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93 Cards in this Set
- Front
- Back
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top 3 ddx for 3 legged lameness
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foot abscess
fracture infection in closed space (ex. septic arthritis) |
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What are the parts of a lameness exam?
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hx
standing exam: visual, palpation, flexion & extension moving: in hand, under tack, on lunge diagnostic anesthesia ancillary diagonstics |
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What are 5 indicators of lameness?
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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 |
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What type of lameness is usually seen w/ laminitis?
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bilateral forelimb lameness
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What are the normal foot angles for:
a. front limb b. hind limb |
a. 45-50 deg.
b. 50-55 deg. |
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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 |
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What is laminitis?
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complex, interrelated series of events --> varying degrees of breakdown of interdigitating 1º & 2º epidermal & dermal laminae of foot (active laminar degeneration)
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What is the pathogenesis of laminitis?
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acute laminar degeneration allows P3 to become displaced ventrally --> painful, crippling lameness --> rotation &/or sinking of P3
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What are 3 factors that complicate laminitis?
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rotation or “sinking” of P3
recurrent or continued metabolic upset inflammation may be present d/t weakening or tearing of remaining healthy laminae |
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** What are the 3 phases of laminitis? **
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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 |
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What are some predisposing factors for development of laminitis?
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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 |
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What are the fundamentals of medical tx of laminitis?
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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 |
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What are 5 basic things to evaluate for tendon/ligament injuries?
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size
shape texture position fiber alignment |
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What is a goal of tx of degenerative tendon injuries?
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treatments should provide a means to improve anabolic capacity of tendon fibrocytes (intrinsic repair)
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What is the medical tx for tendon & ligament injury?
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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 |
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What is the best way to diagnose tendon or ligament injury?
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diagnostic U/S: use linear U/S systems w/ variable focusing capabilities
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What are some surgeries used to tx tendinitis & when should they be done?
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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 |
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How is exercise used in the tx of tendon & ligament injuries?
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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 |
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What are tx goals for synovitis/capsulitis?
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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 |
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What is the normal tx for synovitis?
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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 |
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What are some treatment modalities used in management of osteoarthritis?
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physical therapy: heat, cold, alternating temps, massage
bandaging swimming acupuncture systemic drugs: NSAIDs, PSGAGs, GAGs, hyaluronic acid, steroids intra-articular drugs: sodium hyaluronate, PSGAG (give w/ amikacin), steroids, interleukin-1 receptor antagonist (IRAP) |
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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 |
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What joint is most commonly involved in septic arthritis?
How many cases involve only 1 joint? |
hock
~50% |
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How would one definitively diagnose septic arthritis?
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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 ↑ |
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What is the tx for septic arthritis?
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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. |
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What are some factors assoc. w/ back & upper hindquarter problems?
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type of athletic activity, conformation, equitation induced (rider, saddle), other musculoskeletal problems, shoe imbalance, overtraining, exertional myopathies, trauma, oral/dental irregularities
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What is a hunter's bump?
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exaggeration of tuber sacrale d/t atrophy of gluteal mm.
may indicate ongoing sacroiliac damage |
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What are 3 types of back palpation?
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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 |
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What are some signs of sacroiliac strain?
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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 |
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What is the cause & signs of crowding/overriding dorsal spinous processes?
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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 |
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What are the goals of tx of back pain?
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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 |
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What therapies are used to treat back pain?
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rest
regulated exercise physical therapy chiropractic adjustment drugs: NSAIDs, muscle relaxants, local injections of steroids, HA, nutraceuticals shoeing change swimming acupuncture sx |
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What is the most common type of pelvic fx?
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tuber coxae fx: "knocked down hip"
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What are some potential causes of osteochondrosis?
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rapid growth, genetics, nutrition, toxicoses, abnormal biomechanical forces: created by poor conformation
*mechanical triggering event may also be required |
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What determines if OC or subchondral cystic lesion develops?
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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° |
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What is the presentation of SCL?
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cysts typically occur at sites of maximal wt. bearing
stiff gait, muscle atrophy, intermittent lameness (may move from 1 leg to other) |
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What is the most common location of SCL & what is the tx?
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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 |
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What are principles of emergency management of orthopedic injuries?
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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 |
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How would one dx & tx septic synovial structures (joints, sheaths, bursae)?
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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 |
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What is the tx for fractures of phalanges & distal metacarpus?
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align dorsal cortices
thin padding w/ dorsal splint or Kimzey tightly tape entire length to toe |
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What is the tx for fx of mid-forelimb?
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Robert Jones bandage: 3x normal limb diameter
-several TIGHT layers splint lateral & caudal from elbow to ground |
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What is tx for fx of middle & proximal radius?
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Robert Jones bandage w/ caudal & lateral splints, w/ lateral extension
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What is tx for fx proximal to elbow?
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modified Robert Jones bandage, splint caudal w/ carpus in extension
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What factor is important in px after fx?
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intact skin halves the estimate & doubles the px
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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 |
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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 |
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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 |
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What is the clinical definition of navicular syndrome?
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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 |
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What are some theories of the pathogenesis of navicular syndrome?
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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 genetic distal border fractures |
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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% |
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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 |
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What local anesthetics are used for nerve & joint blocks?
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mepivacaine, xylocaine: intermediate acting (90 min)
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How do you interpret local anesthesia?
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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 |
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What areas are anesthetized by the palmar digital nerve block (PDNB)?
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entire foot except dorsal coronary band & laminae
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What areas are anesthetized by the DIPJ block?
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DIP joint (except collateral ligaments), navicular bone, navicular bursa, toe region of sole, heel region of sole (if 10 cc used), distal DDF tendonitis
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What areas are anesthetized by the navicular bursa block?
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navicular bone, navicular bursa, navicular ligaments, toe region of sole, distal DDF tendonitis
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How can you dx foot pain using local anesthesia?
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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 |
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What is the diagnostic local anesthesia sequence for the lower limb?
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1. PDNB
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 |
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What is the difference b'twn wound contamination & infection?
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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 |
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What are some treatment modalities for navicular pain?
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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 |
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What are the principles of wound lavage?
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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) |
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What are the principles of wound debridement?
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why do it: ↓ # of bacteria, removes contaminants (FB, dead tissue)
sharp, layered debridement is best (scalpel, scissors) |
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What are the types of wound closure?
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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 |
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What factors should one consider when decided TCON (to close or not to close) a wound?
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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 finances |
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What are some reasons for wound dehiscence?
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infection (#1 cause), motion, avascular tissues, too much tension, inappropriate suture selection
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What is the tx for SQ emphysema?
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restricted activity: stall rest
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What are some ways to prevent & tx proud flesh?
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prevention: minimize movement w/ splints & casts, avoid irritating wound medications
tx: topical corticosteroids, sharp excision of excess granulation tissue & pressure bandage, skin grafting |
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What are 2 main uses of skin grafting?
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extensive wounds that won’t close by 2nd intention alone
management of proud flesh |
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What are some advantages & disadvantages of island skin grafts?
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(+): 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 |
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What are some causes of skin graft failure?
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poor recipient bed preparation, infection, motion, fluid accumulation under graft
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What should you always remember to administer in a horse w/ a wound?
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tetanus prophylactic
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What are some causes of acute hemorrhage --> anemia?
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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 |
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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 |
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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 |
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What is the tx for acute hemorrhage?
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stop bleeding
shock: fluid support +/- blood transfusion |
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What is the tx for chronic hemorrhage?
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tx underlying dz
Fe supplements: parenteral ferrous sulfate |
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How would one dx hemolytic dz --> anemia?
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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 |
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EIA
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 |
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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 ABs -drug of choice: oxytetracycline IV for 7 days -doxycycline PO for 14 days supportive care NSAIDs: Flunixin IV for 3 days |
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IMHA
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 |
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What the indications for performing a blood transfusion in animals w/ hemorrhage?
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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 |
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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 steroids CONTRAINDICATED |
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What are some unique properties of the equine cornea?
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slow to heal, prone to infection, high amt. of trauma d/t prominent location of eyes & horses’ propensity to throw their heads
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What is the tx for a superficial uncomplicated corneal ulcer?
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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 |
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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 |
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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)
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What are the 3 main syndromes of ERU?
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“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 |
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What 3 agents are the mainstay of tx for ERU?
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topical corticosteroids, mydriatic/cycloplegics, AND systemic NSAIDs
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What topical meds are used to tx ERU?
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topical:
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 |
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What are some practical & stable management practices to decrease incidence of ERU?
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eliminate environmental triggers (ex. allergens, etc.)
↓ trauma to eyes by eliminating sharp edges, nails, etc. good general health care |
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What systemic drugs are used to tx ERU?
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NSAIDs
-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. |
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What other procedures are used to tx ERU?
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cyclosporine implants: work very well
slow release vitreal implants: constant release of drug can deliver drug for years |
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What differentiates an uncomplicated from a complicated corneal ulcer?
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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 |
