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MSK II > LA Juvenile Orthopedic Disease > Flashcards

LA Juvenile Orthopedic Disease Flashcards

1
Q

describe neonatal septicemia

A
  1. most common problem in neonates
  2. early ID and mgmt is key to success!!
  3. generalized versus localized: naval/joint ill, diarrhea, pneumonia
  4. important risk factors is failure of passive transfer due to poor colostrum ingestion or premature/dysmature foal
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2
Q

what makes a premature foal?

A
  1. born prior to 320 days gestation
  2. thin, with a white silky haircoat, floppy ears, domed head, tendon laxity

3, CUBOIDAL BONES COOK LAST MINUTE so born with cartilage and not bone

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3
Q

describe the etiology of septic arthritis/osteomyelitis in foals

A
  1. hematogenous spread!
  2. failure of passive immunity (like foal septicemia)
  3. mostly due to gram negative
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4
Q

describe the etiology of septic arthritis/osteomyelitis in calves

A

hematogenous spread most common; with concurrent failure of passive transfer, omphalophlebitis, resp, or GI infection

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5
Q

describe clinical signs of spetic arthritis in juveniles

A
  1. septicemia and generalized depression
  2. multisystemic disease
  3. multiorgan failure
  4. local signs: periarticular edema, joint effusion, lameness
  5. polyarthritis common!!
    -equine: tarsus! stifle, fetlock, carpus
    -calves: carpus! stifle, tarsus
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6
Q

what is frequently seen in synoviocentesis of septic joints?

A

super high neutrophils! high total protein, high TNCC!!

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7
Q

what makes a foal/calf at risk? (3)

A
  1. mom history:
    -uterine infection/vaginal discharge
    -illness during pregnancy
    -milk dripping before foaling
  2. delivery:
    -dystocia, red bag
    -early cord rupture
  3. newborn foal: dummy foal
    -meconium staining
    -prolonged time to stand or nurse
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8
Q

describe systemic treatment for septicemia

A
  1. immunoglobulin therapy:
    -colostrum if early enough!
    -plasma: increased non-selective IgG
  2. antibiotics:
    -choice is specific to each case, disease, and region
    -based on isolate and C&S data
    -initial: broad spectrum
    -AMPICILLIN AND AMIKACIN: remain the most appropriate initial antibiotic therapy until C&S results known
    -or a 3rd gen cephalosporin in the field

-can give regional or systemic, interosseous, beads, IA, limb perfusion, etc.

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9
Q

describe surgical intervention for septic arthritis

A
  1. joint drainage: closed needle aspiration; through and through lavage
  2. arthroscopy
  3. arthrotomy

4, +/- biologics

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9
Q

is there any antimicrobial product currently labeled for intra-articular use in cattle?

A

NO!!!; other treatments are also pretty cost prohibitive for cattle, so likely stuck with lavage

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9
Q

describe local treatment of septic arthritis

A

AGGRESSIVE AND URGENT!

solution to pollution is dilution!

needle lavage or arthrotomy

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10
Q

describe prognosis for septic arthritis

A
  1. osteomyelitis: poor
  2. multiple joints: poor
  3. early recognition: good
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11
Q

describe cuboidal bone malformations/incomplete ossification

A

incomplete ossification of the cuboidal bones is a common finding in premature and dysmature foals

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12
Q

describe the etiology of incomplete cuboidal bone ossification (IMPORTANT)

A
  1. bone ossification begins last 2 months of gestation
  2. rapid in last 2 weeks of gestation and continues for approx 1 month post birth
  3. ossification center is spherical, surrounded by cartilaginous precursor
  4. carpal ossification precedes tarsal!!
  5. associated with angular limb deviations, misshapen bones, and juvenile osteoarthritis

so horses would be the WORST species to induce early labor!!!

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13
Q

describe treatment of incomplete cuboidal bone ossification

A

goal: DONT crush cartilage template! potentially sedate and make a bed baby

  1. restrict exercise
  2. bandage with a light splint: not including digit, take caution with tendon laxity (load tendons a little bit while still protecting joints through bones)
  3. repeat radiographs every 1-2 weeks
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14
Q

describe flexor tendon laxity; include treatment

A

common in premature or dysmature foals; see a slight drop in fetlock all the way to fetlock touching the ground

treatment:
1. controlled exercise (10 min daily)
2. protect/monitor wounds
3. trim to get heel off ground
4. heel extensions

15
Q

what are 3 congenital farm animal tendon disorders?

A
  1. hyperextension deformities: seen most commonly in premature calves
  2. flexural deformities: inherited condition, in utero position, overcrowding within uterus
  3. may see cleft palate, dwarfism, or arthrogryposis, always go hunting for more than just ortho issue!
16
Q

describe treatment of hyperextension deformities

A
  1. mild deformity: stall rest
  2. moderate: stall rest and heel extensions
  3. severe: stall rest, heel extensions, arthrodesis (if older in growth period and less to work with)
17
Q

describe angular limb deformities (IMPORTANT)

A

look subjectively from clinical exam and also radiographically

congenital or acquired

*an outward (valgus) or inward (varus) deviation of limb that occurs in the fetlock, carpus, or tarsus

**most common deviation seen in horses is carpus valgus!

but could have a carpal valgus and a fetlock varus; name in relation of distal limb to joint

foals allowed to have up to 4 degree of deviation and still called normal

18
Q

describe the etiology of angular limb deformity in foals

A
  1. perinatal factors:
    -incomplete ossification of cuboidal bones!
    -weak soft tissue structure
    -metaphyseal/epiphyseal dysplasia, physeal trauma
  2. developmental factors:
    -unbalanced nutrition during growth period
    -excess exercise
    -trauma
19
Q

describe the etiology of angular limb deformity in calves

A
  1. most commonly congenital: due to in utero bending stresses
  2. can be due to growth plate abnormalities: normal for calves to have up to 7 degrees of deviation and still called normal though
  3. can be due to fracture or limb rupture
20
Q

describe diagnosis of angular limb deformity

A
  1. thorough physical exam: inspection and manipulation of affected limbs
  2. diagnostic imaging:
    -determine location of deformity
    -determine degree of deformity
    –line drawn through long axis of long bones; where lines cross is the location of the deviation
  3. if have lost of time left in growth period, can do more and have more time to intervene!!
21
Q

describe treatment of angular limb deformity

A

conservative: if still in growth period!
1. stall rest
2. splints and casts: may make worse before get better
3. farrier work: trim which side want to stop leaning toward
-general principles: hoof will turn in direction of the longer claw OR toward side of the wider wall
-valgus correction: lateral claw trimmed shorter than medial claw
-varus correction: medial claw trimmed shorter than lateral claw

surgical: perform when growth period is over
1. perisoteal stripping: controversial: on concave side of deformity
2. transphyseal bridging: temporary fix and MUST remove screws because overcorrection is possible

22
Q

describe congenital flexural limb deformities/contracted tendons

A
  1. flexural deformity at brith
  2. bigger problem in front limbs
  3. causes: abnormal uterine position, genetics, ingestion of toxins during preg, influenza
23
Q

describe congenital flexural limb deformities clinical signs and diagnosis

A

clinical signs: varying degree of flexion
1. fetlock, pastern, and coffin joint: upright walking with no angle to the fetlock, walking on the front of the fetlock, walking on the toe with the heel off the ground

  1. carpus: inability to extend

diagnosis: observation, physical manipulation

24
Q

describe flexural limb deformity TREATMENT

A

mild: trimming, extensions, controlled exercise

moderate: bandaging, splits, sleeve casts

severe: surgery,

24
Q

describe management of flexural limb deformities

A
  1. rest!
  2. congenital with mild limb deformities:-
    -bandage/tube casts
    -tetracycline 44-66mg/kg IV (HELLA HIGH DOSE) worry about in cattle
  3. acquired/secondary to pain:
    -correct primary problem (exercise or calorie restrict)
  4. surgical correction: if no other option work
    -tenotomy: of ulnaris lateralis and flexor carpi ulnaris; poor prognosis for use
25
Q

what are causes of acquired flexural limb deformity?

A
  1. secondary to pain
  2. nutritional: excess energy intake resulting in rapid bone growth (bone grows faster than tendon); mineral imbalance
26
Q

describe management of acquired flexural limb deformities

A
  1. if associated with lameness:
    -manage aggressively! encourage weight bearing on lame limb ASAP! use anti-inflam drugs to relieve pain
  2. nutritional imbalance:
    appropriate mineral intake, decrease excess energy to intentionally stunt growth, increase exercise via NSAIDs
  3. shoeing: more frequent mild changes are better
27
Q

describe prevention of acquired flexural limb deformities

A
  1. appropriate attention to early diagnosis and treatment in young animals!
  2. proper nutrition
28
Q

describe digital subluxation

A
  1. heritable condition of short horn cattle
  2. characterized as VARUS deformity at level of metatarsophalangeal joint
  3. results in difficulty ambulating, abrasions/trauma to limb at level of fetlock
29
Q

describe causes of patellar luxation

A

1, congenital malformation of femeropatellar joint

  1. femoral nerve deficit
  2. trauma
30
Q

describe clinical presentation and diagnosis of patellar luxation

A
  1. unable to extend stifle joint anf pelvis is lowered on affected side
  2. femoral nerve damage: history of dystocia or excesive pulling of calf; atrophy of quads
  3. luxation ID by palpation of patella relative to trochlea: patella luxation should not be inducible normally!
  4. radiographs of stifle:
    -definitive diagnosis
    -determine degree of OA
    -ID any concurrent fractures
    -skyline view allows assessment of lateral and medial trochlea and trochlear groove
31
Q

describe sx treatment of patellar luxation

A

make a new deeper groove and tack it down; doesn’t work well in LA (better if smaller goat, etc.)

for femoral nerve deficits: nonsurgical test of time
-stall rest with good footing, short course of anti-inflam
-if not better within 30d = grave prognosis

MSK II (40 decks)

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