Miscellaneous bone and joint conditions Flashcards
Avascular necrosis (AVN) of the femoral head
Ischaemic necrosis
Small breeds
From 5 months
Pain - hip extension and flexion
Muscle wastage
Radiographic findings of avascular necrosis of the femoral head
Lucent areas initially
Collapse and mushrooming
Treatment of avascular necrosis of the femoral head
Surgery
○ Femoral head and neck excision
○ Total hip replacement
Conservative
○ Cage rest
○ NSAIDs
Panosteitis
Endostosis, fibrous osteodystrophy, juvenile osteomyelitis, eosinophilic panosteitis
Focal areas of endosteal bone proliferation
Age 5-18 months
Species - dogs
Breeds - large especially GSDs
Male > female
Aetiopathogenesis of panosteitis
Viral, excess nutrition, genetic?
Histopathology of panosteitis
Degeneration of medullary adipocytes
Stromal cell proliferation
Intramembranous ossification
Clinical signs of panosteitis
Lame, non-weight bearing, shifting
Dull, anorexia, pyrexia
Physical examinationof panosteitis
Painful bones on palpation
Radiography of panosteitis
Patchy increased density of medullary bone
○ Distal humerus
○ Proximal ulna
○ ‘Thumbprints’
○ Near nutrient foramen
Take radiographs of the whole bone and stand back
Loss of distinction between cortex and medulla
Signalment of craniomandibular osteopathy
Breeds - Terriers, esp. WHW, Scotties, Bostons, and Cairns
Age: 3-8mo
Male = female
Aetiology of craniomandibular osteopathy
Genetic - autosomal recessive - WHWT
Hormones? - low risk after neutering
Infectious? Virus? CDV? - unproven
Irish setters show similar signs with canine leucocyte adhesion deficiency - fatal
Physical examination of craniomandibular osteopathy
Palpably enlarged mandibles
Limited mouth opening
Pain on attempting to open mouth or palpation of jaw
Radiography of craniomandibular osteopathy
Proliferative new bone on mandibles
Sometimes on TMJs
On bullae
Treatment of craniomandibular osteopathy
Analgesia and anti-inflammatories
NSAIDs/steroids
Tramadol/methadone/morphine
Liquefied food, hospitalisation, feeding tube
Usually good prognosis as it is a self-limiting disease
○ Can interfere with prehension/respiration
If very severe - may require euthanasia
Signalment of metaphyseal osteopathy (hypertrophic osteodystrophy)
Breeds - large and giant breeds
○ Occasionally smaller breeds
Age 2-8 months
Male = female
Aetiology of metaphyseal osteopathy (hypertrophic osteodystrophy)
Hypovitaminosis C
Infection - CDV
Hereditary
Excess nutrition
Copper deficiency
Clinical signs of metaphyseal osteopathy (hypertrophic osteodystrophy)
- Wax and wane
- Inappetance
- Pyrexia
- Reluctance to stand
- Reluctance to move
- Prior GIT upset?
Physical examination of metaphyseal osteopathy (hypertrophic osteodystrophy)
Swollen hot metaphyses of lower limb bones
VERY painful - care - may bite!
Pyrexia
Mild lymphomegaly
Radiography of metaphyseal osteopathy (hypertrophic osteodystrophy)
Sclerotic line immediately adjacent to physis
Radiolucent zone adjacent to sclerotic line (Tummerfield zone)
Periosteal new bone formation
Treatment of metaphyseal osteopathy (hypertrophic osteodystrophy)
Balanced diet/no supplements
Rehydrate
Analgesia - NSAIDs/opiates/rest
Antibiotics/steroids
Mild cases will respond, more severe cases may need hospitalisation
Prolonged recovery and may lead to GP closure and deformity
Hypertrophic osteopathy (Marie’s disease) (hypertrophic pulmonary osteoarthropathy)
Hypertrophic new bone formation around distal bones
Secondary manifestation of thoracic (abdominal) disease
In 90% of cases there is pulmonary neoplasia
Pathogenesis of Hypertrophic osteopathy (Marie’s disease) (hypertrophic pulmonary osteoarthropathy)
Neurovascular reflex - afferent vagal and intercostal fibres irritation
Stimulation of efferent fibres in connective tissue and periosteum of limbs
○ Increase in blood flow
○ Overgrowth of vascular connective tissue
○ New bone formation
Prognosis is guarded as it is often a malignant neoplasm
May get regression of bony changes after mass removal
