Foot and miscellaneous orthopaedic conditions Flashcards
Describe the anatomy of the foot
Pes/Manus
5 metacarpal/tarsal bones
1st is always medial – not always present (dew claw)
P1, P2 and P3
Sesamoids
Tarsometatarsal joint
Metacarpal phalangeal joint
Proximal phalangeal joint
Extensor tendons on the dorsal aspect
List the main conditions affecting the foot
- Fractures (MTs/MCs/Phalanges)
- Luxations of joints
- Pad injuries e.g. corn
- FBs
- Nail injuries
What is a corn?
Paw pad keratoma
- focal area of hyperkeratosis
Describe the features of a corn
Excess keratin
Thickening of hard pad
Lameness
Commonly seen in greyhounds
What is keratin?
Structural fibrous protein
Skin, horns, nails, scales etc
Describe some treatments for corns
- Digging out corn -> Incomplete removal - Temporary relief, recurrence common
- Silicone gel implants
- Distal amputations
- Superficial digital flexor tendonectomy
Describe a Superficial digital flexor tendonectomy procedure for corns
- Originally performed when adjacent digit had FT or missing
- Began as a tenotomy: Incidences of corn recurrence
- Developed into SDF tendonectomy = removal of 1cm + of tendon
Describe treatment of single fractures of the MCs/MTs
External coaptation
Describe treatment of multiple fractures of the MCs/MTs
Need internal fixation (plates/wires)
Which bones in the foot are weightbearing?
3rd and 4th metacarpal/tarsal bones
What are some complications of fractures of the metacarpals/tarsals?
Extensive soft tissue injuries-check viability!
Synostosis between bones-painful!
What type of toe amputation is well tolerated?
Single digit
When is toe amputation indicated?
Severe luxations/fracture /neoplasia (STAGE)
What type of incision in a toe amputation preserves that pad?
‘Y’ shape
List some developmental bone diseases
- Panosteitis
- Metaphyseal Osteopathy
- Craniomandibular Osteopathy
- Legg-Calve-Perthes Disease
- Slipped Capital Femoral epiphysis
- Bone Cysts
List some paraneoplastic bone diseases
Hypertrophic Osteopathy (Marie’s disease)
List some nutritional bone diseases
- Nutritional Secondary Hyperparathyroidism
- Renal Secondary Hyperparathyroidism
- Hypovitaminosis D (Rickets)
Describe the clinical signs of panosteitis
- Self-limiting disease seen in young large breed dogs
- Classically shifting lameness
- Varies in severity from mild to non-weight bearing
- Acute onset, no trauma
- Forelimb:hindlimb ratio 4:1
Which bones are most commonly affected by panosteitis?
Ulna 42%
Radius 25%
Humerus 14%
Femur 11%
Tibia 8%
How is panosteitis diagnosed?
Signalment, history and clinical signs
Radiography
How does panosteitis appear on radiography?
Lack of definition between the cortex and medulla
‘thumb print’ radiopacities in the long bones
0 – 10 days: may appear normal
10 – 70 days: subtle, poorly marginated increased radiodensity in medullary cavity with some corticomedullary blurring and periosteal and endosteal new bone formation and thickened cortices
70 – 90 days: remodeling of medullary canal. Medullary canal regains normal appearance
How is panosteitis treated?
Self-limiting
Exercise control/restriction
Analgesics
Describe the signalment of metaphyseal osteopathy
Young rapidly growing medium and large breed dogs
Puppies may present between 2 and 6 months old
Describe the aetiology of metaphyseal osteopathy
Unknown
? Vitamin C deficiency
?Distemper Virus
Inherited immunodeficiency in Weimaraners
Describe the clinical signs of metaphyseal osteopathy
Vary from mild lameness to severe collapse
Pyrexia, anorexia and depression
How is metaphyseal osteopathy diagnosed?
Signalment, history, clinical signs
Radiography
Describe the radiographic appearance of metaphyseal osteopathy
Common in distal radius and ulna
Radiolucent line and increased radiodensity in metaphysis parallel to physis
Epiphysis and growth plates may appear slightly widened
How is metaphyseal osteopathy treated?
Most cases are self-limiting
Supportive care
Analgesics
What is craniomandibular osteopathy?
Non-inflammatory, non-neoplastic proliferative bone disease-immature dogs
Describe the signalment of craniomandibular osteopathy
Usually present between 4 – 10 months of age
Most common in WHWT, Scottish Terrier and Cairn Terrier
Describe the aetiology of craniomandibular osteopathy
Autosomal recessive in WHWT
Describe the clinical signs of craniomandibular osteopathy
Mandibular swelling/thickening
Inability to open mouth/prehend food
Salivation
Anorexia and weight loss
Pain when eating
How is craniomandibular osteopathy diagnosed?
Signalment
History
Clinical findings
Radiography
How does craniomandibular osteopathy appear on radiography?
- Changes usually bilateral
- Palisading proliferation on the mandible and tympanic bullae
- Temporal, frontal and maxillary bones can be affected
- Occasionally affects long bones
Describe the treatment of craniomandibular osteopathy
Supportive care
Analgesics - ?corticosteroids
Surgery not successful
What is the medical condition termed ‘Maries disease’?
Hypertrophic osteopathy
Describe the signalment of Hypertrophic osteopathy
Older dogs and cats
Mean age 9 years (6 month – 15 years))
Describe the aetiology of Hypertrophic osteopathy
- Paraneoplastic: secondary to intrathoracic or abdominal neoplasia
- Increased peripheral blood flow
- Vascular congestion in periosteum
- Calcification of periosteum and connective tissue
- New bone formation on the distal limbs starting from the toes
- Neural mediated: ?vagus, ?intercostal, other afferents
Describe the clinical signs of Hypertrophic osteopathy
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
How is Hypertrophic osteopathy diagnosed?
History and clinical signs
Thoracic radiographs and abdominal ultrasound
Radiography
Describe the radiographic changes seen in Hypertrophic osteopathy
Periosteal new bone formation – 90 degrees
Increased bone density
How is Hypertrophic osteopathy treated?
Symptomatic
Remove primary cause -> resolution of new bone formation
Normal bone production but excessive bone resorption lead to?
Osteopenia
Describe the aetiology of nutritional secondary hyperparathyroidism
- Diets high in phosphorus or low in calcium (Kittens and puppies are fed a non-balanced diet e.g. purely meat
Ideal ratio of calcium:phosphorus is altered) - Usually meat based diets
- Ideal Ca:P ratio 1.2:1 (dogs) and 1:1 (cats)
- Hypocalcaemia -> increased PTH
- Induces progressive skeletal demineralisation
Describe the clinical signs of nutritional secondary hyperparathyroidism
Lameness/ inability to stand
Skeletal pain
Swollen metaphysis
Pathological fracture
Describe the radiographic signs of nutritional secondary hyperparathyroidism
Decreased bone density/thinned cortices
Mushroom shaped metaphysis
Pathological fractures may be seen
How is nutritional secondary hyperparathyroidism treated?
Rest
Diet correction
Oral calcium supplementation
NSAID
What is renal osteodystrophy?
Osteopenia secondary to chronic kidney disease
What are the main causes of renal osteodystrophy
Impaired phosphate excretion
Impaired vitamin D production
Describe how impaired phosphate excretion leads to renal osteodystrophy
Hyperphosphataemia -> hypocalcaemia
Increased PTH secretion
Bone demineralisation
Describe how impaired vitamin D production leads to renal osteodystrophy
Depressed enteric calcium absorption
Impaired osteoid mineralisation
Rickets-osteomalacia
List the orthopaedic clinical signs of renal osteodystrophy
Pliable mandible/maxilla (rubber jaw)
Loose teeth
Skeletal pain
Pathological fractures
Bowing of long bones
How is renal osteodystrophy treated?
Reduce phosphate intake/phosphate binder
Calcium or calcitriol supplementation
Ligament injuries are known as?
Sprains
Tendon injuries are known as?
Strains
Describe the 1st, 2nd and 3rd degree ligament injuries
First degree = Minimal tearing, rapid healing
Second degree = Partial rupture associated with haemorrhage and oedema
Third degree = Complete rupture of ligament or avulsion from bony attachments
Describe the 1st, 2nd and 3rd degree tendon injuries
First degree:
- Healing is rapid- transient lameness
- 1 week restricted exercise and NSAIDS
Second degree:
- Weight-bearing –Support bandage/splint for 3-4 weeks
- Exercise controlled for up to 3 months
Third degree:
- Not weight-bearing, joint alterations
- Surgical repair, reattachment or replacement of ligament usually necessary e.g. ACL/CCL
Describe general treatment of tendon injuries
- In acute phase need to reduce inflammation-alternate cold warm compresses, and immobilisation to prevent further stress
- Surgical treatment for ruptured, severed, displaced, avulsed tendons (in dog)
- Immobilisation for 4-6 weeks post-operatively
- Gradual increase in exercise over the following 2 months
Describe surgical treatments of tendon injuries
Early repair better
Make sure wound clean
Monofilament nylon sutures used to attach ends
Immobilisation necessary for 4-6 weeks
Muscle contractures are seen where anatomically?
Reversible contracture of the flexor carpi ulnaris muscle
Describe the signalment of reversible contracture of the flexor carpi ulnaris muscle
Young dogs 6 – 8 weeks of age
- Skeleton and muscles grow at different rates leading to a flexural deformity
Describe the clinical signs of reversible contracture of the flexor carpi ulnaris muscle
Flexed carpus that cannot be extended
Tendon of FCU is taut on palpation
Describe the treatment of reversible contracture of the flexor carpi ulnaris muscle
Resolution usually occurs after 2 – 3 weeks
Carpal supports
FCU tendinectomy in rare cases
