TB Hip

Tuberculous arthritis of the hip is the most common form of skeletal tuberculosis after spinal TB. It is caused by haematogenous seeding of Mycobacterium tuberculosis to the synovium or adjacent bone of the hip joint, with progressive destruction of articular cartilage, subchondral bone, and surrounding soft tissues if untreated. TB hip remains a significant public health problem in endemic regions including South Asia, Sub-Saharan Africa, and among immunocompromised individuals worldwide.

• Skeletal TB accounts for approximately 1–3% of all TB cases; the hip is the second most common site of skeletal TB after the spine (Pott disease)
• Most common age group: children and young adults in endemic regions; also seen in elderly and immunocompromised patients
• Pathogenesis: haematogenous spread from primary pulmonary focus → synovial or metaphyseal seeding → granulomatous inflammation → caseating necrosis → progressive articular and bony destruction
• Primary pulmonary TB is often quiescent or healed by the time hip TB presents — only approximately 50% of hip TB patients have active pulmonary TB; chest X-ray and Mantoux/IGRA should be performed in all suspected cases regardless
• Risk factors: malnutrition, poverty, overcrowding, HIV/AIDS, diabetes, immunosuppression (biologics, steroids), prior BCG non-vaccination

TB hip progresses through characteristic pathological stages if untreated. Understanding these stages guides both the clinical and radiological assessment.

• Phemister triad (classic radiological triad of TB joint): (1) periarticular osteoporosis; (2) peripheral marginal erosions; (3) gradual joint space narrowing — distinguishes TB from pyogenic arthritis (rapid destruction) and rheumatoid arthritis (bilateral, symmetric)
• Cold abscess: pus from TB infection that tracks along fascial planes without the warmth and erythema of pyogenic abscess; may present as a groin swelling, psoas abscess, or discharging sinus at the hip

• Insidious onset — weeks to months of progressive hip pain; limp; reduced range of motion
• Constitutional symptoms: low-grade fever, night sweats, weight loss, malaise — often subtle or absent; do not exclude TB in the absence of systemic symptoms
• Hip position: progressive flexion, adduction, and internal rotation deformity as disease progresses — muscle spasm and contracture; Thomas test positive (flexion deformity)
• Wasting of thigh muscles: quadriceps and gluteal wasting from disuse; leg length discrepancy in advanced cases
• Cold abscess: soft, non-tender fluctuant swelling in groin or buttock; may track to the medial thigh, perineum, or down the psoas sheath to the iliac fossa
• Sinus tracts: chronic discharging sinuses in neglected cases — secondary infection common; sinus discharge is characteristically thin and watery
• Children: irritable child with limp; refusal to bear weight; may present acutely if superimposed bacterial infection; can mimic transient synovitis or Perthes disease in early stages

• Plain radiographs (AP pelvis + lateral hip): Phemister triad; monitor disease progression; standing films for deformity assessment
• MRI hip: investigation of choice for early disease — synovial thickening and enhancement, bone marrow oedema, subchondral erosions, abscess collections, soft tissue tracking; detects disease before plain radiograph changes
• CT scan: better characterises bony destruction, sequestra (necrotic bone), and abscess extension; guides surgical planning
• Mantoux test (PPD) / IGRA (interferon-gamma release assay): IGRA (QuantiFERON Gold, T-SPOT) more specific than Mantoux; positive result supports TB but does not confirm active joint disease; IGRA unaffected by BCG vaccination status
• Joint aspiration / synovial biopsy: definitive diagnostic procedure — synovial fluid for AFB smear, TB culture (6–8 weeks), PCR (rapid, more sensitive); synovial biopsy shows caseating granulomas; send both fluid AND tissue — AFB culture of synovial tissue has higher sensitivity (up to 90%) than fluid culture alone (50–60%)
• Sputum AFB and culture; urine for TB (renal TB); chest X-ray; CT chest if CXR equivocal
• ESR, CRP: elevated but non-specific; useful for monitoring treatment response
• HIV test: mandatory in endemic regions; TB/HIV co-infection changes management

• Standard RIPE regimen: Rifampicin + Isoniazid + Pyrazinamide + Ethambutol × 2 months (intensive phase) then Rifampicin + Isoniazid × 4 months (continuation phase) — total 6 months minimum for non-spinal TB; most guidelines extend to 9–12 months for skeletal TB
• Pyridoxine (Vitamin B6): given with isoniazid to prevent peripheral neuropathy
• Drug-resistant TB (MDR-TB): resistance to rifampicin and/or isoniazid; requires second-line agents (fluoroquinolones, injectable agents); 18–24 months of treatment; specialist infectious disease input essential
• Medical treatment alone is curative in early stage (Stage I–II) TB hip — serial radiological and clinical monitoring; surgery not required if responsive to chemotherapy
• Response monitoring: clinical improvement (pain, ROM, constitutional symptoms), ESR/CRP trending down; radiological stabilisation of bone destruction

Surgery in TB hip serves two purposes: diagnostic (biopsy/debridement) and therapeutic (abscess drainage, deformity correction, joint reconstruction). Medical treatment should always be initiated or optimised before elective surgery.

• THA in TB hip: safe and effective when disease is quiescent; minimum 2–3 months of anti-TB chemotherapy before elective THA; continue chemotherapy for 6 months post-THA; cementless or cemented both acceptable; reactivation rate approximately 2–5% in most series — lower than historically feared
• Titanium implants: safe in quiescent TB; theoretical concern about reactivation reduced with modern antibiotic protocols

• Fibrous ankylosis: most common outcome in treated but advanced disease; painless ankylosis in a good functional position is compatible with satisfactory function; painful ankylosis requires surgical intervention
• Bony ankylosis: complete fusion of the joint; rare; stable but may cause significant gait abnormality
• Pathological dislocation: from progressive bone and capsule destruction in untreated Stage IV disease; AVN may accompany; requires major reconstructive surgery
• Sinus tract formation: chronic discharging sinus increases risk of secondary bacterial superinfection; sinus epithelialises over time — tract excision needed before THA
• Limb length discrepancy: from growth arrest, bone destruction, or dislocation — particularly significant in children
• AVN: pressure from joint effusion, vascular disruption, and direct metaphyseal involvement can cause AVN of the femoral head — especially in children where the blood supply is more vulnerable

• TB hip in HIV-positive patients: more aggressive disease; faster progression; higher reactivation risk after surgery; immune reconstitution inflammatory syndrome (IRIS) can cause paradoxical worsening after antiretroviral therapy; co-manage with infectious disease specialist; antiretroviral therapy should be optimised before elective surgery
• THA timing in TB hip: the historical dogma of waiting 10+ years after disease quiescence is no longer supported by evidence — modern series demonstrate safe THA after 2–3 months of chemotherapy with continuing antibiotic cover; prolonged waiting disadvantages patients functionally and the evidence does not support it
• Excision arthroplasty (Girdlestone) to THA: conversion of Girdlestone procedure (from previous septic hip or TB hip) to THA is technically demanding — proximal femoral migration, acetabular bone loss, scar tissue, and abductor weakness all complicate reconstruction; modular stems, structural allograft, and augmented acetabular components often required
• Paediatric TB hip deformity: growth disturbance is a major long-term concern; AVN of the femoral head and epiphyseal damage lead to coxa magna, coxa breva, or coxa vara; serial monitoring until skeletal maturity; reconstructive osteotomy or THA deferred until maturity if possible

• Phemister triad: periarticular osteoporosis + marginal erosions + gradual joint space narrowing — classic TB joint radiological triad
• Cold abscess: non-tender fluctuant pus tracking along fascial planes; thin watery discharge from sinus tract
• RIPE × 2 months then RI × 4 months = 6 months total; skeletal TB 9–12 months recommended
• Synovial biopsy: caseating granulomas; AFB culture of tissue (90% sensitivity) superior to fluid alone
• IGRA (QuantiFERON): more specific than Mantoux; unaffected by BCG; supports diagnosis but does not confirm active joint disease
• THA in healed TB hip: safe after 2–3 months chemotherapy; continue for 6 months post-THA; reactivation rate only 2–5%
• Active pulmonary TB present in only approximately 50% of hip TB patients — always investigate regardless
• Children: AVN risk from effusion + vascular disruption; growth disturbance; distinguish from Perthes in early disease
• Sinus tracts: must be excised before THA to reduce reactivation risk
• HIV + TB: IRIS can cause paradoxical worsening; ARV optimisation before elective surgery; specialist co-management