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TRAUMA & ORTHO > 2: Arthritis, Osteomyelitis & Acutely Swollen Joint > Flashcards

2: Arthritis, Osteomyelitis & Acutely Swollen Joint Flashcards

1
Q

what is the pathophysioogy of OA

A

occurs in the synovial joints
- progressive loss of articular cartilage and remodelling of the underlying bone
- active response of chondrocytes in articular cartilage and inflamm cells in the surrounding tissues
- release of enzymes from above cells break down collagen and proteoglycans = destroy articular cartilage
- exposure of underlying subchondral bone = sclerosis = remodelling = osteophytes and progressive loss of joint space

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2
Q

what are the risk factors of OA

A
  • obesity
  • age
  • occupation trauma
  • female
  • FHx
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3
Q

what are commonly affected joints of OA

A
  • Hips
  • Knees
  • Distal interphalangeal (DIP) joints in the hands
  • Carpometacarpal (CMC) joint at the base of the thumb
  • Lumbar spine
  • Cervical spine (cervical spondylosis)
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4
Q

what are the 4 key X-Ray changes of OA

A
  • L – Loss of joint space
  • O – Osteophytes (bone spurs)
  • S – Subarticular sclerosis (increased density of the bone along the joint line)
  • S – Subchondral cysts (fluid-filled holes in the bone)
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5
Q

what is the typical presentation of OA

A
  • joint pain and stiffness which is worse with activity and at the end of the day
  • deformity, instability and reduced function of joint
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6
Q

what are general signs of OA

A
  • bulky, bony enlargement of the joint
  • restricted ROM
  • crepitus on movement
  • effusions around joint
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7
Q

t are

what are signs of OA in the hands

A
  • Heberden’s nodes (in the DIP joints)
  • Bouchard’s nodes (in the PIP joints)
  • Squaring at the base of the thumb (CMC joint)
  • Weak grip
  • Reduced range of motion
  • CMCJ
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8
Q

what is osteomyelitis

A

infection of the bone, either acute or chronic

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9
Q

what are the most commonly affected bones of osteomyelitis in adults and children

A
  • adults: vertbrae
  • children: long bones
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10
Q

what are the 3 main routes by which osteomyelitis can arise

A
  1. Haematogenous spread
  2. Direct inoculation of micro-organisms into the bone (e.g. following an open fracture)
  3. Direct spread from nearby infection (e.g. adjacent septic arthritis)
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11
Q

what are the most common causative organisms of osteomyelitis

A
  • S. aureus
  • streptococci
  • enterobacter
  • P.auerginosa (IV drug users)
  • Salmonella (hx of sickle cell disease)
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12
Q

explain the pathophysiology of osteomyelitis

A
  • bacteria enter bone tissue and express adhesins to bind to the host tissue proteins
  • produce polysaccharide ECM through which pathogens are able to propagate, spread and seed
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13
Q

what can chronic osteomyelitis lead to

A
  • devascularisation of the affected bone = necrosis and resorption of surrounding bone
  • leads to sequestrum (floating piece of dead bone) which acts as resevoir for infected
  • this cannot be penetrated by abx as it is avascular
  • involucrum can also form where the region becomes encased in a thick sheath of new periosteal bone
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14
Q

what are risk factors of osteomyelitis

A
  • DM
  • immunosuppression e.g. long term steroids/AIDS
  • excessive alcohol
  • IV drug use
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15
Q

what is Potts disease

A

infection of the vertebral body and intervertebral disc by Mycobacterium tuberculosis

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16
Q

how does Potts disease present

A
  • back pain +/- neurological features
  • associated low grade fever
  • non-specific infective symptoms
17
Q

how does Potts disease progress

A

initially start in the intervertebral disc before spreading to the para-discal regions
- typically affecting the thoraco-lumbar region of the spine

18
Q

what is the gold standard investigation for Potts disease

A

MRI

19
Q

what is the management of Potts

A
  • prolonged course of anti-TB medication
  • surgical intervention may be required fro abscess drainage in case of extensive spinal destruction
20
Q

what investigations/imaging will patients with suspected acute osteomyelitis undergo

A
  • urgent blood tests, including a FBC and CRP
  • blood cultures
  • plain radiographs (poor accuracy and only visible signs from 7-10 days post infection)
21
Q

what features may be visible on radiography of osteomyelitis

A
  • osteopenia
  • periosteal thickening
  • endosteal scalloping
  • focal cortical bone loss
22
Q

how is diagnosis of osteomyelitis reached

A

MRI
- demonstrates bone marrow oedema 1-2 days post infection
- Nuclear medicine bone scans, e.g. PET-CT or scintigraphy, may also be used in diagnosing osteomyelitis, showing evidence of any active infection

23
Q

what is the gold standard diagnosis of osteomyelitis

A

culture via bone biopsy at debridement
- ensure culture is checked for mycobacterium and fungal causes especially in susceptible cases e.g. immunosuppressed

24
Q

what is the management of osteomyelitis

A
  • if pt clinically well: long term IV abx therapy >4 weeks
  • if pt deteriorates/progressive bone destruction seen then need surgical debridement and send samples for culture/sensitivity
25
Q

what needs to be established when a patient presents with an acutely swollen joint

A
  • onset
  • site
  • timeframe
  • precipitating factors e.g. trauma, surgery
  • level of pain
  • ability to weight bear
  • +/- fever, rigors, lethargy
  • other joint involvement
  • skin changes
  • previous episodes
26
Q

what is involved in the initial assessment of an acutely swollen joint

A
  • A-E
  • inspect: redness, swelling, skin changes
  • feel: focal tenderness and evidence of joint effusion
  • ROM?
  • look for signs of other joint involvement or systemic signs
27
Q

what investigations are done in an acutely swollen joint

A
  • routine bloods: FBC, CRP, ESR (rheum), serum urate (gout)
  • plain film radiographs
  • joint aspiration!
28
Q

what are you looking for in joint aspiration

A
  • visual inspection: opacity, colour, presence of frank pus in the syringe
  • can also be sent for WCC and microscopy, culture & sensitivity and light microscopy for crystals
29
Q

what is gout and where does it commonly affect

A
  • inflammatory arthritis caused by collection of mono sodium urate crystals in a joint
  • caused by hyperuricaemia which leads to crystallisation of urate in joint
  • classically affects 1st MTP joint
30
Q

How is a diagnosis of gout made

A
  • joint aspiration and microscopy which will show thin, needle shaped mono sodium urate crystals in the synovial fluid
  • plain radiographs will often show only a soft tissue swelling
31
Q

How is acute gout treated

A

NSAIDs

32
Q

How are multiple episodes of gout treated

A

Prophylactic agents e.g. allopurinol for prevention

33
Q

What is pseudo gout and how does it differ from gout

A

Inflammatory arthritis caused by deposits of calcium pyrophosphate crystals within the joint
- more likely to affect the proximal joints with knee and wrist being commonly affected

34
Q

What are risk factors for pseudo gout (3)

A
  • advanced age
  • hyperparathyroidism
  • hyperphosphatemia
35
Q

How is pseudo gout diagnosed and treated

A

Joint aspiration and microscopy
- positively birefringent rhomboid-shaped crystals
- treat acutely with NSAIDs

36
Q

What is the diagnostic criteria for RA

A

EULAR classification
- 4 categories: joint distribution, serology, symptom duration, acute phase reactants
- if >6/10 then definite RA

37
Q

What conditions are included in spondyloarthropathies

A
  • psoriatic arthritis
  • ankylosing spondylitis
  • reactive arthritis
  • enteropathic arthropathy
38
Q

What are spondylarthropathies classified as and what are they associated with

A

Seronegative conditions (RF negative) and associated with HLA-B27

39
Q

How might spondyloarthropathies present

A

axial arthritis
- or affecting any joint as an oligoarthritis or monoarthritis
- enthesitis and dactylitis

TRAUMA & ORTHO (11 decks)

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