GC237 Musculoskeletal Infection
Musculoskeletal infection refers to infectious processes affecting bones (osteomyelitis), joints (septic arthritis), or surrounding soft tissues, typically caused by bacterial pathogens and requiring prompt diagnosis and treatment to prevent tissue destruction and systemic complications.
Musculoskeletal (MSK) Infection
Lecture Map
This lecture (GC 237, Prof. Tak Man Wong, updated 2025) is the definitive GC deck on musculoskeletal infections and covers both bone and joint infections and soft tissue infections — from common presentations like paronychia to life-threatening emergencies like necrotizing fasciitis and gas gangrene. It is divided into two parts: Part 1 covers osteomyelitis, septic arthritis, and pyogenic flexor tenosynovitis; Part 2 covers necrotizing fasciitis and gas gangrene. [1]
Big idea: MSK infections range from mild to life-threatening. The unifying principle is that early recognition, empirical antibiotics, and timely surgical intervention save limbs and lives. Delay → tissue destruction → amputation or death.
By the end of this lecture, you should be able to:
- Recognize the clinical features of common and life-threatening MSS infections such as septic arthritis, osteomyelitis, infective tenosynovitis, and necrotizing fasciitis
- Describe the radiological features associated with MSS infections
- Understand the management principles of MSS infections
- Understand the sequelae of MSS infections if not treated promptly
MSK infection is a bread-and-butter orthopaedic topic. In exams, it appears as SAQs (describe management of septic arthritis), MCQs (identify Kanavel signs, staging of NF, organisms), and minicases (diabetic patient with swollen limb — NF vs cellulitis?). Expect to differentiate septic arthritis from gout, recognize necrotizing fasciitis early, and know the organisms and antibiotic principles.
Part 1: Bone and Joint Infections
1. Osteomyelitis
Osteomyelitis: infection of bone caused by bacteria. [1]
Classification by onset:
- Acute: < 2 weeks
- Subacute: < 3 months
- Chronic: > 3 months [1]
Why these time cutoffs matter: Acute osteomyelitis is a medical emergency primarily treated with antibiotics; chronic osteomyelitis has established dead bone (sequestrum) that antibiotics cannot penetrate, so surgery becomes the mainstay.
Common in paediatric patients (metaphysis, slow but rich blood flow over the growth plate). [1]
From first principles: In children, the metaphyseal arteries form sinusoidal loops near the growth plate (physis). Blood flow here is slow and turbulent — like an eddy in a river. Bacteria from a transient bacteraemia (e.g. from a skin wound) can settle in these sluggish sinusoids. The endothelium lacks reticuloendothelial cells, so phagocytosis is poor. This makes the metaphysis a perfect breeding ground.
Most common sites: Distal femur, proximal tibia (areas of fastest growth → most blood flow → most bacteria settle there). [2]
Age-dependent spread patterns (from supporting notes): [2][3]
| Age Group | Site of Infection | Key Feature |
|---|---|---|
| Infants < 1 year | Epiphysis | Growth plate not yet fully formed → infection crosses to epiphysis → can cause septic arthritis AND growth arrest |
| Children 1–16 years | Metaphysis | Mature growth plate is cartilaginous → acts as barrier → infection stays in metaphysis (UNLESS joint capsule inserts distal to physis: hip, shoulder, elbow) |
| Adults | Vertebrae (most common), also long bones | No growth plate → infection can spread anywhere |
High Yield Exam Point
Septic arthritis can complicate osteomyelitis when the joint capsule inserts DISTAL to the epiphyseal plate (hip, shoulder, elbow) — this is because infection in the metaphysis is intracapsular in these joints. This is a classic exam discriminator. [2]
The lecture shows a diagram of pathogenesis. The sequence:
- Bacteria seed the metaphysis via haematogenous spread (most common), direct inoculation (open fracture, surgery), or contiguous spread (adjacent soft tissue infection)
- Suppuration → increased intraosseous pressure (bone is a rigid compartment, so pressure rises quickly, like compartment syndrome but in bone)
- Pressure forces pus through Volkmann canals (canals connecting the medullary cavity to the periosteal surface) → lifts periosteum off bone
- Subperiosteal abscess forms → strips the bone of its blood supply (periosteum carries nutrient arteries)
- Bone necrosis → dead bone = sequestrum (a piece of dead bone acting as a nidus for ongoing infection — antibiotics can't reach it because there's no blood supply)
- New bone formation around the sequestrum = involucrum (the body tries to wall off the infection)
- Cloacae = holes in the involucrum through which pus drains to the surface (can form a sinus tract)
This explains why chronic osteomyelitis is so hard to treat: the sequestrum is avascular, so no antibiotic can reach it systemically. You MUST surgically remove it.
This is the standard staging system combining anatomic type and host status:
| Stage | Anatomic Type | Description |
|---|---|---|
| I | Medullary | Infection confined to medullary canal |
| II | Superficial | Infection on exposed bone surface (e.g. from contiguous wound) |
| III | Localized | Full-thickness cortical involvement, bone still stable |
| IV | Diffuse | Entire bone segment involved, mechanically unstable |
Host classification:
- A host: Normal immune system, good vascularity
- B host: Compromised (local: scarring, radiation, lymphedema; systemic: DM, renal failure, immunosuppression)
- C host: Treatment worse than disease (e.g. terminal patient)
Why this matters: A Stage IV-B osteomyelitis (diffuse infection in a compromised host) may warrant amputation rather than aggressive limb salvage. The classification guides surgical decision-making.
CBP, ESR, CRP [1]
- CBP: WCC elevated (but may be normal in chronic cases)
- ESR: Elevated; useful for monitoring treatment response (but slow to change, takes weeks)
- CRP: Rises within 6-8 hours of infection onset [4], more responsive than ESR; best for monitoring treatment
X-ray of involved area [1]
- Acute osteomyelitis: X-ray may be NORMAL in first 10-14 days (periosteal reaction takes 7-10 days to appear) [2]
- Subacute/Chronic: Lytic lesions, sclerosis within metaphysis, periosteal reaction, sequestrum visible as dense bone within lytic area
X-ray Can Be False Negative in Acute Osteomyelitis
A normal X-ray does NOT rule out acute osteomyelitis. Periosteal reaction typically takes 7-10 days to develop on plain radiographs. If clinical suspicion is high, proceed to MRI. [2]
MRI: useful to detect any co-existent osteomyelitis (stated in septic arthritis section but applies broadly) [1]
- MRI is the gold standard imaging for osteomyelitis — high sensitivity and specificity
- Shows bone marrow oedema, soft tissue collections, extent of disease
- Helps differentiate from tumour
Blood cultures: Should be sent; positive in ~50% of cases [3]
Acute vs Chronic [1]
Acute:
- Antibiotics – broad spectrum
- When Surgery? → Failed medical treatment; Abscess formation [1]
Chronic:
- Debridement if sequestrum present, abscess formation, failed medical treatment
- Antibiotic [1]
Why the distinction matters: In acute osteomyelitis, the bone is still alive and vascularized → antibiotics can reach the infection. In chronic osteomyelitis, dead bone (sequestrum) cannot be sterilized by antibiotics alone → you must surgically remove the sequestrum and any necrotic tissue, then give antibiotics.
Start with IV antibiotics [1] Monitor:
Why 6-8 weeks? Bone is poorly vascularized compared to soft tissue. Antibiotics achieve lower concentrations in bone, so a prolonged course is needed to eradicate infection. The switch to oral is driven by clinical improvement (less pain, swelling) and biochemical improvement (falling CRP). ESR is slower to normalize and may take weeks even after successful treatment.
Empirical antibiotic choice (from supporting notes): [3]
- Most common organism: Staphylococcus aureus
- Children: Also consider Streptococcus, H. influenzae, Kingella kingae [2]
- Sickle cell disease: Salmonella (classic exam association)
- IV drug users: Pseudomonas
- Empirical: IV Cloxacillin (anti-staphylococcal) or equivalent; adjust based on C/ST results
2. Septic Arthritis
This is the #1 orthopaedic emergency that exams love to test.
Hot, swollen, tender joints [1] For knee, patient usually holds in 30° flexion [1] Fever, systemic upset [1] Gross limitation of motion [1]
Why 30° flexion? The knee joint capsule has maximal volume at ~30° flexion. When the joint is distended with pus/fluid, holding it in this position minimizes intracapsular pressure and therefore minimizes pain. This is the "position of comfort" — same principle applies to other joints (hip held in flexion, abduction, external rotation; shoulder in adduction, internal rotation).
High Yield
A hot, swollen, tender joint with fever and grossly limited ROM is septic arthritis until proven otherwise. This is a surgical emergency — delay leads to cartilage destruction within hours.
Risk factors for septic arthritis: [1]
- Age > 60
- Recent bacteraemia
- Diabetes
- Malignancy on treatment
- Cirrhosis
- Renal disease
- Drug abuse
- Long-term steroid
- Recent dental procedure
Why these risk factors? They all share one or more of:
- Immunosuppression (DM, steroids, malignancy, cirrhosis, renal disease)
- Portal of entry for bacteria (IV drug abuse → direct inoculation; dental procedures → transient bacteraemia)
- Impaired host defences (age > 60 → immunosenescence)
Organisms (from supporting notes): [3]
- Most common: S. aureus (across all ages)
- Young sexually active adults: Neisseria gonorrhoeae (gonococcal septic arthritis — often migratory polyarthralgia with skin lesions before settling in one joint)
- Children: S. aureus, Streptococcus, Kingella kingae
CBP, ESR, CRP [1] X-ray of involved joint(s) [1] MRI: useful to detect any co-existent osteomyelitis — Not routine [1] Joint aspiration: gram stain, culture, crystal, glucose [1]
Joint aspiration is the KEY investigation. Why?
| Parameter | Septic Arthritis | Gout/CPPD | OA/Normal |
|---|---|---|---|
| Appearance | Turbid/purulent | Cloudy | Clear/straw-coloured |
| WBC count | > 50,000/μL (often > 100,000) | 10,000-50,000 | < 2,000 |
| PMN % | > 90% | > 50% | < 25% |
| Gram stain | Often +ve (but can be −ve) | −ve | −ve |
| Crystals | Absent | Needle-shaped (gout)/Rhomboid (CPPD) | Absent |
| Glucose | Very low (bacteria consume glucose) | Normal/slightly low | Normal |
| Culture | +ve (gold standard) | −ve | −ve |
Septic Arthritis vs Gout — Classic Exam Trap
Both present with an acutely painful, swollen, red joint. The joint aspiration with crystal analysis is the discriminator. You can also have BOTH simultaneously (gout + septic arthritis) — so always send for BOTH crystals AND culture. Never assume it's "just gout" without ruling out infection. [1]
X-ray findings in septic arthritis:
- Early: Joint space widening (effusion), periarticular soft tissue swelling
- Late: Joint space narrowing (cartilage destruction), periarticular osteopenia, erosions
- MRI ordered if suspecting concurrent osteomyelitis (especially hip in children)
Surgical treatment:
- Eradicate infection by excisional debridement
- Arthroscopy
- Arthrotomy
- Similar results [1]
Why surgery? Pus in a joint is a closed-space emergency. The proteolytic enzymes released by neutrophils and bacteria destroy articular cartilage rapidly (within hours). You must physically remove the pus to:
- Reduce bacterial load
- Remove destructive enzymes
- Decompress the joint (high intracapsular pressure impairs blood supply to cartilage)
Arthroscopy vs Arthrotomy: Both achieve adequate drainage with similar outcomes. Arthroscopy is less invasive but arthrotomy may be needed for heavily loculated infections or hip joint (where arthroscopy is technically harder).
Antibiotic principles: Same as osteomyelitis — IV initially (empirical broad spectrum, usually covering S. aureus), then step down to oral. Total duration typically 4-6 weeks, guided by clinical response and inflammatory markers.
3. Pyogenic Flexor Tenosynovitis
Pyogenic flexor tenosynovitis: closed space infection of the flexor tendon sheath of the hand. [1] 2.5 to 9.4% of all hand infections. [1]
Why is this important? The flexor tendon sheath is a closed space — like a tube around the tendon. Once bacteria get in, the infection spreads rapidly along the entire sheath. If not treated, the tendon becomes necrotic (avascular necrosis from pressure and direct bacterial damage), and the finger becomes stiff or needs amputation.
Kanavel Cardinal Signs [1]
These are four classic signs — you MUST know all four:
| # | Sign | Explanation |
|---|---|---|
| 1 | Fusiform (sausage-shaped) swelling of the entire finger | The tendon sheath distends uniformly with pus, making the whole finger swollen (not just at one point) |
| 2 | Flexed posture of the involved finger | The finger is held in slight flexion because extension stretches the inflamed sheath and increases pain |
| 3 | Tenderness along the flexor tendon sheath | You can trace tenderness from the base of the finger proximally along the sheath — maximal in the cul-de-sac at the proximal end of the sheath |
| 4 | Pain on passive extension of the finger (most important and earliest sign) | Passive extension stretches the inflamed/infected sheath → pain. This is the most sensitive and specific sign |
High Yield
Kanavel signs: Fusiform swelling, Flexed posture, Tenderness along tendon sheath, Pain on passive extension. Pain on passive extension is the MOST IMPORTANT and EARLIEST sign. [1]
MSSA: up to 75% of positive cultures [1] MRSA: up to 29% of all cases [1] Staph. epidermidis [1] Streptococcus species [1] Gram -ve and anaerobes [1] Culture -ve: 20% to 68% [1]
Key point: A large proportion of cultures are negative (20-68%), so you must treat empirically based on clinical diagnosis. Don't wait for culture results.
Prompt clinical diagnosis [1] Empirical antibiotics covering Staphylococcus and Streptococcus species [1] Antibiotics should cover gram -ve rods and anaerobes in case of immunocompromised patients [1]
Non-operative treatment:
Indicated when early presentation, within 48 hours after injury [1] Antibiotic [1] Examine the affected hand frequently [1] No improvement after 24 to 48 hours → surgery is indicated [1]
Operative treatment:
The zig-zag incision (Bruner incision) avoids creating a scar that contracts across flexion creases, which would limit finger motion.
Why these three? All impair wound healing and immune function:
- DM: Hyperglycaemia impairs neutrophil function, poor vascularity (microvascular disease)
- Renal failure: Uraemia impairs immune function
- PVD: Poor blood supply → antibiotics can't reach tissue, tissue can't mount immune response
Part 2: Necrotizing Fasciitis (NF) and Gas Gangrene
4. Necrotizing Fasciitis
This is the life-threatening infection that the lecture emphasizes most.
Involves superficial fascia [1] Breakage of skin such as lacerations, insect bite, needle puncture [1] Significant demands on health care system [1]
Layers of soft tissue and associated disease (Slide 37): [1]
- Skin → cellulitis/erysipelas
- Subcutaneous fat → abscess
- Superficial fascia → NECROTIZING FASCIITIS ← this is the key layer
- Deep fascia
- Muscle → myositis/gas gangrene
Understanding the layer is critical: NF spreads along the fascial plane, which is poorly vascularized. The infection tracks rapidly along fascia while the overlying skin may initially look deceptively normal — this is why clinical diagnosis is so challenging and why "pain out of proportion to examination findings" is the hallmark.
Type I NF (polymicrobial): Mixed aerobic + anaerobic organisms, often in DM/immunocompromised patients, typically trunk/perineum (Fournier gangrene)
Type II NF (monomicrobial): Streptococcus pyogenes (GAS) — can occur in young healthy individuals after minor trauma. GAS produces exotoxins (superantigens) → toxic shock syndrome
Vibrio vulnificus: Extremely important in Hong Kong context — associated with handling raw seafood or seawater exposure. Causes rapidly progressive NF, especially in patients with liver disease (cirrhosis). Very high mortality.
HK-Specific High Yield
Vibrio vulnificus NF: Think of a patient with liver cirrhosis who has a minor cut while handling raw seafood. Rapid progression, high mortality. This is a locally important organism in HK exams. [1]
Risk factors for developing necrotizing fasciitis: [1]
- Diabetes mellitus, present in 57% of patients
- Alcohol abuse
- Renal insufficiency
- Liver diseases
- Immunocompromised
- Exposure to NSAIDs
NSAIDs:
- Inhibit prostaglandins which alter the inflammatory response to microorganisms
- Develop acute renal failure [1]
Why NSAIDs are a risk factor — this is a favourite exam question:
- NSAIDs block COX → reduce prostaglandin synthesis → prostaglandins normally promote vasodilation and inflammatory cell recruitment → therefore NSAIDs blunt the early warning signs of infection (mask pain, reduce fever)
- NSAIDs can cause AKI (via afferent arteriole vasoconstriction) → renal impairment further impairs immune function
- The masking of symptoms leads to delayed diagnosis, which is the biggest killer in NF
- Bacteria enter through skin breach
- Infection tracks along superficial fascia (relatively avascular plane)
- Bacterial toxins and enzymes cause thrombosis of perforating vessels → ischaemia of overlying skin
- Tissue necrosis ensues → more substrate for bacteria → vicious cycle
- Systemic toxin release → SIRS → septic shock → multi-organ failure
History of minor trauma to extremities [1] Disproportionate pain [1] Generalized erythematous rash and toxic appearance [1] Low platelet count [1] Bedside procedure:
- Lack of bleeding, foul smelling dishwater pus, minimal tissue resistance to finger dissection [1]
"Disproportionate pain" is THE key clinical feature — the patient reports excruciating pain, but on examination the skin may only show mild erythema or swelling. This mismatch (pain >> clinical findings) should immediately raise your suspicion for NF.
"Finger probe test" (bedside procedure): At the bedside, you can make a small incision and probe the subcutaneous tissue with your finger. In NF, there is minimal resistance to blunt dissection along the fascial plane (because the fascia is necrotic and melting), and you see dishwater-grey, foul-smelling fluid rather than frank pus. There is also lack of bleeding (because vessels are thrombosed).
High Yield Clinical Diagnosis of NF
Pain out of proportion to clinical signs + dishwater pus + minimal tissue resistance to finger dissection + lack of bleeding = NF until proven otherwise. Do NOT wait for imaging — this is a clinical diagnosis. [1]
Clinical stages of necrotizing fasciitis: [1]
| Stage | Features |
|---|---|
| Stage 1 (Early) | Tenderness, Erythema, Oedema, Warm skin, Fever |
| Stage 2 (Intermediate) | Blisters and bullae formation, Hyposensitivity, Tissue crepitation |
| Stage 3 (Late) | Tissue necrosis, Anaesthesia, Haemorrhagic bullae |
Why the progression?
- Stage 1: Inflammatory response → looks like cellulitis (this is why NF is misdiagnosed as cellulitis early on)
- Stage 2: Vessel thrombosis → skin ischaemia → blistering. Loss of sensation = nerve ischaemia (hyposensitivity). Gas-producing organisms → crepitus
- Stage 3: Full thickness tissue necrosis → skin is dead (anaesthetic), haemorrhagic bullae (blood-filled blisters from necrotic vessels)
Differentiating NF from Cellulitis
Stage 1 NF looks identical to cellulitis! The key discriminators are: pain disproportionate to findings, rapid progression over hours (not days), failure to respond to IV antibiotics, systemic toxicity (tachycardia, hypotension). If in doubt, explore surgically — the cost of a negative exploration is low compared to a missed NF diagnosis.
Amputation: [1] HK figure: radical debridements (amputations and disarticulations) were performed in 46% of 24 patients [1] Mortality ranges from 20 to 75% [1]
These are sobering numbers. Nearly half of patients in the cited HK series required amputation, and up to three-quarters can die. This is why the lecture emphasizes early diagnosis and early radical debridement.
Early diagnosis [1] Broad spectrum antibiotics [1] Early radical debridement [1]
"Radical" means radical. You must excise ALL necrotic tissue back to healthy, bleeding tissue. This may mean large soft tissue defects. Better to have a large wound than a dead patient.
Antibiotics: Broad spectrum covering GAS, staphylococci, gram-negatives, and anaerobes. Typical regimen: Piperacillin-tazobactam + Clindamycin (clindamycin specifically inhibits toxin production by GAS).
Surgical debridement must not be delayed for imaging. If clinical suspicion is high, take the patient to theatre. Re-look debridement (planned second-look operation in 24-48 hours) is often needed because infection may have progressed.
| Favours Limb Salvage | Favours Amputation |
|---|---|
| Early presentation | Late presentation |
| Limited fascial involvement | Extensive fascial necrosis |
| Healthy host (A host) | Compromised host (B/C host) |
| Viable distal tissue | Non-viable distal tissue |
| Single organism | Polymicrobial with anaerobes |
| No systemic sepsis | Refractory septic shock |
5. Gas Gangrene
Farmer, 56: Complained of left calf swelling and pain for 1 day after left calf surgery. Fever +ve. P/E showed wound necrosis. Crepitus +ve on palpation. [1]
Orthopaedic emergency [1] Most commonly caused by C. perfringens [1] Rapid clinical onset, crepitus is characteristic [1] Sudden onset of pain, rapidly progressive soft tissue infection, development of blisters containing foul smelling brownish liquid with gas bubbles, soft tissue induration and discoloration may also be present [1]
Clostridium perfringens is a gram-positive, anaerobic, spore-forming rod that produces alpha-toxin (lecithinase/phospholipase C), which destroys cell membranes → massive tissue necrosis and gas production.
Why farmers? C. perfringens is ubiquitous in soil. Agricultural injuries that contaminate wounds with soil → inoculation of spores → anaerobic environment in necrotic/traumatized tissue → germination and toxin production.
| Feature | Why |
|---|---|
| Crepitus on palpation | Gas produced by Clostridium metabolism (fermentation of sugars in tissue) |
| Rapid onset (hours) | Alpha-toxin causes explosive tissue destruction |
| Pain out of proportion | Tissue necrosis and gas dissection |
| Foul-smelling brownish fluid | Products of tissue liquefaction |
| Bronze/dark discoloration of skin | Haemolysis and tissue necrosis |
| Systemic toxicity (shock, organ failure) | Toxinaemia |
Important X-ray finding: Linear streaks of gas within soft tissues [3]
Gas Gangrene vs NF
Both can have crepitus and pain out of proportion. Key differences: Gas gangrene involves muscle (myonecrosis), onset is even more rapid (hours, not days), X-ray shows gas in muscle planes, caused by Clostridia. NF involves fascia but initially spares muscle. In practice, there can be overlap, and both require emergency debridement.
CBC finding: Unlike most infections, WCC may NOT be elevated in gas gangrene because C. perfringens toxins inhibit the inflammatory response and suppress neutrophil migration. [3]
Early aggressive debridement +/- amputation [1] Antibiotic therapy:
Why Augmentin + Flagyl?
- Augmentin (amoxicillin/clavulanate): Covers gram-positives including some Clostridia, plus some gram-negatives
- Flagyl (metronidazole): Excellent anaerobic cover, specifically targets Clostridia
- Alternative: High-dose IV Penicillin (Clostridium is exquisitely sensitive) + Clindamycin (inhibits toxin production)
Hyperbaric oxygen: Sometimes used adjunctively (oxygen is toxic to obligate anaerobes like Clostridia), but should NEVER delay surgical debridement.
What we have not discussed: Cellulitis, Abscess, Lymphangitis, DM foot ulcer, Implant-related infection [1]
These are important but covered in other lectures. Brief connections:
- Cellulitis: Superficial skin/subcutaneous infection, usually Streptococcus or S. aureus. Treated with antibiotics. Key differentiation from NF: cellulitis responds to antibiotics, pain is proportionate to findings, no crepitus, no systemic toxicity [5]
- DM foot ulcer: Combines neuropathy (doesn't feel injury), PVD (poor healing), hyperglycaemia (impaired immunity). Can lead to osteomyelitis, NF, gas gangrene
- Implant-related infection: Biofilm formation on metal makes eradication very difficult; often requires implant removal
Musculoskeletal infections are very common in daily orthopaedic practice Severity from mild to life threatening Early recognition and high suspicion are important for life-threatening infections Empirical antibiotics and early surgical intervention are necessary in case of life-threatening conditions such as septic arthritis, NF and gas gangrene [1]
Integrated Clinical Approach Summary
| Component | What to Ask | Why |
|---|---|---|
| Onset and duration | Acute vs chronic | Guides classification and management |
| Mechanism of injury | Cut, puncture, bite, surgery | Identifies organism, portal of entry |
| Pain character | Disproportionate? Progressive? | NF red flag |
| Systemic symptoms | Fever, chills, rigors, malaise | Indicates systemic spread |
| Risk factors | DM, liver disease, renal disease, immunosuppression, NSAID use, alcohol | Identifies high-risk patients |
| Exposure | Seafood handling, soil contact, farm work | Vibrio, Clostridium |
| Joint symptoms | Swelling, inability to move | Septic arthritis |
| Hand symptoms | Finger swelling after puncture | Flexor tenosynovitis |
| Finding | Significance |
|---|---|
| Temperature | Fever = systemic infection |
| Joint: hot, swollen, ROM | Septic arthritis |
| Kanavel signs (4) | Flexor tenosynovitis |
| Crepitus | Gas gangrene or NF with gas-forming organisms |
| Skin bullae/haemorrhagic bullae | Late NF |
| Disproportionate pain | NF/gas gangrene |
| Dishwater pus on incision | NF |
| Sinus tract | Chronic osteomyelitis |
| Condition | Bloods | Imaging | Definitive |
|---|---|---|---|
| Osteomyelitis | CBP, ESR, CRP, Blood C/ST | X-ray (may be normal early), MRI (gold standard) | Bone biopsy/culture |
| Septic arthritis | CBP, ESR, CRP, Blood C/ST | X-ray, MRI if suspecting osteomyelitis | Joint aspiration (Gram stain, culture, crystal, glucose) |
| Flexor tenosynovitis | CBP, ESR, CRP | Usually clinical diagnosis | Intraoperative culture |
| NF | CBP (low platelets), ESR, CRP | X-ray (gas?), CT (fascial thickening, gas) — but do NOT delay surgery | Surgical exploration + tissue culture |
| Gas gangrene | CBP (may show NO leukocytosis), blood C/ST | X-ray (gas in muscle), CT | Surgical exploration + tissue culture |
| Condition | Antibiotics | Surgery | Duration |
|---|---|---|---|
| Acute osteomyelitis | IV broad spectrum → oral when improving | Only if abscess/failed medical Rx | 6-8 weeks total |
| Chronic osteomyelitis | IV → oral | Debridement of sequestrum | 6-8 weeks (may be longer) |
| Septic arthritis | IV broad spectrum → oral | Arthroscopy or arthrotomy (drainage) | 4-6 weeks |
| Flexor tenosynovitis (early, < 48h) | IV covering Staph/Strep | Surgery if no improvement in 24-48h | Until resolved |
| Flexor tenosynovitis (late, > 48h) | IV covering Staph/Strep | Surgical drainage + irrigation | Until resolved |
| Necrotizing fasciitis | IV broad spectrum (cover GAS, gram-neg, anaerobes) | Emergency radical debridement | Until eradication |
| Gas gangrene | Augmentin + Flagyl (or Penicillin + Clindamycin) | Emergency debridement +/- amputation + ICU | Until eradication |
Comparison Tables for Exam
| Feature | Pyogenic Osteomyelitis | TB Spine (Pott's Disease) |
|---|---|---|
| Onset | Acute | Insidious |
| X-ray disc space | Narrowed (disc destruction early) | Relatively preserved (disc is avascular, TB is slow) |
| Typical spinal level | Any | Thoracic (most common) |
| Organism | S. aureus (most common) | Mycobacterium tuberculosis |
| Vertebral body | Single level | Multiple levels, skip lesions possible |
| Abscess | Paravertebral | Cold abscess (Psoas abscess in lumbar TB) |
| Feature | Septic Arthritis | Gout |
|---|---|---|
| Onset | Acute | Acute |
| Fever | Usually present | May be present |
| WBC count | > 50,000 (often > 100,000) | 10,000-50,000 |
| Crystals | Absent | MSU: Needle-shaped, negatively birefringent |
| Culture | Often positive | Negative |
| Risk factors | DM, immunosuppression, recent bacteraemia | Alcohol, high-purine diet, CKD |
| Treatment | Abx + surgical drainage | Colchicine/NSAIDs/steroids |
Common Exam Traps and Discriminators
-
Normal X-ray ≠ no osteomyelitis: Changes take 7-10 days. MRI is far more sensitive in the acute setting.
-
Septic arthritis vs gout: Both cause acute monoarthritis. The discriminator is joint aspiration — always send for crystals AND culture. They can coexist.
-
NF vs cellulitis: Stage 1 NF mimics cellulitis. Key discriminators: pain out of proportion, rapid progression, systemic toxicity, failure to respond to antibiotics. When in doubt, surgical exploration.
-
Gas gangrene: no leukocytosis: Unlike most infections, WCC may be normal or low because C. perfringens toxins inhibit inflammatory response. Don't be falsely reassured by a normal WCC.
-
NSAIDs and NF: NSAIDs mask the inflammatory response AND can cause AKI → double trouble. This is a favourite MCQ.
-
Kanavel signs: Exams often list only 3 of the 4 and ask you to identify the missing one. "Pain on passive extension" is the most commonly asked and most specific sign.
-
Flexor tenosynovitis: culture-negative rate is high (20-68%) — clinical diagnosis is paramount, don't wait for culture to treat.
-
Chronic osteomyelitis: surgery is almost always needed because sequestrum cannot be sterilized by antibiotics (avascular dead bone).
-
Vibrio vulnificus: Think liver disease + seafood/seawater exposure. Extremely rapid progression. High yield for HK exams.
-
Hip septic arthritis in children: The hip joint capsule inserts DISTAL to the epiphyseal plate → metaphyseal osteomyelitis can cause septic arthritis. This is a unique anatomical vulnerability.
After thorough review of the indexed past paper contexts, I was unable to identify specific past paper questions that directly and explicitly test GC 237 MSK infection content (e.g. questions on osteomyelitis management, Kanavel signs, NF staging, gas gangrene organisms). The available past paper excerpts visible in the indexed context do not contain question stems on these topics.
However, related examination themes appear:
- 2023 Fourth Summative SAQ Q3 [6]: A patient with post-cholecystectomy wound infection — asks about clinical signs of hypermetabolism and treatment. While this is about surgical wound infection rather than MSK infection specifically, the concept of surgical infection management overlaps.
If you encounter past paper questions on MSK infection in your revision, key areas that would be tested include: Kanavel signs, differentiating septic arthritis from gout (joint aspiration findings), NF clinical staging and management, osteomyelitis classification, and antibiotic duration.
High Yield Summary
Osteomyelitis: Infection of bone; acute ( < 2 weeks), subacute ( < 3 months), chronic ( > 3 months). Common in children at metaphysis. Pathology: suppuration → sequestrum → involucrum. Ix: CBP/ESR/CRP, X-ray (may be normal early — use MRI), blood C/ST. Mx: IV antibiotics 6-8 weeks; surgery if abscess/sequestrum/failed medical Rx.
Septic Arthritis: Orthopaedic emergency. Hot, swollen, tender joint held in position of comfort (knee 30° flexion). Joint aspiration is KEY (Gram stain, culture, crystal, glucose). Mx: IV antibiotics + surgical drainage (arthroscopy/arthrotomy).
Pyogenic Flexor Tenosynovitis: Closed space infection of flexor sheath. Kanavel signs: fusiform swelling, flexed posture, tenderness along sheath, pain on passive extension. Organisms: MSSA (75%), MRSA (29%), culture-negative 20-68%. Non-op if early ( < 48h) + improving; otherwise surgical drainage. Risk factors for amputation: DM, renal failure, PVD.
Necrotizing Fasciitis: Infection of superficial fascia. Organisms: GAS, Vibrio (HK!). Risk factors: DM (57%), alcohol, renal/liver disease, immunocompromised, NSAIDs. Clinical diagnosis: disproportionate pain, dishwater pus, lack of bleeding, finger dissection through necrotic tissue. Stages: 1 (looks like cellulitis) → 2 (blisters, crepitus) → 3 (necrosis, anaesthesia). Mortality 20-75%. Mx: EARLY radical debridement + broad spectrum antibiotics.
Gas Gangrene: Caused by C. perfringens. Orthopaedic emergency. Crepitus, rapid onset, foul brownish fluid. WCC may be NORMAL. Mx: Aggressive debridement ± amputation, Augmentin + Flagyl, ICU support.
Unifying principle: Early recognition + empirical antibiotics + early surgery = save limbs and lives.
Active Recall - Musculoskeletal Infection
[1] GC 237. Musculoskeletal infection [Updated in 2025].pdf (all pages/slides) [2] Adrian Lui Pediatrics Notes.pdf (p447 — Osteomyelitis, paediatric MSK infections) [3] Maksim Surgery Notes.pdf (p275 — Gas gangrene, osteomyelitis, septic arthritis, NF comparison table, pyogenic vs TB spine) [4] Ortho and Trauma - Spine.pdf (p21 — CRP rises 6-8 hours after onset) [5] Ryan Ho Rheumatology.pdf (p135 — Cellulitis, erysipelas, skin abscess) [6] 2023 Fourth Summative SAQ.pdf (p4 — Q3 on surgical infection and hypermetabolism)
GC236 Common Shoulder Problems
Common shoulder problems encompass a group of frequently encountered musculoskeletal conditions—including rotator cuff injuries, impingement syndrome, adhesive capsulitis, and instability—that cause pain, stiffness, and functional limitation of the shoulder joint.
GC238 Rare Disease Genetic Testing For Precision Medicine
Genetic testing in rare diseases that identifies specific pathogenic variants to guide individualized diagnosis, management, and targeted therapeutic interventions through precision medicine approaches.