Equine Lacrimal and Conjunctiva

Nasolacrimal System
Equine Ophthalmology Service
University of Florida
Nasolacrimal System
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Secretory components
– Lacrimal gland, TE gland
– Meibomian glands, Conjunctival goblet cells
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Drainage system: Tears drain
– upper and lower eyelid puncta at the medial canthus
– into the nasolacrimal duct (osseous and soft tissue parts)
– which opens at the nasal punctum located at the mucocutaneous
junction of the ventrolateral portion of the floor of the nasal
vestibule.
Multiple openings in the nasal meatus
The TrilayeredTear Film
Outer lipid layer
 Middle aqueous
layer
 Inner mucin layer
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Keratoconjunctivitis sicca
(KCS): Deficiency or
abnormality of contenct of
the tear
 1. Diagnosis:
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– a. Clinical signs
– squinting, mucoid discharge,
nonhealing ulcers, dry appearance,
dull cornea with vascularization
and pigmentation of cornea;
improvement with any topical
medication.
KCS
It looks dry……….
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Schirmer tear test
– horses: 24 +/- 5 mm wetting /minute
– not a linear test
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Tear film breakup time
(TFBUT)
In KCS the tear film is unstable,
and “breaks” up faster.
A strip of fluorescein is applied in
the lower eyelid fornix and then
removed.
The lid is blinked and held open
until the appearance of a break or
dark spot
Normal is 21.8 ± 10.0 seconds
TFBUT of 10 seconds or less is
consistent with KCS.
b. Rose Bengal stain - epithelium of conjunctiva and cornea
will remain red if exposed due to lack of tear film.
d. USE FLUORESCEIN TO LOOK FOR ULCERS.
Rose Bengal positive
Rose bengal
Tear film integrity
 Mucin layer blocks
RB staining
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KCS
Viral keratitis
Fungal keratitis
Edema
Scar tissue
Qualitative KCS: Rose bengal positive but normal STT
Etiology of Equine KCS:
 a. Congenital: rare
 b. Drug related:
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– Atropine: Topical and systemic
– Anesthesia: reversible
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c. Systemic diseases: locoweed toxicity
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d. Chronic blepharoconjunctivitis - scarring of
lacrimal ducts
e. Neurogenic
– Temporohyoid osteoarthropathy (middle ear disease)
– Fractures of stylohyoid bone (petrosal nerve
dysfunction)
– Parasympathetic facial nerve dysfunction associated
with hypothyroidism. Caused head shaking too.
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f. Immune mediated lacrimal gland adenitis in
eosinophilic keratoconjunctivitis.
g. Trauma to the orbit and eye
Treatment: palliative
 a. Medical
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– 1. Always attempt 1-2 months of medical
treatment because the problem may be
transient. Owner compliance may be difficult.
– 2. Goals to remove pain and maintain vision:
a. Replace tears with SERUM
 b. Control bacterial flora
 c. Control inflammation

– 3. Topical 2% cyclosporine A or .03% tacrolimus:
is a potent immunosuppressive drug with specific T-cell
inhibitory activity
 mechanism of increased tear production not defined
 reduces pigmentary/inflammatory keratitis.
 Antifibroblastic: can reduce corneal scarring
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– dose: BID; may take 3-4 weeks before increasing tear
production.
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Surgical therapy for KCS:
– 1. Nictitans flap - to protect cornea when
ulcerated
– 2. Conjunctival flap - Deep corneal ulcers, to
provide corrective tissue and blood vessels.
– 3. Parotid duct transposition
•Lacrimal gland abscess: STT 4 mm wetting/min postop
Dacryocystitis is inflammation of the lacrimal sac and nasolacrimal
duct, and is seen frequently in horses
Dacrycystitis
Congenital: duct atresia
 Acquired
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– fractures, foreign bodies, neoplasia, granulomas,
sinusitis
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Treatment:
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Systemic antibiotics for
the dacryocystitis.
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Eyelid and Nasal puncta
atresia: Surgical opening of
the tissue and catheter
placement for 4-6 weeks.
Nasolacrimal duct agenesis:
– Conjunctival rhinostomy
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Epiphora: increased tearing
1. Increased tear
production
2. Decreased tear
drainage
Nasolacrimal System Atresia
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Congenital defects in the eyelid puncta, nasolacrimal duct, and the
nasal puncta must be differentiated from acquired obstruction of
the tear drainage system.
Chronic unilateral or bilateral mucoid and eventually purulent
ocular discharge in a young horse (1-2 yrs).
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Culture and antibiotic sensitivity testing.
Contrast dacryocystorhinography
Eyelid puncta atresia: lack of a distal
opening of the nasolacrimal duct within the
nares at the mucocutaneous junction,
Irrigating solution does not exit at the nasal
puncta.
CONJUNCTIVA AND NICTITATING
MEMBRANE
Dennis E. Brooks, DVM, PhD
University of Florida
[email protected]
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Dermoid - Congenital tumor
of dermal origin
– May involve conjunctiva, limbus,
cornea, nictitans.
– The mass may irritate cornea and
palpebral conjunctiva with possible
epiphora, conjunctivitis and/or
keratitis.
– Treatment - surgical removal
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Conjunctivitis – “red eye”
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1. Signs - vary with duration; nonspecific
a. hyperemia (redness). “RED EYE”
b. chemosis (swelling)
c. follicles - usually chronic response
d. discharge-serous = mild
mucoid = chronic, KCS
purulent = bacterial
e. pain - variable, usually mild
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2. Diagnostic tests
– a. STT, RB and fluorescein- routine on all
conjunctivitis cases
– b. Culture/sensitivity - fornix, not routinely
done
– c. Cytology - topical anesthetic, spatula
– d. PCR tests for herpes
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3. Etiologies
– a. Bacterial: purulent discharge
– Staphylococci and Streptococci.
– Primary bacterial conjunctivitis is rare - usually
has an underlying cause, ie foreign body, lid
disease
– Cytology: neutrophils + bacteria
– Treatment: a) Determine cause and treat; b)
Antibiotics - broad spectrum initially; based on
C and S if non-responsive; c) Flush discharge
from eye before application of antibiotics
b. Viral - frequently bilateral, may be
unilateral
 c. Mycotic - rare
 d. Parasitic
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e. Allergic - frequent cause
– 1. may have seasonal occurrence, associated
with many allergens
– 2. cytology - eosinophils, basophils
– Treatment: topical anti-inflammatories
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f. Physical irritation - wind, dust, foreign
bodies, eyelid disease, frequent causes
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With conjunctivitis please don't just treat
the signs! Look for a cause.
– An eye with potentially blinding glaucoma or
uveitis or KCS will be red and mimic simple
conjunctivitis!!!!!
Many ocular diseases have conjunctivitis
associated with them.
 Primary conjunctivitis is a diagnosis made
by excluding secondary causes of
conjunctivitis.
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Follicular Conjunctivitis
Habronema nodules
Lymphoma
SCC
Vitiligo
Lymphocytic conjunctivitis
Icterus
Subconjunctival hemorrhage from dystocia (maiden mares)
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Eversion of TE cartilage
– Cartilage is abnormally formed, causes nictitans
to roll inward or outward.
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Protrusion (prolapse) of the TE - common
complaint, multiple etiologies.
– 1. Decreased orbital mass - dehydration or
emaciation leads to loss of orbital fat and
volume, eye becomes enophthalmic, TE
protrudes bilaterally.
– 2. Decreased ocular mass - microphthalmia or
phthisis bulbi
– 3. Increased orbital mass or pressure retrobulbar neoplasia, retrobulbar cellulitis or
abscess; usually unilateral
Orbital fat
microphthalmos
– 4. Denervation - Horner's
syndrome
– 5. Ocular pain - ulcers
– 6. Tetanus- OU; flicking of the haw
– 7. Conjunctivitis
– 8. Idiopathic
– 9. Generalized illness - the nictitans
is a lymph node
TE SCC
Copper