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Here are complete model answers for both examination papers:

EXAM 04 - Ward Assessment Examination

Bone Tumour, Polytrauma, Mass Casualty, Amputation


Q1. Neoplasm (3.5 marks)

a) Define neoplasm (1.0)
A neoplasm is an abnormal mass of tissue whose growth is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change (Willis definition). It is characterised by excessive, uncontrolled proliferation of cells.

b) Differentiate between benign and malignant neoplasm (1.5)
FeatureBenignMalignant
Growth rateSlowRapid
CapsuleWell encapsulatedNo capsule / invasive
BorderWell definedIll defined
DifferentiationWell differentiatedPoorly differentiated
MitosesRare/absentFrequent, atypical
InvasionNo local invasionLocally invasive
MetastasisDoes not metastasizeMetastasizes
RecurrenceRare after excisionCommon
Effect on hostLocal pressure effectsCachexia, systemic effects

c) Common sites for primary and secondary bone tumour (1.0)
Primary bone tumours:
  • Osteosarcoma: distal femur > proximal tibia > proximal humerus (metaphysis of long bones)
  • Ewing sarcoma: diaphysis of long bones (femur, tibia, humerus); also flat bones (pelvis, ribs)
  • Giant cell tumour (GCT): epiphysis of long bones around the knee, distal radius, proximal humerus
Secondary (metastatic) bone tumours:
  • Common primaries: Breast, Bronchus (lung), Kidney, Thyroid, Prostate (mnemonic: Bad Boys Kick Their Parents)
  • Common sites of metastases: vertebrae, pelvis, ribs, skull, proximal femur

Q2. Classification and Bone Tumours (3.5 marks)

a) Classify bone tumours (1.5)
By tissue of origin:
TissueBenignMalignant
Bone-formingOsteoid osteoma, OsteoblastomaOsteosarcoma
Cartilage-formingOsteochondroma, Enchondroma, ChondroblastomaChondrosarcoma
Fibrous tissueNon-ossifying fibroma, Fibrous dysplasiaFibrosarcoma, MFH
VascularHaemangiomaAngiosarcoma
Marrow cells-Myeloma, Ewing sarcoma, Lymphoma
Unknown originGiant cell tumour, Simple bone cyst, ABC-
Notochordal-Chordoma
Secondary/metastatic: spread from breast, lung, kidney, thyroid, prostate

b) Differentiate between Osteosarcoma and Ewing sarcoma (1.0)
FeatureOsteosarcomaEwing Sarcoma
Age10-20 years (2nd decade)5-15 years (1st-2nd decade)
SiteMetaphysis of long bones (distal femur, proximal tibia)Diaphysis of long bones; flat bones (pelvis, ribs)
X-ray appearanceSunray/spiculation + Codman's triangle; mixed sclerotic/lyticOnion peel layering; permeative lytic
HistologyMalignant osteoid-producing cellsSmall round blue cells
GeneticsComplex karyotypet(11;22) translocation - EWS-FLI1 fusion
Soft tissue massVariableVery common and prominent
TreatmentSurgery + chemotherapy (no radiation)Surgery/radiation + chemotherapy
Prognosis~65-70% 5-year survival~60-65% 5-year survival

c) Radiological findings of Ewing sarcoma (1.0)
  1. Onion peel (onion skin) periosteal reaction - most characteristic: multiple parallel layers of periosteal new bone
  2. Permeative / moth-eaten lytic lesion in the diaphysis
  3. Codman's triangle - elevation of the periosteum at the edge of the tumour (also seen in osteosarcoma)
  4. Soft tissue mass - often large, seen on MRI
  5. "Hair on end" periosteal reaction - spiculated pattern
  6. Bone scan: increased uptake; MRI shows extensive medullary involvement beyond plain film appearance

Q3. Case Scenario - Osteosarcoma (3.5 marks)

20-year-old man, painful/tender/hard swelling in left knee, X-ray shows sun ray appearance in lower end of femur
a) Most probable diagnosis (0.5)
Osteosarcoma (conventional intramedullary osteosarcoma of the distal femur)
The combination of: young male + metaphyseal location (distal femur) + hard swelling + sun ray appearance on X-ray is classic for osteosarcoma.

b) Approach to diagnose such a case (1.5)
History: Duration, nature of pain (worse at night), swelling, systemic symptoms (fever, weight loss), trauma
Examination: Site, size, consistency (hard/bony), tenderness, skin changes, regional lymph nodes, movements of knee joint, neurovascular status
Investigations:
Radiological:
  • Plain X-ray (AP & lateral): sun ray spiculation, Codman's triangle, mixed sclerotic-lytic lesion
  • MRI of affected limb (extent of tumour, neurovascular involvement, skip lesions)
  • CT chest (lung metastases - most common site)
  • Bone scan / PET-CT (systemic staging, skip lesions)
Laboratory:
  • FBC, ESR, CRP
  • Serum ALP (elevated in osteosarcoma)
  • LDH (elevated; poor prognostic marker)
  • Serum calcium, phosphate
Histopathological (definitive):
  • Core needle biopsy (image-guided; performed by surgeon who will do definitive surgery, through the planned incision tract)
  • Open biopsy if needle biopsy inconclusive
  • Biopsy confirms malignant osteoid-producing cells

c) Treatment plan for osteosarcoma (1.5)
Multidisciplinary approach (orthopaedic oncologist + medical oncologist + radiation oncologist + pathologist + physiotherapist)
1. Neo-adjuvant (pre-operative) chemotherapy:
  • MAP regimen: Methotrexate (high-dose) + Adriamycin (doxorubicin) + Cisplatin
  • Given for 3-4 months; shrinks tumour, treats micrometastases, assesses chemosensitivity
2. Surgery (local control):
  • Limb salvage surgery (preferred when wide clear margins achievable, no neurovascular invasion, good chemotherapy response)
    • Wide excision of tumour with surrounding cuff of normal tissue
    • Reconstruction: endoprosthesis (modular tumour prosthesis), allograft, allograft-prosthesis composite
  • Amputation - if limb salvage not feasible (neurovascular invasion, infection, poor response, pathological fracture with contamination)
3. Adjuvant (post-operative) chemotherapy:
  • Same MAP regimen continued for total 6-9 months
  • Histological response to neoadjuvant chemo assessed (>90% necrosis = good prognosis - Huvos grading)
4. Radiotherapy: not routinely used in osteosarcoma (radio-resistant tumour)
5. Follow-up: regular clinical + radiological review for recurrence and metastases

Q4. Mass Casualty / Polytrauma (3.5 marks)

30 patients brought to casualty after a bus accident
a) Categorise patients for management (triage) (1.5)
Triage = sorting patients by severity to allocate resources optimally. Uses START (Simple Triage and Rapid Treatment) or SIEVE and SORT system.
Four categories (METHANE / Colour coding):
CategoryColourDescriptionAction
P1 - ImmediateRedLife-threatening but salvageable (airway obstruction, tension pneumothorax, major haemorrhage)Treat immediately
P2 - UrgentYellowSerious but stable; can wait 1-2 hours (closed fractures, burns <20%, abdominal injury)Treat within 1-2 hours
P3 - DelayedGreenMinor injuries; walking woundedCan wait (self-care)
P4 - Expectant/DeadBlackDead OR unsurvivable injuries given available resourcesExpectant / morgue
Triage sieve criteria (primary triage):
  1. Can they walk? (Yes = Green)
  2. Breathing? (No = Black after airway manoeuvre)
  3. Respiratory rate (>30 or <10 = Red)
  4. Capillary refill >2 seconds OR radial pulse absent = Red
  5. Otherwise = Yellow

b) Indications of amputation (1.0)
Mnemonic: TIMID
  1. Trauma - mangled limb (MESS score ≥7), traumatic amputation, blast injury with non-reconstructible vascular injury
  2. Infection - gas gangrene (clostridial myonecrosis), severe osteomyelitis unresponsive to treatment, necrotising fasciitis
  3. Malignancy - primary bone tumours where limb salvage not feasible; recurrent tumours
  4. Ischaemia - peripheral vascular disease with gangrene; diabetic foot with non-healing ulcer
  5. Deformity/disability - congenital limb deformity, failed reconstructive procedure where amputation + prosthesis gives better function
Others: severe frostbite, chronic intractable pain, extensive burns

c) Complications of amputation of a limb (1.0)
Early:
  • Haemorrhage (primary or reactionary)
  • Infection / wound breakdown / necrosis of flap
  • DVT / pulmonary embolism
  • Gas gangrene
Late:
  1. Phantom limb pain - pain perceived in amputated limb (most common late complication)
  2. Stump neuroma - painful nodule from regenerating nerve
  3. Skin problems - dermatitis, pressure sores, ulceration over stump
  4. Bone problems - bony spur/exostosis, osteomyelitis
  5. Joint contracture - e.g., hip flexion contracture after AK amputation
  6. Psychological - depression, body image issues
  7. Prosthesis problems - ill-fitting prosthesis causing skin breakdown
  8. Causalgia / reflex sympathetic dystrophy
  9. Recurrence of tumour at stump margin (if amputation for malignancy)

Q5. Polytrauma (3.5 marks)

a) Define polytrauma (0.5)
Polytrauma is defined as the simultaneous injury to multiple body regions or organ systems, where at least one injury or the combination of injuries is life-threatening. It is defined by an Injury Severity Score (ISS) ≥16.
The "Berlin definition" (2014) further requires: ISS ≥16 PLUS at least one of: hypotension (SBP ≤90), GCS ≤8, acidosis (BE ≤-6), coagulopathy (INR ≥1.4 or aPTT ≥40s), age ≥70 years.

b) Approach to manage polytrauma (2.0)
Follow ATLS (Advanced Trauma Life Support) protocol:
Primary Survey - ABCDE (simultaneously treat life threats as found):
  • A - Airway with C-spine control: Clear airway (chin lift, jaw thrust), suction, OPA/NPA, intubation if needed; cervical spine immobilisation
  • B - Breathing and ventilation: Inspect, palpate, percuss, auscultate; treat tension pneumothorax (needle decompression), open chest wound (3-sided occlusive dressing), haemothorax (chest drain)
  • C - Circulation + haemorrhage control: IV access ×2 large bore, fluid resuscitation (2L crystalloid then blood), direct pressure to external wounds, pelvic binder for suspected pelvic fracture, tourniquet for limb haemorrhage
  • D - Disability (neurological status): GCS, pupils, limb movements, blood glucose
  • E - Exposure + environment control: Fully undress, log roll to examine back, maintain temperature (warm blankets, warm IV fluids)
Resuscitation: concurrent with primary survey - O2, 2 large IV cannulae, blood samples (FBC, U&E, LFT, clotting, group & cross match, ABG), urinary catheter (monitor urine output)
Secondary Survey (head-to-toe examination):
  • Detailed history (AMPLE: Allergies, Medications, Past history, Last meal, Events)
  • Systematic examination of all body regions
  • Imaging: FAST scan, CT head/chest/abdomen/pelvis (pan-CT "trauma scan")
  • X-rays: CXR, pelvis AP, lateral C-spine
Definitive care:
  • Damage control surgery (haemostasis first, delayed definitive repair)
  • ICU/HDU monitoring
  • Orthopaedic injury management (splinting, temporary external fixation)
  • Multidisciplinary team: trauma surgeon, neurosurgeon, orthopaedic surgeon, anaesthetist

c) Components of Glasgow Coma Scale (1.0)
ComponentResponseScore
Eye Opening (E)Spontaneous4
To voice/command3
To pain2
None1
Verbal Response (V)Orientated5
Confused4
Inappropriate words3
Incomprehensible sounds2
None1
Motor Response (M)Obeys commands6
Localises pain5
Withdrawal from pain4
Abnormal flexion (decorticate)3
Extension (decerebrate)2
None1
  • Total: 3-15 (minimum 3, maximum 15)
  • Normal = 15; Severe TBI = ≤8; Moderate = 9-12; Mild = 13-15
  • GCS ≤8 = indication for intubation (cannot protect airway)

Q6. Short Notes (3.5 marks)

a) GCT - Giant Cell Tumour of bone (1.75)
Definition: Locally aggressive primary bone tumour composed of large osteoclast-like multinucleated giant cells on a background of spindle-shaped mononuclear stromal cells.
Epidemiology:
  • Age: 20-45 years (after physeal closure)
  • Females slightly more common
  • Rare before skeletal maturity
Sites: Epiphysis of long bones - distal femur (most common) > proximal tibia > distal radius > proximal humerus; around the knee is the most frequent location
Clinical features:
  • Pain and swelling around the joint
  • Restricted joint movement
  • Pathological fracture in ~10%
  • "Benign" pulmonary metastases occur in ~3%
Radiological features:
  • Epiphyseal eccentric lytic lesion extending to subarticular bone
  • "Soap bubble" appearance (trabeculation within lytic area)
  • No periosteal reaction (unless fractured)
  • Campanacci grading: Grade I (well defined), Grade II (thin cortex), Grade III (soft tissue extension)
Histology: Uniform distribution of osteoclast-like giant cells throughout the stroma; no malignant osteoid
Treatment:
  • Intralesional curettage + high speed burr + bone graft/cement (with or without phenol/liquid nitrogen as adjuvant) - standard treatment; 15-25% local recurrence
  • Wide excision for Grade III or recurrent cases (distal radius: excision + fibula autograft reconstruction)
  • Denosumab (anti-RANK-L antibody) - for unresectable/recurrent GCT, or pre-operatively to reduce tumour size
  • Radiotherapy - reserved for unresectable sites (risk of malignant transformation)

b) Osteoid Osteoma (1.75)
Definition: A benign bone-forming tumour characterised by a small (<2 cm) vascular nidus of woven bone with surrounding dense reactive cortical bone sclerosis.
Epidemiology:
  • Age: 10-30 years; males > females (3:1)
  • Accounts for ~10% of all benign bone tumours
Sites: Proximal femur (most common - neck of femur), tibia, humerus, spine (posterior elements - may cause painful scoliosis)
Clinical features:
  • Characteristic night pain - worse at night, dramatically relieved by aspirin/NSAIDs (prostaglandin-mediated pain from the nidus)
  • Localised tenderness
  • If near joint: effusion, synovitis
  • If in spine: painful scoliosis
Radiological features:
  • Plain X-ray: small round/oval lucent nidus (<2 cm) surrounded by dense cortical sclerosis (the sclerosis may obscure the nidus)
  • CT scan: best modality - clearly shows the nidus with central calcification
  • Bone scan: intense uptake ("hot spot")
  • MRI: may overestimate extent due to surrounding oedema (less specific than CT)
Treatment:
  • Percutaneous radiofrequency ablation (RFA) - treatment of choice (CT-guided); >90% success rate, minimal morbidity
  • Surgical excision of the nidus (open or arthroscopic) - if RFA not available or fails; complete excision of nidus is curative
  • NSAIDs: long-term medical treatment (symptoms often resolve spontaneously after ~3 years)
  • The lesion may undergo spontaneous resolution after several years


EXAM 03 - Ward Assessment Examination

Bone Infections


Q1. Acute Haematogenous Osteomyelitis - Case (3.5 marks)

7-year-old boy, high fever, pain in upper right leg, tender/red/hot/oedematous area, restricted knee movement for 36 hours
a) Three differential diagnoses (0.5)
  1. Acute haematogenous osteomyelitis (most likely) - of the proximal tibia or distal femur
  2. Septic arthritis of the knee joint
  3. Cellulitis / soft tissue infection
Others to consider: acute rheumatic fever, trauma with haematoma, Ewing sarcoma (unlikely in 36-hour history)

b) Clinical evaluation of this patient (1.5)
History:
  • Onset and duration of symptoms; preceding infection (upper respiratory tract infection, skin infection, dental - bacteraemia source)
  • Site and severity of pain; fever pattern
  • Any trauma
  • Immunisation history; general health status; sickle cell disease
Examination:
  • General: fever (often high, >38.5°C), tachycardia, toxic-looking
  • Local: point tenderness over metaphysis (proximal tibia/distal femur), warmth, erythema, oedema, fluctuation (suggests abscess)
  • Joint: assess range of movement carefully - restricted movement due to pain (not true septic arthritis unless joint involved); if joint infected = severe restriction + pain on all movements
Investigations:
Blood tests:
  • FBC: raised WBC (neutrophilia)
  • ESR and CRP: both elevated (CRP more sensitive/specific for monitoring)
  • Blood culture ×2 (before antibiotics) - positive in ~50%
  • Serum procalcitonin
Imaging:
  • Plain X-ray: normal in first 10-14 days; periosteal elevation appears after 10 days
  • MRI (investigation of choice): shows bone marrow oedema, periosteal reaction, soft tissue involvement, abscess within 24-48 hours
  • Ultrasound: shows subperiosteal collection/abscess; can guide aspiration
  • Bone scan (Tc-99m): "hot" in early osteomyelitis; useful when MRI unavailable
  • CT scan: less useful for soft tissue but shows cortical destruction
Microbiological:
  • Aspiration of subperiosteal abscess / bone under USS guidance: Gram stain + culture + sensitivity
  • Throat swab / skin swab (identify source of bacteraemia)

c) Treatment options for acute haematogenous osteomyelitis (1.5)
General measures:
  • Admit; bed rest; splinting of the affected limb (Thomas splint or POP backslab for comfort)
  • IV access, adequate hydration, antipyretics (paracetamol)
Antibiotics (cornerstone of treatment):
  • Start empirically after blood cultures taken; adjust when sensitivities available
  • In children: Staphylococcus aureus is the most common organism
  • Empirical IV antibiotics: Flucloxacillin (first line) OR Co-amoxiclav OR Cefuroxime; Clindamycin if penicillin allergic
  • MRSA suspected: Vancomycin or Teicoplanin
  • Neonates: cover Gram-negative organisms (Cefotaxime + Flucloxacillin)
  • IV for 2-4 days until clinical improvement, then switch to oral for total 4-6 weeks
  • Monitor CRP response
Surgical treatment (indications):
  • Failure to respond to antibiotics within 24-48 hours
  • Presence of subperiosteal/soft tissue abscess (USS-confirmed)
  • Chronic osteomyelitis developing
  • Procedure: Surgical drainage - incision and drainage of abscess, drilling of bone (multiple drill holes in metaphysis to decompress), lavage, temporary drain placement

Q2. Chronic Osteomyelitis after Open Tibial Fracture (3.5 marks)

25-year-old man, chronic discharging sinus in right leg, H/O open fracture of right tibia 6 months ago
a) Provisional diagnosis (0.5)
Chronic osteomyelitis of the right tibia (post-traumatic / secondary to open fracture)

b) Management plan (1.5)
Investigations first:
  • X-ray tibia (AP + lateral): look for sequestrum, involucrum, cortical thickening, fracture union
  • MRI: extent of bone involvement, soft tissue, abscess, dead bone
  • CT: best for detecting sequestrum and extent of bone destruction
  • Sinus tract sinography: map sinus tract
  • Swab from sinus discharge: culture + sensitivity (note: sinus swabs often colonised; deep tissue biopsy is gold standard for microbiology)
  • FBC, ESR, CRP, blood cultures (if febrile)
Surgical management (mainstay):
  1. Sequestrectomy - removal of all dead bone (sequestrum)
  2. Saucerisation (Saucer + plate technique) - removal of the roof of the involucrum and dead bone, creating a saucer-like cavity that can heal by granulation tissue
  3. Debridement of all infected soft tissue, granulation tissue, scar tissue
  4. Dead space management:
    • Antibiotic-impregnated beads (calcium sulphate or PMMA beads with gentamicin/vancomycin) - local antibiotic delivery
    • Antibiotic-impregnated intramedullary nail (for intramedullary osteomyelitis)
    • Cancellous bone graft after infection controlled
  5. Wound closure: primary if clean; VAC (negative pressure wound therapy) if large defect; flap coverage (local/free flap) if large soft tissue defect
  6. Fracture stabilisation: external fixator preferred over internal fixation in infected setting; Ilizarov ring fixator (allows bone transport if large segment lost)
  7. Bone reconstruction (if large segment lost): Masquelet technique (induced membrane technique) OR Ilizarov bone transport
Medical management:
  • Prolonged antibiotics guided by deep tissue culture (IV 2-6 weeks, then oral; total 6-12 weeks for chronic osteomyelitis)
  • Nutrition optimisation
  • Diabetic control if applicable

c) Complications that may arise (1.5)
  1. Pathological fracture through weakened infected bone
  2. Amyloidosis (secondary/AA amyloidosis) - from chronic infection; affects kidneys, liver, spleen
  3. Malignant transformation - Marjolin's ulcer (squamous cell carcinoma arising in chronic sinus/scar - rare but important)
  4. Septicaemia - haematogenous spread of infection
  5. Septic arthritis - spread to adjacent joint
  6. Non-union / malunion of fracture (especially relevant here - post-open fracture)
  7. Limb length discrepancy (growth disturbance in children; bone loss in adults)
  8. Joint stiffness (disuse, periarticular fibrosis)
  9. Anaemia of chronic disease
  10. Sinus tract recurrence despite treatment
  11. Metastatic infection (lung abscess, endocarditis)

Q3. Osteomyelitis (3.5 marks)

a) Define osteomyelitis (1.0)
Osteomyelitis is an infection of bone (cortex and/or medullary cavity) caused by pyogenic organisms (bacteria, rarely fungi or mycobacteria). It may be acute (days to weeks) or chronic (months to years) and can be classified by route of infection: haematogenous, contiguous (from adjacent soft tissue), or direct inoculation (trauma/surgery).

b) Classify osteomyelitis (1.0)
By duration:
  • Acute (within days to weeks)
  • Subacute (weeks to months)
  • Chronic (months to years; usually with dead bone/sinus)
By pathogenesis (Waldvogel Classification):
  1. Haematogenous osteomyelitis (most common in children)
  2. Contiguous focus osteomyelitis - with vascular insufficiency (diabetic foot, PVD) or without
  3. Direct inoculation - post-operative, post-traumatic (open fractures)
By anatomy (Cierny-Mader Classification):
  • Type I: Medullary (endosteal)
  • Type II: Superficial (cortical)
  • Type III: Localised (cortex + medulla, stable)
  • Type IV: Diffuse (entire bone segment, unstable)
Host classification (Cierny-Mader):
  • A host: Normal immune system
  • B host: Compromised (local or systemic)
  • C host: Treatment worse than disease (surgery not indicated)

c) Pathogenesis of chronic pyogenic osteomyelitis (1.5)
  1. Acute haematogenous osteomyelitis begins - bacteria lodge in metaphyseal sinusoids (slow blood flow + lack of phagocytes in this area)
  2. Bacteria multiply → acute inflammatory response → pus forms (increased intraosseous pressure)
  3. Pus spreads through Haversian and Volkmann canals → lifts periosteum → subperiosteal abscess forms
  4. Periosteal stripping → interrupts blood supply to the cortical bone (periosteal vessels cut off)
  5. Medullary blood supply also compromised by pus under pressure
  6. Cortical bone becomes avascular / necroticsequestrum forms (dead bone, which harbours bacteria and is not reached by antibiotics)
  7. Periosteum lays down new bone (reactive) around the sequestrum → involucrum forms (living bone shell)
  8. Cloacae form - openings in the involucrum through which pus and bone fragments discharge
  9. Sinus tract develops to skin surface → chronic discharging sinus
  10. Bacteria persist within sequestrum (biofilm; avascular; antibiotic-resistant) → perpetuates chronic infection → cycle continues unless sequestrum surgically removed

Q4. Aetiology and Pathology of Osteomyelitis (3.5 marks)

a) Why is AHO common in metaphysis of long bones? (1.0)
Acute haematogenous osteomyelitis is most common in the metaphysis due to its unique vascular anatomy:
  1. Terminal capillary loops: The nutrient artery divides into loops at the metaphysis and turns back sharply toward the diaphysis. This causes marked slowing of blood flow in these sinusoidal loops
  2. Absence of phagocytic lining cells: The metaphyseal sinusoids lack Kupffer-like phagocytic cells (unlike liver/spleen), so bacteria are not cleared
  3. Low oxygen tension: Slow flow → relative hypoxia → favourable for bacterial growth
  4. High vascularity / blood flow: The metaphysis is the most vascular zone of growing bone, so bacteraemic bacteria are delivered in large numbers
  5. Lack of anastomoses: Terminal loops have few collaterals, so once thrombosis occurs due to infection, large areas of bone infarction follow rapidly
  6. Micro-trauma: Minor trauma to metaphysis (common in active children) may cause small intraosseous haematomas that act as a focus for bacterial seeding

b) Common organisms responsible for osteomyelitis (1.5)
SituationOrganism
Most common overallStaphylococcus aureus (accounts for >80% of all ages)
Neonates (<3 months)S. aureus, Group B Streptococcus, E. coli, Gram-negatives
Children (>1 year)S. aureus (predominant), Streptococcus pyogenes, H. influenzae (now rare with vaccination)
Sickle cell diseaseSalmonella species (characteristically) + S. aureus
Immunocompromised / IV drug usersPseudomonas aeruginosa, Candida, S. aureus
Post-operative / post-traumaticS. aureus, S. epidermidis (coagulase-negative staph), Gram-negatives
MRSACommunity-MRSA becoming increasingly common
Subacute osteomyelitis (Brodie abscess)S. aureus (low virulence)
TuberculosisMycobacterium tuberculosis (Pott's disease of spine)

c) Define acute osteomyelitis. What is sequestrum and involucrum? (1.5)
Acute osteomyelitis: Infection of bone occurring within days to a few weeks of onset, characterised by acute inflammation (pus formation, oedema, vascular congestion) in the bone, without dead bone formation. If treated promptly, may resolve completely without chronic sequelae.
Sequestrum:
  • A fragment (or mass) of dead, avascular, necrotic bone that has separated from the living bone
  • It is the result of cortical bone losing its blood supply (both periosteal and medullary) due to subperiosteal abscess and increased intraosseous pressure
  • Sequestrum is dense and white on X-ray (appears more radio-opaque than surrounding bone because it has not been resorbed)
  • Bacteria colonise the sequestrum forming a biofilm - this is why osteomyelitis is so difficult to treat and becomes chronic: antibiotics cannot penetrate avascular bone
  • Treatment: surgical removal (sequestrectomy) is essential for cure
Involucrum:
  • A sheath of new periosteal bone (reactive bone) laid down by the elevated periosteum around the sequestrum
  • The periosteum, despite being stripped from the cortex by pus, remains viable and capable of bone formation
  • The involucrum encloses the sequestrum and pus within it
  • It has openings called cloacae through which pus and sequestrum fragments may be discharged (forming sinuses to the skin surface)
  • On X-ray: involucrum appears as a layer of new bone surrounding the lucent area of osteomyelitis

Sources: Bailey and Love's Short Practice of Surgery 28th Edition; Miller's Review of Orthopaedics 9th Edition; Campbell's Operative Orthopaedics 15th Ed 2026; Rockwood and Green's Fractures in Adults 10th ed 2025; Goldman-Cecil Medicine
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