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]

The lecture shows a diagram of pathogenesis. The sequence:

1. Bacteria seed the metaphysis via haematogenous spread (most common), direct inoculation (open fracture, surgery), or contiguous spread (adjacent soft tissue infection)
2. Suppuration → increased intraosseous pressure (bone is a rigid compartment, so pressure rises quickly, like compartment syndrome but in bone)
3. Pressure forces pus through Volkmann canals (canals connecting the medullary cavity to the periosteal surface) → lifts periosteum off bone
4. Subperiosteal abscess forms → strips the bone of its blood supply (periosteum carries nutrient arteries)
5. 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)
6. New bone formation around the sequestrum = involucrum (the body tries to wall off the infection)
7. Cloacae = holes in the involucrum through which pus drains to the surface (can form a sinus tract)

What the pathogenesis panels show: metaphyseal seeding → subperiosteal abscess → central sequestrum wrapped by involucrum with a draining sinus/cloaca — chronic OM is a plumbing problem until dead bone is removed. ^[1]

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:

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

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:

• Clinical signs such as pain, swelling, range of motion
• Biochemical markers including ESR, CRP Change to oral form if showing improvement ^[1] Total 6-8 weeks, depends on clinical condition ^[1]

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

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).

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?

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)

Antibiotic ^[1] Surgical management ^[1]

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:

1. Reduce bacterial load
2. Remove destructive enzymes
3. Decompress the joint (high intracapsular pressure impairs blood supply to cartilage)

This arthroscopic staging system guides whether arthroscopic washout alone is sufficient or open arthrotomy is needed:

Stages I–II generally respond to arthroscopic washout; Stages III–IV may require arthrotomy or repeated procedures.

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.

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.

Mechanism of tendon ischaemia (Slide 25): The flexor tendon receives its blood supply via vincular branches of the digital arteries. When pus accumulates within the synovial sheath, the increased pressure compresses these vincular branches → tendon ischaemia → necrosis. This is why prompt drainage is essential to preserve tendon viability. ^[1]

Haematogenous ^[1] Direct inoculation:

• Laceration
• Puncture wound
• Bites ^[1]

Most cases are from direct inoculation (e.g. thorn prick, knife cut, animal/human bite). Human bites over MCP joints ("fight bite") are particularly dangerous.

Kanavel Cardinal Signs ^[1]

These are four classic signs — you MUST know all four:

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:

Surgical drainage and irrigation ^[1] Zig-zag incision ^[1]

The zig-zag incision (Bruner incision) avoids creating a scar that contracts across flexion creases, which would limit finger motion.

Key decision point: The number of Kanavel signs present (1–2 vs 3–4) determines initial operative vs non-operative management.

DM ^[1] Renal failure ^[1] Peripheral vascular disease ^[1]

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

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]

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.

Note: The slide diagram (Slide 37) places NF at the deep fascia layer. The superficial fatty fascia layer corresponds to cellulitis. This distinction explains why NF is deep to clinical inspection and why skin signs lag behind fascial destruction. ^[1]

Group A Streptococcus ^[1] Vibrio species ^[1]

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.

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:

1. 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)
2. NSAIDs can cause AKI (via afferent arteriole vasoconstriction) → renal impairment further impairs immune function
3. The masking of symptoms leads to delayed diagnosis, which is the biggest killer in NF

1. Bacteria enter through skin breach
2. Infection tracks along superficial fascia (relatively avascular plane)
3. Bacterial toxins and enzymes cause thrombosis of perforating vessels → ischaemia of overlying skin
4. Tissue necrosis ensues → more substrate for bacteria → vicious cycle
5. 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).

Clinical stages of necrotizing fasciitis: ^[1]

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)

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.

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.

Important X-ray finding: Linear streaks of gas within soft tissues ^[3]

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:

• Empirical antibiotic should cover Clostridia and gram +ve cocci
• Augmentin + Flagyl ^[1] Intensive care support ^[1]

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.