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MSK2 > Small animal MSK disease 2 > Flashcards

Small animal MSK disease 2 Flashcards

1
Q

Outline the aetiology of carpal hyperextension injuries

A
  • Usually traumatic, associated with fall from height

- Can be degenerative (Collies)

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2
Q

What other injuries may be associated with carpal hyperextension injuries?

A

Carpal bone fractures esp. when traumatic as well as the rupture of palmar ligaments and fibrocartilage

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3
Q

Describe the diagnosis of carpal hyperextension injuries

A
  • Characteristic seal stance
  • Careful palpation
  • Radiographic examination including stressed views - establish joints involved and therefore required treatment
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4
Q

Outline the treatment of carpal hyperextension injuries

A
  • Pancarpal arthrodesis most common
  • Use bespoke plates, bone graft, removal of all articular cartilage
  • Further support until partial arthrodesis occurred
  • Splints an support bandages will fail
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5
Q

Explain the difference between luxation and subluxation

A
  • Luxation: cartilage surfaces not in contact at all

- Subluxation: partial contact of cartilage surfaces

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6
Q

What is meant by joint incongruency?

A

Abnormal shape to bones and cartilage so cartilage does not fit together properly

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7
Q

What are the possible underlying aetiologies of luxations?

A

Trauma (common), congenital (rare), developmental (frequent)

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8
Q

Describe how traumatic luxations occur

A

Associated with third degree sprain (except in elbow luxation), joint capsule and other peri-articular structure damage

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9
Q

Outline the consequences of traumatic luxation

A
  • Traumatic arthritis
  • Individual ligaments may never heal
  • Capsule thickens to assume some function of the supporting ligaments
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10
Q

Outline the treatment of traumatic luxation

A
  • Surgery to restore acceptable function of ligaments
  • May require salvage procedures
  • Talocrural/tibiotarsal luxation - fixator will restore acceptable function
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11
Q

Explain the cause of congenital luxations

A
  • Malformation of joint, bone or soft tissue leading to abnormal articular surfaces
  • Often severe associated bone deformity
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12
Q

Describe the typical presentation of congenital luxations

A
  • May be symmetrical
  • Small breed dogs (e.g. cavvie) with shoulder luxations are rarely lame (mechanical rather than painful lameness)
  • Congenital elbow luxation in Staffies
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13
Q

Outline the treatment options for congenital luxations

A
  • Conservative: first option, pain releif and weight management
  • If unsuccessful, attempt surgical but poor success due to abnormal joint surfaces
  • Salvage procedures typically required
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14
Q

What is the prognosis for surgical treatment of congenital luxations?

A

Guarded

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15
Q

Explain the cause of developmental subluxations/incongruencies

A
  • Common
  • Hip/elbow dysplasia
  • Incongruency of joints leading to joint effusion and luxation
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16
Q

Describe the typical presentation of developmental subluxation

A
  • Commonly bilaterally symmetrical

- Develop secondary arthritis

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17
Q

Outline the treatment of developmental luxations

A
  • Conservative/medical management of the arthritis

- Salvage surgical procedures

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18
Q

Explain the cause of degenerative luxation

A

Very common e.g. cranial cruciate ligament degeneration/rupture leading to cranial subluxation of the tibia

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19
Q

Which joints are predisposed to luxation in dogs and cats?

A
  • Hip and tarsus

- Patella (intermittent)

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20
Q

Outline the assessment for luxation in dogs and cats

A
  • Clinical examination (+/- GA): pain,asymmetry
  • Laxity (depends on chronicity of disease)
  • Orthogonal radiographs of limb, +/- stressed views
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21
Q

When qould thoracic and abdominal radiographs be indicated when investigating joint luxation in cats and dogs?

A

Where traumatic luxation has occurred

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22
Q

What test would indicate hip luxation on clinical examination of a cat/dog?

A
  • Finger and thumb placed between ischial tuberosity and greater trochanter, hold both HLs
  • When HLs extended behind animal, luxated limb will be shorter due to dorsal luxation
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23
Q

Explain why laxity may not always be a good indicator of joint luxation

A
  • Depends on chronicity of condition

- With time, partiarticular fibrosis and muscle contraction can stabilise the joint

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24
Q

Outline the principles of repair of acquired/traumatic luxations

A
  • Reduce joint into normal anatomical alignment, maintain reduction while capsule and other soft tissues heal
  • Re-attach bone if avulsion present
  • May require prosthetic ligament
  • Post-op support as for sprains
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25
Q

What are the 3 main stabilisers of the hip?

A
  • Round ligament
  • Joint capsule
  • Acetabular rim
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26
Q

List the options for the management of hip luxation

A
  • Closed reduction
  • Open reduction and stabilisation such as:
  • Salvage procedures
  • Transarticular pin
  • Rectus femoris or ilio-femoral suture for craniodorsal luxation
  • Hip toggle
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27
Q

Describe closed reduction of hip luxation

A
  • Manipulate hip back into acetabulum without surgery within 1 day of luxation
  • Always readiograph after
  • Care re/ soft tissue injuries and re-luxation
  • May also require Ehmer sling
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28
Q

What is the success rate for closed reduction of hip luxation?

A

50%, higher in dogs than cats

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29
Q

Describe open reduction and stabilisation of hip luxation and give success rare

A
  • Always includes soft tissue repair/imbrication
  • E.g. transarticular pin, toggle, rectus femoris or ilio-femoral suture
  • 75-85% success
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30
Q

What salvage procedures may be used for hip luxation?

A

Replacementof excision

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31
Q

Discuss the use of transarticular pins for hip luxation

A
  • Most suitable for cats/small dogs
  • Gives reasonable function but limited adduction
  • Causes arthritis
  • If incongruent may damage articular surface
  • Requires 2nd procedure 3 weeks later to remove pin
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32
Q

Describe the use of rectus femoris or ilio-femoral suture for craniodorsal hip luxation

A
  • Suture placed through tunnel in base of greater trochanter and either: origin of rectus femoris, or hole made in ventral aspect of ilium
  • Suture tightened with hip slightly internally rotated
  • May cause slight internal rotation of paw (resolves with suture absorption)
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33
Q

Discuss the use of hip toggles for canine hip luxation

A
  • Challenging
  • Medium to large dogs best
  • Can cause articular damage if hip not congruent
  • Very stable, functional joint if correct
  • Braided multifilament suture use so some risk of infection
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34
Q

Outline the method for the hip toggle in dogs

A
  • Drill hole through acetabular notch
  • Then another from origin of teres ligament, through femoral neck to base of trochanter
  • Then place suture through hole, as pushed through pull on loop, toggle comes into right angle to hole
  • Tightening holds head in acetabulum
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35
Q

Outline the approach to traumatic elbow luxation

A
  • Treat Asap, always GA, pre-op radiographs including thorax
  • Closed or open reduction can be used
  • Check collateral ligaments
  • Post-op radiographs required
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36
Q

Outline the approach to congenital elbow luxation

A
  • Can be treated conservatively if dog is coping

- Surgery can be beneficial, but residual lameness common so little benefit over conservative

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37
Q

Outline the general approach to acquired luxations

A
  • Reconstruct supporting structures if possible
  • Support repair
  • Physio improves recovery
  • DJD inevitable, warn owner
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38
Q

Outline the general approach to subluxations

A
  • very common
  • medically manage if milk
  • Salvage surgery if not coping
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39
Q

Outline the general approach to congenital luxations

A
  • Very rare
  • Poorer prognosis
  • Grossly dysplastic joint and better left alone
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40
Q

What diagnostic techniques can be used for the evaluation of acutely traumatised joints?

A
  • Careful physical examination
  • Manipulation under GA
  • Radiography
  • Ultrasound
  • arthroscopy
  • CT
  • MRI
  • Need to look for concurrent injuries
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41
Q

Outline the use of ultrasonography for the evaluation of acutely traumatised joints

A
  • Damage to tendons, rarely for ligaments
  • Linear scanner
  • Bicipital, gastrocnemius and flexor tendons in particular
42
Q

Outline the use of arthroscopy for the evaluation of acutely traumatised joints

A
  • Examine intra-articular ligaments e.g. cruciates

- And those withinn the joint capsule such as glenohumeral ligaments of the shoulder

43
Q

Outline the use of CT for the evaluation of acutely traumatise joints

A
  • Limited ability to examine soft tissue structures
  • Good for demonstration of tendon sheath effusions and tendon mineralisation e.g. around shoulder joint (mineralisation of suprascapularis tendon or infraspinatus)
44
Q

Outline the use of MRI in the evaluation of acutely traumatised joints

A
  • Good for soft tissues

- Best modality for tendons and ligaments

45
Q

List the different types of non-inflammatory joint disease

A
  • DJD/OA: instability, trauma or developmental disease

- Coagulopathic joint disease

46
Q

List the different types of inflammatory joint disease

A
  • Septic arthritis
  • Non-bacterial: rickettsia, viral, protozoal
  • Sterile: IMPA
  • Neoplastic arthritis
  • Crystal induced arthritis
47
Q

Explain how tick borne diseases lead to arthritis

A

Immune mediated responses that cause polyarthritis

48
Q

What is the main type of neoplastic arthritis?

A

Synovial cell sarcomas

49
Q

What tumours may cause neoplastic arthritis?

A
  • Synovial cell sarcomas
  • Fibrosarcomas
  • Haemangiosarcomas
  • Osteosarcomas
50
Q

Describe the common presentation for neoplastic arthritis

A
  • Dogs (rare in cats, large animals)
  • Large joints of limb usually (e.g. stifle)
  • lameness, joint effusion, soft tissue swelling, lytic areas of bone destruction on radiograph both sides of joint
51
Q

In which species does true gout occur?

A

Those without uricase enzyme: humans, birds, reptiles

52
Q

How does gout occur in reptiles?

A
  • Production of uric acid normal, secrete as urates in proximal renal tubules
  • Damage to kidney raises uric acid in blood
  • Deposits in various parts of body incl. kidney, pericardial space, joints
53
Q

Outline crystal induced arthritis in dogs

A
  • White, peri-articular deposits lead to inflammatory reaction
  • Rare in dogs
  • Peri-articular synovial deposits of calicum pyrophosphate, or Ca phosphate
  • Single or multiple can be affected
54
Q

Outline the aetiology of IMPA

A
  • Usually type III hypersensitivity reaction
  • Immune complex deposition in synovial basement membrane, complement cascade activation
  • Recruitment of inflammatory cells
  • Leads to release of nitric oxide, free radicals, proteases, leading to tissue damage
55
Q

Give examples of erosive immune mediated polyarthritis

A
  • Idiopathic erosive polyarthritis
  • Rheumatoid arthritis
  • Semi-erosive polyarthritis of greyhounds
  • Periosteal proliferative polyarthritis in cats (rare)
56
Q

Describe type I non-erosive IMPA

A

Idiopathic IMPA, most common

57
Q

Describe type II non-erosive IMPA

A
  • Associted with infection remote from joint (25% of cases)

- Not septic, is an immune reaction

58
Q

Describe type III non-erosive IMPA

A
  • Associated with GI disease (15% of cases)

- Immune complexes deposited in joint

59
Q

Describe type IV on-erosive IMPA

A

Associated with neoplastic disease i.e. paraneoplastic syndrome (rare)

60
Q

Describe the involvement of SLE in joint disease

A
  • Multisystemic immune mediated disease, rare
  • Joint disease + glomerular disease, or joint disease + skin lesions
  • IMHA +/- thrombocytopaenia
  • Combination of clinical signs increases potential for multisystemic disease
61
Q

List some unusual syndromes of non-erosive immune mediated polyarthritis

A
  • Polyarthritis/meningitis syndrome
  • Polyarthritis/polymyositis syndrome
  • Breed associated non-erosive IMPA
  • Familial Shar-Pei fever
  • Drug induce IMPA
62
Q

List the breeds that are associated with breed related non-erosive IMPA

A
  • Weimaraner
  • Boxer
  • Akita
  • Bernese MD
  • GSD
  • Spaniels
  • Beagles
63
Q

Outline drug induced IMPA

A
  • Immune complex deposition as a result of drug-antibody interaction
  • Reported with sulohonamides esp in Doberman
  • Post live Calicivirus vaccines in cats
64
Q

Outline the aetiology of septic arthritis in small animals

A
  • trauma
  • Post-surgery
  • Intra-articualr injection
  • Idiopathic
65
Q

What may lead to idiopathic septic arthritis?

A

Underlying OA in dogs

66
Q

What may cause septic arthritis in multiple joints of adult small animals?

A
  • Haematogenous spread of infeciton in debilitated/immunosuppressed animals
  • Non-bacterial causes e.g. Rickettsia, Mycoplasma, fugnal , viral, protozoal (rare)
67
Q

What clinical signs may be seen in cats with septic arthritis as a result of Calcivirus?

A
  • Inflammatory joint disease
  • Pyrexia
  • Other flu symptoms
68
Q

What may lead to septic arthritis in large animal neonates?

A
  • Failure of passive transfer of immunity
  • Umbilical infection
  • Haematogenous spread of infection
  • Osteomyelitis
69
Q

Describe the signalment for IMPA

A
  • Larger breed dogs <6yrs old
  • (Also seen in smaller breeds and mixed beedds)
  • More dogs than cats
70
Q

What would a shifting lameness that may wax and wane be suggestive of?

A

Immune mediated disease

71
Q

Describe the lameness commonly seen in IMPA

A

Often look stiff rather than lame, more than one limb affected

72
Q

In a case of arthritis in a small animal, what should be included in the physical examination?

A
  • Assess for pyrexia
  • Number of limbs/joints affected
  • Palpation to assess heat, swelling, ROM, pain, joint affected
  • Neck/muscle pain
  • Lymph nodes assessed
73
Q

When performing arthrocentesis for the diagnosis of an inflammatory arthritis in small animals, what parameters of the synovial fluid needs to be assessed?

A
  • Colour
  • Total and differential white cell counts
  • Cell morphology
  • Culture and sensitivity
74
Q

When would radiography be indicated in the work up for a case of inflammatory arthritis?

A
  • If joint palpation reveals crepitus, instability, poor ROM, deformity
  • If there is poor response to treatment
75
Q

Compare the radiographic findings expected for erosive vs. non-erosive IMPA

A
  • Erosive: subchondral defects, collapsed joint spaces, proliferation and calcification of periarticular soft tissue
  • Non-erosive: joint effusion likely only finding
76
Q

When might a diagnosis of erosive IMPA be missed on radiography?

A

If radiographs taken too early in course of disease - if not responding well to treatment, may be appropriate to repeat radiographs of multiple joints

77
Q

What additional imaging modalities may be required in the investigation of IMPA and why?

A
  • If suspicious of type II, III or IV IMPA or multi-systemic immune mediated disease
  • Thoracic radiographs: mets of neoplastic disease, endocarditis
  • Abdominal ultrasound
  • Echocardiography
78
Q

When might contrast studies be useful in the investigation of inflammatory joint disease?

A
  • Septic arthritis
  • Especially in horse
  • Look for communication between tracts/sinuses and a joint
  • May be able to identify a foreign body
79
Q

Outline the laboratory tests that may be used in the investigation of inflammatory joint disease

A
  • Haematology: inflammatory leukogram? Anaemia of chronic disease? IMHA?
  • Biochem: changes consistent with systemic disease
  • Urinalysis: proteinuria/evidence of glomerulonephropathy
  • Serology: ANA and rheumatoid factor (non-specific in dogs)
  • Histopathology: tissue biopsy for unusual syndrome
80
Q

Compare the findings in haematology and biochemistry for IMPA vs non-inflammatory joint disease

A
  • More likely to find changes with IMPA
  • Leukocytosis
  • Hyperglobulinaemia
  • Mild hypoalbuminaemia
81
Q

What are the key aspects of investigation that may aid the identification of IMPA?

A
  • Full flexion of carpi and squeezing to assess pain response
  • Subtle enlargement of LNs
  • Aspiration of multiple joints
  • Changes in >1 joint, no bacteria on cytology or culture
82
Q

Outline the key aspects of the treatment of septic arthritis in small animals

A
  • Must be fast and aggressive
  • Systemic and intra-articular antibiotics
  • Joint lavage and drainage to clean joint
  • Post-op care important
83
Q

Discuss the use of lavage in the treatment of septic arthritis in horses, farm animals and small animal cases

A
  • Horses: antibiotics rarely enough, lavage used as minimum

- Farm and severe small animal: lavage possible, often not cost effective in farm animals

84
Q

Outline the use of arthroscopy in the treatment of septic arthritis

A
  • Direct visualisation of joint
  • Removal of fibrin
  • Foreign material or articular fractures
  • Used in chronic or complicated cases
  • Ideally in every equine case
85
Q

Outline the use of systemic antibiotics in the treatment of septic arthritis in small animals

A
  • Broad spec
  • C+S takes time, start before results available
  • Amoxyclav common in small animals (penicillin + aminoglycoside in large)
  • Start IV/IM admin, switch to oral after 5-7 days, total duration 2-4 weeks min.
86
Q

Outline the use of local antibiotics in the treatment of septic arthritis in small and large animals

A
  • Intra-synovial admin common in large animals
  • High doses with low cost and toxicity achieved
  • Gentamycin, amikacin, ceftiofur in horses
  • Higher risk of nephrotoxicity in dogs
  • PMMA beads useful in chronic/difficult cases
87
Q

Outline the post-operative care in cases of septic arthritis in small animals

A
  • NSAIDs
  • Rest, controlled exercise, physio
  • Avoid intra-articular medication, esp. in early stages as will predispose to infection (esp. HAs, PsGAGs, corticosteroids)
88
Q

Discuss the prognosis for septic arthritis in small animals

A
  • Following systemic antibiotics only: 56% full clinical recovery, 32% persistent mild lameness, 12% poor response (consider lavage)
  • Factors affecting outscome: duration, severity, multiple joints affected, concurrent problems (e.g. bacterial endocarditis)
89
Q

Outline the general treatment of IMPA

A
  • Treat/remove underlying cause or antigenic trigger
  • Analgesia while managing primary disease
  • Nutritional support where needed
90
Q

Outline the treatment of type I IMPA

A
  • No underlying cause therefore immunosuppressive treatment
  • Single agent e.g pred
  • Combination therapy may be needed in refractory cases/side effects e.g. pred + ciclosporin/azathioprine
  • Newer single agent therapy e.g. mycophenolate, luflenomide
91
Q

Outline the monitoring required when treating IMPA

A
  • Clinical sings
  • Physical examination findings, owner reports
  • Follow up arthrocentesis
  • Serum C reactive protein
92
Q

Evaluate the use of serum C reactive protein for the monitoring of IMPA

A
  • Good surrogate marker for synovial inflammation
  • Good correlation with pain scores and joint cellularity
  • Objective and non-invasive method to monitor cases
93
Q

Discuss the prognosis for erosive and non-erosive IMPA

A
  • Good for non-erosive, but may relapse

- Poor for erosive, surgical salvage procedures often required, euthanasia is reasonable alternative

94
Q

Compare the joints typically affected by IMPA and septic arthritis

A
  • IMPA: smaller distal joints e.g. hocks, carpi, stifle

- Septic: more proximal larger joints e.g. elbow

95
Q

Compare the synovial fluid analysis of IMPA and septic arthritis

A
  • IMPA: ~300 cells x10^9/l, <95% neutrophils, usually non-degenerate
  • Septic: cell count variable but usually very high, most cells are degenerate neutrophils
96
Q

Outline why septic arthritis may not also be demonstrable by bacteria on smears

A

Pathology is more to do with sensitive location of bacteria, rather than their number so may be a small load

97
Q

What may help indicate that blood in synovial fluid following arthrocentesis is as a result of sampling?

A
  • Blood streak in otherwise clear fluid

- Sample starts clear then changes to bloody

98
Q

Compare the findings on a smear for an iatrogenic/very acute haemoarthrosis vs a long standing one

A
  • Iatrogenic/very acute: platelets present

- Chronic: no platelets (clotted) , increased white cells, erythrophagocytosis, haemosiderin, haematoidin

99
Q

How can bacteria be distinguished from artefacts on a synovial smear?

A
  • Artefact of fluid not lying flat on slide leading to dotty granular background
  • May resemble bacteria, but is pink and irregular vs bacteria which are blue and regular
100
Q

Explain why neutrophils may be confused with lymphocytes in synovial smears

A

Slow drying leads to lobes of neutrophilic nucleus becoming folded, so may look similar to lymphocyte

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