LA Ophthalmology Flashcards

1
Q

what are 4 things to pay attention to when examining large animals?

A
  1. ocular comfort: eyelash position
    -will be pointing down or in if discomfort
    -do before sedation
  2. 3rd eyelid: retropulse globe to produce passive prolapse! can take a lot of force
  3. sedation can decrease IOP
  4. taking pressures without blocking auriculopalpebral n can result in increased IOP due to strain of pushing eyelids open (in horses)
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2
Q

what types of sedation are used for ophtho exam in horses?

A
  1. xylazine: 0.5-1mg/kg IV
  2. detomidine: usually only required for badly behaved patients or when extra sedation needed for procedure
    -0.02-0.04 mg/kg IV
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3
Q

what nerve blocks are used in horse ophthalmic exams?

A
  1. auriculopalpebral
    -palpebral branch of facial nerve; paralyzes orbicularis oculi muscle
    -they can still blink just not resist
    -sensation to eyelids persists and some palpebral function
    -usually palpate along zygomatic arch roughly halfway between the eye and ear, strums like a rubber band
    -inject approx 1ml of lidocaine
  2. block various branches of CN V to block sensation to eyelids
    -frontal (supraorbital) branch: sensory to upper eyelid
    -lacrimal branch: sensory to lateral upper eyelid
    -infratrochlear branch: sensory to medial canthus
    -zygomatic branch: sensory to lower eyelid
    -nasociliary branch: sensory innervation to cornea
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4
Q

describe orbital fractures in large animals

A

they happen!

if closed: pop it back in

if open: call a surgeon

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4
Q

describe anatomical differences

A
  1. orbit: laterally on skull
    -mononuclear vision enhanced
    -horse, sheep, cattle, and goat all have enclosed orbit (completely encompassed by bone)
  2. iris: oval in horizontal plane in oxen, horses, sheep, goats
    -granula iridica/corpora nigra present in herbivores: series of black masses on upper edge of pupil (NOT a tumor!)
  3. retinal vessels
    -horses paurangiotic
    -cows, sheep, goat: holangiotic
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5
Q

describe lid lacerations in large animals

A
  1. COMMON
  2. do NOT trim tissues!! if you sew it, it WILL heal
  3. two layer closure required!!
    -if only close skin side, conjunctiva will grow across inner portions and it will dehisce
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6
Q

describe entropion in large animals

A
  1. most common neonatal eyelid abnormality
  2. temporary tacking sutures until grown
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7
Q

describe keratitis- superficial, uncomplicated corneal ulcers in large animals

A
  1. same as in dogs:
    -no stromal involvement
    -acute onset
    -no signs of infection (stromal loss, cellular infiltrate, stromal defects)
  2. treatment:
    -topical broad spectrum Abx q6-8 hrs: ofloxacin or neopolybac
    -atropine PRN to keep pupil dilated
    -systemic NSAIDs if reflex uveitis present (much more common in horses than dogs and cats!)
    -NO steroids or topical NSAIDS!
    -may consider a prophy antifungal!
  3. if nonhealing/indolent:
    -start with cytology!
    -never drag needle across horse cornea though horsey eye
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8
Q

describe bacterial keratitis in horses

A
  1. stromal involvement: corneal melting, edema, cellular infiltrate
  2. anterior uveitis: miosis, flare, hypopyon, hypotony
  3. treatment:
    -broad spectrum Abx: ofofloxacin or moxifloxacin q1-4h
    -anti-melt (anti-collagenase): serum, EDTA, N-acetylcysteine, or topical oxytet q1hr
    -atropine: as needed to dilate pupil, typically q4-6hr to start, then decrease to q12-24hr
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9
Q

describe fungal keratitis in horses

A
  1. common in horses, esp in SE!!: warm and wet = fungus festival
  2. most commonly involve aspergillus or fusarium spp.
  3. clinical appearance:
    -progressive, subacute keratitis
    -painful
    -severe secondary uveitis
    -ulcer present for longer than 1-2 weeks
    -may have healed but fungus set up shop and caused stromal abscess (fl. neg.)
    -love to grow to descemet’s membrane = hard to cut out
  4. treatment: DIFFICULT
    -poor prognosis and requires long-term aggressive therapy
    -goals: kill fungus, kill bacteria, and control secondary uveitis
    -can take 4-8 weeks or more to resolve
    -will heal with scarring (bc lost cornea, decreases visual capabilities and calls into question soundness to be ridden)
    -subpalpebral lavage needed
    -also control melting with topical serum
    -control uveitis with oral banamine
    -topical atropine too but be careful of slowing gut!!
  5. surgical treatment:
    -keratectomy + corneal or conjunctival graft: indicated when there is no response to medical management, formation of deep corneal furrow, or lesion is deep within the cornea
    -deep lesions: penetrating keratoplasty, lamellar keratoplasty, or deep lamellar keratoplasty
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10
Q

describe stromal abscesses in horses

A
  1. usually the result of tiny penetrating injury which inoculates corneal stroma with infectious agent; entry subsequently heals but a few weeks later an abscess forms
  2. diagnosis:
    -clinical appearance
    -culture and cytology useless as epithelium is intact!
  3. treatment:
    -if well vascularized: oral and topical antibiotics/antifungals/atropine
    –why we often mix antifungals with DMSO (draw across epi surface)
    -if non-vascularized, severe abscess: keratectomy and graft, or penetrating keratoplasty if deep endothelial
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11
Q

describe equine recurrent uveitis

A
  1. major disease of horses; leading cause of blindness
    -2-10% prevalence in US
  2. immune-mediated, panuveitis characterized by recurring episodes of intraocular inflammation that develop weeks to months after an initial episode of uveitis

*uveitis is also number 1 cause of cataracts in horses

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12
Q

how do you decide that a horse with uveitis has equine recurrent uveitis? (5)

A
  1. history of repeated episodes of redness (may have been previously diagnosed as allergies)
  2. signs of chronic inflammation
  3. signs of inflammation in contralateral eye
  4. presence of chorioretinal scarring: butterfly scarring
  5. the only “true” way to diagnose ERU is by documented repeated episodes of uveitis
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13
Q

describe clinical signs of ERU

A
  1. photophobia
  2. blepharospasm
  3. corneal edema
  4. aqueous flare
  5. hypopyon
  6. miosis
  7. vitreous haze
  8. chorioretinitis
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14
Q

describe pathogenesis, diagnosis, and retinal changes of ERU

A

pathogenesis:
1. unknown but several theories: molecular mimicry, bystander activation, epitope spreading

diagnosis:
1. based on presence of characteristic clinical signs
2. history of documented recurrent or persistent episodes of uveitis

retinal changes:
1. peripapillary chorioretinal scars (butterfly lesions)
2. exudative retinal detachments

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15
Q

describe treatment of ERU

A
  1. AGRESSIVE
  2. topical and systemic anti-inflam meds
    -steroids: pred, neopolydex
  3. NSAIDs
    -dlicofenac or flubiprofen
    -bromfenac but expensive!!
  4. systemic therapy:
    -ORAL, IM or IV banamine
    -phenylbutazone or aspirin much less effective
  5. cyclosporine A
    -imm. modulatory meds
    -poor penetration topically
    -sustained release devices/implants bypass blood ocular barrier, high concentrations of drug achieved in eye without systemic side effects
    -placed in or near subchoroidal space
    -may need to replace implant in 2 years
16
Q

describe insidious ERU

A
  1. inflammation never resolves, low-grade inflam response leads to chronic clinical signs
  2. horses to not have overt signs of discomfort so owners do not notice until cataract formation causes blindness
  3. often seen in Appaloosas and draft breeds
17
Q

describe squamous cell carcinoma

A
  1. most common neoplasm of equine eye and adnexa!
    -rarely metastasize by can ride down NLD and into guttural pouch so want to cut out pretty early
  2. risk factors:
    -lack of periocular pigment
    -age
    -breed: draft or Appaloosa
    -geographic location: increased elevation, decreased latitude, mean annual solar radiation
  3. most common locations:
    -3rd eyelid
    -lateral canthus
    -limbus
    -lower eyelid
  4. progression: solar keratitis causes carcinoma in situ then becomes LARGE and invasive
  5. treatment:
    -intralesional chemotherapy: BCG, cisplatin
    -surgical excision +/- cryotherapy
    -hyperthermia
    -CO2 laser
    -brachytherapy
18
Q

describe sarcoids

A
  1. cutaneous tumor of fibroblastic origin; periocular!!
  2. metastasis rare, recurrence rrequent
  3. result in pathology by disrupting eyelid function or direct contact with the eye
  4. quarter horses, appaloosas, arabians
  5. management difficult:
    -DONT biopsy, once you touch they awaken
19
Q

describe cancer eye/lymphosarcoma

A
  1. affects retrobulbar tissues, most common cause of exophthalmos in cattle
  2. caused by BLV; biopsy - definitive diagnosis
  3. treatment: usually palliative, prognosis approx 6 months
    -exteneration indicated to relieve pain from exposure/panophthlamitis, not curative
20
Q

what is the most common tumor of eye and eyelids in cattle?

A
  1. squamous cell carcinoma!
  2. signalment:
    -age related: uncommon in young
    -degree of periocular pigmentation drastically affects risk factor
  3. risk factors:
    -age, gender, breed, perioular and corneascleral pigmentation, exposure to sunlight, viral infeciton, nutrition
  4. clinical presentation
    -75% precursor lesions affect bulbar conjunctiva and cornea
    -remaining 25% palpebral conjunctiva, nictitating membrane, eyelids
  5. progression of disease:
    -benign plaques that progress to carcinoma in situ then to invasive carcinoma
    -rarely metastasize (only very alte in the process, local invasion may be particularly aggressive)
  6. diagnosis:
    -histopath eval: excisional biopsy
    -eval extent of lesion: topical anesthesia, gloves, lube, then palpate
    -not all preacnacerous lesions progress to SCC
  7. treatment: surgery!
    -excisional biopsy then treat with adjunctive therapy
    -salvage procedures:
    –enucleation to prolong life
    –exteneration if orbital involvement is suspected
21
Q

describe infectious bovine keratoconjunctivitis/bovine pink eye

A
  1. caused by moraxella bovis: gram negative bacillus
  2. transmission:
    -usually a new animal or carrier animal within herd
    -can reside in herd for months in the winter with no clinical signs
    -fomites, direct contact, mechanical (fly) vectors: face fly (musca autumnalis)
  3. predisposition
    -breed: bos indicus breeds (herefords and hereford crosses)
    -age
    -UV light
  4. pathogenesis:
    -corneal lesions from bacterial cytotoxicity: melting precipitated by collagenase relased by damaged cells and neutrophils
    -cows do not have lysozyme, depend on lactoferring and secretory IgA to control infection
    -pathogenic factors include pilin and cytotoxin (hemolysin, cytolysin)
  5. clinical signs:
    -corneal vesicles that form corneal ulcers that form corneal abscesses that result in perforation
    -uveitis
    -mucopurulent discharge, blepharospasm
    -75% of cases are unilateral!
22
Q

describe treatment of IBK

A
  1. medical therapy:
    -oxytet can be used in pregnant
    -topical meds like terramycin and vetericyn pink eye spray
    -duration of carrier state reduced by admin of 2 injections of long acting oxytet
  2. surgical:
    -third eyelid flap or temporary sew eyelids shut