Miscellaneous orthopedic conditions Flashcards
1
Q
What is an osteochondrodysplasia?
A
A heritable disease that is characterized by abnormal endochondral or intramembranous ossification (dwarfism).
2
Q
What are potential causes of retarded growth/dwarfism?
A
Proportionate: Metabolic disease, endocrinopathy, polysystemic diseases.
Disproportionate: Osteochondrodysplasia, nutritional disease
3
Q
What minimum database should be performed in a patient with osteochondrodysplasia?
A
Family and nutritional history, CBC/biochem, urinalysis, radiographs (to document delayed development of epiphyseal growth centers, and abnormal growth morphology), TSH/T4, growth hormone, insulin-like growth factor.
4
Q
How is a presumptive diagnosis of osteochondrodysplasia made?
A
Clinical signs, history/family history, evidence of abnormal endochondral +/- intramembranous ossification of rads
5
Q
What are dystoses?
A
Group of bone dysmorphologies characterized by abnormal development of individual bones or parts of bones.
6
Q
What are some types of axial dystoses?
A
Hemivertebrae, block vertebrae, butterfly vertebrae, transitional vertebrae, spina bifida, facet aplasia, and dens malformation
7
Q
What are the different classifications of dystoses?
A
Amelia: complete absence of limb
Hemimelia: absence or partial absence of bone
Dimelia: duplicated limb
Ectrodactyly: congenital digital cleft extending between metacarpal bones
Polydactyly: additional digits
Syndactyly: fused digits
8
Q
What are the different classifications of amelia?
A
Thoracic limb: Monobrachia (one limb), abrachia (both limbs)
Pelvic limb: Monopodia, apodia
9
Q
In which breed might amelia be heritable in?
A
Beagles
10
Q
What are the classifications of hemimelia?
A
11
Q
What are some examples of hereditary hemimelia?
A
Bilateral terminal preaxial thoracic limb hemimelia in Chihuahuas, radial hemimelia in DSH and Siamese cats.
12
Q
What are signs associated with radial hemimelia?
A
Marked varus and flexural deformity of the elbow and carpus
13
Q
What are treatment options for radial hemimelia?
A
Young patient (<4-6 months): external coaptation to allow fusion of the antebrachiocarpal joint in a standing position.
Older patient: conservative therapies or surgery (declawing, reconstruction or amputation [can consider ectoprostheses after amputation]), distraction osteogenesis to repair the radial defect.
14
Q
Name the dystoses shown in the radiographs.
A
15
Q
Is ectrodactyly inherited in dogs and cats?
A
Possibly in cats, not in dogs
16
Q
Between which bones is ectrodactyly most frequent reported?
A
First and second metacarpals
17
Q
What are treatment options for ectrodactyly?
A
Young patient (<4-6months): splinting as for hemimelia.
Older patient: conservative or surgical (amputation or reconstruction) treatment.
18
Q
What conditions are often seen in conjunction with ectrodactyly?
A
Elbow joint incongruity and luxation, syndactyly, digital contractures, missing carpal bones, short ulna
19
Q
Is polydactyly considered an inherited trait?
A
Yes for preaxial (medial) polydactyly in dogs. Considered autosomal dominant in cats.
20
Q
What are the classifications of syndactyly?
A
- Simple: interconnection between digits only consists of skin and fibrous tissue.
- Complex: both soft tissues and bone are fused (further subclassified into complicated when other defects are involved, or uncomplicated)
a. Complete: digits are connected along their entire length
b. Incomplete: digits are only partially connected
21
Q
How is simple syndactyly treated?
A
Separation of the digits and use of a skin flaps or skin grafts to close the resultant defect.
22
Q
What is the most likely signalment for a patient with HOD?
A
Large or giant breed breed, young (2-6 months), male dog (2.3 times more likely than females)
23
Q
Which bones are most frequently affected by HOD?
A
Distal radius and ulna, tibia
24
Q
What are some proposed causes of HOD?
A
Vitamin C deficiency, overnutrition (both largely refuted), inherited (particularly Weimeraners), infectious, inflammation, vaccinations.
25
What are some systemic clinical signs associated with HOD?
Swelling of the metaphyseal region(s). Lethargy, depression, diarrhea, inappetence/anorexia, hyperthermia.
In severe cases carpal or tarsal limb valgus may develop.
26
What are radiographic signs associated with HOD?
Lucent line parallel to the physis, metaphyseal flare (in advanced cases).
27
What is the treatment for HOD?
Mildly affected dogs: analgesics, balanced diet.
Severely affected dogs: supportive care (IV fluids, feeding tube placement, opioids, antacids, antimicrobials [in cases with bactermia], NSAIDs/steroids).
Normally resolves within days to weeks, but can take months. Recurrence may occur.
28
Are corticosteroids or NSAIDs thought to be more effective in treating non-bacteremic, systemically affected Weimeraners with HOD?
Corticosteroids associated with better response (unless HOD associated with bacteremia).
29
What is the typical signalment for dogs affected by panosteitis?
Large to giant breed, young (5-12 months), male dogs (4:1 male to female ratio)
30
Which bones are most frequently affected by panosteitis?
Thoracic limbs more commonly affected (4:1).
Ulna (42%), radius (25%), humerus (14%), femur (11%), and tibia (8%).
31
What is the pathogenesis of panosteitis?
Vascular proliferation and bone formation around the nutrient foramen result in increases in intramedullary pressures. This causes further local bone formation and enlargement of the haversian system. These eventually coalesce, joining the endosteum and being remodelled resulting in reformation of the medullary canal and bone marrow.
32
What are the typical radiographic findings associated with panosteitis?
Increased medullary opacity with granular pattern or loss of the normal trabecular pattern.
33
What is the treatment for panosteitis?
Rest and analgesia (self limiting).
34
Which breeds of dogs are at highest risk for craniomandibular osteopathy?
West highland whites, cairn terriers, scottish terriers (generally less than 6 months of age)
35
Is craniomandibular osteopathy suspected to be inherited?
Yes - strong breed predisposition suggests this
36
What characterizes craniomandibular osteopathy?
Unilateral or bilateral symmetric irregular osseous proliferations of mostly the mandibles and/or tympanic bullae.
Can also affect the temporal bones, frontal bones, maxillary bones, long bones.
37
When does craniomandibular osteopathy typically become self limiting by?
11-13 months of age
38
What is the treatment for craniomandibular osteopathy?
Supportive care (soft food, gruel/syringe feeding, placement of a feeding tube, analgesia +/- antimicrobials and NSAIDs when febrile).
39
What is the expected signalment for a patient with a retained ulnar cartilaginous core?
Large or giant breed dog, young.
40
What is the cause of a retained ulnar cartilaginous core?
Failure of hypertrophic chondrocytes to convert into metaphyseal bone (may be a manifestation of osteochondrosis). Can result in similar limb deformities as are seen with premature closure of the distal ulnar physis.
41
What is the treatment for retained cartilaginous core?
No limb deformity: no treatment.
Limb deformity: ALD correction.
Cores may disappear spontaneously.
42
What is the most likely signalment for a patient with Legg-Calve-Perthes disease (avascular necrosis of the femoral head)?
Toy breed or small breed dog, 4-11 months of age, no sex predisposition
43
What is the pathogenesis of avascular necrosis of the femoral head?
Necrosis of the trabeculae of the femoral head followed by fragmentation and collapse of the epiphyseal subchondral bone during loading and cleft formation on the articular surface. Trabecular thickening and necrosis may also be found in the metaphyseal region resulting in fracture. Remodelling results in partial or complete malformation of the femoral head.
44
What are radiographic signs associated with avascular necrosis of the femoral head?
Flattening and mottling of the femoral head, collapse and thickening of the femoral neck, potential femoral neck fractures.
45
Is surgical or conservative management recommended in the treatment of avascular necrosis of the femoral head?
Surgical (FHO or THR). Conservative treatment associated with only 25% success rate
46
What is the normal signalment for a patient suffering from a slipped capital femoral epiphysis?
Male, neutered, overweight cats (normal age 4.5-42 months)
47
What differentiates slipped capital femoral epiphysis from a Salter Harris fracture?
Slipped capital femoral epiphysis is the slow progressive displacement of the proximal femoral metaphysis from the epiphysis through the growth plate. Often bilateral. Salter Harris fractures are traumatically induced.
48
What is the proposed pathogenesis of slipped capital femoral epiphysis?
Unclear but might be related to delayed closure of the growth plate following gonadectomy and hypotestosteronism
49
What is the treatment for slipped capital femoral epiphysis?
Surgical repair with K-wires may be considered in early cases.
FHO typically performed due to progressive resorption of the femoral neck. If the femoral neck remains intact can consider THR
50
What are multiple cartilaginous exostoses?
Cartilage capped bony protuberances that arise from the surfaces of any bone formed by endochondral ossification
51
What are the primary differences between multiple cartilaginous exostoses in dogs as compared to cats?
In dogs normally they only form during growth and stop once endochondral ossification ceases. In cats they are normally found after skeletal maturity.
52
Can multiple cartilaginous exostoses undergo malignant transformation?
Yes - to osteosarcomas or chondrosarcomas
53
What bones do multiple cartilaginous exostoses most frequently affect?
Vertebra, ribs and long bones
54
Formation of multiple cartilaginous exostoses has been associated with what disease in cats?
FeLV.
55
How is multiple cartilaginous exostoses diagnosed?
Histopathology.
DDx include osteomyelitis, neoplasia, disseminated idiopathic skeletal hyperostosis, hypervitaminosis A, skeletal coccidioidomycosis, and bone cyst.
56
What is the treatment for multiple cartilaginous exostoses (osteochondromatosis)?
Can be excised if solitary or impeding function, otherwise monitoring with serial radiography is recommended.
Continued growth of an exostoses following closure of the growth plates is suggestive of malignant transformation.
57
What is the suspected cause of swimmer syndrome?
Unknown, but environmental conditions (area with poor traction) and genetics may be involved.
58
What is the treatment for Swimmer syndrome?
Hobbles and physical rehabilitation.
Prognosis is good with prompt intervention.
59
What are the two forms of puppy carpal laxity syndrome?
Hypoextension: less than 180 degrees
Hyperextension: greater than 180-190 degrees
60
What is the cause of puppy carpal laxity syndrome?
Unknown.
61
What is the typically signalment for a patient with puppy carpal laxity syndrome?
Large breed dogs between 6-16 weeks of age
62
What are the treatments for puppy carpal laxity syndrome?
Typically exercise, splinting and change to adult diet is adequate for most patients.
If severe hyperextension may require carpal arthrodesis.
Severe hypoextension can perform tenotomy but rarely indicated.
63
When should a metabolic bone disease be considered?
In dogs with generalized osteopenia, brittle bones, pathologic fractures, limb deformities, and/or excessive new bone formation (hypervitaminosis A).
Work-up may include; CBC, biochem, ionized calcium, parathyroid hormone, Vitamin D assays, biomarkers of bone metabolism, complete body radiographs, abdominal ultrasound, type-1 collagen analysis (for osteogensis imperfecta), bone mineral density measurements and/or bone biopsy.
64
Where is hypertrophic osteopathy most frequently seen?
Distal extremities and long bones.
Characterized by periosteal reaction.
65
What is the proposed pathogenesis of hypertrophic osteopathy?
Increased peripheral blood flow due to a neurally mediated increase in peripheral blood flow. This is thought to occur secondary to a primary lesion (neoplasia) causing irritation to afferent nerves. The increase in blood flow results in vascular congestion in the periosteum.
66
What is the most common site of neoplasia in cases of hypertrophic osteopathy?
Pulmonary or metastatic neoplasia most common
67
What are clinical signs associated with hypertrophic osteopathy?
Taut skin over the distal extremities with firm swelling advancing proximally as the disease progresses.
Hyperthermia, weight loss, and depression also common.
Clinical signs of lameness typically appear before respiratory signs.
68
In what direction is new bone often deposited in relation to the long axis of the bone in cases of hypertrophic osteopathy?
Perpendicular (pallisade formation)
69
What is the treatment for hypertrophic osteopathy?
Treatment is directed at managing the primary problem with secondary improvements in the hypertrophic osteopathy typically occurring within 1 week.
70
What is disseminated idiopathic skeletal hyperostosis?
A spinal and extraspinal manifestation of heavy bone formation.
71
Which breed is predisposed to disseminated idiopathic skeletal hyperostosis?
Boxers (large and giant breed dogs most commonly affected)
72
What structure does disseminated idiopathic skeletal hyperostosis most frequently affect?
Ventral longitudinal ligament of the vertebrae
73
What is the most common differential for disseminated idiopathic skeletal hyperostosis?
Spondylosis deformans
74
What criteria (the presence of 4 of 5) are used for diagnosis of disseminated idiopathic skeletal hyperostosis?
(1) Continuous or “flowing” calcification and ossification of at least three contiguous vertebral bodies
(2) relative preservation of intervertebral disc width
(3) periarticular osteophytes surrounding the zygapophyseal joints
(4) formation of pseudoarthrosis between the bases of spinous processes
(5) periarticular osteophytes and calcification and ossification of soft tissue attachments (enthesophytes) in both axial and peripheral skeleton
75
What is the treatment for disseminated idiopathic skeletal hyperostosis?
1. Palliative or supportive care.
2. Enthesophytectomy in cases of impaired range of motion.
3. Foraminotomy in instances of nerve root compression, neurological deficits or pain.
76
What are the classifications of bone cysts?
Simple, aneurysmal and subchondral. Simple most commonly reported in dogs and cats.
77
What is the cause of bone cysts?
Unknown, but may be due to metaphyseal venous obstruction with secondary osteolysis.
78
What is the mots common signalment for patients with bone cysts?
Young large breed dogs are most commonly reported. A 2:1 male to female ratio is reported.
79
Which breed is predisposed to polyostotic bone cysts?
Dobermans.
80
How are bone cysts diagnosed?
Radiography (whole body radiography may be considered due to risk of polyostotic lesions), ultrasound, angiography (useful for aneurysmal cysts), and MRI.
Histology and/or cultures obtained via FNA or biopsy (although hemorrhage with aneurysmal bone cysts, or pathologic fracture is a risk) is recommended before definitive treatment.
81
What are DDx for bone cysts?
Trauma, hypertrophic osteodystrophy, hemangioma, infectious causes, multiple cartilaginous exostoses, and neoplasia.
82
What are surgical treatment options for bone cysts?
Asymptomatic patients can be monitored with serial radiography.
Treatment options include; surgical drainage, curettage, placement of cancellous bone graft, radiation, total excision and amputation.
83
Which breeds are most frequently affected by acute caudal myopathy?
Labrador retrievers and pointers.
Normally affect dogs with a history of recent hunting or swimming, hard workout, prolonged cage transport, or exposure to wet or cold weather.
84
How is acute caudal myopathy diagnosed?
1. History and clinical signs (limp tail, nociception present, pain on palpation near the base).
2. Decreased tail temperature and mildly elevated CK.
3. Isotope uptake in the tail on scintigraphy.
4. Increased signal intensity on T1-weighted MRI images.
85
What are DDx for acutal caudal myopathy?
Lumbosacral disease, spinal disease (intervertebral disc disease, radiculitis, neoplasia), pelvic disease (fracture, neoplasia), anal gland disease, and prostatic disease.
86
What is the treatment for acute caudal myopathy?
Nothing, most dogs spontaneously recover
87
What is the iliopsoas muscle maneuver?
Simultaneous internal rotation and extension of the hip joint.
If the hip joint is the source of pain the iliopsoas manoeuvre will not elicit a response.
88
Dysfunction of what nerve has been associated with iliopsoas muscle injury?
Femoral nerve.
89
How is iliopsoas muscle injury diagnosed?
1. Pelvic radiographs: may show avulsion or mineralization at the inerstion of the tendon on the lesser trochanter of the femur.
2. Ultrasound: hypoechoic or hyperechoic areas within the tendon depending on severity.
3. CT: enlargement of the iliopsoas.
4. MRI: increased signal intensity.
90
What are treatment options for iliopsoas muscle injury?
1. Conservative management with rest and NSAIDs.
2. Tenomyectomy. Possible complications include intraoperative hemorrhage and incomplete severance of the tendon.
91
In a study by Roberston 2023 in JSAP, were male or female dogs more likely to be affected by hypertrophic osteodystrophy? What were the 4 most common clinical signs? How many patients suffered relapses prior to skeletal maturity?
Male dogs were more frequently affected.
The most common clinical signs were pyrexia, lethargy, pain and non-ambulatory.
8/25 cases suffered relapse prior to skeletal maturity.
Median hospitalization was 5 days. 4/25 cases developed future autoimmune disease.
92
In a study by Pilot 2022 in JFMS, what was an occasional concurrent finding in cats with PADS (patellar fracture and dental anomaly syndrome)? What treatment was frequently required?
Chronic paronychia was identified in some cats with PADS. This is inflammation of the folds of tissue surrounding the nail. Often affected multiple digits.
Medical management was only successful in 17% of cases, with the remaining 83% requiring digital amputation.
