Spinal TB (Pott’s) — Anterior vs Posterior

Spinal tuberculosis (Pott`s disease — named after Percivall Pott who described it in 1779) is the most common form of extrapulmonary skeletal tuberculosis, accounting for approximately 50% of all musculoskeletal tuberculosis. It remains a major global health problem, particularly in resource-limited settings, and is increasingly seen in immunocompromised patients (HIV, organ transplant, biologic therapies) and in high-prevalence immigrant populations in developed countries. The disease causes progressive vertebral body destruction, paravertebral abscess, and kyphotic deformity (gibbus deformity) — and threatens the spinal cord with compressive myelopathy.

• Pathophysiology: Mycobacterium tuberculosis reaches the spine via haematogenous spread from a primary pulmonary (or rarely gastrointestinal) focus; the bacilli seed the metaphyseal region of the vertebral body (the most vascular region in childhood) or the anterior subchondral bone via Batson`s venous plexus (retrograde flow); infection starts in the anterior aspect of the vertebral body and spreads: to adjacent vertebrae under the anterior longitudinal ligament (the typical `two-level` involvement) or across the disc (children — disc is vascular; adults — disc is avascular and relatively resistant); the disc is eventually involved but later in the disease process than in pyogenic discitis; granuloma formation with central caseating necrosis destroys the anterior vertebral body; as the anterior column collapses, kyphosis develops
• Distribution: thoracolumbar junction most common (~50% of cases — T8-L2); pure thoracic 20%; cervical 12% (dangerous — may cause quadriplegia from cord compression + instability); lumbar 25%; sacral rare; cervical tuberculosis may present with dysphagia from a retropharyngeal abscess or with dyspnoea from airway compression; always consider in the differential of any spinal disease in patients from endemic regions
• HIV association: patients with HIV co-infection have a dramatically higher risk of tuberculosis reactivation and dissemination; TB spine in HIV+ patients may be multifocal (several non-contiguous spinal levels involved — unlike typical two-level involvement in immunocompetent patients); paradoxical reactions (immune reconstitution inflammatory syndrome — IRIS) can occur after antiretroviral therapy (ART) is initiated, causing worsening of TB manifestations as immunity recovers

• Clinical features: insidious onset over weeks to months; back pain (the most common symptom — initially dull aching, eventually constant and severe); constitutional symptoms — fever, night sweats, weight loss, fatigue (approximately 40–50% of patients); neurological deficit — weakness, sensory loss, paraplegia (Pott`s paraplegia) from spinal cord compression by abscess, granulation tissue, or bony collapse; abscess presentation — a psoas abscess may track along the psoas muscle sheath to present as a groin swelling (psoas sign), or it may present as a fluctuant cold abscess in the iliac fossa, posterior chest wall, or paravertebral region; `cold abscess` — unlike pyogenic abscess, TB abscess is typically not hot, minimally tender, and does not cause severe acute local signs — the `cold` nature is characteristic and important diagnostically
• Gibbus deformity: progressive angular kyphosis caused by anterior vertebral body collapse; the thoracolumbar junction involvement produces a sharp, angular posterior hump (gibbus — Latin for hump); this is the classic physical sign of severe Pott`s disease; gibbus deformity is the most common cause of acquired kyphosis in developing countries; the angular kyphosis can cause late neurological deterioration even after the infection is cured — through progressive mechanical cord compromise and ischaemia
• Pott`s paraplegia — classification: (1) Active (early onset — within 2 years of disease onset): caused by cord compression from abscess, granulation tissue, or caseous material; responds to anti-TB chemotherapy and/or surgical decompression; (2) Healed/Late onset: caused by mechanical compression from bony deformity (severe kyphosis), fibrous bands, or rarely by ischaemia of the cord from arteritis; occurs years after the infection has been treated; does NOT respond to chemotherapy; requires surgical decompression and deformity correction
• MRI features: T1 — hypointense (oedema/necrosis/pus); T2 — heterogeneous high signal; gadolinium enhancement — rim-enhancing paravertebral or epidural abscess (ring enhancement); loss of vertebral body height with anterior wedging; disc involvement (T2 high signal in disc if disc involved — but disc may be preserved early); paraspinal/psoas abscess (often large — `large abscess, little pain` is characteristic of TB); epidural extension with cord compression; calcification within the abscess (indicates chronic TB); relative preservation of the disc early (contrast with pyogenic — which destroys the disc rapidly) is a useful feature but not absolute

• Standard regimen: 2HRZE/10HR — the WHO-recommended regimen for spinal TB: Intensive phase: 2 months of Isoniazid (H) + Rifampicin (R) + Pyrazinamide (Z) + Ethambutol (E); Continuation phase: 10 months of Isoniazid + Rifampicin (total = 12 months); spinal TB requires a longer duration of treatment than pulmonary TB (6 months) due to the poor vascularity of the affected bone and the difficulty of achieving adequate drug levels in caseous tissue; some guidelines recommend 18 months for severe spinal TB, particularly in HIV+ patients; directly observed therapy (DOT) is essential to ensure compliance and prevent drug resistance
• Drug toxicity monitoring: Isoniazid — peripheral neuropathy (pyridoxine supplementation essential), hepatotoxicity; Rifampicin — hepatotoxicity, drug interactions (enzyme inducer — reduces efficacy of warfarin, OCP, antiretrovirals), orange discolouration of body fluids; Pyrazinamide — hepatotoxicity, hyperuricaemia/gout; Ethambutol — optic neuritis (monitor visual acuity and colour vision — must be checked before and during treatment; contraindicated in children under 5 years where visual monitoring is unreliable)
• Multidrug-resistant TB (MDR-TB): resistance to Isoniazid AND Rifampicin; requires second-line agents (bedaquiline, fluoroquinolones, aminoglycosides, cycloserine); treatment duration 18–24 months; much lower cure rates; requires specialist infectious disease management; MDR-TB prevalence is highest in Eastern Europe and Central Asia; Xpert MTB/RIF provides rapid rifampicin resistance detection, alerting clinicians to likely MDR-TB

The MRC (Medical Research Council) Hong Kong trials of the 1970s–1980s established that chemotherapy alone can achieve bony fusion in most cases of spinal TB without surgery. However, surgery is indicated in specific circumstances — and when surgery is required, the debate between anterior and posterior approaches (and combined approaches) is central.

• Pott`s disease: haematogenous spread of M. tuberculosis to vertebral body; thoracolumbar junction most common (T8-L2, ~50%); anterior vertebral body destroyed first; disc relatively preserved early (unlike pyogenic); `cold abscess` — not hot, minimally tender
• Gibbus deformity: sharp angular kyphosis from anterior vertebral collapse; most common cause of acquired kyphosis in developing countries; can cause late paraplegia even after infection treated (mechanical cord compression)
• Pott`s paraplegia: active (early — abscess/granuloma → chemotherapy ± surgery; responds); healed/late (mechanical — bony deformity/fibrous bands → surgery only; does NOT respond to chemotherapy)
• MRI: ring-enhancing abscess; anterior vertebral destruction; disc preserved early; large psoas/paravertebral abscess; epidural extension; skip lesions in HIV+
• Standard chemotherapy: 2HRZE/10HR (12 months total); Isoniazid + Rifampicin + Pyrazinamide + Ethambutol × 2 months, then Isoniazid + Rifampicin × 10 months; DOT mandatory; MDR-TB (INH + RIF resistant) → second-line drugs 18–24 months
• Surgical indications: neurological deficit; severe kyphosis or instability; failed medical therapy; diagnostic failure; large abscess
• Anterior approach: direct anterior column debridement + bone graft; gold standard for anterior cord compression; higher morbidity (thoracotomy); does not provide posterior stability alone
• Posterior approach: better deformity correction; 3-column control; familiar corridor; cervical TB; growing evidence for posterior-only for selected cases; instrumentation in infected field is safe with concurrent chemotherapy
• Combined anterior-posterior: severe pan-vertebral disease; kyphosis >60°; maximum debridement + 360° fixation; highest morbidity; specialist centres
• MRC Hong Kong trials: established chemotherapy alone achieves bony fusion in most spinal TB; radical anterior surgery + chemotherapy superior to chemotherapy alone for neurological recovery in severe disease; landmark evidence for conservative vs surgical management
• Ethambutol monitoring: optic neuritis risk; check visual acuity and colour vision (Ishihara charts) before and during treatment; avoid in children <5 years (unreliable monitoring)