Equine ophthalmology, renal, neuro (CVM, seizures, EHV neuro, spinal cord trauma, shivers, stringhalt, nerve inujuries, botulism, tetanus) Flashcards
Which lenses show which parts of the eye in a horse with close direct ophthalmology?
0 to -3D: fundus
+2D to +6D: vitreous
+7D to +8D: lens
+10D: cornea
What is a slit lamp used for?
To assess depth of lesions
What to assess on ophthalmic exam?
Symmetry, angle of eyelashes (normally horizontal/slightly down)
Ocular reflexes:
- PLR (direct and indirect)
- dazzle reflex
- menace response
- palpebral reflex
- corneal reflex
Check for cleft above upper eyelid (if not there may be swollen)
Third eyelid
Check tear duct opening is patent in nostril
Check eye from outside in
What nerve blocks can be used to help examine horse’s eye?
Auriculopalpebral nerve block (actually just palpebral)
- bundle near zygomatic arch above eye, inject S/C near nerve
- motor only
- won’t take away pain if suturing etc
Frontal nerve block
- feel over frontal orbit area
- S/C injection near supraorbital foramen
- sensory and motor?
How do ulcers appear with fluorescein?
Superficial ulceration - sharp edges, no epithelial under-run, no stain migration
Indolent ulcer - epithelial under-run
Deep stromal ulceration - very intense staining with stain migration (5-15 mins)
Descematocele - walls of ulcer stain intensely with stain migration (5-15 mins), central ulcer transparent and takes up no stain
What is the Seidal test?
Block eye so stays open
Fluorescein over whole eye
See aqueous draining through where a foreign body has penetrated
What is Rose Bengal used for?
Assesses tear film quality (stained areas haven’t got good tear film cover)
Assesses margins of conjunctival and corneal neoplasia (SCC)
Fungal ulcers
How to do cytology/C+S for the eye?
Sedate and block eye
Don’t put LA on eye if want to do culture
Cotton bud, brushes
What midriatic is used to dilate the pupil to examine the fundus?
Tropicamide
Not atropine as can leave dilated for 4 weeks
When is a CT useful for eyes?
Cases of exophthalmos
When is electroretinogram (ERG) useful?
To check retina working before cataracts surgery etc
Eyelid lacerations - When is management easier/prognosis better? How to manage?
Lower (easier to manage) and lateral better (medial tear duct can be affected)
Never cut tissue from eyelid - minimal debridement as most tissue likely to survive
Iodine povidone
Suture carefully to appose eyelid margins accurately
Use very thin suture material
Common eyelid masses?
Sarcoids
Melanomas - surgery easier as don’t need as wide margins
Lymphoma (third eyelid)
Hamangiosarcoma
Layers of the cornea?
Epithelium
Stroma
Descemet membrane
Endothelium
Ulcerative keratitis (corneal ulcers) - How common in horses? Clinical signs? Diagnosis? Depths? Treatment?
Very common
Pain, blepharospasm, epiphora, photophobia
Fluorescein (and rose bengal)
Superficial ulcer
- epithelium only
- painful (most nerve endings are in epithelium)
- well defined margins with fluorescein
- tend to heal with no complications if treated appropriately
- topical antimicrobial (e.g. chloramphenicol) +/- topical atropine (pre-emptive for uveitis but not generally necessary)
- healing rate approx 0.6mm/day
- no corneal scar
Deeper ulcer:
- epithelium and stroma
- same treatment as superficial but for longer period of time
- gentamicin
- EDTA and plasma?
- more likely to have uveitis so atropine may be more warranted
- scarring likely (collagen heals in different directions): if small = like chip in windscreen
- can get keratomalacia
What is keratomalacia? Why happens? Appearance? Treatment?
Complication of deep ulcers
= Melting ulcers (collagen being broken down)
Due to activation/production of proteolytic enzymes by corneal epithelial cells, leucocytes or microbial organisms (pseudomonas)
Can happen within hours
Gel like appearance and consistency on eye
Needs early aggressive therapy:
- topical serum
- topical EDTA (better in ambulatory setting, put saline in blood tube)
- topical tetracycline or doxycycline
- systemic NSAIDs (flunixin)
What is a descemetocele? Appearance? Presentation? Treatment?
Ulcer reached Descemet membrane (thickness of 4 cells)
Looks like a crater, black in centre
Fluorescein negative
Not necessarily very painful
Aggressive therapy necessary (same as for deep melting ulcers):
- topical serum q2h
- topical EDTA (better in ambulatory setting, put saline in blood tube) 2h
- topical tetracycline or doxycycline or gentamicin q 6h
- atropine? q4h
- systemic NSAIDs (flunixin)
Surgery therapy may be necessary:
- conjunctival flap
What can follow on from a descemetocele?
Full thickness corneal laceration -> iris prolapse
Risk of infection getting into eye - need antibiotics
Risk of uveitis and recurrent ocular pain
So should fix:
- push back in, stitch cornea, reinflate
Stromal abscess - Appearance/clinical signs? Treatment?
Circular white-yellow lesion in cornea
Constricted pupil
Invading blood vessels
Fluorescein negative
Medical therapy - antibiotics (needs to penetrate through cornea so must be lipophilic e.g. chloramphenicol, NOT gentamicin)
Surgery if not improving/very painful- debridement or corneal grafting techniques
What causes viral keratitis? Appearance? Diagnosis?
EHV-2 (common in horses eyes without causing signs)
Multiple superficial, white, punctate or linear (dendritic) opacities
Fluorescein, rose bengal
Varying (normally high) degree of ocular pain
Difficult to diagnose - virus isolation and/or PCR
Treatment:
- topical Idoxuridine
- topical Trifluorothymidine
- topical Aciclovir (best)/Ganciclovir
- topical Interferon Y
Fungal keratitis - Risk factors? Presentation? Diagnosis? Treatment?
Rare in UK
USA risk factors:
- hot and humid
- previous administration of antibacterial and/or corticosteroids
May be fluorescein -ve initially (rose bengal +ve)
Poor vascularisation of lesions
Cytology essential +/- culture
Slow to resolve
Surgery usually necessary - keratectomy +/- conjunctival flap
Signs usually deteriorate 24h after starting anti fungal therapy due to massive fungus death with a dramatic PMN response and secondary uveitis
Topical:
- miconazole
- natamycin
- fluconazole
- itraconazole
- amphoteericin B
- voriconazole (best, use as many times per day as poss)
Still guarded prognosis
Immune mediated keratopathies - Presentation? Clinical signs? Treatment?
Insidious onset Usually unilateral Slight ocular discomfort (no uveitis) Vary from irregular corneal surface to deep bullae formation, vascularisation and oedema (yellow/green haze is pathognomonic for deep stromal) Medical: - topical corticosteroids - cyclosporin A - doxycycline Surgery: - keratectomy - cyclosporin A implant Characterised by WBCs, vascularisation and oedema
What is Equine recurrent uveitis (ERU)?
Uncommon in UK
Most referred cases are just an acute uveitis not treated sufficiently -> chronic uveitis
ERU - at least 2 separate episodes of uveitis (normal in between)
Active
Quiescent
Insidious - Appaloosas and Warmbloods
Causes of uveitis? Treatment for uveitis?
Primary or secondary to other eye disease (e.g. ulcer) or systemic disease (e.g. Rhodococcus)
Strong immune mediated component
Leptospira involved in many cases in Europe and USA (less in UK)
Recurrence episodes likely
Treatment:
- topical corticosteroids (if no ulcer present)
- topical NSAIDs? (if ulcer present, or better to treat ulcer first then use steroids)
- topical antimicrobials only needed if ulcer
- topical atropine (if responds quickly = mild, if needs lots to respond = severe case, danger of colic due to effect on gut motility, check other eye before each dose as if dilated then have systemic absorption)
- systemic NSAIDs (flunixin>bute)
Surgery:
- suprachoroidal cyclosporin A implant (works for mild cases)
- pars plana vitrectomy
- enucleation?
Clinical signs of anterior uveitis?
Pain - blephorospasm and epiphora
Chemosis - red eye
Constricted pupil
Aqueous flare - milky appearance of anterior chamber
Blood (hyphaema), pus (hypopyon) or fibrin in anterior chamber
Clinical signs of posterior uveitis?
Subtle Pain variable (often mild) Vitritis Retinal changes Typically diagnosed late in the course of the disease
Long term complications of uveitis?
Atrophy granula iridica Synechiae Cataracts Glaucoma Retinal pathology Blindness Phthisis bulbi
Types of cataracts in horses? Significance? Treatment?
Acquired or secondary cataracts (uveitis, trauma, tumour)
Developmental opacities, including congenital cataracts
Most are not progressive
Little effect on vision unless complete
Most do not require treatment
Treat primary cause if secondary
Surgery can be performed in foals (before 4mo)
Surgery in adults
- not if uveitis
- phacoemulsification
Lens anatomy?
Epithelium grows from centre to side of lens and becomes fibres - squeezes nucleus
Suture line at front looks like a Y (same at back but tilted)
Diagnosis of cataracts?
Retroillumination using light reflected from the tapetum - opacities appear dark
Transillumination (direct focal illumination) using direct beam light at 45 degrees angle into the lens - cataracts appear white
Types of cataract location/extent?
Photos
What is glaucoma? How common in horses? Significance? Signs? Diagnosis?
Increased IOP (normal 15-30mm/Hg) Relatively uncommon in horses - conventional (60%) and unconventional (40%) aqueous humour drainage Pain not as common sign as in other species Horses relatively more tolerant of higher pressures Signs: - hydrophthalmos or buphthalmos - corneal oedema - corneal striae - lens luxation - blindness Diagnosis: - signs - tonometry - US
Treatment for glaucoma in horses?
Medical:
- carbonic anhydrase inhibitors: topical (dorzolamide) and/or systemic (acetazolamide)
- B blockers: topical timolol
- NSAIDs and/or corticosteroids (topical and/or systemic)
- prostaglandin derivatives contraindicated in horses!
Surgery:
- laser destruction of ciliary body
- aqueous shunts
- enucleation
Chemical ciliary body destruction - intravitreal gentamicin injection
Fundus anatomy?
Photo Tapetal region - stars of Winslow Non tapetal region Retinal vessels Optic nerve - oval (roundish in foals), salmon pink, 3-5mm vertically and 5-8mm horizontally
What is the blood supply to the horse fundus?
Equine retina paurangiotic: 30-60 vessels radiate from optic nerve:
- 1-2 disc diameters
- less prominent dorsally and ventrally
- may be absent at 6 o’clock
Rest of retina avascular:
- stars of Winslow (from choroid vessels)
Layers of the retina? Colours? Why relevant?
Upper neurosensory retina = cling film (less shiny) Lower retinal pigment epithelium = black Tapetum behind retina in tapetal fundus = blue, green, amber Choroid = red Sclera = white Colours relevant as allows assessment of depth of lesions Pigment accumulation (clumping) indicates pathology
Most common pathology of the fundus in horses?
Bullet hole lesions
Butterfly wings of optic nerve - may be secondary to uveitis, herpes, may not be significant
Senile retinopathy - old horses, looks like cracks of non tapetal fundus, typically not a problem
How does forebrain disease present in horses?
Disorders of behaviour and personality - aggression, compulsive walking, loss of learnt behaviour, yawning
Seizures
Blindness
Altered states of consciousness: alert -> quiet -> depressed -> obtunded -> comatose
Head posture - head and neck turn, head pressing
Causes of forebrain disease in adult horses?
Trauma - most common
Abscess
Cholesterol granuloma (common to have but uncommon to have signs) - obstruct CSF flow -> hydrocephalus
Verminous
Infectious meningoencephalomyelitis - rare
Neoplasia - rare
Toxins - uncommon
Intracarotid injection
Sleep disorders - narcolepsy, sleep deprivation
Metabolic (common) - hepatic encephalopathy, intestinal hyperammoniaemia, electrolyte imbalances
(Trauma and metabolic most common)
What is cataplexy?
Sudden loss of muscle tone
Difference between narcolepsy and sleep deprivation?
Sleep deprivation - horses always need to eventually lie down for full cycle of sleep, happens if can’t lie down
Narcolepsy - sudden onset of sleep (diagnose by response to treatment), less common
Typical signs of hepatic encephalopathy?
Head pressing Yawning Saliva drooling Reduced consciousness state Blindness (central)
What causes neonatal seizures and epilepsy?
Low seizure threshold
Most common: perinatal asphyxia syndrome (NMS/HIE), sepsis, trauma
Also metabolic (hypoNa, hypoglycaemia), drug associated, idiopathic
Juvenile idiopathic Arab epilepsy - benign, up to 12mo
What do seizures look like?
Typically start at nose/mouth
May progress to leg thrashing
Signs of brainstem and cranial nerve disease
Vestibular disease - head tilt to affected side, nystagmus, loss of physiological nystagmus, ventral strabismus (check by raising head), ataxia
Facial nerve paralysis (VII and VIII frequently affected together)
Pharyngeal/laryngeal deficits - dysphagia
Other CN deficits
Severe brainstem lesions - gait abnormalities, coma (RAS)
What does vestibular ataxia look like?
Hypermetria (not flexing very much), wobbly, wide based stance, affected side weaker so go towards that side and forms circles
Can be compensated by vision - e.g. if treated and walking ok test with blindfold and only sign off if still walking ok
Worse up ramps
Causes of vestibular disease?
Trauma - central or peripheral
Idiopathic
Otitis media/interna (temporohyoid osteoarthropathy)
Causes and signs of facial nerve injuries? What prolonged/permanent deficits can be caused?
Commonly iatrogenic due to halters left on during field anaesthesia Trauma (+/- vestibular) THO (+/- vestibular) Signs: - dropped ear - ptosis - nostril deviation Possible deficits: - exposure keratitis - dysphagia (feed pouching) - poor performance: nostril collapse
