Miscellaneous Orthopaedic Conditions 2022 PDF

Summary

This document is a lecture overview of miscellaneous orthopaedic conditions in small animals. It covers topics like developmental bone disease, paraneoplastic bone disease, and nutritional bone disease, and includes specific examples such as Panosteitis, Metaphyseal Osteopathy, and others. The lecture is presented by Andrew Tomlinson, a senior lecturer in small animal surgery at the University of Liverpool.

Full Transcript

MISCELLANEOUS ORTHOPAEDIC CONDITIONS ANDREW TOMLINSON BVSC CERTAVP(GSAS) DIPECVS FHEA MRCVS SENIOR LECTURER IN SMALL ANIMAL SURGERY LECTURE OVERVIEW Developmental Bone disease: Paraneoplastic Bone Disease Nutritional Bone Disease: • Panosteitis • Hypertrophic Osteopathy • Nutritional Seconda...

MISCELLANEOUS ORTHOPAEDIC CONDITIONS ANDREW TOMLINSON BVSC CERTAVP(GSAS) DIPECVS FHEA MRCVS SENIOR LECTURER IN SMALL ANIMAL SURGERY LECTURE OVERVIEW Developmental Bone disease: Paraneoplastic Bone Disease Nutritional Bone Disease: • Panosteitis • Hypertrophic Osteopathy • Nutritional Secondary • Metaphyseal Osteopathy • Craniomandibular Osteopathy • Legg-Calve-Perthes Disease • Slipped Capital Femoral epiphysis • Bone Cysts Hyperparathyroidism • Renal Secondary Hyperparathyroidism • Hypovitaminosis D (Rickets) PANOSTEITI S Clinical signs: Diagnosis: • Classically shifting lameness • Signalment, history and clinical signs • Varies in severity from mild to nonweight bearing • Acute onset, no trauma • Radiography I. 0 – 10 days: may appear normal II. 10 – 20 days: subtle, poorly marginated • Forelimb:hindlimb ratio 4:1 increased radiodensity in medullary cavity • Most commonly affected bones: with some corticomedulalry blurring 1. Ulna 42% III. 20 – 70 days: obvious increase in medullary 2. Radius 25% radiodensity, periosteal and endosteal new 3. Humerus 14% bone formation and thickened cortices 4. Femur 11% 5. Tibia 8% IV. 70 – 90 days: remodeling of medullary canal. Medullary canal regains normal appearance PANOSTEITI S Treatment: • Self-limiting • Exercise control/restriction • Analgesics Prognosis: • Good for complete resolution METAPHYSEAL OSTEOPATHY Signalment: Clinical signs: • Young rapidly growing medium and large • Vary from mild lameness to severe breed dogs • Puppies may present between 2 and 6 months old collapse • Pyrexia, anorexia and depression • Swollen metaphysis Aetiology: • Unknown Diagnosis: • ? Vitamin C deficiency • Signalment, history, clinical signs • ?Distemper Virus • Confirmed by radiography • Inherited immunodeficiency in Weimaraners Radiography: METAPHYSEAL OSTEOPATHY • Common in distal radius and ulna • Band of increased radiodensity immediately adjacent to physis • Radiolucent line in metaphysis parallel to physis • Epiphysis and growth plates may appear slightly widened • Latter stages calcification proximal to the metaphysis Treatment Prognosis: Most cases are self-limiting • Good – excellent in mild cases • Supportive care • Analgesics • 25% - 33% euthanasia due to severity of clinical signs • Possible angular limb deformities CRANIOMANDIBULAR OSTEOPATHY Non-inflammatory, non-neoplastic proliferative bone disease of immature dogs Signalment: • Usually present between 4 – 10 months of age • Most common in WHWT, Scottish Terrier and Cairn Terrier Aetiology: • Autosomal recessive in WHWT Clinical signs: Diagnosis: • Mandibular swelling/thickening • Signalment • Inability to open mouth/prehend food • History • Salivation • Clinical findings • Anorexia and weight loss • radiography • Pain when eating CRANIOMANDIBULAR OSTEOPATHY Radiography: • Changes usually bilateral • Palisading proliferation on the mandible and tympanic bullae • Temporal, frontal and maxillary bones can be affected • Occasionally affects long bones Treatment: Prognosis: • Supportive care • Self-limiting at 11 – 13 months • Analgesics • Can be good • ?corticosteroids • Surgery not successful • Euthanasia may be requested LEGG-CALVE-PERTHES DISEASE Signalment: Developmental avascular/ischaemic necrosis of the femoral head • Onset of lameness 4 – 11 months • Commonly affects miniature poodle, WHWT, Cairn Terrier, Manchester Terrier and Yorkshire Terrier • No sex predilection Clinical signs: • Mild cases can be subclinical • Mild intermittent lameness to acute nonweight bearing lameness • Pelvic limb muscle atrophy • Pain and crepitus on manipulation of hip Aetiopathogenesis: • Autosomal recessive mode of inheritance in Manchester Terrier and WHWT • Vascular supply to femoral head from epiphyseal vessels that enter at the level of the joint capsule. • Temporary vascular compromise is suspected: I. Necrotic II. Creeping substitution: bone resorption/bone formation III. Articular cartilage collapse due to failure of subchondral bone support LEGG-CALVE-PERTHES DISEASE Diagnosis: • History, signalment, clinical signs • Confirmation via VD extended or frog leg view Radiography: • Focal bone lysis – “apple core” appearance Treatment: • Conservative • Femoral head and neck ostectomy • Total hip replacement SLIPPED CAPITAL FEMORAL EPIPHYSIS Feline Metaphyseal Osteopathy/Femoral Neck Metaphyseal Osteopathy Signalment: Clinical signs: • Neutered male, overweight cats • Subtle lameness progressing to acute • < 2 years of age • ?Siamese over-represented non-weight bearing • Inability to jump • Pain and crepitus on hip manipulation Aetiopathogenesis: • Unknown • Delayed physeal closure • Gonadectomy • Hypotestosteronism • ?Physeal dysplasia Diagnosis: • History, signalment and clinical signs • Confirmed radiographically SLIPPED CAPITAL FEMORAL EPIPHYSIS Radiographic changes: • Early – mild widening and lateral displacement of the capital femoral growth plate • Late – displacement of proximal femoral metaphysis, resorption and sclerosis of femoral neck Treatment: • FHNE • THR HYPERTROPHIC OSTEOPATHY Hypertrophic Pulmonary Osteoarthropathy/Marie’s Disease Signalment: • Older dogs and cats • Mean age 9 years (6 month – 15 years) Aetiology: • Paraneoplastic: secondary to intrathoracic or abdominal neoplasia • Neural mediated: ?vagus, ?intercostal, other afferents  Increased peripheral blood flow  Vascular congestion in periosteum  Calcification of periosteum and connective tissue Clinical signs: • Lameness can develop over several months • Can be non-ambulatory • Single or multiple limbs • Firm swelling along bone of distal extremities • Pain in early stages • ?hyperthermia, weight loss, depression HYPERTROPHIC Hypertrophic Osteopathy OSTEOPATHY Diagnosis: • History and clinical signs • Thoracic radiographs and abdominal ultrasound • Radiographic changes: • Periosteal new bone formation • New bone laid down at right angles to periosteum • Increased bone density Treatment: • Symptomatic • Remove primary cause  resolution of new bone formation BONE CYSTS Simple, unicameral bone cysts: • Fluid filled cavity lined by fibrous connective tissue • Monostotic or polyostotic Aneurysmal bone cyst: • Benign expansile osteolytic lesions containing blood sinusoids Subchondral bone cysts: • Adjacent to synovial membrane • May communicate with joint space • Associated with OCD • Only one reported veterinary case Clinical signs: • May be asymptomatic • Lameness • Painful swelling • Acute lameness  pathological fracture Treatment: • Asymptomatic no treatment  repeat imaging in 4 – 6 weeks • Surgical drainage, curettage, cancellous bone grafting • Radiation therapy • Excision • Amputation BONE CYSTS Radiographs: • Expansile, locally aggressive lucent lesion with little periosteal reaction • Typically metaphysis and diaphysis • Eccentrically located • Thinned cortices Prognosis: • Good to excellent in most cases MUSCLE CONTRACTURES Reversible contracture of the flexor carpi ulnaris muscle Signalment: • Young dogs 6 – 8 weeks of age Aetiopathogy: • Unknown Clinical signs: • Flexed carpus that cannot be extended • Tendon of FCU is taught on palpation Treatment: • Resolution usually occurs after 2 – 3 weeks • Carpal supports • FCU tendinectomy in rare cases NUTRITIONAL DISORDERS OF BONE Nutritional Secondary Hyperparathyroidism Normal bone production but excessive bone resorption  osteopenia Aetiology: • Diets high in phosphorus or low in calcium • Usually meat based diets • Ideal Ca:P ratio 1.2:1 (dogs) and 1:1 (cats) • Hypocalcaemia  increased PTH • Induces progressive skeletal demineralisation Clinical signs: • Lameness/ inability to stand • Skeletal pain • Swollen metaphysis • Pathological fracture Diagnosis: • History (inappropriate diet) and clinical signs • Radiography NUTRITIONAL DISORDERS OF BONE Nutritional Secondary Hyperparathyroidism Radiography: • Decreased bone density and thinned cortices • Mushroom shaped metaphysis • May have slight relative increase in opacity • Pathological fracture may be seen Treatment: • Rest • Diet correction • Oral calcium supplementation • NSAID NUTRITIONAL DISORDERS OF BONE Hypovitaminosis D (Rickets) Insufficient calcium, phosphorus or both is available for mineralisation of newly formed osteoid Aetiology • Dietary deficiency in Vitamin D Radiography: Clinical signs: • Cupping of adjacent metaphysis • Lameness • Osteopenia, thinned cortices • Pathological fracture or bowing of long bones • Bowed diaphysis • Thickening of growth plates • Enlarged costochondral junction and metaphysis • Delayed dental eruption, weakness, listlessness, and neurological signs Treatment: • Balanced diet NUTRITIONAL DISORDERS OF BONE Renal Osteodystrophy Osteopenia secondary to chronic kidney disease Impaired phosphate excretion: Orthopaedic clinical signs: • Hyperphosphataemia  hypocalcaemia • Pliable mandible/maxilla • Increased PTH secretion • Bone demineralisation (rubber jaw) • Loose teeth • Skeletal pain Impaired vitamin D production: • Depressed enteric calcium absorption • Impaired osteoid mineralisation • Rickets-osteomalacia • Pathological fractures • Bowing of long bones Treatment: • Reduce phosphate intake/phosphate binder • Calcium or calcitriol supplementation The End! 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