Small Animal Miscellaneous Juvenile Diseases

Question 1

describe avascular necrosis of the femoral head/Legg-Calve-Perthes Disease etiology

Answer 1

etiology: cause not fully understood

pathogenesis: non-inflammatory ischemia and necrosis resulting in deformation of the femoral had and neck (trabecular necrosis leads to fragmentation that leads to reossification and a malformed femoral head)

Question 2

describe signalment, history, and clinical signs of avascular necrosis

Answer 2

signalment:
-small breed dogs
-4-11 months old

history:
-lameness, usually unilateral
-NO trauma

clinical signs: looks like a joint problem!!
1. non-weight bearing lame
2. pain with hip extension
3. crepitus
4. muscle atrophy

Question 3

describe diagnostics of avascular necrosis

Answer 3

radiographic findings:
1. osteolysis: subtractive process (UNLIKE the additive process of osteophytes with joint pathology)
2. malformed femoral head
3. femoral neck fractures are possible

CT:
1. may be more sensitive earlier n the disease process
-similar lesions as radiographs

Question 4

describe treatment and prognosis of avascular necrosis

Answer 4

1. conservative is RARELY (25%) successful
2. surgery: FHO/FHNE!!! or total hip replacement

prognosis: excellent with surgery; lameness resolve in 84-100% cases

Question 5

describe Pes Varus (inward foot) signalment, history, and clinical signs

Answer 5

signalment: juvenile dachshunds

etiology:
1. NO history of trauma!!!! genetic!!! runs in litters
2. suspected autosomal recessive gene
3. unilateral or bilateral

clinical signs: angular limb deformity!!
1. medial bowing of distal tibia
2. deviation of feet toward midline (varus deformity)
3. +/- lameness; abnormal biomechanics lead to osteoarthritis! (cartilage weardown)

Question 6

describe pes varus diagnostics

Answer 6

physical exam:
1. angular change typically visible
2. pain may or may not be present (depends on presence of OA)

radiographs:
1. shortening of medial tibia
2. medial bowing of distal tibia
3. +/- degenerative changes in the tibial-tarsal joint

Question 7

describe pes varus treatment and prognosis

Answer 7

1. dictated by severity and clinical signs:
   -lameness = surgery
   -no lameness = maybe not surgery?
2. technique: medial opening wedge osteotomy followed by fixation with either bone plate or ESF

prognosis: excellent results for dachshunds!!!

Question 8

describe carpal laxity syndrome presentation

Answer 8

can look like one of two things:

1. hyperextension: dropped carpus
2. hypoextension:
   -carpal flexural deformity
   -carpal flexion syndrome

Question 9

describe signalment and exam findings of carpal laxity syndrome

Answer 9

1. young, rapidly growing dogs: 6-16 weeks of age (PUPPIES)
2. males > females
3. medium to large breed dogs: dobies, german shepherds, great dane, shar pei

exam findings:
1. unilateral or bilateral changes to carpal joint
2. +/- pain: will be painful if try to overstretch/correct

Question 10

describe etiology of carpal laxity syndrome

Answer 10

exact etiology unknown: but due to genetics, environment (cage size and floor surface), stress, poor muscle tone, UNBALANCED growth, DIET

clinically: asynchronous growth/development between bones and soft tissues (muscles and tendons)
-hyperflexed: bone grow faster than tendons

Question 11

describe treatment of carpal laxity syndrome

Answer 11

1. balanced diet
2. exercise on surface that allows traction: carpet, grass, etc.
3. splints;
   -NO: usually not needed
   -consider ONLY in cases of severe carpal hypoextension (carpal flexural deformity) where the radiocarpal joint cannot be completely extended during physical exam; splint for 2 weeks then reassess

Question 12

describe etiology and signalment of craniomandibular osteopathy (CMO)/Lion Jaw

Answer 12

etiology:
1. non-neoplastic proliferative bone disease
2. typically affects multiple bones of head
3. genetic origin: autosomal recessive similar to paget’s disease in humans

age: dogs 4-10 months of age

breeds:
1. WESTIES!!!
2. scottish terrier!
3. cairn terrier!
4. boston terrier, shetland sheepdog, labs, great danes, english bulldogs, doberman pinscher, irish steer (CAN happen in any dog)

Question 13

describe history, exam, and diagnostics of CMO

Answer 13

history/owner complaints:
1. moderate pain and difficulty with prehension (eating)
2. inability to eat or drink
3. generalized facial swelling
4. excessive drooling
5. other: intermittent hyperthermia, depression, weight loss, pain, exophthalmia, strabismus (systemic signs indicate more severe)

physical exam:
1. bilaterally enlarged mandibles
2. moderate to extreme pain on opening of the jaw
3. emaciation and dehydration: secondary to inadequate intake

radiographs:
1. proliferative new bone formation
2. mandible, temporal bones, occipital bones, bulla
3. new bone margins are slightly spiculated

Question 14

what bones are commonly affected with CMO? which are less commonly affected?

Answer 14

common:
1. skull: madible, temporal, occipital bones
-may result in ankylosis of TM joint
-tympanic bulla? >50% have mandible and tympanic bullae affected

less common:
femur, radius, ulna; usually due to extension of CMO or HOD

Question 15

describe treatment and prognosis of CMO

Answer 15

treatment:
1. no specific:
-may become self limiting when dog is 11-13 months old
-bony proliferations often regress completely or partially over time
2. analgesics to reduce pain
3. hand-feeding or tube-feeding if necessary

prognosis:
1. mild lesions: fair to good; able to eat until progression stops
2. severe/extensive lesion: guarded to poor; unable to eat, aspiration pneumonia, starvation

Question 16

describe etiology, signalment, and clinical signs of retained cartilaginous core (RCC)

Answer 16

etiology:
1. failure of growth plate cartilage to ossify
2. likely vascular etiology
3. physeal osteochondrosis potentially

breed: young, large/giant breed dogs

clinical signs: often nothing until limb deformed
1. lameness
2. angular limb deformity
3. most common location: distal ulnar physis

Question 17

describe diagnostics and clinical consequences of RCC

Answer 17

radiographs: radiolucent triangle extending proximally from physis

clinical consequences:
-option 1: angular limb deformity: due to affect on growth of distal ulna only, while radius continues on growing normally
1. distal ulnar physis: procurvatum, valgus, elbow incongruity

-option 2: incidental finding with no clinical impact

Question 18

describe treatment and prognosis of RCC

Answer 18

treatment:
1. incidental finding with NO clinical impact: no treatment needed, monitor growth; consider treatment if changes develop

2. clinical impat present:
   -consider surgical correction of an angular limb deformity
   -surgical choices depend on timing and severity:
3. catch early with minor changes: ulnar ostectomy can be considered (growth still occurring, take out a big section of ulna to snap rubber band and allow normal growth)
4. catch late with moderate to severe changes: more advanced corrections needed

prognosis for non-incidental cases:
-depends on severity of deformity and pre-existing OA

Question 19

describe hypertrophic osteodystrophy (HOD); include etiology, signalment, and clinical signs

Answer 19

-also called metaphyseal osteopathy, skeletal scurvy, juvenile scurvy, infantile scurvy, Moller Barlow’s disease, and osteodistrophy II

etiology:
-unknown
-possible causes: infectious, nutritional, vascular abnormalities, genetics, metaphyseal bone, histologic changes, metaphyseal trabecular necrosis, hemorrhage

signalment:
breed: large/giant breed dogs
age: 2-8 months old
sex: Males>females

clinical signs:
1. lameness: intermittent or shifting
2. swelling and pain of the metaphyseal region of long bones!!
3. one or multiple limbs
4. systemic illness

Question 20

describe exam and ortho findings of HOD

Answer 20

general physical exam findings:
1. hyperthermia
2. lethargy
3. diarrhea

orthopedic findings:
1. lameness
2. single or multi limb; often bilateral
3. metaphyseal swelling
4. painful
5. distal radius/ulna or tibia are most common sites!

radiographic findings:
1. radiolucent metaphyseal line is pathognomonic!!! double physeal line
2. increased opacity between radiolucent line and physis
3. metaphyseal enlargement

Question 21

describe treatment and prognosis of HOD

Answer 21

treatment:
1. usually self limiting so treat sympotmatically
2. rest and anti-inflam (NSAIDs and corticosteroids
–weimeraners in particular appear to respond better to corticosteroids (also irish setters and australian kelpies)
3. hospitalization may be required for severe cases: IV fluids, +/- antibiotics

prognosis:
1. good with treatment; usually self limiting but can recur
2, can impact growth and result in angular limb deformity!!- once resolved may require surgery to straighten limb
3 severe cases can result in euthanasia

Question 22

describe the pathophysiology of panosteitis

Answer 22

1. inflammatory disease of bone marrow of LONG BONES
2. histologic changes:
   -vascular proliferation and congestion
   -bone formation around nutrient foramen
3. secondary periosteal reaction

Question 23

describe signalment and clinical signs of panosteitis

Answer 23

signalment:
1. large/giant breed dogs
2. 5-12 months old
3. male >female

clinical signs:
1. forelimbs > hindlimbs
2. SHIFTING LEG LAMENESS
3. waxing and waning severity
4. PAIN ON LONG BONE PALPATION
5. bones affected: ulna, radius, humerus, femur, tibia

Question 24

describe radiographic findings of panosteitis (4)

Answer 24

1. increased medullary cavity opacity: splotchy
2. loss of trabecular pattern
3. periosteal bone formation (smooth)
4. may look normal early in disease; radiographic severity does not correlate well with severity of lameness

Question 25

describe panosteitis treatment and prognosis

Answer 25

1. generally self limiting
2. key treatments for most patients are rest and NSAIDs!!
3. supportive care: IV fluids, hospitalization, +/- opioids

prognosis:
1. generally good: self limiting
2. usually self limiting but can recur in different bones
-IMPORTANT: can recur in different bones of the same limb!!! (in femur and then tibia, in ulna and then radius)

Question 26

describe slipped capital femoral epiphysis; include etiology

Answer 26

also called femoral neck metaphyseal osteopathy, spontaneous femoral capital physeal fracture, and femoral capital physeal dysplasia syndrome

etiology:
1. slow progressive displacement of femoral epiphysis through the growth plate/physis
2. exact cause unknown but may be related to delayed physeal closure
3. often bilateral but can be unilateral
4. nontraumatic: NOT the same as traumatically induced salter harris type I fracture of femoral capital physis
5. MOST commonly reported in CATS!: has been reported in dogs but might not be same etiology

Question 27

describe signalment and clinical signs of clipped capital femoral epiphysis

Answer 27

signalment:
1. siamese cats are overrepresented
2. younger animals (avg 22 months old +/- 6.5 months)
3. males&raquo_space;»»> females
-most common in males neutered less than 6 months old
4. more common in overweight cats

clinical signs:
1. pelvic limb lameness
2. not jumping up/down
3. decreased activity

Question 28

describe treatment and prognosis of slipped capital femoral epiphysis

Answer 28

treatment:
surgery: FHNE or total hip replacement; stabilization not usually an option

prognosis: excellent with surgery

Question 29

describe swimmer syndrome; include etiology and clinical signs

Answer 29

-also called twisted legs, flat-pup syndrome, or turtle-pup

etiology:
1. poorly describe condition of neonatal cats and dogs
2. the cause of decreased muscle tone is unknown, but environmental conditions such as confinement in an area with poor traction and genetics may be involved

clinical signs:
1. apparent in first 1-2 weeks after birth (BABY babies)
2. affected animals remain in sternal recumbency with the pelvic limbs and also often the thoracic limbs splayed laterally
3. attempts to walk often result in a paddling motion

Question 30

describe treatment and prognosis of swimmer syndrome

Answer 30

1. should be started within the first 3-4 weeks of life!!!!
   -if recognized and treatment is started early, prognosis can be good
   -treatment recommendations include hobbles and physical rehab
   -response often seen in 2-4 weeks
2. if not recognized and aggressively treated early:
   -chronic changes will make changes more complicated
   -severe/chronic cases are often euthanized

Question 31

describe ectrodactyly

Answer 31

also called split hand deformity, cleft hand, lobster claw deformity, oligodactyly, or hypodactyly

1. a congenital digital cleft extending between metacarpal bones
2. dogs: no evidence indicating heritability
3. cats: may be an autosomal dominant defect with variable expression

KEY: UNILATERAL disease affecting ONE thoracic limb
-can be mild and nonpainful or super severe and very painful

Question 32

describe treatment and prognosis of ectrodactyly

Answer 32

1. early recognition is KEY: splinting until 4-6 may help prevent muscle contracture
2. mild cases: conservative management may be considered in non-painful and limb use acceptable: splint until can do definitive surgery in adult hood
3. severe cases with pain or limited use:
   -surgical correction may be possible but amputation is often choses

prognosis depends on the severity of the limb deformity and any secondary OA that develops, may need to perform arthrodesis