato nabirajo v èlodcu in iz njih nastajajo dla~ne kepe
(„hairballs“); pomešajo se s hrano in se izlo~ijo z iztrebki
ali pa jih ma~ka izbruha.
male slinske `leze:
~eljustna ali mandibularna (glandula mandibularis). Leì rahlo kavdalno in medialno od ~eljustnega kota (angulusa mandibule). Pred njo in
delno pod njo so lnn. mandibulares (~eljustne
bezgavke). POZOR: Pri palpaciji prihaja velikokrat
do zamenjave in ~eljustne bezgavke ocenimo kot
pove~ane, ker dejansko otipamo ~eljustno slinsko `lezo!!! êljustna `leza je okroglasta, pogosteje je ve~ja kot podušesna slinska `leza in je
tudi svetleje obarvana.
podjezi~na ali sublingvalna (glandula sublingualis). Sestoji iz 2 delov, glandula sublingualis
polystomatica in glandula sublingualis monostomatica.
li~na ali zigomati~na (glandula zygomatica) –
podušesna ali parotidna (glandula parotis) – otipamo jo le, kadar je pove~ana. To je majhna trioglata `leza, ki obdaja bazo uhlja.
molarna – prisotna je le pri ma~ki. ê se nahaja
na bukalni strani spodnjega molarja, govorimo
o bukalni ali li~ni molarni slinski `lezi. Kadar se
nahaja na notranji strani spodnje ~eljusti, na
lingvalni strani molarjev, govorimo o lingualni
molarni slinski `lezi. Kakšna je specifi~na vloga
molarne slinske `leze, ni znano. Po kirurški
odstranitvi niso opazili nobenih klini~nih sprememb v funkcioniranju jezika, vla`nosti ustne
votline ali nastajanju trdih zobnih oblog.
Slina
Slinske `leze proizvajajo slino, ki ima zapleteno sestavo
in številne naloge. Odvisno od hidracijskega stanja ìvali
in jemanja vzorca je lahko slina prozorna in vodena ali pa
gosta in sluzasta. Male slinske `leze proizvajajo predvsem
mukozno (sluzasto, èlatinasto) slino, velike slinske `leze
pa bolj vodeno slino (serozno), ki vsebuje encim ptialin,
ki igra pomembno vlogo pri razgradnji ogljikovih hidratov.
92
90
ZBORNIK REFERA
TOV
REFERATOV
Slina vlaì ustno sluznico, navlaì in oblikuje bolus hrane,
kar olajša `ve~enje in potovanje bolusa skozi ustno votlino in poìranje. Slina ima pomembno zaš~itno nalogo
pred bakterijami, saj vsebuje encime, lizosome in imunoglobuline. Slina tudi mehansko spira ustno votlino (sluznico in zobe) in na ta na~in zmanjšuje število prisotnih bakterij. Proteini, ki se nahajajo v slini, se veèjo na mikroorganizme in na ta na~in prepre~ujejo njihovo lepljenje na
tkiva ustne votline. Slina deluje proti glivicam in virusom.
Zobje
Na splošno velja, da zobje pri ma~ki izrastejo 2 – 4 tedne
prej kot pri psu. Zobovje pri ma~ki je glede na zobovje pri
psu zreducirano zaradi kratkih, stisnjenih ~eljusti in to na
vsaki strani za en zgornji premolar in en zgornji molar ter
na obeh straneh za dva spodnja premolarja in dva spodnja molarja. Ker navedeni zobje manjkajo, je zobovje pri
ma~ki skrajno sekodontno (pomeni, da imajo ostre grbice, (izbokline) s katerimi ma~ka reè meso podobno
giljotini. Sekodontno zobovje imajo tipi~ne zveri. Pri rezanju hrane sodelujeta predvsem prvi molar v spodnji
~eljusti in ~etrti premolar v zgornji ~eljusti.). Ma~ke imajo
tako kot psi heterodontno zobovje, kar pomeni, da imajo
ve~ skupin razli~no zgrajenih zob.
Incizivi ali sekalci so razmeroma majhni zobje, primerni
za „rezanje“. Imajo le eno, dolgo korenino in kratko, ostro zobno krono. Incizivi v zgornji ~eljusti so ve~ji od
incizivov v spodnji ~eljusti in po velikosti naraš~ajo od
prvega do tretjega inciziva. Pes in ma~ka imata po šest
sekalcev v zgornji in v spodnji ~eljusti, pri ma~ki so mnogo
manjši.
Kaninusi ali grabilci so najdaljši zobje in imajo eno mo~no
korenino, ki je lahko do dvakrat daljša od zobne krone.
Zobna krona je koni~na in ukrivljena. Z grabilci pes zgrabi
in drì plen ter trga meso, pri ma~ki pa sluìjo predvsem
za drànje in ubijanje plena. Pes in ma~ka imata štiri grabilce, ki so pri ma~ki mnogo ostrejši.
Predmeljaki ali li~niki imajo lahko eno, dve ali tri korenine. Njihova zobna krona je koni~na in ima ve~ grbic.
Odrasel pes ima šestnajst predmeljakov, po štiri levo in
desno v spodnji in zgornji ~eljusti, pri ma~ki pa manjkata
prvi premolar v zgornji ~eljusti na obeh straneh ter prvi
in drugi premolar v spodnji ~eljusti na obeh straneh, tako
ima ma~ka 10 predmeljakov.
Meljaki ali ko~niki imajo pri psu – izvzemši prvi meljak v
spodnji ~eljusti – ravne grizne ploskve, primerne za drobljenje hrane. êprav se zobna gniloba (karies) pri psu v
primerjavi z ljudmi pojavlja zelo redko, se najpogosteje
pojavlja na griznih ploskvah meljakov.
V zgornji ~eljusti ima odrasel pes po dva meljaka na levi
in na desni strani, v spodnji ~eljustnici pa po tri na levi in
desni strani. Ma~ka ima v zgornji in spodnji ~eljusti samo
po en meljak na vsaki strani. Ker nima zob z ravnimi
ploskvami, ki sluìjo drobljenju hrane, ima ma~ka zna~ilen
ugriz, pri katerem hrano reè. Pri spodnjem molarju je
rezilna ploskev izoblikovana z dvema skoraj enakima deloma krone, glavno in distalno grbico, ki ju podpira velika
mezialna korenina, distalna pa je zelo majhna. Zgornji
~etrti premolar, ki se imenuje tudi drobilec, zdrsne s svojo palatinalno ploskvijo mimo bukalne ploskve spodnjega
prvega ko~nika. Skupaj delujeta kot škarje; na tem mestu
je stisk ~eljusti najmo~nejši. Tu ma~ke trgajo meso in
drobijo kosti. Temeljito `ve~enje pri mesojedih ni potrebno, ker goltajo cele kose mesa in kosti.
Pri mle~nem zobovju ni meljakov, to velja za ma~ke in
pse.
Obolenja ustne votline pri ma~ki
1.) Parodontalna bolezen
Je najpogostejše vnetno obolenje ustne votline ma~ke,
gre za vnetje obzobnih tkiv, do ~esar pride zaradi kopi~enja
mehkih zobnih oblog na zobeh ob robu dlesni. Mehke
zobne obloge so sestavljene iz ostankov hrane in predvsem bakterij, ki se razmnoùjejo v hrani. V ustni votlini
ìvali so našli ve~ kot 500 vrst razli~nih bakterij, nekatere
povzro~ajo smrad, druge pa vdirajo v dlesni in druga
obzobna tkiva. Ko se v mehke zobne obloge vgradijo minerali, postanejo te trde in predstavljajo zobni kamen. Zobni kamen sam ne povzro~a obolenj obzobnih tkiv, res pa
je, da postane površina zobne krone hrapava in se zato
nanjo še bolj lepijo ostanki hrane in bakterije. Parodontalna bolezen se za~ne kot vnetje dlesni (gingivitis). Vneta
dlesen je temno rde~a, nabrekla in zelo rada krvavi. Vnetje
dlesni lahko povsem pozdravimo s primerno ustno
higieno, lahko pa napreduje v globino, kjer povzro~i
postopno propadanje obzobnih tkiv (vezivnega tkiva, kosti in zobnega cementa), ki drìjo zob v ~eljustni kosti.
Takšni zobje postanejo majavi, se navidezno podaljšajo,
med zobom in dlesnijo nastanejo razli~no globoki „èpi“
in bole~e gnojne otekline. ê se ne zdravi pravo~asno,
zobje na koncu izpadejo. Z ustreznim in pravo~asnim
ukrepanjem lahko parodontalno bolezen prepre~imo ali
jo nadziramo.
Mehke zobne obloge je treba s š~etkanjem odstranjevati
vsak dan, veterinar pa naj po potrebi opravi zobni poseg.
Pri napredovali parodontalni bolezni je treba izdreti mo~no
prizadete zobe, ki se majejo.
2.) Resorpcija zob pri ma~ki (FORL – Feline odontoclastic
resorptive lesions )
Je ena najpogostejših obolenj ustne votline pri ma~ki,
prizadene 25 – 75 % ma~k. Za bolezen ni pasemske predispozicije, oba spola sta prizadeta enako, vendar število
prizadetih ma~k naraš~a s starostjo. Resorpcije zob ne
smemo zamenjevati s kariesom, ki se pri ma~kah ne po-
93
91
ZBORNIK REFERA
TOV
REFERATOV
javlja. Resorpcija zob se pojavlja tudi pri starejših psih, a
veliko redkeje.
Navadno se pri~ne na skleninsko cementni meji ali pod
njo, navadno na li~ni strani zoba. FORL je bolezen sodobnega ~asa, saj je na zobeh pri najdenih lobanjah izpred leta 1950 skoraj ni najti.
3.) Kroni~ni gingivostomatitis pri ma~ki, tudi
limfocitno plazmocitni gingivostomatitis
Stomatitis (vnetje ustne sluznice zaradi katerega koli vzroka) je zelo pogosto obolenje pri ma~kah, medtem ko se
pri psih pojavlja le pri ìvalih z oslabljenim imunskim sistemom, navadno ob kontaktu sluznice z zobmi, ki so
prekriti z zobnim plakom.
Pri ma~kah opazimo lokalno ali difuzno kroni~no vnetje
dlesni in ustne sluznice. Za enkrat ni znano, kaj je
povzro~itelj tega obolenja. Opazimo razli~ne stopnje vnetja
dlesni (gingivitis), li~ne sluznice, podro~ij lateralno od
glosopalatinalnih gub, ki se ga pogosto napa~no
poimenuje „faucitis“, jezika (glositis), trdega in mehkega
neba ali kombinacije teh. Poškodbe so navadno simetri~ne
in ve~krat izraène na mehkih tkivih v podro~ju premolarjev in molarjev kot pa incizivov in grabilcev.
Prizadete ma~ke te`ko jemljejo hrano, imajo teàve pri
poìranju, se slinijo in so brez apetita. Zanimivo je, da so
bolj prizadete ma~ke, ki ìvijo skupaj z drugimi ma~kami,
kot tiste, ki ìvijo same. Pri klini~nem pregledu ugotovimo zna~ilno vneto ustno sluznico, ìval ima lahko tudi
pove~ane bezgavke. Pregled krvi mnogokrat pokaè hipergamaglobulinemijo, ki je posledica kroni~ne antigenske stimulacije. Pri prizadetih ma~kah opravimo test za
FeLV/FIV, da izklju~imo moèn vzrok obolenja.
Literatura
1. Bonello D. Feline inflammatory, infectious and other oral conditions. V: Tutt C, Deeprose J, Crossley DA, eds. BSAVA Manual of
canine and feline dentistry. Glouchester: BSAVA, 2007: 126–47.
2. Gorrel C. Oral examination and recording. V: Gorrel C ed. Veterinary dentistry for the nurse and technician. Edinburg: Elsevier,
2005: 41–54.
3. Gracis M. Orodental anatomy and physiology. V: Tutt C, Deeprose J, Crossley DA, eds. BSAVA Manual of canine and feline dentistry.
Glouchester: BSAVA, 2007: 1–21.
4. König HE, Sautet J, Liebich HG. Digestive system (apparatus digestorius). V: König HE, Sautet J, eds. Veterinary anatomy of
domestic mammals. Stuttgart: Schattauer, 2004: 277-342.
5. Rigler L. Anatomija doma~ih ìvali. Splanhnologija. Ljubljana: Veterinarska fakulteta,1987: 22–53.
6. Rothuizen J, Schrauwen E, Theyse LFH, Verhaert L. Digestive tract. V: Rijnberk A, van Sluijs FJ, eds. Medical history and physical
examination in companion animals. Edinburg: Elsevier, 2009: 86–100.
94
92
ZBORNIK REFERA
TOV
REFERATOV
MAJHNE SKRIVNOSTI ZA BOLJŠE POÛTJE MA^K
Sara Suhadolc Scholten
Ma~ke veljajo za misteriozna in fascinantna bitja, ki v ljudeh, ki jih ne poznajo, vzbujajo strah ali celo nelagodje.
Zgodovina jih povezuje s ~arovnicami, zato so bile dolgo
~asa tako ma~ke, kot ~arovnice preganjane. Ko pa so se
ma~ke prikradle, bolje re~eno »pripredle« v naše domove,
so se nam za~ela postavljati nova vprašanja, kakšne te
ìvali sploh so.
Prvi znani predniki iz druìne ma~k (znanstveno ime Felidae) segajo 45 milijonov let nazaj. Predniki ma~ke, kakršno poznamo danes, pa segajo “samo” 8 do 10 milijonov
let nazaj. Podatki o za~etkih udoma~evanja ma~k so razli~ni
vendar nekatere teorije predpostavljajo da se je to dogajalo è 7000 let pred Kristusom.Nekateri pravijo, da ma~ke
ne bodo nikoli popolnoma udoma~ene, ker so samozadostne. Ljudje so ma~ke tolerirali, nikoli pa popolnoma
sprejeli. Zgodovinsko je trajalo kar nekaj let, da so zavzele takšno pozicijo in ugled, kot ga uìvajo danes (1).
Svetovni splet nam ponudi nekaj zanimivih številk o razširjenosti ma~k:
-
na svetu je pribli`no 200 milijonov ma~k
-
naši sosedje Italijani jih imajo 7 milijonov
Razmerja v številu ljudi in ma~k so slede~a:
-
svet 1:34
-
Avstrija 1:1
-
Evropa, Amerika 1:4 (2).
V ZDA je leta 2007 ìvelo pribli`no 81 milijonov ma~k,
povpre~no število ma~k na gospodinjstvo je 2,2 in za
obiske pri veterinarju so porabili 81 dolarjev (3).
Z ma~kami rokujemo ne`no, previdno in brez strahu. Ko
se jim pribliùjemo, jih nagovarjamo, in ko smo se
prepri~ali, da se ji lahko pribliàmo, to tudi storimo. Ker
so to ~iste ìvali, zahtevajo tudi v okolju, kot je veterinarska klinika, red in ~isto~o. Svojega novega domovanja na
kliniki se morajo privaditi, tako vizualno, kot tudi olfaktorno. Vonjave razkuìl, dišav, drugih ìvali, neo~iš~enih
straniš~ in stare hrane so za njih zelo mote~e. Kletka,
posode, straniš~e morajo biti vsaj enkrat dnevno
o~iš~ene. Njihovo vidno polje iz kletke naj bo ~im širše,
omogo~imo jim opazovanje z višine, ponudimo jim
skrivališ~e, kamor se lahko umaknejo. Ob vsakem hranjenju ma~ko vzamemo iz kletke, ~e je le mogo~e ji za~asno
odstranimo zaš~itni ovratnik, ponudimo ji ve~ razli~nih
vrst hrane, se z njo ukvarjamo. Po kon~anem hranjenju
ma~ko o~istimo. ê jo hranimo prisilno, lahko uporabimo ovratnik ali slin~ek, ki omogo~ata, da ostane dlaka in
okolica ma~ke ~ista. Lastniki, ki ma~ko na kliniki obiš~ejo,
naj bodo z njo sami. ê je le mogo~e, jih namestimo v
drug prostor, kjer se ma~ka druga~e ne zadrùje.
Higiena venske kanile in njene obveze se izvaja vsaj enkrat dnevno, obvezo odvijemo, preverimo stanje koè pod
obvezilnim materialom, preverimo ote~enost šape. ê
bolezen in karakter ma~ke dopuš~ata, ji omogo~imo sprehod po prostoru. Za nekatere ma~ke je priporo~ljivo, da
jih opazujemo na daljavo. Kontaktov z drugimi ma~kami
ali ìvalskimi vrstami se izogibamo pa ~eprav v doma~em
okolju z nekaterimi sobivajo.
Torej, za ma~ko, ki biva pri nas, si moramo vzeti ~as.
V Veliki Britaniji ìvi pribli`no 8 milijonov ma~k, od tega
92 % nepasemskih. Glavna razloga, zaradi katerih imajo
ljudje na Otoku ma~ke, sta ljubezen do ma~k (27%) in
uìvanje v njihovi dru`bi (27%) (4).
Literatura
Sara Suhadolc Scholten, dr.vet.med.
SI-1000 Ljubljana
1. Introduction to Feline Behaviour.In: Bonnie V. Beaver. Feline
behaviour:a guide for veterinarians,second edition.St. Louis,
Missouri:Saunders,2003:p.1-7
2. http://www.suite101.com/blog/shaya_weaver/
how_many_cats_are_there
3. http://www.avma.org/reference/marketstats/ownership.asp
4. http://www.pfma.org.uk/overall/pet-population-figures-.htm
[email protected]
95
93
ZBORNIK REFERA
TOV
REFERATOV
CELOSTNA OBRAVNAVA GERIATRI^NEGA STOMATOLOŠKEGA
PACIENTA – KLINI^NI PRIMER
Martina Krofi~, Nina Mlakar, Katerina Tomsi~, Alenka Seliškar,
Zlatko Pavlica, Nataša Tozon
UVOD
ANESTEZIJA IN POOPERACIJSKA OSKRBA
Adultna parodontalna bolezen (AP) je najpogostejša
bolezen ustne votline odraslih ma~k, saj prizadene
pribli`no 85 % populacije (1), sledi ji odontoklasti~na resorptivna poškodba (ORL), ki prizadene okoli 29 % populacije (2, 3). V prispevku je opisana celostna obravnava
ma~ka z napredovalo parodontalno boleznijo in ORL.
Deset dni po prvem pregledu smo opravili stomatološki
poseg v splošni anesteziji. Ma~ka smo premedicirali z
metadonom (Heptanon, Pliva) 0.125 mg/kg s.c. in po
preoksigenaciji s 100 % kisikom uvedli v anestezijo s propofolom (Propofol 1%, Fresenius Kabi) 6,25 mg/kg i.v.
Anestezijo smo vzdrèvali z izofluranom (Forane, Abbott
Laboratories Ltd.) v 100 % kisiku. Med anestezijo smo
ma~ku i.v. injicirali Hartmanovo raztopino v odmerku 5
ml/kg/h. Zaradi sistoli~nega šuma na srcu smo odmerek
izotoni~ne raztopine med anestezijo prepolovili, saj bi z
ve~jim odmerkom lahko preobremenili sr~noìlni sistem
in povzro~ili plju~ni edem. Po uvodu v anestezijo smo
ma~ku aplicirali antibiotik amoksicilin s klavulansko kislino (Augmentin, GSK) 20 mg/kg i.v. Med anestezijo smo
spremljali delni tlak izdihanega CO2 (ETCO2), koncentracijo
vdihanega in izdihanega izoflurana ter telesno temperaturo. Elektri~no aktivnost srca smo merili z elektrokardiografom, z Dopplerjevim merilcem pa smo neinvazivno
merili sistoli~ni arterijski tlak. Frekvenca srca je bila med
posegom med 120 in 140 utripov na minuto. Ma~ek je
med anestezijo dihal spontano s frekvenco okoli 20 vdihov na minuto, ETCO2 pa je bil med 33 in 40 mmHg.
Arterijski tlak je bil po uvodu v anestezijo nizek (70 mmHg),
verjetno zaradi vazodilatativnega u~inka propofola in izoflurana, zato smo ma~ku aplicirali sinteti~ni koloid (Gelofusine, B Braun Melsungen AG) v odmerku 0,3 ml/kg v
10 min. Po tem se je arterijski tlak zve~al na 90 mmHg.
KLINI^NI PREGLED IN PREDOPERACIJSKA
PRIPRAVA
Zaradi zmanjšanega apetita in ìvahnosti so na pregled
pripeljali ma~ka, kastrata, starega 20 let, s telesno maso
5,6 kg. Ma~ek je shujšal, v zadnjem mesecu ve~ pil in
uriniral ter imel zadah iz gob~ka. Pri pregledu smo ugotovili dehidracijo, tahikardijo, levostranski sistoli~ni šum
II. stopnje, vnetje dlesni in trde zobne obloge.
Hematološki, biokemi~ni (se~nina, kreatinin, alkalna fosfataza, alanin aminotransferaza, skupne beljakovine, albumini, koncentracija kalcija) in urinski parametri (kemi~na
analiza urina s testnim trakom, specifi~na teà urina,
merjena z refraktometrom in urinski sediment) ter raven
skupnega tiroksina (T4) v serumu so bili znotraj referen~nih
vrednosti, test na prisotnost specifi~nih protiteles proti
virusu ma~je imunske pomanjkljivosti (FIV) in prisotnost
virusa ma~je levkoze (FeLV) je bil negativen. Ma~ku smo
s.c. aplicirali 100 ml izotoni~ne infuzijske raztopine (Hartmanova raztopina, B Braun Melsungen AG) in nesteroidni analgetik meloksikam (Metacam, Boehringer Ingelheim
Vetmedica) 0,2 mg/kg. Zdravljenje z meloksikamom smo
nadaljevali 2 dni v odmerku 0,1 mg/kg p.o. Za zmanjšanje števila bakterij v ustni votlini smo predpisali mazanje
dlesni z gelom s klorheksidinom (Stomodine gel, ICF). @e
po enem dnevu se je ma~ku klini~no stanje izboljšalo,
samostojno je za~el jesti in postal je ìvahnejši.
Martina Krofi~, dr.vet.med., Nina Mlakar, dr.vet.med., Katerina Tomsi~, dr.vet.med., doc.dr.
Alenka Seliškar, dr.vet.med., prof.dr. Zlatko Pavlica, dr.vet.med., prof.dr. Nataša Tozon,
dr.vet.med.
SI-1000 Ljubljana
Med prebujanjem smo ma~ku aplicirali meloksikam v
odmerku 0,1 mg/kg i.v., 6 ur po premedikaciji pa smo
ponovili aplikacijo metadona. Aplikacijo antibiotika smo
ponovili 2 in 8 ur po prvem odmerku. Teko~insko homeostazo smo po posegu vzdrèvali z injiciranjem Hartmanove raztopine v odmerku 2 ml/kg/h i.v. Ma~ka smo
odpustili v doma~o oskrbo še isti dan in mu predpisali
analgetika meloksikam v odmerku 0,075 mg/kg/24 h p.o.
in tramadol (Tramal, Krka) 2,5 mg/kg/12 h p.o. za dva
dni. Antibioti~no zdravljenje smo nadaljevali deset dni z
amoksicilinom s klavulansko kislino (Synulox, Pfizer) 20
mg/kg p.o Lastnici smo svetovali, naj ma~ka pribli`no
teden dni hrani z mehko hrano.
96
94
ZBORNIK REFERA
TOV
REFERATOV
STOMATOLOŠKI POSEG
Ma~ek je imel kljub visoki starosti še vse zobe, ki so bili
prekriti z mehkimi in trdimi zobnimi oblogami. Na nekaterih zobeh smo z zobno sondo odkrili erozije sklenine,
ki so segale tudi v dentin. Dlesen ob njih je bila mo~no
pordela in je ob dotiku z inštrumentom zakrvavela. Vizualno in s pomo~jo parodontalne sonde smo dolo~ili
indeks vnetja dlesni in indeks mehkih ter trdih zobnih
oblog, izmerili globino dlesninega èpa, hkrati pa ugotovili mo`no razkrito razcepiš~e korenin in majavost zob.
Na vseh grabilcih je bila vidna recesija dlesni in posledi~no
izpostavljene korenine. Vsi li~niki in ko~niki, z izjemo spodnjega desnega ~etrtega li~nika in prvega ko~nika, so imeli
globino sondiranja 2 mm ali ve~.
Zaradi brezupne napovedi izida zdravljenja AP in ORL smo
se odlo~ili za izdrtje vseh grabilcev in vseh li~nikov razen
408 ter ko~nikov 209 in 309. Najprej smo z zvo~nim
luš~ilcem odstranili mehke in trde zobne obloge nad in
pod dlesnijo ter ustno votlino temeljito sprali z vodnim
sprejem. Enokoreninske li~nike in ko~nike smo izdrli z
metodo zaprte tehnike izdiranja, ve~koreninske li~nike ter
ko~nike pa smo najprej razdelili v enokoreninske fragmente in jih nato izdrli z metodo odprte tehnike izdiranja.
Prav tako smo z odprto tehniko izdrli grabilce, kjer smo
pri spodnjih odstranili del kosti z lingvalne strani.
RAZPRAVA
Parodontalno bolezen predstavljajo vnetne spremembe
parodoncija (dlesni, alveolarne kosti, cementa in pozobnice) povzro~ene z mehkimi zobnimi oblogami (4). Parodontitis odraslih ma~k AP je ena od oblik te bolezni, ki se
pri~ne è kmalu po erupciji stalnih zob, vendar se zaradi
po~asnega napredovanja klini~no pokaè šele kasneje (1).
Pri ma~ki z omenjeno boleznijo klini~no opazimo mehke
in trde zobne obloge, razli~ne stopnje vnetja dlesni, majavost zob, lahko pa tudi è izpostavljeno koreninsko
razcepiš~e. Na podlagi ocene parodontalnega statusa se
odlo~imo za obseg zdravljenja, saj bolezen predstavlja vir
kroni~ne oku`be organizma. Sistemski u~inki se pojavijo
zaradi delovanja eksotoksinov in endotoksinov ter prehodne bakteriemije ob grizenju in stomatoloških posegih. Zaradi parodotitisa se lahko pojavijo bolezni srca in
oìlja (endokarditis, okluzije koronarnih arterij, miokardni infarkt, diseminirana intavaskularna koagulacija, šok),
bolezni dihal (kroni~ni bronhitis, kroni~no obstruktivno
obolenje plju~, fibroza, emfizem), ledvic (degeneracija
tubulov, limfoplazmocitni intersticijski nefritis, pielitis),
jeter (vnetje parenhima, fibrozacijske spremembe portalnega sistema), sladkorna bolezen in druge (5).
pozni fazi, ko zajame sklenino ali vrat zoba, saj je pogosto pokrita z vneto in hiperplasti~no dlesnijo. Lahko vodi
tudi do zloma krone oz. njene popolne resorpcije in pokritja
ostanka zoba z dlesnijo (6). Najpogosteje sta prizadeta
spodnja tretja li~nika. Pri ve~ini ma~k se ORL pojavlja
simetri~no (7). Do danes še ni u~inkovite preventive ORL,
zato moramo prizadete zobe najve~krat izdreti. V primeru ankiloze koreninskega dela zoba pa se lahko na podlagi rentgenskega izvida odlo~imo le za amputacijo krone
(4).
Ma~ek je ob prvem pregledu kazal nezna~ilne klini~ne
znake. V primeru take klini~ne slike moramo predvsem
pri geriatri~nih pacientih izklju~iti kroni~no ledvi~no
odpoved in bolezni jeter, kar smo izklju~ili na osnovi laboratorijskih preiskav krvi in urina (8). Pri starejših ma~kah
pogosteje pri~akujemo hipertireoidizem, še posebej, ~e
se pojavijo nekateri ali vsi od naštetih klini~ni znakov: tahikardija, sistoli~ni sr~ni šum, poliurija, polidipsija in
neješ~nost (9). Ker je bil ma~ek v stiku z drugimi ma~ki,
smo opravili test na FeLV in FIV, saj se kroni~ni gingivitis,
stomatitis in parodontitis lahko pojavijo tudi v povezavi s
tema boleznima. FeLV in FIV sta pogostejši pri mlajših
ma~kah, kljub temu pa je poznavanje stanja pomembno
za prognozo zdravljenja sprememb v ustni votlini (10,
11).
Glede na slabo splošno stanje ma~ka ob prvem pregledu
smo ga najprej rehidrirali in mu nudili ustrezno analgezijo, zaradi ~esar je ma~ek pri~el jesti è naslednji dan. Po
stomatološkem posegu smo teàve v ustni votlini odpravili.
Vzrok vnetja in bole~ine je bil dokon~no odstranjen, ìval
pa je lahko ponovno zaìvela kvalitetno ìvljenje.
ORL je do danes znana kot idiopatska resorpcija zobnih
struktur z odontoklasti, ki se pri~ne na koreninskem cementu, nadaljuje v dentin, prizadene pa tudi sklenino.
Uni~en cement in pozobnico nadomesti kosti podobno
tkivo, kar privede do zraš~anja zoba z okolno kostjo (ankiloza zoba) (4). Poškodba na zobu postane vidna šele v
97
95
ZBORNIK REFERA
TOV
REFERATOV
LITERATURA
1. Wiggs RB, Lobprise HB. Domestic feline oral and dental disease. In: Wiggs RB, Lobprise HB, eds. Veterinary Dentistry Principles
and Practice. Philadelphia: Lippencott-Raven, 1997; 485.
2. Ingham KE et al. Prevalence of odontoclastic resorptive lesions in a population a clinically healthy cats. JSAP 2001; 42, 439-443.
3. Reiter AM, Nachreiner RF. Evaluation of calciotropic hormones in cats with odontoclastic resorptive lesions. American Journal of
Veterinary Research 2005; 66, 1446-1452.
4. Gorrell C. Small animal dentistry, Saunders solutions in veterinary practice. Elsevier Health Sciences, 2008.
5. Pavlica Z. Sistemski u~inki parodontalne bolezni pri psih. Veterinarske novice 2002; 28: 53- 61.
6. Dumais Y. Feline odontoclastic resorptive lesions. WSAVA, Vancouver, 2001.
7. Gorrel C. Feline odontoclastic resorptive lesions. WSAVA, Bangkok 2003.
8. Feldman EC. Polyuria and polydipsia. In: Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, 6th ed.,
Philadelphia: Elsevier, 2006; 102-105.
9. Rijndberk, A. Thyroids. In: Rijndberk A, Kooistra H, eds. Clinical endocrinology of dogs and cats. 2nd edition,
Hannover: Schlutersche, 2010; 73.
10. Sellon RK., Hartmann K. Feline Immunodeficiency virus infection. In: Greene CE: Infectious diseases of the dog and cat.
Georgia: Saunders, 2006; 131-143.
11. Hartmann K.. Feline Viral Leukemia virus infection. In: Greene CE: Infectious diseases of the dog and cat.
Georgia: Saunders, 2006; 105-130.
98
96
ZBORNIK REFERA
TOV
REFERATOV
KVANTITATIVNO DOLOÂNJE KONCENTRACIJE CRP PRI
PSIH Z UPORABO NOVE IMUNOKEMIJSKE METODE
Alenka Nemec Svete, Barbara Lukanc, Katerina Tomsi~, Alenka Seliškar
Izvle~ek
Uvod
C-reaktivni protein (CRP) je najpomembnejši protein akutne
faze vnetja, tako pri ljudeh kot tudi pri psih. Pove~ano
koncentracijo CRP pri psih so ugotovili po kirurških posegih, pri infekcijskih in vnetnih boleznih. Za dolo~anje
koncentracije pasjega CRP obstajajo številne imunokemijske metode. Ve~ina teh je zelo zamudnih in zahtevajo
posebej izurjeno osebje in aparature. V naši raziskavi smo
preizkusili najnovejšo imunokemijsko metodo, osnovano
na merjenju magnetne permeabilnosti, ki omogo~a dolo~anje koncentracije CRP v serumu psov v samo 11 minutah
C-reaktivni protein (CRP) spada med najpomembnejše
proteine akutne faze vnetja, tako pri ljudeh kot tudi pri
psih. Sintetizira in sproš~a se iz hepatocitov kot odgovor
na pove~an nivo proinflamatornih citokinov (IL-6, TNFα) v sistemskem krvnem obtoku. Ime je dobil zaradi svoje
lastnosti, da reagira s somatskim C-polisaharidom
pnevmokoka (Streptococcus pneumoniae) (1,2,3). V humani medicini sluì dolo~anje CRP kot pokazatelj vnetnega dogajanja. Koncentracija CRP se zna~ilno pove~a pri
poškodbah tkiva zaradi bakterijske infekcije in po operacijah. Pri virusnih oku`bah praviloma ni povišanja CRP,
zato lahko pri ljudeh hitro in zanesljivo razlikujemo med
bakterijskimi in virusnimi infekcijami (1).
Abstract
C-reactive protein (CRP) is the major acute phase protein
in man and dog. Increased concentration of CRP was
determined in dogs after surgery and dogs with infectious disease and chronic inflammatory disease. There
are several immunochemistry methods for determination
of canine serum or plasma CRP concentration, majority
of them are time consuming, require well-trained personnel and specialized equipment. New immunochemistry method, based on the measurement of magnetic permeability, which enables the determination of canine CRP
concentration in 11 minutes, was used in the present
study.
Pri zdravih psih je CRP prisoten v nizkih koncentracijah.
Koncentracija CRP se zna~ilno pove~a pri psih po kirurških posegih, pri infekcijskih in vnetnih boleznih (2,4).
Študije potrjujejo uporabnost dolo~anja CRP pri spremljanju poteka zdravljenja s kortikosteroidi, saj le-ti vplivajo na število levkocitov in absolutno število nevtrofilcev,
na parametra, ki se sicer uporabljata za spremljanje poteka vnetnih bolezni (5,6). Za dolo~anje serumske oziroma
plazemske koncentracije CRP pri psih obstajajo številne
komercialno dostopne imunokemijske metode (7,8,9), ki
pa so zaradi na~ina izvajanja zelo zamudne, zahtevajo
ustrezne aparature in so namenjene analizi ve~jega števila
vzorcev hkrati, kar je za klini~no prakso nesprejemljivo.
Uporaba humanih imunokemijskih metod ni priporo~ljiva
zaradi razli~nih antigenskih lastnosti pasjega in ~loveškega
CRP (10).
V okviru preliminarne raziskave smo preizkusili najnovejšo imunokemijsko metodo, osnovano na merjenju magnetne permeabilnosti, ki omogo~a dolo~anje koncentracije
CRP v serumu psov v samo 11 minutah (11).
doc.dr. Alenka Nemec Svete, univ.dipl.in`.kem.in`., asist.dr. Barbara Lukanc, dr.vet.med.,
Katerina Tomsi~, dr.vet.med., doc.dr. Alenka Seliškar, dr.vet.med.
SI-1000 Ljubljana
[email protected]
99
97
ZBORNIK REFERA
TOV
REFERATOV
Materiali in Metode
Rezultati in Razprava
V raziskavo smo vklju~ili 18 psov razli~nih pasem, spola
in starosti, pri katerih smo opravili razli~ne kirurške in
stomatološke posege (Tabela 1). Zdravstveni status smo
dolo~ili na osnovi klini~nega pregleda ter rezultatov hematoloških in biokemijskih preiskav (podatki, razen števila
levkocitov, niso prikazani). Serumsko koncentracijo CRP
smo dolo~ali z imunokemijsko metodo (LifeAssays Canine CRP Test Kit, Sweden). Spodnja meja detekcije metode je 10 mg/L, zgornja pa 140 mg/L.
Koncentracija CRP je bila pri psih (n=12), pri katerih s
klini~nim pregledom in laboratorijskimi preiskavami nismo ugotovili sprememb splošnega zdravstvenega statusa, v mejah normalnih vrednosti (7,8,12) to je v razponu od < 10 mg/L do 17 mg/L (Tabela 1). Pri ostalih
psih smo, v skladu z literaturnimi podatki, dolo~ili
pove~ano koncentracijo CRP (2).
Tabela 1: Koncentracija CRP in število levkocitov pri zdravih in bolnih ìvalih
CRP (mg/L)
levkociti (x 109/L)
Podatki o psu
Poseg
1
psica, X, 5 mesecev, zdrava
ovariektomija
17,0
8,98
2
pes, X, 10 let, zdrav
higiena ustne votline in orhiektomija
70,0
9,62
3
psica, X, 2 leti, zdrava
ovariektomija
13,0
6,69
4
psica, YT, 4 leta, zdrava
ovariektomija
16,0
7,24
5
pes, YT, 7 let, parodontalna bolezen,
epileptik
higiena ustne votline, ekstrakcija zob
76,0
9,28
6
pes, TM, 2 leti, zdrav
zobna akrilatna opornica
32,0
/
7
psica, GR, 6 let, ileus
mediana laparotomija, gastrotomija,
resekcija dela ~revesja
270,0
22,19
8
pes, X, 11 let, lumbosakralna stenoza
dorzalna laminektomija
<10,0
6,04
9
psica, X, 8 let, kroni~ni apikalni
parodontitis 208
ekstrakcija zoba
<10,0
8,25
10
psica, NB, 4 leta, ruptura kolenskih
kri`nih vezi levo, kroni~ni gonitis
tehnika »over the top« ter delna
odstranitev ve~jih kostnih izrastkov
<10,0
10,18
11
psica, JKP, 5 let, raztrganina na
levem stegnu
šivanje rane
<10,0
/
12
psica, X, 14 let, ruptura kolenskih
kri`nih vezi levo, epileptik
tehnika po Gambardelliju,
oànje kapsule
<10,0
13,34
13
pes, IS, 14 let, atrofija mod in
nadmodkov ter vaskularni hamartom
desnega nadmodka
orhiektomija in elektrokemoterapija
<10,0
9,18
14
psica, X, 7 let, ugrizne rane
šivanje ran
78,0
18,94
15
pes, BS, 8 let, ko`ni hemangiopericitom
na desnem komolcu
odstranitev novotvorbe, torakalni
aksialni dorzalni reènj
<10,0
12,57
16
pes, GR, 12 let, prostati~na cista
orhiektomija, biopsija prostate
16,0
12,37
17
pes, MO, 5 let, parodontalna bolezen,
osteomielitis susp.
higiena ustne votline, gingivektomija
21,0
13,24
18
pes, X, 9 let, ruptura kolenskih
kri`nih vezi desno
tehnika »over the top«, meniskotomija
<10,0
8,99
19
psica, X, 13 let, gnojno vnetje maternice
ovariohisterektomija
155,0
30.37
20
psica, CAT, 12 let, gnojno vnetje
maternice
ovariohisterektomija
92,0
22,29
100
98
ZBORNIK REFERA
TOV
REFERATOV
Zaklju~ek
Nova imunokemijska metoda za dolo~anje CRP v serumu
psov je enostavna in hitra za uporabo. Za ugotavljanje
diagnosti~ne uporabnosti metode pri razli~nih boleznih
oziroma spremljanja poteka zdravljenja bodo potrebne nadaljnje študije.
Literatura
1. Pepys MB, Hirschfield GM. C-reactive protein: a critical update. J Clin Invest 2003; 111: 1805-1812.
2. Nakamura M, Takahashi M, Ohno K, e tal. C-reactive protein concentration in dogs with various diseases. J Vet Med Sci 2008; 70:
127-131.
3. Yamashita K, Fujinaga T, Miyamoto T, Hagio M, Izumisawa Y, Kotani T. Canine acute phase response: relation between serum
cytokine activity and acute phase response. J Vet Med Sci 1994; 56: 487-492.
4. Yamamoto S, Shida T, Miyaji S, et al. Changes of serum C-reactive protein levels in dogs with various disorders and surgical
traumas. Vet Res Commun 1993a; 17: 85-93.
5. Ohno K, Yokoyama Y, Nakashima K, Setoguchi, Fujino Y, Tsujimoto H. C-reactive protein in canine idiopathic polyarthritis. J Vet
Med Sci 2006; 68: 1275-1279.
6. Kjelgaard-Hansen M, Jensen AL, Houser GA, Jessen LR, Kristensen AT. Use of serum C-reactive protein as an early marker of
inflammatory activity in canine type II immune-mediated polyarthritis: a case report. Acta Vet Scand 2006; 48:9 doi:10.1186/17510147-48-9
7. Kjelgaard-Hansen M, Kristensen AT, Jensen AL. Evaluation of a commercially available enzyme-linked immunosorbent assay (ELISA)
for the determination of C-reactive protein in canine serum. J Vet Med 2003; 50: 164-168.
8. Yamamoto S, Shida T, Okimura T, Otabe K et al. Determination of C-reactive protein in serum and plasma from healthy dogs and
dogs with pneumonia by ELISA and slide reverse passive latex agglutination test. Vet Q 1994; 16: 74-7.
9. Eckersall PD, Conner JG, Harvie J. An immunoturbidimetric assay for canine C-reactive protein. Vet Res Commun 1991; 15: 17-24.
10. Yamamoto S, Miyaji S, Abe N, Otabe K, Furukawa E, Naiki M. Canine C-reactive protein (CRP) does not share common antigenicity
with human CRP. Vet Res Commun 1993b; 17: 159-66.
11. Ibraimi F, Kriz K, Merin H, Kriz D. Magnetic permeability based diagnostic test for the determination of the C-reactive protein
concentration in undiluted whole blood. J Magn Mahn Mater 2009; 321: 1632-1634.
Otabe K, Sugimoto T, Jinbo T, et al. Physiological levels of C-reactive protein in normal canine sera. Vet Res Commun 1998;
22: 77-85.
101
99
ZBORNIK REFERA
TOV
REFERATOV
HEMOBARTONELOZA PRI MA^KI – KLINI^NI PRIMER
Urška Ravnik, Sara Suhadolc Scholten, Nataša Tozon
Hemobartonelozo povzro~ajo gram – negativni epicelularni mikroorganizmi, uvrš~eni v rod Mycoplasme. Zaradi afinitete do eritrocitov jih ozna~ujemo s predpono hemo
– hemoplazme oziroma hemotrofne mikoplazme. S
pomo~jo molekularnih metod so pri ma~kah potrdili dve
razli~ni vrsti: Haemobartonela felis large = Mycoplasma
haemofelis (M. haemofelis) in Haemobartonela felis small
= Mycoplasma haemominutum (M. haemominutum).
Ve~ino klini~no zaznavnih oku`b povzro~a M. haemofelis, medtem ko oku`ba z M. haemominutum obi~ajno
poteka klini~no nezaznavno in/ali z minimalnimi laboratorijskimi odstopanji, razen pri so~asni oku`bi z virusom
FeLV.
Najpogostejša pot oku`be naj bi bila s krvosesnimi zajedalci (bolhe, klopi), vendar omenjenega na~ina prenosa
eksperimentalno niso mogli potrditi. Opisujejo tudi
mo`nost vertikalnega prenosa, ki ravno tako ostaja nepotrjen.
Ni povsem raziskano, ali je Mycoplasma haemocanis (M.
haemocanis), prej Haemobartonela canis, samo izolat M.
haemofelis, ali gre za drugo vrsto. Bolezen, ki jo povzro~a,
pa je pri psih bistveno redkejša in manj pomembna.
Klini~ni znaki hemobartoneloze pri ma~kah so odvisni od
stopnje anemije, faze bolezni in imunskega statusa ìvali.
Najpogostejši klini~ni znaki so neposredno povezani z
anemijo: blede sluznice, depresija, neješ~nost, oslabelost,
lahko ikterus in splenomegalija. Akutno oku`bo obi~ajno
spremlja povišana temperatura, ki se lahko intermitentno
pojavlja tudi pri kroni~ni oku`bi. Ma~ke v kroni~ni fazi so
lahko subklini~no okuène. Pri njih lahko pride do izbruha klini~ne oblike bolezni po razli~nih stresnih stanjih ali
ob so~asnem pojavu druge bolezni.
Diagnozo postavimo z mikroskopskim pregledom razmaza
periferne krvi pobarvanega s klasi~nimi metodami barvanja, pri katerem vidimo povzro~itelja na površini eritrocitov. Ker število organizmov variira, je lahko rezultat mik-
Urška Ravnik, dr.vet.med., Sara Suhadolc Scholten, dr.vet.med., prof.dr. Nataša Tozon,
dr.vet.med.
SI-1000 Ljubljana
roskopskega pregleda la`no negativen v do 50 % primerov, zato je pri mo~nem sumu ob negativnem rezultatu
potreben dnevni pregled krvnih razmazov 7 dni zapored.
Zanesljivejša metoda dokaza oku`be je PCR, ki je
ob~utljivejša in s katero lahko lo~imo med posameznimi
vrstami povzro~itelja.
V prispevku opisujemo klini~ni primer oku`be z M.
haemofelis pri doma~em kratkodlakem ma~ku, starem 2
leti, ki je bil na Kliniki za kirurgijo in male ìvali sprejet
zaradi apati~nosti, inapetence in kaheksije. V anamnezi
so lastniki povedali, da je ma~ek kastriran, prete`no zunanji, cepljen proti panlevkopeniji in oku`bam zgornjih dihal,
redno razglisten, FeLV/FIV negativen. Prve teàve so opazili pred štirimi meseci, ko je bil ma~ek sprejet pri drugem veterinarju, kjer so ugotovili povišano telesno temperaturo, pove~ane površinske bezgavke in anemijo. Ob
sprejemu na naši kliniki je bil ma~ek afebrilen, apati~en,
kahekti~en, tahikarden, z izrazito anemi~nimi sluznicami
in ikteri~nimi belo~nicami.
Vzorec polne krvi z EDTA smo analizirali s hematološkim
analizatorjem (Technicon H-1TM System). Prvi rezultati
hematološke analize krvi pri ma~ku so pokazali levkocitozo (19,40x109 g/L; referen~na vrednosti 5,5-19,5x109 g/
L) in anemijo (število eritrocitov 0,66x1012/L; referen~na
vrednost 5-10x1012/L, hematokrit 0,05 L/L; referen~na
vrednost 0,30-0,45L/L). Odstotek retikulocitov v razmazu polne krvi je znašal 0,4 %, dejanska vrednost, popravljena na obstoje~i hematokrit, je torej 0,04 %, kar kaè na
neregenerativno anemijo (referen~na vrednost 0,4-6,4%).
Mikroskopska preiskava krvnega razmaza je pokazala prisotnost zna~ilno razporejenih epieritrocitnih mikroorganizmov, kar potrjuje sum na M. haemofelis.
Ma~ek je bil hospitaliziran, pri~eli smo s terapijo z doksiciklinom (Clinofug D 50 mg ®, Dr. August Wolff) 10
mg/ kg tt/24 ur. Dnevno spremljanje hematokrita ni pokazalo bistvenega porasta, zato smo ma~ku kljub izboljšanju klini~nega stanja po šestih dneh dali transfuzijo polne
krvi (30 ml). Hematokrit je bil dan po transfuziji ni`ji od
pri~akovanega, zato smo terapijo dopolnili z metilprednizolonom (Medrol®, Pfizer Luxemburg) v imunosupresivni dozi 2mg/kg tt/24 ur. Ma~ek se je na terapijo dobro
102
100
ZBORNIK REFERA
TOV
REFERATOV
odzval in bil po dveh dneh odpuš~en v doma~o oskrbo.
Antibioti~no zdravljenje je nadaljeval še 3 tedne, imunosupresivno pa do prve kontrole, 10 dni po pri~etku zdravljenja. Prva kontrola hematokrita je pokazala porast,
klini~no stanje ma~ka je bilo odli~no, zato smo se odlo~ili,
da imunosupresivno zdravljenje postopno zmanjšamo
(2mg/kg tt/48ur) in po enem mesecu popolnoma ukinemo. Ob popolni ukinitvi terapije je prišlo do relapsa.
Ma~ek tako ostaja na terapiji z metilprednizolonom v dozi
1mg/kg tt/24 – 48 ur od novembra 2008, se odli~no
po~uti, hematokrit je v mejah referen~nih vrednosti. V
obdobju zdravljenja pa do danes prejema ma~ek še podporno terapijo, ki vsebuje vitamine in makro elemente
(Hemolitan pet®, Vetnil Brazilija) v dozi 1gtt/kg tt/12 ur.
Anemija pri hemobartonelozi se obi~ajno pojavlja cikli~no,
kar je rezultat cikli~nega pojavljanja povzro~itelja v krvnem
obtoku. Epizode anemije so obi~ajno povezane s povišano temperaturo in levkocitozo ter nastanejo kot posledica sekvestracije okuènih eritrocitov v retikuloendotelnem sistemu in skrajšani ìvljenjski dobi celic. Pomembnejša od neposredne poškodbe eritrocitov pa je imunsko pogojena poškodba, ki je posledica vezave povzro~itelja
na steno eritrocita, kar lahko razkrije ali spremeni eritrocitne antigene, zaradi ~esar pride do nastanka antieritrocitnih protiteles. Razvije se sekundarna avtoimuna
hemoliti~na anemija (sAIHA), ki zaradi mo`nosti prehoda bolezni v kroni~no obliko lahko zahteva doìvljenjsko
zdravljenje.
Zdravljenje hemobartoneloze s hujšo obliko anemije je
sicer priporo~ljivo è v za~etni fazi kombinirati z imunosupresivnimi zdravili, s katerimi zmanjšamo eritrofagocitozo. Po zvišanju hematokrita poskusimo imunosupresivna zdravila postopno ukiniti, vendar moramo pacienta
spremljati. Kljub morebitnemu negativnemu krvnemu
razmazu na prisotnost povzro~itelja je namre~ lahko prisoten imunski odgovor organizma in posledi~no sAIHA,
kar zmanjša mo`nost popolne ukinitve zdravil.
Brez ustreznega zdravljenja zaradi anemije pogine
pribli`no tretjina ma~k z akutno hemobartonelozo. Tiste,
ki akutno fazo preìvijo, imajo dobro prognozo, vendar
lahko doìvijo relaps ob pojavu druge bolezni oziroma
stresnega stanja. Zato je pomembno, da pri pacientu, pri
katerem diagnosticiramo hemobartonelozo, ne zanemarimo morebitne prisotnosti primarne bolezni, ki je potencialno pripeljala do akutizacije hemobartoneloze.
LITERATURA
1. Harvey JW. Haemobartonellosis. In: Greene CE, ed. Infectious Diseases of the Dog and Cat, 2nd edition, Philadelphia: Saunders
Company, 1998: 166 – 71.
2. Geiger U. Regenerative Anemias Caused by Blood Loss or Hemolysis. In:Ettinger SJ, Feldman EC, eds. Veterinary Internal Medicine,
6th edition, Missouri: Elsevier Saunders, 2005:1902 – 4.
103
101
ZBORNIK REFERA
TOV
REFERATOV
HIPERALDOSTERONIZEM PRI MA^KAH –
POGOSTEJŠI KOT SI MISLIMO ?
Tanja Plavec
UVOD
Primarni hiperaldosteronizem je posledica novotvorbe ali
hiperplazije klob~i~aste plasti nadledvi~ne `leze, ki vodi v
pove~ano izlo~anje aldosterona in posledi~no motnjo homeostaze natrija in kalija. Klini~ni znaki so ve~inoma odraz
hipokaliemije ter hipernatriemije. Bolezen diagnosticiramo klini~no, laboratorijsko in s pomo~jo slikovne diagnostike. Zdravljenje je v primeru enostranskega tumorja
kirurško, v primeru obojestranske hiperplazije pa medikamentozno.
Izlo~anje aldosterona iz klob~i~aste plasti (cone glomeruloze) nadledvi~ne `leze v fizioloških pogojih poteka pod
vplivom stimulacije sistema renin-angiotenzin-aldosteron (RAAS) (1-3), kalija in ACTH (1,4). Aldosteron je glavni
mineralokortikoid, ki deluje na mineralokortikoidne receptorje v distalnih tubulih ledvic, v kolonu in slinskih `lezah
ter s tem vzpodbuja reabsorbcijo natrija ter izlo~anje kalija in vodika. Retencija natrija vodi v ekspanzijo volumna
ekstracelularne teko~ine (1,3).
Poznamo primarni ali sekundarni hiperaldosteronizem. Pri
primarnem hiperaldosteronizmu (PHA), tumorske ali
hiperplasti~ne celice klob~i~aste plasti avtonomno izlo~ajo
aldosteron. Mehanizem negativne povratne zveze vodi v
nizko ali normalno aktivnost plazemskega renina (PRA)
(2,5,6), sekundarni hiperaldosteronizem pa se pojavi kot
odgovor na aktivacijo sistema renin-angiotenzin-aldosteron, ki ga sproì hipovolemija ali zmanjšanje u~inkovitega volumna krvi, pri ~emer pri~akujemo visoko PRA
(6). Stanja so lahko posledica jetrne ciroze, popuš~anja
ledvic ali kongestivnega popuš~anja srca (3).
Primarni hiperaldosteronizem (tudi Connova bolezen) lahko delimo na dva glavna podtipa: enostranski, ki je posledica adenoma ali adenokarcinoma nadledvi~ne `leze, ali
obojestranski, ki je posledica hiperplazije nadledvi~ne `leze
(tudi idiopatski hiperaldosteronizem). Obe patologiji vodi-
asist.dr. Tanja Plavec, dr.vet.med.
SI-1000 Ljubljana
[email protected]
ta v pove~ano izlo~anje aldosterona, ki ni ve~ pod vplivom
fizioloških spodbujevalnih/zaviralnih mehanizmov. In ker
je aldosteron glavni regulator homeostaze natrija
(pove~ano zadrèvanje v organizmu in posledi~no
pove~anje ekstracelularne prostornine teko~ine) in kalija
v organizmu (pove~ana kaliureza), so klini~ni znaki posledica motnje homeostaze teh dveh mineralov (2).
V veterinarski literaturi je trenutno opisanih 31 primerov
PHA pri ma~kah. Le-to povzro~ajo unilateralni karcinomi
skorje nadledvi~ne `leze (10/31), manj je unilateralnih
adenomov skorje (6/31), bilateralnih adenomov (2/31) in
bilateralne hiperplazije skorje nadledvi~ne `leze (3/31); pri
ostalih primerih vzrok ni opisan (6).
Klini~ni znaki, ki se ob primarnem hiperaldosteronizmu
pojavijo, so tipi~no posledica sistemske hipertenzije zaradi
volumske ekspanzije krvi (z o~esnimi krvavitvami, slepoto, odstopom mre`nice, nevrološkimi znaki in motnjami
obnašanja) in/ali polimiopatije zaradi hipokaliemije (ventrofleksija glave, oslabelost okon~in, ataksija) (2,3), pojavljajo se tudi poliurija, podipsija, polifagija in hujšanje
(7); hipokaliemija pa lahko vodi tudi v razli~ne sr~ne aritmije ali kaliopeni~ne nefropatije. Ti znaki so lahko hudi in
se pojavijo akutno, lahko pa se znaki pojavijo intermitentno in v bla`ji obliki (2).
Bolezen diagnosticiramo na podlagi klini~nih znakov, laboratorijske potrditve kipokaliemije, povišane vrednosti kreatin kinaze, hipernatriemije, povišane koncentracije plazemskega aldosterona in zniàne aktivnosti plazemskega renina ter povišanim razmerjem med tema dvema vrednostma (3), pojavljajo se lahko tudi alkaloza, hipofosfatemija,
ter hipomagnezemija (8). Referen~ne vrednosti za PAC
so 110 – 540 pmol/l oziroma 40 – 195 pg/ml, za PRA 60
– 630 fmol/l/s oziroma 0,3 – 3 ng/ml/s, za razmerje
PAC:PRA pa 0,3 – 3,8 (9). V študiji, kjer je bilo opisanih
11 ma~k s primarnim hiperaldosteronizmom najverjetneje zaradi bilateralne hiperplazije klob~i~aste plasti (histološka diagnoza potrjena samo pri treh ma~kah v tej
študiji) vrednosti aldosterona niso bile tako povišane kot
pri ma~kah s tumorji nadledvi~ne `leze in tudi vrednosti
PRA niso bile toliko zniàne kot v primeru tumorjev (4).
Ultrazvo~no ali s pomo~jo ra~unalniške tomografije ali
magnetne resonance lahko ugotovimo pove~anje ene ali
obeh nadledvi~nih `lez, z venografijo preko vene saphe104
102
ZBORNIK REFERA
TOV
REFERATOV
nae lateralis pa lahko ugotovimo potencialno invazivno
rast v v. cavo caudalis (3,5). Normalna dolìna nadledvi~ne
`leze pri odraslih, zrelih ma~kah je 10,7 ± 0,4 mm, maksimalni premer oziroma debelina pa 4,34 ± 0,3 mm (10).
Zdravljenje je v primeru enostranskega pove~anja
nadledvi~ne `leze kirurško (enostranska adrenalektomija
in po potrebi trombektomija) (7), v primeru obojestranske hiperplazije ali tumorja nadledvi~ne `leze z zasevki pa
simptomatsko: nadomeš~anje kalija v obliki kalijevega
glukonata (2 6 mmol PO BID) in/ali kalijevega klorida,
aplikacija antagonistov aldosterona (npr. spironolakton 2
4 mg/kg PO SID) in zdravil za zniànje krvnega tlaka (npr.
amlodipin 0,125 mg/kg PO SID – BID). Klini~ni znaki
polimiopatije se dobro odzovejo na nadomeš~anje kalija
in zdravljenje s spironolaktonom, ~eprav serumska koncentracija kalija v veliki ve~ini primerov ostane pod
referen~nimi vrednostmi (3).
Prognoza ma~k, ~e preìvijo akutno perioperativno obdobje, kjer je glavna komplikacija krvavitev, je dobra in ni
odvisna od tipa tumorja (adenom ali karcinom) (3).
ZAKLJUÊK
Primarni hiperaldosteronizem moramo vklju~iti med diferencialne diagnoze pri vseh srednje starih in starih ma~kah
s hipokaliemi~no polimiopatijo in/ali sistemsko hipertenzijo in je ne smemo ve~ smatrati za redko bolezen. Po
adrenalektomiji lahko doseèmo zelo dobre ~ase remisije
(do pet let), vendar sam poseg s sabo nosi precejšnje
tveganje med in postoperativnih krvavitev. Medikamentozno zdravljenje s spironolaktonom in nadomeš~anjem
kalija v ve~ini primerov odpravi znake polimiopatije, zdravljenje z amlodipinom pa znake arterijske hipertenzije,
~eprav je ta v nekaterih primerih refrakterna na zdravljenje (3).
LITERATURA
1. Flood SM, Randolph JF, Gelzer ARM, Refsal K. Primary hyperaldosteronism in two cats. J Am Anim Hosp Assoc 1999; 35: 411-6.
2. MacKay AD, Holt PE, Sparkes AH. Successful surgical treatment of a cat with primary aldosteronism. Case report. Journal of Feline
Medicine and Surgery 1999; 1: 117-22.
3. Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. Journal of Feline Medicine and Surgery
2005; 7: 173-82.
4. Javadi S, Djajadiningrat-Laanen SC, Kooistra HS et al. Primary hyperaldosteronism, a mediator of progressive renal disease in cats.
Domestic Animal Endocrinology 2005; 28: 85-104.
5. Moore LE, Biller DS, Smith TA. Use of abdominal ultrasonography in the diagnosis of primary hyperaldosteronism in a cat. J Am Vet
Med Assoc 2000; 217 (2): 213-5.
6. Briscoe K, Barrs VR, Foster DF, Beatty JA. Hyperaldosteronism and hyperprogesteronism in a cat. Case report. Journal of Feline
Medicine and Surgery 2009; 11: 758-62.
7. Rose SA, Kyles AE, Labelle P et al. Adrenalectomy and caval thrombectomy in a cat with primary hyperaldosteronism. J Am Anim
Hosp Assoc 2007; 43 (4): 209-14.
8. DeClue AE, Breshears LA, Pardo ID, Kerl ME, Perlis J, Cohn LA. Hyperaldosteronism and hyperprogesteronism in a cat with an
adrenal cortical carcinoma. J Vet Intern Med 2005; 19: 355-8.
9. Javadi S, Slingerland LI, van de Beek MG et al. Plasma renin activity and plasma concentrations of aldosterone, cortisol, adrenocorti
cotropic hormone, and á-melanocyte-stimulating hormone in healthy cats. J Vet Intern Med 2004; 18: 625-31.
10. Barthez PY, Nyland TG, Feldman EC. Ultrasonography of the adrenal glands in the dog, cat, and ferret. Vet Clin North Am Small
Anim Pract 1998; 28 (4): 869-85.
105
103
ZBORNIK REFERA
TOV
REFERATOV
DIAGNOSTIKA KLAMIDIJSKIH OKU@B PRI MA^KAH
Cvetka Marhold1, Brigita Slavec1, Jo`ko Ra~nik1, Marko Zadravec1,
Maja ôn~, Marko Oman2 in Alenka Dov~1
1. UVOD
3. DIAGNOSTIKA KLAMIDIJ
Z imenom klamidije (gr.: chlamys -÷ëáìõó - plaš~)
poimenujemo razli~ne skupine bakterij iz druìne Chlamydiaceae. Sprva so klamidije uvrš~ali med viruse, saj so
organotrofni obligatni znotrajceli~ni organizmi evkariontskih gostiteljev. Klamidije so majhne, kokoidne po
Gramu negativne bakterije (1).
Oku`be s klamidijami lahko ugotovimo z razli~nimi laboratorijskimi metodami za dokazovanje klamidijskih antigenov in protiteles proti klamidijam. Uporaba dolo~ene
diagnosti~ne metode je odvisna od vrste in koli~ine vzorca ter opreme posameznega laboratorija.
3.1 Metode za dokazovanje klamidijskih antigenov
Znotraj druìne Chlamydiaceae sta dva rodova: Chlamydophila (Cp) in Chlamydia (C). V rod Chlamydia uvrš~amo
C. trachomatis, C. muridarum in C. suis. V rod Chlamydophila pa so uvrš~ene Cp. psittaci, Cp. pneumoniae, Cp.
pecorum, Cp. abortus, Cp. felis in Cp. caviae. Infekcije
povzro~ene s Cp. psittaci, Cp. abortus in Cp. felis predstavljajo potencialna zoonozna obolenja (1).
2. KLAMIDIJSKE OKU@BE PRI MA^KAH
Klamidijske oku`be pri ma~kah najpogosteje povzro~ajo
izolati Cp. felis. Primarni gostitelj te bakterije je doma~a
ma~ka in je endemi~no razširjena po vsem svetu. Pri
ma~kah povzro~ajo obolenja zgornjih dihalnih poti, kar
se klini~no zazna z nosnim izcedkom, kihanjem in vnetjem
o~esne veznice. Pri samicah oku`ba s Cp. felis lahko
povzro~i tudi kroni~no vnetje rodil (2).
Klamidijske oku`be se z ma~k lahko neposredno z o~esnim
in nosnim izcedkom prenese na ljudi, pri katerih najpogosteje povzro~ijo vnetje o~esnih veznic, redkeje tudi
plju~nice. Za obolenje klamidijskih oku`b so dovzetnejši
ljudje z oslabelim imunskim sistemom (2).
Ob~utljivost in specifi~nost diagnosti~nega testa za dokaz
klamidijskega antigena je posredno odvisna od ustreznosti
vzorca. Za diagnostiko so primerni izlo~ki in eksudati, ki
vsebujejo epitelne in mukozne celice. Pri ma~kah se
odvzame bris vnete o~esne veznice in/ali vnete nosne
sluznice. Najprimerneje je, da se vzorec po odvzemu in
med prenosom v laboratorij hrani v prenosnem gojiš~u
saharozno fosfatni pufer (2SP) pri 4º C. ê vzorcev ne
moremo prenesti v laboratorij znotraj 48 ur, jih zamrznemo (3).
a) Hitri komercialni encimsko imunski testi
S hitrimi komercialnimi encimsko imunskim testi (najpogosteje se uporablja Clearview® Chlamydia MF) lahko
v brisu ku`nine zaznamo klamidijski antigen. Slabost teh
testov so številni la`no pozitivni rezultati. Da se ovrèjo
morebitni la`no pozitivni rezultati, se za potrditev rezultatov hitrih testov uporabljajo specifi~ne diagnosti~ne
metode, kot so direktna imunoflourescenca in molekularne metode veri`ne reakcije s polimerazo (4).
b) Direktna imunofluorescenca (DIF)
Cvetka Marhold, dr.vet.med., asist.dr. Brigita Slavec, dr.vet.med.,
asist.dr. Jo`ko Ra~nik, dr.vet.med., Marko Zadravec, dr.vet.med.,
Maja ôn~, študentka VF LJ, asist. Marko Oman, dr.vet.med.,
doc.dr. Alenka Dov~, dr.vet.med.
1
Univerza v Ljubljani, Veterinarska fakulteta, Inštitut za zdravstveno varstvo perutnine,
2
Zavetiš~e za zapuš~ene ìvali Ljubljana, Gmajnice 30, SI-1000Ljubljana
[email protected]; [email protected];
[email protected]; [email protected]
Z DIF ugotavljamo antigen s pomo~jo specifi~no
ozna~enih protiteles in dolo~imo poloàj antigena v tkivu
ali celici. Strogo specifi~na vezava omogo~a, da kompleks antigen–protitelo ostane ~vrsto vezan tudi v nadaljnjem postopku obdelave. Pri spiranju se odstranijo nevezana protitelesa, ki motijo pri ocenjevanju reakcije. Metoda
je hitra, vendar manj ob~utljiva kot molekularna metoda
veri`ne reakcije (5).
c) Molekularne metode veri`ne reakcije
Zaradi znotrajceli~nega na~ina ìvljenja, klamidij ne more-
106
104
ZBORNIK REFERA
TOV
REFERATOV
mo gojiti na umetnih gojiš~ih. Razmnoùjemo jih lahko v
celi~nih kulturah, v kokošjih embrijih in v laboratorijskih
ìvalih. Do razvoja molekularnih diagnosti~nih testov je
bila izolacija „zlati standard“ med neposrednimi metodami
za dokaz oku`be s klamidijami (6).
Dokazovanje povzro~itelja oku`b z metodo veri`ne reakcije
s polimerazo (PCR) ima številne prednosti pred drugimi
metodami, s katerimi dokazujemo antigene. Izolacija na
tkivnih kulturah in kokošjih embrijih zahteva infektivno
obliko bakterij, vzorec pa lahko razglasimo za negativnega šele po enem tednu. Pri tem pa je izvajalec izpostavljen ve~ji nevarnosti oku`bi s patogeni. Z metodo PCR
lahko teoreti~no zaznamo è eno samo klamidijo v vzorcu. Test PCR je hiter in ga lahko zaklju~imo è v dveh
dneh. Pridobivanje rezultatov še v krajšem ~asu omogo~a
metoda PCR v realnem ~asu. Njena uporaba mo~no
naraš~a, saj postaja dostopna tudi za manjše diagnosti~ne
laboratorije. Metoda daje hkrati kvalitativno in kvantitativno informacijo ter ne zahteva dodatne obdelave vzorcev
po pomnoèvanju, kot je npr. lo~evanje amplikonov na
gelu. Na ta na~in se mo~no zmanjša mo`nost laboratorijske kontaminacije s PCR produkti (7).
4. ZAKLJUÊK
Klamidije povzro~ajo številne bolezni pri ljudeh in ìvalih.
Nekatere med njimi so povzro~itelji zoonoz. Hitra in zanesljiva laboratorijska diagnostika klamidij v veterinarski medicini ni pomembna le za spremljanje zdravstvenega stanja
ìvali, temve~ tudi za preventivno ukrepanje pred prenosom oku`b z ìvali na ljudi (2).
3.2 Serološke metode
Pri seroloških testiranjih ima ve~ji diagnosti~ni pomen
porast titra protiteles pri ponovnem pregledu iste ìvali,
kot pa sama ugotovitev pozitivnih titrov protiteles. Serološki testi dopolnjujejo molekularno diagnostiko in so
pomembni tudi za epidemiološke študije. Specifi~na in
hitro izvedljiva serološka reakcija je indirektna imunofluorescenca (2).
a) Indirektna imunofluorescenca (IIF)
Osnova pri IIF metodi je vezava serumskih protitels s
specifi~no ozna~enimi kompleksi. Pozitiven serološki test
kaè, da je bila ìval okuèna s klamidijami, ni pa nujno,
da pri ìvali tudi trenutno poteka aktivna oku`ba. La`no
negativni rezultati pri ìvalih z akutno oku`bo se pokaèjo,
kadar so vzorci odvzeti pred serokonverzijo. Zdravljenje
s protimikrobno u~inkovino lahko zmanjša odgovor protiteles. Povišan titer protiteles pri parnih serumskih vzorcih ali kombinacija titra protiteles in dokaz antigena potrjuje oku`bo s klamidijjo (5).
LITERATURA
1. Everett K. D., Bush R. M., Andersen A. A. 1999. Emended description of the order Chlamydiales, proposal of Parachlamydiaceae fam.
nov. and Simkaniaceae fam. nov., each containing one monotypic genus, revised taxonomy of the family Chlamydiaceae, including a
new genus and five new species, and standards for the identification of organisms. Int. J. Syst. Bacteriol. 49: 415-40
2. Rodolakis A, Mohamed K. Y. 2010. Zoonotic potential of Chlamydophila. Veterinary Microbiology 140: 382-91
3. Keše D., Petrovec M., Avši~-@upanc T. 1999. Posebnosti pri odvezmu in prenosu ku`nin za dokaz klamidij, rikecij in erlihij. V:
Mikrobiološka analiza ku`nin. Nova Gorica, Zavod za zdravstveno varstvo: 55-56
4. Greguri} G. G.., Vlahovi} K., Slavec B., Gra~ner D., Dov~ A. 2010. PCR confirmation of Chlamydophila felis from nasal and
conjunctival swab samples of a domestic cat in Croatia. Acta vet. (Beogr.), vol. 60, no. 1: 23-29
5. Dov~ A. 1998. Klamidioza (Chlamydia psittaci) pri doma~ih in divjih pernatih ìvali v Sloveniji. Doktorska disertacija. Ljubljana.
Veterinarska fakulteta: 157
6. Everett K. D. E. 2000. Chlamydia and Chlamydiales: more than meets the eye. Veterinary Microbiology. 75: 109-126
7. Berg H. F., Maraha B., Bergmans A. M., van der Zee A., Kluytmans J. A., Peeters M. F. 2003. Extraction of Chlamydia pneumoniae
DNA from vascular tissue for use in PCR: an evulation of four procedures. Clinical Microbiology and Infection, 9, 2: 135-139
107
105
ZBORNIK REFERA
TOV
REFERATOV
ZDRAVSTVENA PROBLEMATIKA ZAPUŠÊNIH
MA^K V LJUBLJANI
Marko Oman1, Alenka Dov~2, Pavel Kvapil1, Marjan Kastelic3, Barbara Miheli~1
UVOD
Za zapuš~ene ma~ke na obmo~ju Mestne ob~ine Ljubljana (MOL) skrbi Zavetiš~e za zapuš~ene ìvali Ljubljana
(zavetiš~e). Zavetiš~e zapuš~enim ma~kam nudi potrebno veterinarsko oskrbo v skladu z minimalnim zdravstvenim varstvom, ki je opredeljeno v Pravilniku o pogojih za
zavetiš~a za zapuš~ene ìvali (1).
Zakon o zaš~iti ìvali definira zapuš~ene ìvali kot ìvali,
ki so najdene, oddane ali odvzete hišne ìvali, kamor spadajo tudi doma~e ma~ke. Posebna kategorija so “prostoìve~e ma~ke” – ma~ke potomke udoma~enih in zapuš~enih ma~k, ki nimajo lastnika in ìvijo prosto v okolici, so najdene in se štejejo kot zapuš~ene ma~ke. Ulov in
oskrbo prostoìve~ih ma~k izvajamo po rednem programu in v okviru projekta “Prostoìve~e ma~ke v Mestu
Ljubljana”.
PROJEKT PROSTO@IVEÊ MA^KE
Program je nastal na podlagi pobude ob~anov MOL. Glavni
namen projekta je vzpostaviti nadzor nad populacijo z
uvedbo registriranih hranilnih mest in prepre~evati nenadzorovano razmnoèvanje ter širjenje ku`nih bolezni z veterinarsko oskrbo prostoìve~ih ma~k. V tem prispevku
prikazujemo rezultate prevalence prisotnosti protiteles
proti ma~jemu virusu imunske pomanjkljivosti (FIV) in
antigena virusa ma~je levkoze (FeLV).
Projekt smo v okviru rednega programa izvajali è leta
2008. Na podlagi pridobljenih dodatnih sredstev za namen projekta smo v letu 2009 obseg oskrbe ma~k podvojili. V letu 2008 je bilo steriliziranih oz. kastriranih in
vrnjenih v okolje 688 ma~k, v letu 2009 pa 1165.
asist. Marko Oman, dr.vet.med., doc.dr. Alenka Dov~, dr.vet.med., asist. Pavel Kvapil,
dr.vet.med., asist. Marjan Kastelic, dr.vet.med., Barbara Miheli~, uni.dipl.biol.
1
ZOO Ljubljana, Ve~na pot 70, SI-1000 Ljubljana
Projekt se izvaja ob sodelovanju s ~lani interesnih zdruènj
(društvo Ma~jelovka in drugi), zainteresiranimi fizi~nimi
osebami ter najditelji. Zavetiš~e jim nudi opremo za ulov
in transport ma~k, prevoz ma~k ter hrano. Vsak najditelj
ob predaji ma~ke v zavetiš~e poda osebne podatke in
podatke o ma~ki, vklju~no s to~no lokacijo mesta najdbe,
ki jo ozna~imo s koordinatami (2). Podatke vpišemo v
evidence.
Na podlagi obdelave pridobljenih podatkov smo izdelali
karto naseljenosti ma~k. Najve~ ma~k (med 50 in 86) je
bilo v letih 2008 in 2009 ulovljenih na posameznih
obmo~jih: Trata, ~rnuški vrti~ki, Fuìne, Moste – Toplarna, Moste, KC, Trnovo, Spodnja Šiška in Podutik. Ma~ke
so bile lovljene na 379 mestih, to je skupaj na 133 razli~nih
lokacijah. V obdelavo smo vklju~ili tudi pridobljene pozitivne rezultate hitrih komercialnih testov za ugotavljanje
prisotnosti protiteles proti FIV in antigena FeLV.
Najve~ (med 8 in 12 ma~k) FIV pozitivnih ma~k smo ugotovili na obmo~jih Trata, Dravlje, ~rnuški vrti~ki, Zelena
jama, KC in Trnovo, skupno na 85 lokacijah. Menimo, da
pogostnost primerov sovpada z ve~jo gostoto populacije.
V okviru zavetiš~a se je ma~ke steriliziralo oz. kastriralo
in vra~alo v okolje è od leta 2004 (do leta 2008 skupaj
1.983 ma~k). Zaradi nepopolnosti podatkov o dejanski
števil~nosti populacije ne moremo govoriti, saj je neznano
število ma~k oskrbljenih tudi s strani zasebnih veterinarskih organizacij. Na podlagi neuradnih podatkov naj bi
bilo od leta 2004 skupno steriliziranih oz. kastriranih okrog 5.000 ma~k.
Najve~ (med 4 in 7 ma~k) FeLV pozitivnih primerov smo
ugotovili na posameznih obmo~jih: Stegne, ~rnuški vrti~ki,
Nove Jarše, Zgornja Zadobrova, Zavoglje in Kosovo polje, skupno na 38 lokacijah. Najmo~nejše prekrivanje FeLV
s FIV je na obmo~ju ~rnuških vrti~kov, kar je verjetno
posledica koncentracije populacije zaradi rušenja tamkajšnjih objektov.
FIV IN FeLV
2
Univerza v Ljubljani, Veterinarska fakulteta, Inštitut za zdravstveno varstvo perutnine,
3
Ambulanta BUBA d.o.o. Ro`na dolina 5, SI-1290 Grosuplje
[email protected]; [email protected]; [email protected]; [email protected];
[email protected]
FIV se ve~inoma prenaša s parenteralno inokulacijo virusa iz sline ali krvi, to je najpogosteje pri ugriznih ranah ob
pretepih; posledi~no je prevalenca oku`b višja pri samcih. Poro~ajo tudi o oku`bah preko sluznice ob spolnem
108
106
ZBORNIK REFERA
TOV
REFERATOV
kontaktu, vertikalno preko placente in s sesanjem pri novorojenih mladi~ih. Po vdoru v organizem sledi viremija
in v dveh do osmih tednih nastanejo specifi~na protitelesa (3).
ma~kah na obe bolezni. Glede na vse v letu 2009 oskrbovane prostoìve~e ma~ke je prevalenca FIV 8,4 % in je
višja kot v letu 2008, prevalenca FeLV 1,6 % (ni`ja kot v
letu 2008) in prevalenca dvojne oku`be 0,5 %.
FeLV se prenaša se enako kot FIV, oziroma tudi z urinom
in blatom. Po za~etni infeciji, ki je ve~inoma po oronazalni poti, se virus replicira v limfati~nem tkivu orofarinksa. Pri ve~ini imunokompetentnih ma~k se virusna replikacija ustavi zaradi mo~nega imunskega odgovora. ê
pa imunski odziv ni zadosten, se FeLV znotraj mononuklearnih celic razširi sistemsko. Tar~na tkiva so timus,
vranica, bezgavke in slinske `leze (primarna viremija).
Lahko se virus razširi v kostni mozeg in inficira hematopoetske prekurzorske celice. Okuèni trombociti in granulociti cirkulirajo v krvi in predstavljajo sekundarno viremijo. ê gostitelj ni sposoben eliminirati virusa, lahko preide v stanje latentne infekcije oziroma lahko se razvije perzistentna viremija (4).
Od 141 bolnih samcev je bil ugotovljen pozitiven rezultat
na FIV v 53 %, na FeLV v 6,3 %, na obe bolezni v 3,5 %.
Od 136 bolnih samic je bil pozitiven rezultat na FIV
ugotovljen v 25,7 %, na FeLV v 9,6 % in na obe bolezni v
1,5 %.
V letu 2008 smo, kot prejšnja leta, vse ma~ke testirali s
hitrim imunokromatografskim testom za ugotavljanje FIV
in FeLV. V letu 2009 smo testirali le ma~ke, ki kaèjo
kakršnakoli klini~na znamenja bolezni. Literatura navaja,
da je prevalenca FIV in FeLV precej višja pri ma~kah, ki
kaèjo klini~ne znake, zato je ta odlo~itev smiselna. Pri
ma~kah mlajših od 6 mesecev smo testirali le FeLV. Uporabljamo Speed Duo FeLV – FIV, BVT (Virbac Group), ki
je primerljiv z drugimi podobnimi testi (4). Velika prednost testa je enostavno skladiš~enje in preprosta uporaba.
Glede na vse oskrbovane samce (530) je prevalenca FIV
pri njih 14,1 % (višja kot v letu 2008), FeLV 1,7 % in na
obe bolezni 0,9 %. Pri samicah (774) je prevalenca FIV
4,5 % (ostaja na ravni leta 2008), FeLV 1,7 % in na obe
bolezni 0,2 %.
Rezultati potrjujejo v literaturi navedeno ve~jo prevalenco
za FIV pri samcih. Tudi v naši raziskavi se je v primerjavi
z letom 2008 prevalenca pri samcih pove~ala, pri samicah pa ostaja na enaki ravni. Rezultati potrjujejo tudi
navedeno ve~jo prevalenco pri bolnih ma~kah. Verjetno
bi bila prevalenca FIV še višja, ~e bi virus ugotavljali s
PCR metodo, ki je bolj ob~utljivejša in bolj specifi~na kot
komercialni hitri testi (3, 5, 6, 7).
Pri FeLV je zanimivo, da smo ugotovili enako prevalenco
pri obeh spolih glede na celotno populacijo. Razlogi za
tak pojav nam niso znani. Prav tako nam niso znani razlogi za precej ni`jo prevalenco FeLV, kot jo navaja literatura, po kateri naj bi bilo 61,1 % zunanjih ma~k pozitivnih. Z uporabo PCR metode bi verjetno prišli do rezultatov, bolj podobnih študijam drugih avtorjev (3).
V letu 2008 je bilo testiranih 775 prostoìve~ih ma~k (241
samcev in 447 samic). Pozitiven rezultat na FIV je bil ugotovljen pri 7,2 % ma~kah. Pri samcih je bil FIV ugotovljen
v 11,8 %, pri samicah pa v 4,5 %.
FeLV je bil ugotovljen pri 3,2 %, pri 1,7 % samcev in 1,5
% samic. FIV in FeLV sta bila ugotovljena pri 0.8 %, pri
samcih v 0,1 % in pri samicah v 0,7 %.
V letu 2009 smo testirali samo klini~no obolele ma~ke.
Od skupno 1304 ma~k smo testirali le 277 (21,2 %) ma~k.
Pri 50,2 % bolnih ma~kah je bil ugotovljen pozitiven rezultat. Od tega je bil pri 39,7 % bolnih ma~kah ugotovljen
pozitiven rezultat na FIV. Pri 7,9 % bolnih ma~kah je bil
ugotovljen pozitiven rezultat na FeLV in pri 2,6 % bolnih
LITERATRURA
1. Veterinarska zbornica. Oman M, Lindtner Knific R et al. (2010). Zbornik 6. Podiplomskega izpopolnjevanja veterinarske zbornice,
139- 44.
2. Geopedia - interaktivni spletni atlas in zemljevid Slovenije: http://www.geopedia.si
3. Tozon N, Nemec Svete A, Zemlji~ M, Zakošek M , Barli~ Magajna D, (2008). High Prevalence of feline Imunodeficiency virus (FIV) and
feline leukemia virus (FeLV) in Slovenia. Acta vet. (Beogr.), 58(2-3): 191-201.
4. Greene C E, (2006), Infectous Diseases of the dog and cat, Third edition, 105-31.
5. Hartmann K, Griessmayr P, Schulz B, Greene C E, Vidyashankar A N, Jarrett O, Egberink H F (2007), Quality of different in-clinic test
system for feline immunodeficiency virus and feline leukemia infections virus J Feline Med Surg. 9: 439-45.
6. Muraj J K, Roberts M A, Skillings E, Morrow L D, Gruffydd-Jones T J (2009), J Feline Med Surg. 11 (6): 467-73.
7. Lara V M, Taniwaki S A, Araujo jr. J P (2008), Occurrrence of feline immunodeficiency virus infection in cats. Ciencia Rural, Santa
Maria 38 (8) 2245-49.
109
107
ZBORNIK REFERA
TOV
REFERATOV
110
108
ZBORNIK REFERA
TOV
REFERATOV
111
109
ZBORNIK REFERA
TOV
REFERATOV
112
110
ZBORNIK REFERA
TOV
REFERATOV
113
111
ZBORNIK REFERA
TOV
REFERATOV
114
112
ZBORNIK REFERA
TOV
REFERATOV
115
ZBORNIK REFERA
TOV
REFERATOV
116
ZBORNIK REFERA
TOV
REFERATOV
117
ZBORNIK REFERA
TOV
REFERATOV
118
ZBORNIK REFERA
TOV
REFERATOV
119
ZBORNIK REFERA
TOV
REFERATOV
120
ZBORNIK REFERA
TOV
REFERATOV
121
ZBORNIK REFERA
TOV
REFERATOV
122
ZBORNIK REFERA
TOV
REFERATOV
123
ZBORNIK REFERA
TOV
REFERATOV
124
ZBORNIK REFERA
TOV
REFERATOV
125
ZBORNIK REFERA
TOV
REFERATOV
126
ZBORNIK REFERA
TOV
REFERATOV
127
ZBORNIK REFERA
TOV
REFERATOV
128
ZBORNIK REFERA
TOV
REFERATOV
129
ZBORNIK REFERA
TOV
REFERATOV
130
ZBORNIK REFERA
TOV
REFERATOV
131
ZBORNIK REFERA
TOV
REFERATOV
132
ZBORNIK REFERA
TOV
REFERATOV
133

ZBORNIK REFERA ZBORNIK REFERATOV XXIII. SIMPOZIJ O

Transcription

Similar documents

tukaj - Fotografsko društvo Grča

Fosilni ostanki jamske `ivali Marifugia cavatica v

showtime - EST - English student theatre

Petindvajseta številka - Društvo za osvoboditev živali

SLOVAŠKO-SLOVENSKI KONVERZACIJSKI PRIROČNIK KOT

Pomembno odkritje slovenskih znanstvenikov

Organizacijski odbor posveta - Sindikat policistov Slovenije

Notice - Phainomena