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93 Cards in this Set

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  • Back
top 3 ddx for 3 legged lameness
foot abscess
infection in closed space (ex. septic arthritis)
What are the parts of a lameness exam?
standing exam: visual, palpation, flexion & extension
moving: in hand, under tack, on lunge
diagnostic anesthesia
ancillary diagonstics
What are 5 indicators of lameness?
head nod: usually indicates forelimb lameness
asymmetrical pelvic movements: usually indicates hindlimb lameness
changes in stride length or height: length almost always shortened in affected limb, & height thru which it moves is often lowered
changes in joint range of motion
abnormal tracking of limbs: usually indicates hindlimb lameness
What type of lameness is usually seen w/ laminitis?
bilateral forelimb lameness
What are the normal foot angles for:

a. front limb
b. hind limb
a. 45-50 deg.
b. 50-55 deg.
What are the results of therapeutic shoeing to:

a. increase hoof angle
b. decrease hoof angle
a. ↓ strain on DDF tendon but ↑ strain on suspensory ligament, promotes heel 1st landing

b. ↑ strain of DDF tendon w/ no effect on suspensory ligament, promotes toe 1st landing & ↑ vibration/friction in navicular bursa
What is laminitis?
complex, interrelated series of events --> varying degrees of breakdown of interdigitating 1º & 2º epidermal & dermal laminae of foot (active laminar degeneration)
What is the pathogenesis of laminitis?
acute laminar degeneration allows P3 to become displaced ventrally --> painful, crippling lameness --> rotation &/or sinking of P3
What are 3 factors that complicate laminitis?
rotation or “sinking” of P3
recurrent or continued metabolic upset
inflammation may be present d/t weakening or tearing of remaining healthy laminae
** What are the 3 phases of laminitis? **
development phase: begins by contact w/ inciting agent & ends w/ onset of clinical signs
acute phase: clinical signs of laminitis (medical emergency!)
chronic phase: separation of P3 from hoof wall
What are some predisposing factors for development of laminitis?
more prevalent in intact mares & stallions & ponies
assoc. w/ horses that are heavyweight, small-footed, fed grain predominantly, or stressed
inappropriate management practices: grain overload, grazing lush pastures
disease states: any cause of endotoxemia, colic, Cushing’s
toxicity/adverse drug rxn: ex. black walnut shavings for bedding
What are the fundamentals of medical tx of laminitis?
confine horse immediately: do NOT walk for 6-8 weeks
NSAIDS: phenylbutazone, flunixin, aspirin, ketoprofen, firocoxib
other options: cryotherapy, mineral oil, anti-endotoxin therapy, vasodilator therapy, anticoagulant therapy, ABs (limited value), surgical tx (not very helpful)
must also include mechanical support (farriery) w/ medical tx
-frog support using foam pads: raises heels, thus reducing pull of DDF tendon
-want horse to stand on caudal portion of hoof to ↓ pressure in toe region & protect painful sole from ground contact while supporting horses’ wt
What are 5 basic things to evaluate for tendon/ligament injuries?
fiber alignment
What is a goal of tx of degenerative tendon injuries?
treatments should provide a means to improve anabolic capacity of tendon fibrocytes (intrinsic repair)
What is the medical tx for tendon & ligament injury?
early: cold therapy then alternating temp therapy, bandaging, NSAIDs, short acting steroids, DMSO
intralesional injection of anti-inflammatories: insulin like growth factor, Adequan (PSPG), hyaluronic acid, ACell Vet, stem cells, platelet rich plasma
extracorporeal shock wave therapy: used for acute tendon injury
What is the best way to diagnose tendon or ligament injury?
diagnostic U/S: use linear U/S systems w/ variable focusing capabilities
What are some surgeries used to tx tendinitis & when should they be done?
should be done during subacute period to ensure injured area of tendon revascularizes as much as possible
tendon splitting
superior check ligament desmotomy
anular ligament resection
How is exercise used in the tx of tendon & ligament injuries?
controlled exercise initiated during remodeling phase
excessive exercise will stimulate fibrous tissue production, not remodeling
very light exercise up to 6-8 weeks
at 60 days, gradually ↑ loads applied
What are tx goals for synovitis/capsulitis?
alleviate immediate compromising effects of inflammation, incl. pain & ↓ function
prevent development of permanent fibrosis in joint capsule, which in turn --> ↓ motion & compromised shock absorption
prevent or minimize development of OA
What is the normal tx for synovitis?
prevention/tx of 1º problem
tx active dz state, esp. soft tissue component
-may be primarily symptomatic: rest, immobilization?, physical therapy (heat, cold, massage, stretching), sx, drugs
tx cartilage degeneration: infrequently done
What are some treatment modalities used in management of osteoarthritis?
physical therapy: heat, cold, alternating temps, massage
systemic drugs: NSAIDs, PSGAGs, GAGs, hyaluronic acid, steroids
intra-articular drugs: sodium hyaluronate, PSGAG (give w/ amikacin), steroids, interleukin-1 receptor antagonist (IRAP)
What are some common causes of septic arthritis in:

a. adults
b. juveniles
a. wounds, iatrogenic (intra-articular meds)

b. common
hematogenous seeding (dystocia, premature birth, inadequate colostrum production or ingestion, patent urachus (most common)
also GI or resp. dz, infected umbilicus
What joint is most commonly involved in septic arthritis?

How many cases involve only 1 joint?

How would one definitively diagnose septic arthritis?
localizing clinical signs, synovial fluid findings compatible w/ septic arthritis, positive culture from synovial fluid (may be negative 25-70% of time)
total protein > 4 g/dl
WBC > 30,000/mm3 (predominantly PMNs)
peripheral WBC count usually ↑
What is the tx for septic arthritis?
principles: eliminate causative organism, remove inflammatory by-products from joint
IV ABs, IA ABs for 1st 3-5 days; total tx: 2-3 weeks
lavage w/ a balanced electrolyte sol’n

also NSAIDs, DMSO, etc.
What are some factors assoc. w/ back & upper hindquarter problems?
type of athletic activity, conformation, equitation induced (rider, saddle), other musculoskeletal problems, shoe imbalance, overtraining, exertional myopathies, trauma, oral/dental irregularities
What is a hunter's bump?
exaggeration of tuber sacrale d/t atrophy of gluteal mm.

may indicate ongoing sacroiliac damage
What are 3 types of back palpation?
dorsiflexion: dipped back
-elicited by pressure in mid-thoracic region

ventroflexion: arched back
-elicited by squeezing at tail head or applying local stimulus to ventral abdomen

lateral flexion: apply firm pressure along length of each longissimus dorsi m.
-compare degree of contraction & relaxation in different segments
What are some signs of sacroiliac strain?
common, chronic
not curable, but manageable

-intermittent pelvic limb lameness
-poor gluteal muscle cover & asymmetry w/ tilting or rotation of pelvis &/or muscle wastage of 1 quarter
-lack of impulsion of 1 or both hind limbs at slower paces
-sacroiliac joint not fully load bearing
What is the cause & signs of crowding/overriding dorsal spinous processes?
very common

repeated contact of dorsal spinous processes beneath saddle area & extending from T12-L2 predisposes to low back pain

horse resents dorsal & lateral flexion
chronic cases assoc. w/ ↑ atrophy of longissimus dorsi muscles
What are the goals of tx of back pain?
attempt to ID & correct cause: observe horse-rider unit & type of work attempted
reduce or correct impact of other musculoskeletal problems (ex. hock DJD, shoeing, foot imbalance)
relieve pain
What therapies are used to treat back pain?
regulated exercise
physical therapy
chiropractic adjustment
drugs: NSAIDs, muscle relaxants, local injections of steroids, HA, nutraceuticals
shoeing change
What is the most common type of pelvic fx?
tuber coxae fx: "knocked down hip"
What are some potential causes of osteochondrosis?
rapid growth, genetics, nutrition, toxicoses, abnormal biomechanical forces: created by poor conformation

*mechanical triggering event may also be required
What determines if OC or subchondral cystic lesion develops?
skeletal location
OCD develops at sites of shear stress, while SCL develops at sites of substantial & consistent compressive loads
mechanical trauma at point of maximal wt. bearing may cause fatigue failure of subchondral bone unrelated to OC
likely that OC is 1° problem & SCL is 2°
What is the presentation of SCL?
cysts typically occur at sites of maximal wt. bearing
stiff gait, muscle atrophy, intermittent lameness (may move from 1 leg to other)
What is the most common location of SCL & what is the tx?
medial femoral condyle
usually assoc. w/ onset of training

removal of fibrous contents of cyst by surgical curettage eliminates mediators but healing may be slow & incomplete
arthroscopic injection of MPA (Depo Medrol) &/or triamcinolone into cyst cavity: yields similar change of success as debridement but w/ less chance of lesion enlarging & less disruption of articular surface
What are principles of emergency management of orthopedic injuries?
preserve vascular & neural supply
prevent skin penetration of bone fragment
protect from contamination
stabilize limb: splinting
initial exam: twitch/sedation (xylazine); assess damage
therapeutics: ABs, anti-inflammatories, shock
How would one dx & tx septic synovial structures (joints, sheaths, bursae)?
dx: arthrocentesis: TCC, diff cell count, TP, gram stain, C/S, fluid pressure study
rads: survey, stressed, & contrast
U/S: sterile wound prep & sterile shroud

tx: most commonly opt for aggressive intervention: arthroscopy, synovectomy, or open arthrotomy
What is the tx for fractures of phalanges & distal metacarpus?
align dorsal cortices
thin padding w/ dorsal splint or Kimzey
tightly tape entire length to toe
What is the tx for fx of mid-forelimb?
Robert Jones bandage: 3x normal limb diameter
-several TIGHT layers
splint lateral & caudal from elbow to ground
What is tx for fx of middle & proximal radius?
Robert Jones bandage w/ caudal & lateral splints, w/ lateral extension
What is tx for fx proximal to elbow?
modified Robert Jones bandage, splint caudal w/ carpus in extension
What factor is important in px after fx?
intact skin halves the estimate & doubles the px
pedal osteitis

a. etiology
b. signs
c. tx
a. generalized or localized osteolysis in distal phalanx in response to:
-focal trauma (ex. puncture, fx)
-chronic subsolar bruising
b. chronic palmar foot pain in presence of weak soles
often positive response to hoof testers
c. tx 1º cause
if sequestrum has formed, foot should be fenestrated to provide access for surgical debridement & drainage
generalized form: shoeing w/ anticoncussive pads or pour-in sole pads
traumatic & degenerative arthritis of DIP joint

a. etiology
b. signs
c. tx
a. significant cause of racing lameness; also assoc. w/ jumping
b. insidious onset of mild to moderate bilateral forelimb lameness
acute unilateral lameness w/ localizing signs in case of sprain
frequently palpable effusion of DIP joint
often no rad signs
c. tx primary condition
intra-articular drugs (PSGAG, sodium hyaluronate, steroids)
associated foot imbalances must be treated w/ corrective trimming & shoeing
collateral ligament desmitis of DIP joint

a. etiology
b. signs
c. regional anesthesia results
d. tx
a. horses used for jumping appear to be at ↑ risk
desmitis: bone attachments intact, injury in middle of ligament
enthesitis: inflammation at bone ligament interface (worse px)
b. mostly no localizing signs
mild to moderate, chronic foot lameness w/o rad abnormalities
often bilateral
c. ASNB: 100%, PDNB: 72%, DIPJ: 24%, bursa & DFTS: 0%
d. rest: 3-6 mo.
immobilization of lower limb in cast is indicated for 1st 4-6 wks
extracorporeal shockwaves
intra-articular medication of coffin joint w/ IRAP
What is the clinical definition of navicular syndrome?
chronic lameness d/t pain in palmar aspect of front feet of > 2 mo. duration
lameness abolished by PDNB, DIPJ anesthesia & navicular bursa anesthesia
+/- radiological abnormalities
What are some theories of the pathogenesis of navicular syndrome?
biomechanical: pressure & friction b’twn DDFT, navicular bone, & middle phalanx
vascular: arteriosclerosis & thrombosis of nutrient arteries
unification: remodeling of navicular bone d/t overworking
neurologic modulation
distal border fractures
distal deep digital flexor tendintits

a. etiology
b. signs
c. regional anesthesia results
a. horses used for high-level jumping overrepresented
~50% are acute onset, 50% chronic
b. lameness ranges from mild to severe
half unilateral, half bilateral
localizing signs very rare
60% of horses have navicular bone edema
c. ASNB: 100%, navicular bursa: 67%, DIPJ: 63%, PDNB: 60%
distal deep digital flexor tendonitis

a. dx
b. tx
a. MRI
b. 3-12 mo. rest
pastern cast w/ raised heels
shoes w/ raised heels, but horses may deteriorate
What local anesthetics are used for nerve & joint blocks?
mepivacaine, xylocaine: intermediate acting (90 min)
How do you interpret local anesthesia?
lame – no sensation
sound – no sensation
improved – no sensation: mechanical gait restriction, complementary lameness, partial desensitization, severe pain, accommodation to chronic pain
lame – still sensation: poor technique, aberrant innervation
What areas are anesthetized by the palmar digital nerve block (PDNB)?
entire foot except dorsal coronary band & laminae
What areas are anesthetized by the DIPJ block?
DIP joint (except collateral ligaments), navicular bone, navicular bursa, toe region of sole, heel region of sole (if 10 cc used), distal DDF tendonitis
What areas are anesthetized by the navicular bursa block?
navicular bone, navicular bursa, navicular ligaments, toe region of sole, distal DDF tendonitis
How can you dx foot pain using local anesthesia?
sound to PDNB: pain in heel region
sound to DIPJ: pain in DIPJ or navicular apparatus
sound to bursa: pain in navicular apparatus
sound to PDNB, not to DIPJ or bursa: pain in heel region excluding navicular apparatus
What is the diagnostic local anesthesia sequence for the lower limb?
2. pastern ring block or ASNB

if horse is sound at this stage, following blocks may add further info:
DIPJ block
navicular bursa block
PIPJ block
digital sheath block

if lameness has failed to improve
3. fetlock joint block
4. L4PNB
5. subcarpal lateral & medial palmar metacarpal nn.
6. lateral palmar n. at accessory carpal level OR ulnar n. block OR direct infiltration of proximal suspensory region
What is the difference b'twn wound contamination & infection?
contaminated: presence of microorgs in wound w/o active multiplication or trauma to host (all wounds contaminated)

infected: microorgs are actively multiplying & invading healthy host tissues, overwhelming host’s immune response
What are some treatment modalities for navicular pain?
rest alone: suitable for collateral desmitis & DDFT injuries (3-6 mo.)
foot should be trimmed to obtain straight hoof-pastern axis, maintain heel mass, & shorten toe to facilitate breakover (egg bar shoes)
vasoactive meds
intrabursal meds: steroids
tildren: bisphosphonate
extracorporeal shockwaves
navicular burscopy
stem cell injection
navicular suspensory desmotomy
palmar digital neurectomy: tx of last resort w/ navicular dz in which lameness is completely resolved by PDNB
What are the principles of wound lavage?
use sterile isotonic saline: usually enough
if desired, use antiseptics (povidine-iodine or chlorhexidine): must dilute
deliver fluid to wound at 10-15 psi pressure: 18G needle or catheter on 60 cc syringe, spray bottle, Water Pik (not bulb syringe)
What are the principles of wound debridement?
why do it: ↓ # of bacteria, removes contaminants (FB, dead tissue)
sharp, layered debridement is best (scalpel, scissors)
What are the types of wound closure?
1º closure: wound closed immediately & completely using aseptic technique
delayed 1º closure: wound treated as open for 3-5 days to allow debridement & reduction in contamination, then is closed primarily
secondary 1º closure: wound closed 4-7 days after injury, after granulation tissue forms
2nd intention healing: wound allowed to heal by contraction, granulation, & epithelialization
skin grafting
scar revision
What factors should one consider when decided TCON (to close or not to close) a wound?
mechanism of injury: laceration, penetration, impact
location of wound
degree of contamination
duration of wound: “golden period” of 6-8 hrs. is not really relevant
tension on tissues
What are some reasons for wound dehiscence?
infection (#1 cause), motion, avascular tissues, too much tension, inappropriate suture selection
What is the tx for SQ emphysema?
restricted activity: stall rest
What are some ways to prevent & tx proud flesh?
prevention: minimize movement w/ splints & casts, avoid irritating wound medications
tx: topical corticosteroids, sharp excision of excess granulation tissue & pressure bandage, skin grafting
What are 2 main uses of skin grafting?
extensive wounds that won’t close by 2nd intention alone
management of proud flesh
What are some advantages & disadvantages of island skin grafts?
(+): often can harvest & place w/o general anesthesia, need minimal equipment, survive in suboptimal conditions, simple donor site management, unimpaired drainage of graft
(-): poor cosmetic results, hair tufts, incomplete hair coverage
What are some causes of skin graft failure?
poor recipient bed preparation, infection, motion, fluid accumulation under graft
What should you always remember to administer in a horse w/ a wound?
tetanus prophylactic
What are some causes of acute hemorrhage --> anemia?
trauma: most common cause
uterine artery rupture: pregnant mares late gestation
renal medullary necrosis: NSAID toxicity
GI bleeding: NSAID toxicity (very rarely causes enough hemorrhage to cause acute signs)
exercise induced pulmonary hemorrhage
guttural pouch mycosis: internal carotid rupture (life threatening)
coagulopathy: usually no clinical signs
What clinical signs dominate in

a. acute hemorrhage
b. chronic hemorrhage
a. signs of SHOCK dominate:  hypotension, tachycardia, tachypnea, pale mm, prolonged CRT, poor peripheral pulses, cool extremities, trembling weakness, depression
b. signs of ANEMIA dominate:  pale mm, tachycardia, tachypnea, weakness, exercise intolerance, anorexia, depression, physiologic heart murmur
How would one dx

a. acute hemorrhage --> anemia
b. chronic hemorrhage --> anemia
a. evidence of hemorrhage
-if internal hemorrhage suspected: peritoneal or abdominocentesis, thoracic or abdominal U/S, fecal occult blood, U/A, rectal exam, endoscopy (guttural pouch)

regenerative anemia & hypoproteinemia w/o evidence of hemolysis
-regeneration hard to detect in horses: no reticulocytes in peripheral blood
-if MCV > 60: assume regenerative anemia

b. evidence of hemorrhage
evidence of Fe def: non-regenerative anemia, low serum Fe, low serum transferring saturation, high Fe binding capacity
What is the tx for acute hemorrhage?
stop bleeding
shock: fluid support
+/- blood transfusion
What is the tx for chronic hemorrhage?
tx underlying dz
Fe supplements: parenteral ferrous sulfate
How would one dx hemolytic dz --> anemia?
anemia w/ normal TP, hyperbilirubinemia
hemoglobinemia &/or hemoglobinuria: if intravascular hemolysis
-hemoglobinemia may be reflected in high MCHC: artifact
altered RBC morphology: spherocytes, eccentrocytes, Heinz bodies
R/O liver dz: direct & indirect bilirubin, serum hepatic enzymes, bile acids
R/O anorexia

a. pathophysiology
b. clinical signs: acute
c. clinical signs: chronic
d. dx
e. tx
a. retrovirus transmitted by arthropods or contaminated instruments
infects BM: lives in MPs
immune complex dz --> anemia, vasculitis
new antigenic variants assoc. w/ new clinical episodes
b. icterus, depression, fever, edema (d/t vasculitis), petechia
c. intermittent fever, icterus, wt. loss, lethargy, pale mm
d. Coggins: screening test
if positive, ELISA used to confirm w/in 15 days
e. euthanasia, sale for slaughter, or brand & permanent quarantine
Anaplasma phagocytophila

a. pathophysiology
b. signs
c. dx
d. tx
a. vector borne: Ixodes ticks
organism is tropic for granulocytes: proliferates in BM
b. acute depression, high fever, petechiae, icterus, ataxia (d/t hemorrhage or edema in spinal cord), edema (older animals more severely affected)
c. blood smear showing neutrophilic inclusions (morulae): present early in dz, then less frequently seen
serology: NOT helpful
PCR: very sensitive & specific
d. almost always successful
-drug of choice: oxytetracycline IV for 7 days
-doxycycline PO for 14 days
supportive care
NSAIDs: Flunixin IV for 3 days

a. pathophysiology
b. signs
c. dx
d. tx
a. IC mediated destruction of RBCs: direct (intravascular) or phagocyte mediated (extravascular: more common)
induced by drugs (penicillin most common), infections (esp. Strep equi), neoplasia, or may be idiopathic
b. fever, icterus, lethargy, tachycardia, tachypnea, pale mm, splenomegaly, +/- hemoglobinemia or hemoglobinuria (if intravascular)
c. autoagglutination may be evident
Coombs test: IMHA confirmed if either test is positive
-direct: agglutination of patient’s RBCs in presence of antiglobin reagent
-indirect: agglutination of test RBCs in presence of patient’s serum
d. remove or tx underlying cause
supportive care, fluids
immunosuppressive therapy: dex IV (steroid of choice), prednisolone PO, +/- cyclophosphamide, plasmapheresis (if refractory)
ABs if d/t Strep equi
+/- blood transfusion, diuretics
What the indications for performing a blood transfusion in animals w/ hemorrhage?
PCV < 15 if acute
PCV < 8-10 if chronic
HR > 90 even after circulatory support
PCV ↓ to less than 20% in 12 hrs

requires crossmatch: universal donor is Aa neg, Qa neg, & Ca neg, non-TB
if crossmatch not possible, use gelding of same breed & mix donor serum & patient blood to look for agglutination
red maple toxicosis

a. pathophysiology
b. signs
c. dx
d. tx
a. caused by wilted red maple leaves: seasonal
oxidative injury to Hg --> methemoglobinemia
b. icterus, weakness, ataxia, brown mm, methemoglobinemia, methemoglobinuria, tachypnea, tachycardia, colic (very common), oliguria/anuria, DIC/acute death
c. hx, clinical signs, methemoglobinemia, methemoglobinuria, Heinz bodies
d. remove source, ↓ absorption (mineral oil &/or charcoal)
fluids: circulatory support & diuresis
+/- blood transfusion: base decision on clinical signs, not PCV d/t methemoglobinemia
diuretics (always use): furosemide IV +/- dopamine if oliguric
+/- vitamin C, other antioxidants
What are some unique properties of the equine cornea?
slow to heal, prone to infection, high amt. of trauma d/t prominent location of eyes & horses’ propensity to throw their heads
What is the tx for a superficial uncomplicated corneal ulcer?
topical broad spectrum ABs QID: triple AB, gentamicin
topical 1% atropine SID to BID: dilates pupil, ↓ pain assoc. w/ 2º uveitis
systemic NSAIDS: flunixin
NEVER USE TOPICAL CORTICOSTEROIDS!: delays healing, promotes infection
fungal keratitis

a. most common organisms
b. predisposing factor
c. dx
d. tx
e. px
a. Aspergillus, then Fusarium
b. topical steroid use
c. ulcer present for 7-14 d. & now getting worse
clinical appearance, culture (best test), cytology (hyphae), histo of corneal bx
d. as for other ulcers: ABs, atropine
antifungal therapy: all are expensive
1% miconazole IV, natamycin (only available ophthalmic antifungal), fluconazole (topical or oral), itraconazole IV, voriconazole (topical or systemic)
debridement or superficial keratectomy +/- conjunctival flap
-↓ amt. of fungus, removes inflammatory debris
-most take 4-8 wks to heal & result in corneal vascularization w/ a significant scar
equine recurrent uveitis

a. pathogenesis
b. dx
a. ocular insults (trauma, infections (ex. Lepto, Strep), corneal dz, etc.) --> disruption of blood-aqueous barrier --> acute uveitis --> return to normal (most horses) OR immune rxn --> multiple recurrent episodes (ERU)
What are the 3 main syndromes of ERU?
“classic” anterior uveitis: recurring bouts of inflammation & pain followed by variable periods of quiescence
subclinical panuveitis: no observed bout of inflammation/pain (common in Appaloosas)
1º posterior uveitis: least common: mild to no anterior clinical signs, retinal detachment common
What 3 agents are the mainstay of tx for ERU?
topical corticosteroids, mydriatic/cycloplegics, AND systemic NSAIDs
What topical meds are used to tx ERU?
prednisolone acetate 1%
dexamethasone HCl 0.5-1% q 1-6 hrs.
-potent anti-inflammatory w/ excellent ocular penetration
-predisposes to corneal fungal infection
flurbiprofen, voltaren, or other topical NSAIDs: ↓ corneal epithelialization
cyclosporine A 0.02-2% q 6-12 hrs.
-strong immunosuppressant, weak anti-inflammatory effect
-poor eye penetration
atropine HCl 1% q 6-48 hrs.
-cycloplegic, mydriatic: pain relief, ↓ synechia formation
What are some practical & stable management practices to decrease incidence of ERU?
eliminate environmental triggers (ex. allergens, etc.)
↓ trauma to eyes by eliminating sharp edges, nails, etc.
good general health care
What systemic drugs are used to tx ERU?
-flunixin meglumine
-potent ocular anti-inflammatory
-long term use may predispose to gastric & renal toxicity
-phenylbutazone: good ocular anti-inflammatory

steroids: use w/ caution & only as last resort
-prednisolone, dexamethasone
-frequent side effects: laminitis, etc.
What other procedures are used to tx ERU?
cyclosporine implants: work very well
slow release vitreal implants: constant release of drug
can deliver drug for years
What differentiates an uncomplicated from a complicated corneal ulcer?
uncomplicated: no microorganisms on culture or cytology, no cellular infiltrate, no FB, no 2º uveitis
complicated: don’t heal w/in 72 hrs, have a collagenase component (ex. melting corneal ulcers), have a mechanical obstruction to healing (ex. FB, indolent), are infected, or are in danger of perforation