Orthopaedics
Trauma and orthopaedics for the Indian MBBS final-year exam — fractures, dislocations, bone and joint infection, tumours, the spine, arthritis, paediatric and regional orthopaedics. Full-length explanation-first answers with diagrams.
Definition & Epidemiology
Acute haematogenous osteomyelitis is an acute pyogenic infection of bone reaching it through the bloodstream. It is chiefly a disease of children, affecting the metaphysis of a rapidly growing long bone (lower femur, upper tibia). The commonest organism at all ages is Staphylococcus aureus; in neonates group B streptococcus and Gram-negatives, and in sickle-cell disease Salmonella.
Why the Metaphysis?
The metaphyseal ends of growing long bones have a rich but sluggish circulation — the afferent arterioles make sharp hairpin loops into wide venous sinusoids, where blood flow is slow and phagocytic defence is poor. Blood-borne bacteria therefore settle and multiply here.
Haematogenous osteomyelitis begins in the metaphysis, where sluggish venous sinusoids let blood-borne bacteria lodge; pus then spreads to strip the periosteum. Pathology (sequence of events)
Infection begins as inflammation and suppuration in the metaphysis. Rising intra-osseous pressure and pus spread through the Haversian and Volkmann canals to the surface, lifting the periosteum. Stripping of the periosteum cuts off the periosteal blood supply, and with the endosteal supply also thrombosed the cortex dies, forming a sequestrum (dead bone). New bone laid down by the stripped periosteum forms an involucrum around it. Untreated, the disease becomes chronic. In infants and adults (where metaphyseal vessels cross the physis or the physis is closed) infection may reach the joint, causing septic arthritis.
Clinical Features
A child presents with severe constant pain near a large joint, refusal to move or bear weight (pseudoparalysis in infants), and systemic toxicity — high fever, malaise, tachycardia. There is exquisite metaphyseal tenderness, warmth and later swelling; the child holds the limb still.
⚠️Early X-rays are normal — bony changes (rarefaction, periosteal reaction) appear only after 10–14 days. Do not exclude osteomyelitis on the basis of a normal early radiograph; treat on clinical grounds and use MRI, which shows changes within days.Investigations
Blood tests: raised WCC, CRP and ESR; blood cultures (positive in ~50%). Imaging: radiographs are normal early (soft-tissue swelling first, bony changes after 2 weeks); MRI is the most sensitive early investigation (marrow oedema); ultrasound detects a subperiosteal collection; bone scan is an alternative. Aspiration of the metaphysis / subperiosteal pus gives the organism and sensitivities.
Management
Prompt empirical intravenous antibiotics (after cultures) directed against Staph. aureus — e.g. a penicillinase-resistant penicillin or first-generation cephalosporin, adjusted to sensitivities and local resistance (add MRSA cover where prevalent). Supportive care includes analgesia, rest/splintage of the limb and fluids. Surgical drainage is indicated if there is an abscess, if the child fails to improve within 24–48 hours of antibiotics, or if pus is aspirated — the bone is drilled/decompressed and pus evacuated. Antibiotics are continued (IV then oral) for several weeks guided by clinical and CRP response.
💡The dictum is ‘diagnose early, treat aggressively’. Antibiotics started before pus forms can abort the disease; once an abscess or sequestrum forms, surgery is needed and chronicity may follow.Complications
Chronic osteomyelitis (the most important), septic arthritis (especially in infants and where the metaphysis is intracapsular, e.g. the hip), pathological fracture, growth disturbance from physeal damage (limb shortening or deformity), metastatic infection/septicaemia, and (historically) amyloidosis.
Time Pathological change Day 1–3 Inflammation, oedema, pus in medulla Day 3–7 Pus under periosteum, vessel thrombosis Day 7–14 Bone necrosis begins — sequestrum forming After 2–3 weeks Involucrum, cloacae, chronicity Commonest organism Staphylococcus aureus 🔑KEY POINTS TO REMEMBER- Children; metaphysis of long bones; commonest organism Staph. aureus (Salmonella in sickle-cell).
- Metaphyseal sluggish venous sinusoids let bacteria settle; pus strips periosteum → sequestrum.
- Severe pain, fever, refusal to move; X-ray normal for 10–14 days — use MRI.
- Treat early with IV antistaphylococcal antibiotics; drain if abscess or no response in 24–48 h.
- Complications: chronic osteomyelitis, septic arthritis, growth arrest, pathological fracture.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Chronic osteomyelitis is long-standing bone infection, usually following inadequately treated acute haematogenous osteomyelitis, an open fracture, or surgery/internal fixation. Its hallmark is the presence of dead, infected bone (a sequestrum) that harbours organisms protected from antibiotics and host defences, so the infection persists and relapses.
Key Pathological Terms
Sequestrum — a piece of dead, avascular bone separated from living bone; it acts as a reservoir of infection. Involucrum — a sheath of new living bone laid down by the periosteum around the sequestrum. Cloaca — an opening in the involucrum through which pus discharges. Sinus — a track from the cloaca to the skin surface discharging pus. Brodie’s abscess — a localised, walled-off chronic metaphyseal abscess.
Chronic osteomyelitis: dead bone (sequestrum) surrounded by new bone (involucrum), which is perforated by a cloaca that drains through a sinus. Clinical Features
A history of previous acute infection or open injury, with recurrent pain, swelling and discharging sinuses punctuated by quiescent periods. The skin around the sinus is adherent, puckered and pigmented; there may be seropurulent discharge and occasionally a discharged sequestrum. Systemic upset is usually mild between flares.
Investigations
Radiographs show a mix of bone destruction and sclerosis, cavities, sequestra (dense fragments) and involucrum. CT best demonstrates a sequestrum and its position; MRI defines the extent of active infection and soft-tissue involvement; a sinogram may map the track. Inflammatory markers (CRP/ESR) are raised in flares. Culture of deep tissue (not superficial swabs) guides antibiotics.
⚠️A long-standing discharging sinus can, after many years, undergo malignant change to a squamous cell carcinoma (Marjolin’s ulcer) at the sinus mouth — be alert to a change in the discharge, bleeding or a heaped-up margin, and biopsy it.Management
The principle is eradication of infection by removing all dead and infected tissue, combined with prolonged antibiotics. Surgery: sequestrectomy and thorough debridement/saucerisation of the cavity, with dead-space management (muscle flap, antibiotic beads/cement, bone graft). Culture-directed antibiotics are given for a prolonged course (weeks). Adequate soft-tissue cover and skeletal stabilisation are essential; segmental defects may need bone transport (Ilizarov). Recurrence is common, so long follow-up is needed.
💡Antibiotics alone cannot cure chronic osteomyelitis — the avascular sequestrum shields organisms. Surgical removal of dead bone is the cornerstone; antibiotics are an adjunct.Complications
Recurrent flares and sinus formation, pathological fracture, growth disturbance and deformity, joint stiffness, secondary amyloidosis, and Marjolin’s ulcer in a long-standing sinus.
Term Meaning Sequestrum Dead, avascular bone fragment Involucrum New bone formed by periosteum around sequestrum Cloaca Opening in involucrum discharging pus Sinus Track from bone to skin surface Brodie abscess Localised subacute intraosseous abscess 🔑KEY POINTS TO REMEMBER- Follows untreated acute infection, open fracture or surgery; hallmark = infected dead bone.
- Sequestrum (dead bone), involucrum (new bone), cloaca (opening), sinus (skin track).
- X-ray/CT show sequestrum; culture deep tissue, not superficial swabs.
- Cure = surgical debridement + sequestrectomy + dead-space/soft-tissue management + antibiotics.
- Beware Marjolin’s ulcer (SCC) in a chronic sinus.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Importance
Septic (pyogenic) arthritis is infection within a joint. It is an orthopaedic emergency because pus and bacterial enzymes destroy articular cartilage within days, leading to permanent joint damage. It is commonest in young children and in immunocompromised or prosthetic-joint adults; the usual organism is Staphylococcus aureus (in sexually active young adults consider Neisseria gonorrhoeae).
Routes of Infection & Pathology
The joint is infected haematogenously, by spread from adjacent osteomyelitis (especially where the metaphysis is intracapsular — hip, shoulder, elbow, ankle), or by direct inoculation (penetrating injury, injection, surgery). Bacterial multiplication provokes a purulent effusion; enzymes and the host inflammatory response digest the proteoglycan and collagen of cartilage, and raised intra-articular pressure can compromise the epiphyseal blood supply.
Clinical Features
Acute onset of a hot, swollen, exquisitely painful joint held still, with severe pain on the least passive movement and inability to bear weight, accompanied by fever and systemic upset. In an infant the only signs may be pseudoparalysis, irritability and refusal to feed. The hip, being deep, may show only a flexed, abducted, externally rotated posture with pain.
Kocher criterion (child’s hip) Cut-off Points Non-weight-bearing Cannot bear weight 1 Fever > 38.5 °C 1 ESR > 40 mm/h 1 WCC > 12 × 10⁹/L 1 💡The Kocher criteria help distinguish septic arthritis of the hip from transient synovitis in a child: the probability of infection rises steeply with the number of positive predictors (all four present makes septic arthritis very likely). CRP is a useful additional marker.Investigations
Urgent joint aspiration is the key investigation: the fluid is turbid/purulent with a very high white-cell count (predominantly neutrophils); send it for Gram stain, culture and crystals (to exclude gout/pseudogout). Blood tests show raised WCC, CRP and ESR; take blood cultures. Ultrasound confirms an effusion and guides aspiration of the hip; radiographs are often normal early but exclude other pathology.
⚠️A hot, acutely painful joint with fever is septic arthritis until proven otherwise — aspirate before starting antibiotics where possible, and treat as an emergency. Delay beyond a few days risks irreversible cartilage destruction and, in the hip, avascular necrosis.Management
This is an emergency requiring urgent joint decompression and antibiotics. The joint is drained and thoroughly washed out — by arthroscopic or open arthrotomy lavage (repeated aspiration is an option in accessible joints); the hip must be formally drained without delay. Empirical IV antibiotics against Staph. aureus are begun after cultures and adjusted to sensitivities, then continued (IV then oral) for several weeks. The joint is rested then mobilised early to preserve movement once infection is controlled.
Complications
Cartilage destruction and secondary osteoarthritis, joint stiffness or ankylosis, avascular necrosis (notably of the femoral head), growth disturbance in children, dislocation of the septic hip, and systemic sepsis.
Differential Diagnosis & Special Situations
The main differentials are transient synovitis (in children), acute osteomyelitis, crystal arthropathy (gout/pseudogout — hence always send fluid for crystals), reactive arthritis and haemarthrosis. Special situations to recognise: gonococcal arthritis in sexually active young adults (may be migratory with tenosynovitis and a rash), and prosthetic joint infection, which needs specialist combined medical and surgical management (debridement with implant retention, or one-/two-stage revision). Immunocompromise, diabetes and intravenous drug use predispose to atypical organisms and sites (e.g. sternoclavicular, sacroiliac).
Aspirate every acutely hot swollen joint — delay destroys cartilage. 🔑KEY POINTS TO REMEMBER- Orthopaedic emergency — pus destroys cartilage within days.
- Commonest organism Staph. aureus; gonococcus in sexually active young adults.
- Hot, painful, swollen joint held still; Kocher criteria differentiate the child’s septic hip.
- Urgent aspiration (Gram stain, culture, crystals) then emergency drainage + IV antibiotics.
- Complications: cartilage loss/OA, stiffness, AVN, growth disturbance.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Epidemiology
Tuberculosis of the spine (Pott’s disease) is the commonest and most dangerous form of skeletal tuberculosis. It is caused by Mycobacterium tuberculosis reaching the vertebra haematogenously (usually from a pulmonary or other focus). The thoracolumbar region is most often affected. It is important because of the risk of vertebral collapse, deformity and paraplegia.
Pathology
Infection typically begins in the paradiscal region of the vertebral body. Caseating granulomatous destruction spreads to involve the disc (narrowing) and adjacent vertebrae. Anterior vertebral body collapse produces the characteristic angular kyphosis (gibbus / knuckle deformity). Caseous material and pus form a cold abscess (no heat or redness, unlike a pyogenic abscess) that tracks along fascial planes under gravity — e.g. a psoas abscess presenting in the groin.
Pott’s spine: paradiscal destruction and anterior wedge collapse cause an angular kyphosis (gibbus); a cold abscess tracks distally along fascial planes. Clinical Features
Insidious back pain and stiffness with constitutional symptoms — evening rise of temperature, night sweats, weight loss, malaise. There may be a visible/palpable gibbus, muscle spasm, a cold abscess, and — most seriously — signs of cord compression (Pott’s paraplegia): weakness, sensory level, bladder/bowel involvement and upper-motor-neuron signs.
⚠️Pott’s paraplegia is the feared complication. ‘Early-onset’ paraplegia (during active disease, from abscess/oedema/caseum) has a better prognosis than ‘late-onset’ paraplegia (from bony collapse, deformity or fibrosis years later). New or progressing neurology mandates urgent imaging and decompression.Investigations
Radiographs show paradiscal erosion, reduced disc space, vertebral collapse and a paravertebral (fusiform) soft-tissue shadow. MRI is the investigation of choice — it shows marrow oedema, abscesses, disc and cord involvement early. Raised ESR; a positive Mantoux/IGRA supports the diagnosis. CT-guided biopsy for histology (caseating granuloma) and culture/GeneXpert confirms the diagnosis and drug sensitivity.
Management
The mainstay is anti-tuberculous chemotherapy — standard multi-drug therapy (isoniazid, rifampicin, pyrazinamide and ethambutol in the intensive phase, then continuation), given for a prolonged course (commonly 9–18 months for spinal TB). Most patients respond to drugs plus rest/bracing. Surgery is indicated for neurological deficit (cord compression), a large abscess, instability or severe/progressive deformity, and failure of medical treatment — decompression, abscess drainage and stabilisation (e.g. anterior debridement and fusion). Nutrition and general care are important.
💡The classic triad of angular kyphosis (gibbus), cold abscess and paraplegia characterises advanced Pott’s disease. A ‘cold’ abscess lacks the heat and redness of a pyogenic abscess and tracks far from the vertebral focus.🔑KEY POINTS TO REMEMBER- Commonest skeletal TB; thoracolumbar; begins in the paradiscal vertebral body.
- Anterior collapse → angular kyphosis (gibbus); cold abscess tracks along fascial planes.
- Constitutional symptoms + back pain; MRI is the imaging of choice; biopsy confirms.
- Pott’s paraplegia: early-onset (better prognosis) vs late-onset.
- Mainstay = multi-drug ATT (9–18 mo); surgery for deficit, abscess, instability or deformity.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & General Features
Tuberculosis of bones and joints (osteoarticular TB) is a chronic granulomatous infection by Mycobacterium tuberculosis, usually secondary to a pulmonary or lymph-node focus and spread haematogenously. After the spine, the hip and knee are the commonest sites. It is a disease of insidious onset with constitutional symptoms (evening pyrexia, night sweats, weight loss) and a monoarticular, destructive but ‘cold’ course.
Pathology & Stages
Infection starts in the synovium or in the juxta-articular bone, producing a caseating granulomatous pannus that erodes cartilage from the margins. Because there is little reactive new bone, TB causes osteoporosis and destruction rather than sclerosis. Clinically it evolves through stages: synovitis → early arthritis (cartilage loss) → advanced arthritis with marked destruction, deformity and, ultimately, fibrous ankylosis.
Feature Tuberculous arthritis Pyogenic (septic) arthritis Onset Insidious (weeks–months) Acute (hours–days) Local signs ‘Cold’ — little heat/redness Hot, red, acutely tender Systemic Evening fever, night sweats, wt loss High swinging fever, toxaemia X-ray Osteoporosis, marginal erosion Rapid destruction, later new bone Ankylosis Fibrous Bony Clinical Features (hip & knee)
There is pain (often referred to the knee in hip disease), a limp, muscle wasting and progressive restriction of movement, with night cries in children (painful spasm on relaxation during sleep). The hip passes through a sequence of apparent deformities — early flexion, abduction and external rotation (stage of synovitis), later flexion, adduction and internal rotation (stage of destruction). A cold abscess or discharging sinus may develop.
Investigations
Raised ESR; positive Mantoux/IGRA; radiographs show juxta-articular osteoporosis, marginal erosions and reduced joint space (Phemister’s triad). MRI shows synovitis, effusion, abscesses and early bone involvement. Synovial biopsy/aspiration for histology (caseating granuloma), AFB, culture and GeneXpert confirms the diagnosis and drug sensitivity.
Management
The basis of treatment is anti-tuberculous chemotherapy (multi-drug regimen for a prolonged course), with rest and splintage of the joint in a functional position to relieve pain and prevent deformity, followed by guarded mobilisation. Surgery (synovectomy, joint debridement, abscess drainage, and later arthrodesis or arthroplasty for a destroyed joint) is reserved for advanced disease, deformity or failure of drug treatment. Good nutrition and general care aid recovery.
⚠️Do not attempt joint arthrodesis or arthroplasty during active infection — control the disease with chemotherapy first. Reconstructive surgery for a destroyed joint is undertaken only once the disease is quiescent.Complications
Untreated or advanced osteoarticular TB leads to progressive joint destruction with deformity and shortening, fibrous ankylosis in a non-functional position, cold abscesses and chronic discharging sinuses (with risk of secondary pyogenic infection), and, in the spine, paraplegia. Early diagnosis and full chemotherapy prevent most of these, which is why constitutional symptoms with a chronic monoarthritis should prompt investigation for TB rather than prolonged empirical treatment.
Principles of Anti-Tuberculous Therapy
Skeletal TB is treated with the same multi-drug regimen as other forms of tuberculosis, for a prolonged course. An intensive phase of four drugs (isoniazid, rifampicin, pyrazinamide and ethambutol) is followed by a continuation phase of isoniazid and rifampicin, the total duration commonly extended for bone and joint disease. Adherence is critical to prevent drug resistance; directly observed therapy and drug-sensitivity testing (including GeneXpert for rifampicin resistance) are important. Adequate nutrition and treatment of coexisting conditions (HIV, diabetes) improve outcome.
Spine is the commonest skeletal site. 🔑KEY POINTS TO REMEMBER- Osteoarticular TB: after spine, hip and knee commonest; monoarticular, insidious, ‘cold’.
- Causes osteoporosis and destruction, not sclerosis; Phemister’s triad on X-ray.
- Stages: synovitis → early → advanced arthritis → fibrous ankylosis.
- Confirm by biopsy/culture; MRI for extent. TB arthritis is cold, pyogenic is hot.
- Treat with ATT + rest/splintage; reconstructive surgery only once disease is quiescent.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definitions
In osteomyelitis, a sequestrum is a fragment of dead, avascular bone that has become separated from the surrounding living bone. It arises because pus strips the periosteum and thromboses the vessels, depriving a segment of cortex of its blood supply. An involucrum is the sheath of new, living bone formed by the stripped-but-viable periosteum around the sequestrum.
The dead sequestrum lies within a new-bone involucrum, which is perforated by a cloaca. Why They Matter
The sequestrum is the key to chronicity: being avascular, it is inaccessible to antibiotics and to host defences, so it harbours bacteria and perpetuates the infection until it is surgically removed. A cloaca is an opening in the involucrum through which pus (and sometimes small sequestra) discharges, connecting to the skin via a sinus. On radiographs a sequestrum appears as a dense, sclerotic fragment (it cannot decalcify because it has no blood supply) lying within a lucent cavity.
💡A radiodense fragment surrounded by lucency is a sequestrum; the surrounding sheath of new bone is the involucrum. Removing the sequestrum (sequestrectomy) is essential to cure chronic osteomyelitis — antibiotics alone will not eradicate it.⚠️Because the sequestrum is avascular, it stays dense on X-ray while the surrounding living bone becomes osteoporotic — this contrast is a useful diagnostic clue.🔑KEY POINTS TO REMEMBER- Sequestrum = dead avascular bone; involucrum = new living bone around it.
- Cloaca = opening in the involucrum; sinus = track to the skin.
- Sequestrum harbours infection and causes chronicity — remove it surgically.
- On X-ray the sequestrum is dense within a lucent cavity.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
A Brodie’s abscess is a form of subacute / chronic osteomyelitis in which the infection is localised and walled off as a chronic bone abscess, usually in the metaphysis of a long bone (classically the upper tibia). It represents a balance between a relatively low-virulence organism and good host resistance, so a discrete cavity forms rather than widespread infection.
Clinical Features
The presentation is indolent: intermittent, deep pain (often worse at night) over months, with little or no fever and few systemic signs. There may be local tenderness and mild swelling. The insidious course and the radiographic appearance can mimic a bone tumour.
Investigations
Radiographs show a well-defined, round or oval radiolucent cavity in the metaphysis surrounded by a rim of reactive sclerosis. MRI demonstrates the abscess and any ‘penumbra sign’. Inflammatory markers may be normal or mildly raised. The cavity contains pus or granulation tissue; Staph. aureus is the usual organism.
💡A well-circumscribed lucent metaphyseal lesion with a sclerotic rim and night pain in a young patient suggests a Brodie’s abscess — a key differential for a bone tumour or osteoid osteoma.Management
Treatment is curettage/drainage of the abscess cavity combined with antibiotics directed against the cultured organism. Small, clearly infective lesions may respond to antibiotics with immobilisation, but most require surgical evacuation to confirm the diagnosis (and exclude a tumour) and to clear the infection.
Differential Diagnosis
Because of its indolent course and radiographic appearance, a Brodie’s abscess must be distinguished from an osteoid osteoma (also causes night pain, but shows a small nidus with dense surrounding sclerosis), eosinophilic granuloma, and low-grade bone tumours. When doubt exists, biopsy at the time of curettage both confirms infection and excludes a tumour, which is why operative evacuation is usually preferred over antibiotics alone.
💡Because a solitary lytic lesion can be a tumour, the safe rule for a suspected Brodie’s abscess is to obtain tissue — curettage provides both the cure (evacuation) and the diagnosis (histology and culture), avoiding the trap of treating a neoplasm as an infection.Night pain relieved by aspirin mimics osteoid osteoma. 🔑KEY POINTS TO REMEMBER- A localised, walled-off subacute/chronic bone abscess, typically metaphyseal (upper tibia).
- Indolent deep pain, often nocturnal, with minimal systemic upset.
- X-ray: lucent cavity with a sclerotic rim; mimics a tumour or osteoid osteoma.
- Treat by curettage/drainage + culture-directed antibiotics.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
A cold abscess is a collection of tuberculous pus (caseous material) that forms without the classic signs of acute inflammation — hence ‘cold’: there is no heat, redness or acute tenderness, unlike a pyogenic (‘hot’) abscess. It is a hallmark of skeletal tuberculosis, especially of the spine.
Formation & Behaviour
Caseation and liquefaction in a tuberculous focus produce pus that, under gravity and along tissue planes, tracks far from its origin before pointing. A classic example is a psoas abscess from lower thoracic/lumbar Pott’s disease, which follows the psoas sheath to present as a swelling in the groin or iliac fossa, or a retropharyngeal abscess from cervical spine disease. It is characteristically fluctuant but painless and cool.
💡The tendency of a cold abscess to track along fascial planes means the presenting swelling may be remote from the diseased vertebra — always seek the underlying focus (e.g. spinal TB in a groin abscess).⚠️Do not incise and drain a cold abscess through healthy skin as a first move — it risks a persistent tuberculous sinus and secondary infection. Aspirate through a ‘non-dependent’ route where drainage is needed, and treat the underlying TB with chemotherapy.Management
The cornerstone is anti-tuberculous chemotherapy directed at the underlying disease. Small abscesses resorb on treatment; larger or symptomatic ones may be aspirated (avoiding a dependent drainage track) or drained at the time of spinal decompression. Confirm the diagnosis by AFB smear, culture and GeneXpert on the aspirate.
Contrast with a Pyogenic Abscess
The distinction from a pyogenic (‘hot’) abscess is fundamental. A pyogenic abscess is acute, hot, red, tender and systemically toxic, forming close to its origin. A cold abscess is chronic, cool, painless and fluctuant, forms in the setting of constitutional TB symptoms, and characteristically migrates along fascial planes. Recognising the ‘cold’ nature prevents inappropriate incision and points to an underlying tuberculous focus that must be sought and treated.
Absence of inflammatory signs gives it the name. 🔑KEY POINTS TO REMEMBER- Cold abscess = tuberculous pus without heat/redness (cf. hot pyogenic abscess).
- Tracks along fascial planes under gravity (e.g. psoas abscess to the groin).
- Hallmark of skeletal TB, especially spinal (Pott’s) disease.
- Treat the underlying TB with chemotherapy; avoid dependent incision (sinus risk).
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Importance
Septic arthritis of the hip in a child is a surgical emergency: the deep, intracapsular position of the proximal femoral metaphysis means infection readily reaches the joint, and pus rapidly destroys cartilage and can devascularise the femoral head. The main clinical challenge is distinguishing it from the far more common, benign transient synovitis.
Kocher predictor Present if Non-weight-bearing Child refuses to bear weight Fever Temperature > 38.5 °C ESR > 40 mm/h WCC > 12 × 10⁹/L Kocher Criteria
The Kocher criteria use four predictors — inability to bear weight, fever > 38.5 °C, ESR > 40 mm/h and WCC > 12 × 10⁹/L. The probability of septic arthritis rises steeply with the number present: roughly <3% with none, but very high (>90%) when all four are positive. A raised CRP is a useful additional predictor.
Clinical Features & Investigations
The child is unwell and febrile, holds the hip flexed, abducted and externally rotated, and resists all movement with severe pain. Investigations: FBC, CRP, ESR and blood cultures; ultrasound confirms an effusion and guides aspiration; radiographs exclude other causes. Ultrasound-guided aspiration of the joint is diagnostic (Gram stain and culture).
⚠️If septic arthritis of the hip is confirmed or strongly suspected, proceed to emergency arthrotomy and washout — the hip cannot be adequately decompressed by aspiration alone, and delay risks cartilage destruction and avascular necrosis of the femoral head.Transient Synovitis – the Key Differential
Transient synovitis (irritable hip) is the common benign mimic: a child, often after a viral illness, with a limp and mild hip discomfort but who is systemically well, afebrile and can usually bear weight. Inflammatory markers are normal or only mildly raised. The Kocher criteria and CRP help separate the two, but where doubt remains the safe course is aspiration, because missing a septic hip is far more damaging than a negative tap.
All four criteria give over 99% probability of septic arthritis. 🔑KEY POINTS TO REMEMBER- Emergency; deep intracapsular hip is readily infected and pus damages cartilage/femoral head.
- Kocher criteria (weight-bearing, fever >38.5, ESR >40, WCC >12) grade probability vs synovitis.
- Hip held flexed, abducted, externally rotated; ultrasound + aspiration confirm.
- Confirmed septic hip → emergency arthrotomy and washout + IV antibiotics.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Gas gangrene (clostridial myonecrosis) is a rapidly progressive, life-threatening infection of muscle caused by Clostridium perfringens (and other clostridia), spore-forming anaerobes. It follows deep, contaminated wounds with devitalised muscle and poor oxygenation — war wounds, crush and open fractures, and contaminated agricultural injuries.
Pathophysiology
In the anaerobic environment of dead muscle, clostridia proliferate and release powerful exotoxins (notably alpha-toxin, a lecithinase) that cause myonecrosis, haemolysis and profound systemic toxicity, while fermentation produces gas within the tissues. The infection spreads with alarming speed along muscle planes.
Clinical Features
A short incubation (hours to a few days) then sudden severe pain, tense swelling and a brownish, foul (‘sweetish’) serous discharge. The skin becomes discoloured and there is crepitus from gas in the tissues. The patient is strikingly toxic — tachycardic, hypotensive, and may become jaundiced and shocked, often out of proportion to the local appearance early on.
⚠️Gas gangrene is a surgical emergency with high mortality. Do not delay for investigations — the priorities are immediate radical surgical debridement/excision of all dead muscle (amputation may be life-saving), high-dose antibiotics and resuscitation.Management
Treatment combines aggressive surgical debridement (excision of all necrotic muscle, leaving wounds open; amputation where limb-threatening), high-dose intravenous antibiotics (penicillin with clindamycin), and resuscitation of the toxic, shocked patient. Hyperbaric oxygen is a useful adjunct where available. Prevention rests on thorough debridement of contaminated wounds and not closing them primarily.
Investigations & Prevention
The diagnosis is clinical and must not be delayed, but a plain radiograph or CT may show gas in the muscle planes, and a Gram stain of the discharge reveals Gram-positive bacilli with few inflammatory cells. Prevention is key: thorough debridement of contaminated wounds, leaving them open, adequate oxygenation and perfusion, and tetanus prophylaxis. A high index of suspicion in war, crush and agricultural injuries allows life-saving early intervention.
Radical debridement is the only life-saving measure. 🔑KEY POINTS TO REMEMBER- Clostridial myonecrosis (C. perfringens) of muscle after deep, contaminated wounds.
- Exotoxins cause myonecrosis + gas; spreads rapidly with severe systemic toxicity.
- Severe pain, crepitus, foul brown discharge, marked toxaemia.
- Emergency: radical debridement/amputation + high-dose penicillin/clindamycin + resuscitation ± HBO.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Tuberculosis of the hip is, after the spine, one of the commonest sites of osteoarticular TB. It is a chronic granulomatous monoarticular infection that, untreated, progresses to destruction of the joint and fibrous ankylosis in a deformed position.
Clinical Stages & Features
Presentation is insidious, with a limp, pain (often referred to the knee), muscle wasting and night cries in children. The hip passes through recognised stages of apparent deformity: the stage of synovitis (early) holds the hip in flexion, abduction and external rotation (the position of greatest capacity); the stage of arthritis/destruction shifts it to flexion, adduction and internal rotation, producing apparent shortening. Constitutional TB symptoms are usually present.
Investigations & Management
Raised ESR, positive Mantoux, and radiographs showing juxta-articular osteoporosis, marginal erosions and reduced joint space; MRI shows early synovitis and abscesses; aspiration/biopsy confirms. Treatment is anti-tuberculous chemotherapy with rest and traction/splintage to relieve spasm and prevent deformity, then guarded mobilisation. A destroyed joint (once disease is quiescent) may need arthrodesis or arthroplasty.
💡The early ‘FABER’ posture (flexion, abduction, external rotation) of the synovitic hip gives way to flexion, adduction and internal rotation as the joint is destroyed — a useful clinical marker of stage.Complications
If diagnosis or treatment is delayed, the hip is progressively destroyed, leaving a stiff, painful, deformed joint with true shortening and fibrous ankylosis, sometimes with a wandering acetabulum (migration of the femoral head through an eroded acetabular floor), cold abscess or sinus. Even after cure, a badly damaged joint may need arthrodesis or, in suitable patients, arthroplasty once the disease is fully quiescent.
⚠️Reconstructive surgery (arthrodesis or arthroplasty) is undertaken only when the disease is quiescent after adequate chemotherapy — operating on an actively infected joint risks flaring the infection and implant failure.Early stage shows apparent lengthening; later, true shortening. 🔑KEY POINTS TO REMEMBER- Common osteoarticular TB; insidious limp, referred knee pain, night cries.
- Synovitis stage: flexion, abduction, external rotation → destruction: flexion, adduction, internal rotation.
- X-ray: juxta-articular osteoporosis + marginal erosion; confirm by biopsy/culture.
- ATT + rest/traction; arthrodesis or arthroplasty for a destroyed joint once quiescent.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Purpose
The Cierny–Mader classification stages chronic (adult) osteomyelitis to guide treatment and prognosis. It combines the anatomical extent of bone involvement with the physiological status (host) of the patient, recognising that both determine the outcome of surgery.
Anatomical type Description I – Medullary Infection confined to the medullary canal II – Superficial Surface of exposed, infected cortical bone III – Localised Full-thickness cortical sequestrum; bone still stable IV – Diffuse Circumferential/through-and-through; bone unstable Host (Physiological) Class
The patient is graded as A (normal host, good immunity and healing), B (compromised — systemic Bs, e.g. diabetes, malnutrition, immunosuppression; local Bl, e.g. scarred/irradiated tissue, arteriopathy; or both), or C (treatment is more morbid than the disease, so palliation/suppression is chosen). The combination (type + class) gives the clinical stage.
💡Cierny–Mader reminds us that success in chronic osteomyelitis depends not only on the anatomy of the infection but also on optimising the host (nutrition, glycaemic control, smoking cessation, vascular status) before undertaking major reconstruction.Clinical Use
The stage guides the aggressiveness of treatment: medullary and localised disease in a good host may be cured by debridement and antibiotics, whereas diffuse disease in a compromised host requires major reconstruction and carries a higher failure rate — and a class-C host may be best served by suppressive therapy rather than radical surgery.
Contrast with Paediatric Classification
Cierny–Mader applies to adult osteomyelitis and deliberately incorporates the host, reflecting that comorbidity and tissue quality drive outcome in adults. This contrasts with the simpler descriptive approach to acute haematogenous osteomyelitis in children, where the host is usually healthy and treatment centres on early antibiotics and drainage. The staging is most useful when planning reconstructive surgery and counselling on the likelihood of cure.
Combines bone involvement with host status to guide treatment. 🔑KEY POINTS TO REMEMBER- Stages chronic osteomyelitis by anatomy (I medullary – IV diffuse) + host (A/B/C).
- Host class reflects immunity, comorbidity and local tissue quality.
- Guides whether to attempt cure vs suppression, and the scale of surgery.
- Optimising the host is as important as addressing the anatomy.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.