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Locomotor > Small Animal > Flashcards

Small Animal Flashcards

1
Q

What is the key feature of distinguishing which limb in a forelimb lameness?

A

Head and weight goes down on sound limb- sinking.

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2
Q

Why does a forelimb lameness give the appearance of a degree of lameness in the hindlimb?

A

Tend to balance diagonally therefore if e.g. lame on R TL and so on L TL for longer, also likely to be on R HL for longer

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3
Q

What are the key features of distinguishing which limb in a hindlimb lameness?

A

Iliac crest/ gluteal area sinks on sound side. Tarsus (calcaneus) acts as a spring- sinks on sound side

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4
Q

Why is grading the lameness important?

A

Graded out of 10. Regrade in a few weeks following tx

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5
Q

What is the presentation of bone disease in small animals?

A

Young animals. Deviation of limbs, poor posture, weakness. Axial and appendicular. Dietary problems. Comparison with littermates. Pathological fractures. Generalised dz.

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6
Q

Define osteomyelitis

A

Infection of the cortical bone and medullary cavity

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7
Q

Define osteitis

A

Inflammation of the cortex w/out involvement of the red/ yellow BM, can be septic/ aseptic

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8
Q

Describe the acute presentation of osteomyelitis

A

Occurs in LAs and SAs
Single limb lameness rapid onset, short duration
Often hx of laceration or sx

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9
Q

Describe the clinical exam findings for an acute presentation of osteomyelitis

A

Heat, pain, swelling on palpation of bones
Joints structures may be normal
Febrile

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10
Q

Describe the chronic presentation of osteomyelitis

A

Occurs in LA and SA.
Moderate/ intermittent lameness of days/ weeks duration
Often a hx of laceration or sx

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11
Q

Describe the clinical exam findings for a chronic presentation of osteomyelitis

A 
Possible heat, pain, swelling on palpation of bones
Joint structures may be normal
Pain, discharge, sinus tract formation
Pathological fracture (becomes acute)
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12
Q

In bone disease, the combination of pathogenic process and bones reaction leads to what two things?

A 
Bone loss (lysis)
Bone formation
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13
Q

What are some diagnostic options/ plans for bone disease?

A

Radiography. C+S (tracts, pieces of necrotic material). Biopsy (chronic osteomyelitis and OSA will look similar on radiograph, this helps distinguish between the 2). Radionuclide scan

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14
Q

What is the tx for osteomyelitis?

A

Early intervention w/ BS abx (change of culture and consider local delivery)
Surgical debridement, immobilisation, lavage
Rehabilitation of entire limb

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15
Q

Why it is important to get a bone biopsy when presented w/ radiographic appearance of osteomyelitis?

A

OSA and chronic osteomyelitis are radiographically similar (combo of lysis and formation of bone)

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16
Q

With suspected bone neoplasm, what should be included in the investigation?

A

Clinical evaluation (LN, degree of disability)
Radiography
Swab tracts, C+S on samples
Biopsy (jamshidi needle, get a no of planes)
Ddx based on biopsy and culture
Staging/ evaluation of px

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17
Q

Why is it important to get multiple planes of the lesion in a bone biopsy?

A

You need to get a representative sample of the lesion in order to help the pathologist make a ddx

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18
Q

What are some tx options for OSA?

A 
Amputation (4m)
Amputation and chemo (12-14m)
Limb sparing and chemo (12-14m)
Radiotherapy (palliative only)
NSAIDs/ bisphosphonates (palliative only)
Euthanasia
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19
Q

Define dysplasia.

A

It is an abnormality of development.

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20
Q

Describe hip dysplasia.

A

Hereditary disease that causes ligament hypertrophy (slack ligaments), subluxation, destruction of cartilage and changed shape of the joint surface. This leads to secondary osteoarthritis (bony AND fibrous) in the joint.

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21
Q

What are the clinical signs of hip dysplasia in puppies less than 6 months of age?

A

Generally only an abnormal gait is noticeable, caused by subluxation of the hip joint.

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22
Q

What are the clinical signs of hip dysplasia in puppies 6-16 months of age?

A

Progresses from just abnormal gait due to subluxation, to damage and inflammation causing pain and lameness as well.

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23
Q

What are clinical signs of hip dysplasia in dogs 16 months and older?

A

Abnormal joint with secondary OA causing pain and lameness, OR muscular/fibrous stabilization of the joint, resulting in pain free joint with restricted range of motion.

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24
Q

What is the treatment for hip dysplasia for puppies 0-6 months old?

A

Conservative; diet and exercise.

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25
Q

What is the treatment for hip dysplasia for dogs 6-16 months old?

A
  • Conservative; diet and exercise (consider pain relief)

- Surgical; anatomical correction (arthroplasty)

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26
Q

What is the treatment for hip dysplasia for dogs 16 months old and older?

A
  • Conservative; diet and exercise (pain relieving drugs)

- Surgical; hip replacement (arthroplasty)

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27
Q

What are some examples of osteochondrosis?

A
  • Osteochondritis dessicans; detachment of a chondral or osteochondral fragment from the articular surface
  • Subchondral bone cysts (SBCs)
  • Peri-articular fragmentation/fracture; detachment of a chondral or osteochondral fragment from the peri-articular area
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28
Q

What is canine elbow dysplasia and what conditions are included?

A

Elbow dysplasia is a generalized incongruency of the elbow joint in young, large, rapidly growing dogs that is related to abnormal bone growth, joint stresses, or cartilage development. Humeral osteochondritis dessicans, fragmented coronoid process, united anconeal process, 2ry osteoarthritis

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29
Q

What joints can be affected in fast growing high performance dogs?

A

Elbow
Shoulder
Stifle
Tarsus

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30
Q

What conditions can be seen in fast growing high performance dogs?

A
  • Osteochondritis dessicans
  • Fragmented coronoid process
  • Ununited anconeal process
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31
Q

Name the two types of synoviocytes.

A

Type A and type B

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32
Q

Describe the role of type A synoviocytes.

A

These are non-fixed cells that can phagocytose actively cell debris and wastes in the joint cavity, and possess an antigen-presenting ability; they are derived from blood-borne mononuclear cells, can be considered resident macrophages (tissue macrophages.

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33
Q

Describe the role of type B synoviocytes.

A

These are involved in producing the synovial fluid found in joints (hyaluronan, collagen, fibronectin).

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34
Q

Describe joint fluid.

A

It is a dyalisate from plasma, and is filtered by vascular endothelium and synovial interstitium. It contains proteins, electrolytes, enzymes, water, and HA, as well as synovial lining cells.

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35
Q

What are the classifications of arthritis?

A

Non-inflammatory (WBC less than 3000/ul) and inflammatory (WBC greater than 3000/ul).

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36
Q

What are the different types of non-inflammatory arthritis?

A
  • Traumatic
  • DJD
  • Hemarthrosis (bleeding into the joint space)
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37
Q

What are the different types of inflammatory arthritis?

A
  • Infectious (bacterial, viral, fungal, rickettsial, protozoal, borrelial, mycoplasma)
  • Non infectious (immune based and non-immune based)
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38
Q

What are the different types of non-infectious immune based canine arthritis?

A

Erosive or Non-erosive

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39
Q

Name some causes of erosive immune based arthritis

A

Rheumatoid arthritis
PA of greyhound
Feline chronic progressive PA

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40
Q

Name some causes of non-erosive immune based arthritis

A 
SLE
Idiopathic
PA/PM syndrome
PA/ meningitis syndrome
PA of akitas
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41
Q

What posture will a dog w/ a CCL rupture assume when sitting down?

A

The dog will abduct the injured leg out when asked to sit down as painful to flex stifle

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42
Q

What clinical sign is very distinctive to IMPA?

A

Affected animals look like they walk on eggshells. Painful to flex tarsus. Sit w/out putting weight at the back

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43
Q

What clinical sign would be associated with hip dysplasia?

A

Flex/ extend hips, so swing when walking

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44
Q

What can be used to diagnose joint disease?

A

Radiography
Arthrocentesis
Joint fluid analysis (cytology, cell count, chemical analysis, culture)

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45
Q

Describe how joint fluid is obtained via arthrocentesis?

A

Sedation/ GA
Sterile technique
Use of landmarks to determine where joint capsule is

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46
Q

What does presence of macrophages in joint fluid cytology mean? And neutrophils?

A

Macrophages- non-inflamm process (DJD)

Neutrophils- inflamm process (look at degenerate vs non-degenerate)

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47
Q

When is therefore decreased glucose in joint fluid?

A

Septic arthritis

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48
Q

When is there increased TP in joint fluid?

A

Inflammatory arthritis

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49
Q

How reliable is culture of joint fluid and what can be done to improve it?

A

23% false -ve
Be careful w/ false +ve also. If really suspect infectious but culture -ve then can use synovial membrane biopsy. Special culture media incr change of +ve culture

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50
Q

How do bacteria gain entry to the joint?

A

Direct penetration (trauma)
Spread from adjacent tissue
Haematogenous
OA- reaction in joint predisposes to infection

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51
Q

What are common pathogens in bacterial joint infection?

A

Staphylococcus
Streptococcus
Pasteurella

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52
Q

Why is radiography useful in dx of joint disease?

A

Erosive vs non-erosive- won’t see bony changes on radiography w/ non-erosive
Acute- effusion
Chronic- degenerative changes + OA

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53
Q

What diagnostic test can be used for infectious arthritis or when suspecting IMPA?

A

Serology for infectious agents- Lyme dz, Ehrlichiosis, Leishmania

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54
Q

When suspecting erosive PA, what test can be done to definitively diagnose?

A

High titres for Ab against IgG in rheumatoid arthritis (up to 70%) along w/ radiographic changes

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55
Q

What is the ANA titre test used to diagnose?

A

Systemic lupus erythematosus (which will cause other clinical signs incl PA)

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56
Q

What are the diagnostic criteria for SLE?

A

Major signs- skin lesions, glomerulonephritis, PA, haemolytic anaemia, polymyositis, leukopenia, thrombocytopenia
Minor signs- fever of unknown origin, CNS signs, seizures, oral ulcerations, lymphadenopathy, pericarditis, pleuritis
Serologic evaluation- ANA, lupus erythematosus cell preparation

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57
Q

What should you do when you suspect an immune-mediated polyarthritis?

A 
Radiograph affected joint(s)
Rheumatoid factor
ANA titres
Image body cavities (rads, US, CT)
And depending on signs, CSF, muscle biopsy etc
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58
Q

How many limbs are involved in septic arthritis?

A

Usually only one

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59
Q

What is DJD?

A

End stage of joint dz and one of the most common orthopedic conditions vets deal with in practice. Incurable but ideally is manageable

60
Q

What is the progression of osteoarthritis?

A

Thickened capsule, erosion of cartilage and osteophytes leading to complete loss of cartilage and bone spur. Joint disappearing w/ fusion of joint space= ankylosis

61
Q

What is cartilage matrix composed of?

A

Mainly water.

Type II coll fibres, PGs, elastic and reticular fibres, chondrocytes

62
Q

Name some common conditions that can cause DJD?

A 
Trauma (acute/ repetitive)
Infectious/ inflamm
Non-infectious inflamm
Developmental disease (dysplasia, angular limb deformity, flexural limb deformity, osteochondrosis
Other
63
Q

What should be included in the physical exam when DJD is suspected?

A

Wt and BCS. Lameness exam (identify, score and localise). Palpation and manipulation of joint (pain, heat, swelling, crepitus, joint thickening/ effusion, reduced ROM). Check for muscular atrophy in area of joint.

64
Q

What types of diagnostic testing can be used to investigate DJD?

A

Synovial fluid analysis
Local analgesia (esp in equine)
Diagnostic imaging (rad, US, MRI/CT)
Arthroscopy (synovial biopsy)

65
Q

What are the goals of treatment of DJD?

A

Pain reduction
Stop inflamm processes
Chondroprotection (dz modification, try to arrest or slow down cartilage degeneration). Can’t be fully cured

66
Q

What are the recommended tx strategies for DJD?

A

Weight control. Exercise modification/ physio. Strategic analgesia (achieve acceptable level for exercise). Joint supplements. Salvage procedures. Control flare ups- initial analgesia (5-10d), gradually resume controlled exercise, swimming/ hydrotherapy

67
Q

What is the most common medication for orthopaedic problems?

A

NSAIDs, mostly because they are inexpensive and efficient.

68
Q

How can tendon/ ligament disease present?

A

Lameness (acute/ chronic)
Swelling
Specific functional disability (unable to extend a specific joint)

69
Q

How long does tendon take to heal?

A

6 weeks to regain 50% normal strength

1 year to regain 80% normal strength

70
Q

What is the treatment for tendon injury?

A

Rest. Specific support to protect tendon from loading (dressings, casts, trans-articular fixator). Primary surgical repair for lacerations. Ultrasound for monitoring

71
Q

What is the pathophysiology of tendon repair?

A

Fibroblasts and collagen fibres lining up along line of action. Sheathed tendons have poorer BS and heal slower

72
Q

Name some suture patterns used in tendon repair.

A

Locking loop

3 loop pulley

73
Q

What is sprain vs strain?

A

Sprain- ligament

Strain- tendon

74
Q

What is important to perform on physical exam of an animal you suspect has a sprain?

A

Range of motion

75
Q

What further diagnostics can be done for tendon/ ligament injury?

A

Radiography (stressed views)
Ultrasound
Manipulation under anaesthesia (most important thing to help diagnose problem)

76
Q

What is the treatment for sprain (ligament) injury?

A

Rest, reduce swelling (drugs and cooling)
External coaptation (support)
Ligament repair
Internal ligament splintage
Arthrodesis (as salvage procedure)
Degree of tx depends on instability and pain

77
Q

What is the most common ligament injury in SAs?

A

Cranial cruciate ligament rupture

78
Q

What is the most common ligament injury in small animals and what common injury can occur alongside this?

A

Cranial cruciate ligament rupture

Medial meniscus can occur alongside the CCLR

79
Q

What is the position of cranial cruciate ligament and the caudal cruciate ligament?

A

Cranial- runs from proximal and lateral to distal and medial

Caudal- runs in opposite direction

80
Q

What is a common presentation seen with cranial cruciate ligament rupture?

A
  • Middle aged dogs (2-10 years)
  • Overweight dogs, neutered dogs
  • Medium to large breed dogs (not seen in sighthounds)
  • Typically insidious onset pelvic limb lameness; can be bilateral; acute onset lameness can also occur
81
Q

What muscles can be atrophied in a CCLR?

A

Quadriceps and hamstrings

82
Q

What are possible physical exam findings with CCLR?

A 
Pelvic limb lameness
Muscle atrophy
Stifle effusion
Medial buttress
Craniocaudal stifle instability
Pain on manipulation
83
Q

What are two manoeuvres that can positively diagnose a CCLR in a patient?

A

Cranial drawer

Tibial thrust- flex hock and put finger on stifle

84
Q

When is conservative treatment appropriate in CCLR?

A

Minimal lameness
Low grade controllable pain
Valid reason to avoid sx (medical/ age/ finances)

85
Q

What are some complications of conservative tx for CCLR?

A

V slow return to function
Stifle will always be unstable
Continuous stimulation of OA change
No control of meniscal damage

86
Q

What are the advantages of surgical treatment?

A

Should improve joint stability
Should speed up recovery
Allows meniscal lesions to be tx

87
Q

What are the surgical options for CCLR?

A

Lateral tibio-fabella suture

TPLO (tibial plateau levelling osteotomy)

88
Q

Describe the lateral tibio-fabella suture procedure

A

Placed in same line as the cruciate ligament but is extracapsular. Meniscus is normally inspected first via an arthrotomy then the joint is closed and suture placed

89
Q

Describe the TPLO procedure

A

The angle that the tibia meets the femur at the stifle is changed by making a tibial osteotomy and then fixing it with a plate at the desired angle

90
Q

What is a TTA?

A

Line of patella tendon is advanced making it parallel to the line of force transfer across the joint. Tension in the tendon cancels out the compression across the joint negating the caudal movement of the femur.

91
Q

What is arthralgia?

A

Joint pain

92
Q

How can you tell the difference between immune mediated dz and a septic processs using arthrocentesis?

A

In both, there is an increase of neutrophils present in the synovium
Septic- degenerate
Immune mediated- non degenerate

93
Q

What are the causes of septic arthritis?

A

Haematogenous

Traumatic (esp horse): lacerations, puncture wounds, iatrogenic

94
Q

What is the recommended treatment for septic arthritis?

A

Abx (amoxicillin/calv). No diff between surgical and medical tx. May need to remove implants if infections associated w/ them. 6 wk course of abx based on culture

95
Q

What is the aetiology of IMPA?

A

Ag/ab complex–> formation of inflamm products. Host IgG and M bind to altered autologous IgG. Ag/Ab complex deposited on synovium–> neutrophil/ macrophage chemotaxis. Release of chondrodestructive collagenases/ proteases. Failure of self-tolerance or production of immunogenic Ig

96
Q

What are the risk factors for autoimmune disease?

A 
Hereditary component. Certain infectious- GpA strep pharyngitis--> acute rheumatic fever
Bacterial endocarditis
Discospondylitis
Immune mediated bowel dz
Neoplasia
Chronic hepatitis
97
Q

What is a hypersensitivity reaction type I?

A

Immediate/ anaphylactic reaction. IgE–> mast cells, basophils

98
Q

What is a hypersensitivity reaction type II?

A

Ab-dependent cytotoxic reaction. IgG or IgM against a cell-surface component

99
Q

What is a hypersensitivity reaction type III?

A

Immune complex mediated reaction. Lg amounts of IgG or IgM plus Ag–> microprecipitates

100
Q

What is a hypersenstivity reaction type IV?

A

Cell-mediated/ delayed-type reaction. Intra-cellular organism

101
Q

What is immune-mediated arthritis?

A 
Polyarticular dz (6+ joints), occasionally pauciarticular (2-5), rarely monoarticular
Chronic dz due to continual/ recurrent presence of inciting ageents. Failure of normal down-regulation.
102
Q

How does immune-mediated arthritis present?

A

Stiffness, difficulty rising. Multi system pyrexia, depression, anorexia. Palpation and manipulation +/- sedation. ROM, pain, heat, swelling and crepitus. Some lame and joint effusions. Ligamentous laxity.

103
Q

What are the types of non-erosive polyarthritis?

A

Type I- uncomplicated idiopathic
Type II- associated w/ remote infections (reactive)
Type III- associated w/ GI dz/ hepatic
Type IV- associated w/ remote neoplasia
Signs often most severe in type I and II, milder in III and IV

104
Q

What are the main stages in investigation of polyarthropathy?

A

Arthrocentesis, joint radiography, synovial biopsy

Underlying dz hunt- haem/biochem/ UA, thoracic rads, abdo US.

105
Q

What are other examples of non-erosive PA?

A

SLE, lyme dz (borrelia), drug-associated, caliciviral in kittens, associated w/ steroid-responsive meningitis-arteritis, IBD, vaccine induced

106
Q

How does erosive joint disease?

A

Chronic synovitis leads to production of proliferative granulation tissue (pannus), which invades articular cartilage and can erode sub-chondral bone. Produce enzymes incl proteases and colalgenases. Similar changes in septic arthritis

107
Q

What radiographic changes occur in erosive arthritis?

A

Sub-chondral bone erosions. Destructive symmetric multi-joint arthrophaty. Early- may be only soft tissue changes. Chronic- collapse of joint space, joint deformity or sub-luxation, peri-articular new bone formation, calcification of peri-articular soft tissues.

108
Q

What is the mainstay of treatment for inflammatory arthritis?

A

Prednisolone- immunosuppressive doses initially, gradually taper +/- cytotoxic drugs (-> BM suppression), cyclophosphamide (-> haemorrhagic cystitis use for <3m), azathioprine (not cats).
In areas where tick-borne or Lymes dz are prevalent empirical tx may be necc- cyclophosphamide, sulfasalazine

109
Q

What is crystal-based arthritis?

A

True gout in sp w/out uricase e.g. humans, birds and reptiles. Reptile- renal damage–> decr excretion of urate. White, periarticular deposits (urate crystals)–> inflamm reaction.
Tx- fluid therapy, avoid meds that incr renal excretion

110
Q

Define arthroplasty.

A

Replacement or excision of a joint; ‘joint moulding’.

111
Q

Define arthrodesis.

A

The artificial induction of joint ossification between two bones via surgery.

112
Q

In which species are arthroplasties indicated?

A
  • Dogs
  • Cats
  • (small ponies?)
  • Alpacas
113
Q

In which species is arthrodesis indicated?

A

All species, depending on the joint (usually only in low motion joints).

114
Q

In which species is amputation indicated?

A
  • Dogs
  • Cats
  • Occasionally in larger animals (not usually possible, QOL issues)
115
Q

What are the indications for arthroplasty?

A
  • Dysplasia (juvenile pain)
  • Intractable arthritis/joint pain
  • Articular fracture that is unreconstructable
  • Persistent luxation
  • Avascular necrosis
116
Q

What is the primary aim of arthroplasty?

A

Remove pain and restore/maintain normal movement to the affected joint.

117
Q

What are some examples of joints on which excision arthroplasty can be performed?

A
  • Hip
  • Temporomandibular joint
  • Radial head (common in humans)
  • Shoulder
  • MT/MC phalangeal joint
  • Phalangeal joints
118
Q

What are the indications for femoral head and neck excision?

A
  • Hip dysplasia
  • Intractable osteoarthritis/DJD
  • Femoral head and neck fracture
  • Persistent luxation
  • Legg-Calve-Perthes disease (avascular necrosis of the femoral head)
119
Q

What is the outcome of FHNE influenced by?

A
  • Obesity
  • Pre-operative muscle wastage
  • Other orthopedic problems
120
Q

What is the goal of a FHNE?

A

A fibrous connection between the two surfaces; in order to keep the fibrous reaction from getting over-aggressive, the patient will need to keep moving.

121
Q

What are the artificial joints currently available for replacement arthroplasty?

A
  • Canine and feline hip
  • Canine stifle
  • Canine elbow
  • (Canine hock reported anecdotally)
122
Q

When can a total hip replacement be performed?

A

Any time after skeletal maturity.

123
Q

What is the ideal patient for a total hip replacement?

A
  • Non responsive hip pain
  • Large breed dog
  • Previously active lifestyle
  • Sensible, well-trained dog
  • Compliant owners
  • (insured)
124
Q

What are the indications for arthrodesis?

A
  • Intractable arthritis/joint pain
  • Articular fracture (unreconstructable)
  • Persistent luxation or instability
  • Low grade pain interfering with performance
  • Revision of failed joint surgery
125
Q

What are the principles of arthrodesis?

A
  1. Absolute stability, ideally through compression
  2. Remove cartilage from contact areas
  3. Contour opposing joint surfaces
  4. Use of bone graft if necessary
  5. Fuse at a functional angle
126
Q

What are some long-term complications of arthrodesis?

A
  • May require transarticular support (ESF, cast)
  • Implants mechanically vulnerable (may break or back out over time)
  • Problems with high motion joints
127
Q

What are the indications for amputation?

A
  • Neoplasia (malignant or locally invasive)
  • Trauma (excessive tissue damage or ischemia)
  • Paralysis (brachial plexus avulsion)
  • Unmanageable joint conditions, intractable pain, congenital deformity
  • Client finances
128
Q

What are some considerations that need to be taken into account with amputation?

A
  • Temperament
  • Other orthopedic disease
  • Owner
  • Mechanically better to lose a pelvic rather than a thoracic limb
129
Q

What are the amputation sites for the forelimb?

A
  • Forequarter amp. (cosmetic and margin advantage)

- Mid humerus

130
Q

What are the amputation sites for the hindlimb?

A
  • Mid/high femur
  • Trans-articular
  • Hemipelvectomy
131
Q

What are the amputation sites for the digit?

A
  • Proximal interphalangeal joint with cartilage removal in cattle
  • Distal P1 or P2 in small animals
132
Q

Describe the principles of amputation.

A
  • Choose suitable margin of excision (nb neoplasia)
  • Local block and fresh scalpel for neurectomies
  • Make sure it’s not possible for stump to get traumatized post op, and leave sufficient tissue (muscle and skin) to cover it
  • Careful reconstruction of tissue to eliminate dead space +/- drain
133
Q

What are the pros of amputation?

A
  • Predictable
  • Straightforward
  • Minor complications
  • Cost effective
  • Instant palliation of signs
  • Short recovery period
134
Q

What are the possible cons of amputation?

A
  • Worse balance
  • Temperament change
  • Knock-on effects on other joints/spine
  • Posturing problems
  • Neuropathic pain (?)
135
Q

What are the typical fracture patterns?

A 
Transverse
Oblique
Spiral
Comminuted
Segmental
Buckle/ greenstick
Avulsion
Compression
136
Q

What are the forces which act on fractures?

A

Bending, rotation, compression/ shear and distraction

137
Q

What are the basic guidelines for coaptation of fractures?

A

Reduction- best for minimally displaced, repeat radiographs ensure apposition adequate for healing
Alignment- failure to aligns results in rotational/ angular malunion, causes functional gait abnormal, also painful lameness from 2ry OA
Standing position- apply in normal position
Joints above and below must be immobilised

138
Q

What are the advantages of external coaptation?

A 
Rel inexpensive (as long as no complications)
Avoids sx
139
Q

What are the disadvantages of external coaptation?

A

Only for stable, minimally displaced, may result in bone/ limb malalignment. Complications more expensive/ difficult to tx than original fracture
Difficult to manage- slips, gets wet, removed by animal!

140
Q

How would you minimise the risks of using external coaptation after sx?

A

Don’t place cast immediately. Place RJ dressing for 3-5d to allow swelling to reduce. Place cast. Monitor for 24hr before sending home. Keep dry. Change cast weekly. Remove at 6wks post-op or before if complications

141
Q

What complications can occur with external coaptation?

A

Distal limb soft tissue swelling, distal limb oedema, skin rubs/ ulceration/ necrosis, soft tissue necrosis, slippage of cast. W/ several amputation can be the only option

142
Q

What are the different types of external coaptation?

A

Robert jones bandage, modified RJ (less cotton padding), reinforced RJ, spica splint, full leg cast, half-cast, bivalved cast, walking bar (aluminium bar at end of cast)

143
Q

What are the different layers of external coaptation made up of?

A

1ry- allevyn/ melolin- covers a protects skin, absorb discharge
2ry- absorption, support, pressure. Conforming gauze wrapped over this to provide stability and occasionally compression
3ry- hold inner layers together, barrier against physical abrasion and environmental contaminants.

144
Q

What is a Salter Harris Fracture?

A

One which involces the epiphyseal plate

145
Q

Which side of the bone should implants be placed on?

A

The tension side= otherwise they will be subject to repeated bending and compressive forces and they will break

Locomotor (4 decks)

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