Week 11 Flashcards
How does acute compartment syndrome present?
It is elevated interstitial pressure within a closed facial compartment resulting in microvascular compromise
Common sites are leg, forearm and thigh
CFs:
- disproportionate pain, pain on passive stretching of the compartment, pallor, parasthesia, paralysis and pulselessness
- swelling, shiny skin
- autonomic responses- sweating, tachycardia
Mostly diagnoses clinical
Describe the pathophysiology of ACS:
Causes:
- increased internal pressure
- eg bleeding, swelling, iatrogenic infiltration
- increased external compression
- eg casts/bandages, full thickness burns
- combination
Pressure within compartment exceeds pressure within the capillaries, muscle becomes ischaemic and develops oedema through increased endothelial permeability
Necrosis begins in the ischaemic muscles after 4 hours
Decreased perfusion Muscle ischaemia Muscle swelling Increased permeability – fluid leaks into interstitial space Increased pressure Autoregulatory mechanisms overwhelmed Muscle necrosis and myoglobin release Loss of function , extremity or loss of life.
How is ACS managed?
Open any constricting dressings / bandages
Reassess
Surgical release:
- full length decompression of all compartments
- excise any dead muscle
- leave wounds open
- repeat debridement until pressure down and all dead muscle excised
Later wound closure
Skin grafting / Plastic surgery input
Describe the presentation and pathology of tendinopathy:
Chronic tendon injury of overuse, due to loss of balance between micro-damage from overuse and reparative mechanisms
Probably not inflamation – tendinosis not tendinitis
Deranged collagen fibres / Degeneration with a scarcity of inflammatory cells
Increased vascularity around the tendon
Failed healing response to micro tears
Inflammatory mediators released IL-1, NO, PG’s – cause apoptosis, pain and provoke degeneration through release of matrix metalloproteinases
CFs:
Pain
Swelling
Thickening
Tenderness
Diagnosed with imaging (Xray, US, MRI) also helps exclude other pathologies
Describe the management of tendinopathy:
Non-op:
NSAID’s
Activity modification
Physiotherapy – stretching , eccentric exercises
GTN patches (vasodilator so increased local perfusion)
PRP injection
Prolotherapy – irritant injection, dextrose
Extracorporeal Shockwave Therapy
Topaz – radiofrequency coblation
Op:
Debridement
Excision of diseased tissue
Possible to debride 50% of tendon without loss of function
(tendon transfers)
What is the clinical significance of ACS?
1 hour- nerve conduction normal, muscle viable
4 hours- neuropraxia in nerves (reversible) and reversible muscle ischaemia
8 hours- nerve axonotmesis and irreversible changes, irreversible muscle ischaemia and necrosis
End stage: stiff fibrotic muscle compartments, impaired nerve function, clawing of limbs, loss of function
Describe the presentation of septic arthritis:
Pain, fever, swollen joint, loss of function, acutely inflamed (<24 hours)
Caused by S. aureus, N, gonorrhoea, H. influenzae
Knee is affected in >50% of cases
RFs: pre-exisiting joint disease, DM, immunosuppression, CKD, recent joint surgery, prosthetic joints
Describe the presentation of reactive arthritis:
Sterile synovitis which occurs following an infection
Trigger organisms- salmonella, shigella, yersinia, chlamydia trachomatis
Preceding illness usually an urethritis or diarrhoeal
CFs: acute, asymmetrical lower limb arthritis, days-weeks post infection
Also presents with enthesisitis (plantar fasciitis), sacroilitits, spondylitis, anterior uveitis, conjunctivitis, keratoderma blenorrhgaica
Describe the presentation of gout:
Typically acute monoarthropathy with severe joint inflammation
>50% occur at the MTP joint of big toe
Other common joints are ankle, foot, knee, elbow, wrist or small joints of the hand
Can be polyarticular
What are the appropriate investigations for patients who present with acute joint pain and swelling?
The synovial fluid must be aspirated, Gram-stained and cultured prior to starting antibiotics, warfarin does not contraindicate needle aspiration
Neither the absence of organisms on Gram stain nor a negative subsequent synovial fluid culture excludes the diagnosis of septic arthritis
Specimens must be sent fresh to the laboratory and obtained prior to starting antibiotics
Polarising microscopy should always be carried out
Blood cultures should always be taken
The white cell count, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) should be measured- inflammatory markers are useful for monitoring response to treatment
The serum urate level is of no diagnostic value in acute gout or sepsis
Electrolytes and liver function should be measured to detect end organ damage because renal function may influence antibiotic choice
If the history suggests non-articular infection, then appropriate cultures and swabs should be taken prior to starting antibiotics
Plain radiographs of the affected joint are of no benefit in diagnosing septic arthritis but may show chondrocalcinosis. They should be performed as a baseline investigation- usually MRI
What are the treatments for gout and when is urate lowering therapy introduced?
NSAIDs – high doses rapidly reduce pain and swelling
Alternatives – colchicine, corticosteroids
If attacks are repeated –
Allopurinol – xanthine oxidase inhibitor
Uricosuric agent (probenecid) – increases secretion of uric acid into urine
Describe the normal structure and function of bone:
Functions:
Structural; support, protection and movement
Mineral Storage; calcium and phosphate
Structure
Diaphysis (shaft)
Epiphysis (end)
Metaphysis (transitional flared area between diaphysis and epiphysis)
Cortical/compact outside with spongy/cancellous in the medullary cavity
Compare and contrast direct and indirect bone healing:
Indirect: formation of bone via a process of differential tissue formation until skeletal continuity is restored
INFLAMMATION, REPAIR, REMODELLING
Direct: surgical situation- direct formation of bone without the process of callus formation to restore skeletal continuity, relies on compression of the bone ends
Direct formation of bone via osteoclastic absorption and osteoblastic formation (cutting cones)
How can medication affect bone healing?
NSAIDs, steroids and bisphosphonates
NSAIDs reduce local vascularity at fracture site
Additional reduction in healing effect independent of blood flow
COX 2 NSAIDS inhibit fracture healing more than non-specific NSAIDS
Magnitude of effect is related to duration of treatment
Bisphosphonates:
Inhibit osteoclastic activity
Delay fracture healing as a result
Long half life
What factors compromise bone healing?
a
Describe avascular necrosis:
a
Describe secondary tumours in the bone:
Present in 60% of patients dying of cancer
Metastatic carcinoma: bronchus, breast, prostate, kidney, thyroid
Often mets to bones with good blood supply- long bones/vertebrae
CFs: often asymptomatic, bone pain, bone destruction, pathological fracture in long bones, hypercalcaemia
Spinal mets: vertebral collapse, spinal cord compression, nerve root compression, back pain
Can by lytic or sclerotic destruction
Lytic: osteoclast activity, stimulated by cytokines from tumour cells and inhibited by bisphosphonates
Describe myeloma:
Commonest malignant primary bone tumour
Monoclonal proliferation of plasma cells
Solitary: plasmacytoma or multiple myeloma
Orthopaedic and medical consequences
Medical: pancytopenia due to destruction of bone marrow
Orthopaedic: bone lesions (punched out lytic foci and generalised osteopenia)
What are the common radiological features of OA/DJD?
Joint space narrowing, characteristically asymmetric
Sclerosis: occur at joint margins and present unless severe OP is present
Osteophytosis; DIP, PIP and base of thumb should be bilateral
Joint erosions; temperomandiubular, acromioclavicular, sacroiliac and symphysis pubis joints
Sub-chondral cyst; DJD, RA, CPPD,
What are the common radiological features of RA?
Loss of joint space
Mild subarticular sclerosis
Lack of osteophyte
Symmetrical disease MCP joint erosions MCP ulnar deviation Deformed thumbs Erosions distal ulna Erosive changes wrists 2o degenerative changes
What are the common radiological features of Paget’s disease?
Blade of grass or candle flame sign: begins as a subchondral area of lucency with advancing tip of V-shaped osteolysis, extending towards the diaphysis in long bones
Skull:
osteoporosis circumscripta: large, well-defined lytic lesion
cotton wool appearance: mixed lytic and sclerotic lesions of the skull
What are the common radiological features of ankylosing spondylitis?
Bi-lateral sacro-iliitis
Squaring of vertebral bodies
Bamboo spine
Peripheral large joint arthritis
Romanus lesions and spinal fractures in spine
How can USS be used in early diagnosis of arthritis?
a