Describe Leprosy — Musculoskeletal Aspects in detail.

Definition & Relevance

Leprosy (Hansen’s disease) is a chronic granulomatous infection by Mycobacterium leprae that characteristically affects peripheral nerves and skin. It remains an important cause of hand and foot deformity and disability in endemic regions (including parts of India). The orthopaedic burden arises almost entirely from peripheral nerve damage — producing sensory loss, motor paralysis and autonomic dysfunction — and its consequences.

Nerve Involvement & Deformities

M. Leprae has a predilection for cooler, superficial nerves at characteristic sites, which become thickened and palpable: the ulnar nerve (at the elbow), the median, the common peroneal (at the fibular neck), the posterior tibial, and the facial nerve. The resulting deformities include the claw hand (ulnar ± median palsy), foot drop (common peroneal palsy), lagophthalmos (facial nerve), and the consequences of anaesthesia.

Trophic Ulcers & Secondary Damage

Because the anaesthetic sole cannot feel pressure or injury, painless trophic (neuropathic) ulcers develop over pressure points (e.g. The metatarsal heads), and repeated unperceived trauma and secondary infection cause absorption/shortening of digits and destruction of the foot — not from the bacillus ‘eating’ the tissue but from insensitivity and injury.

Management

The infection is treated with WHO multi-drug therapy (MDT) — combinations of rifampicin, dapsone and clofazimine — which cures the infection and prevents further nerve damage. The orthopaedic role is prevention and correction of deformity and disability: protection and care of anaesthetic hands and feet (protective footwear, daily inspection, wound care) to prevent trophic ulcers; physiotherapy and splinting; and reconstructive surgery (tendon transfers for claw hand and foot drop, correction of deformity, ulcer surgery). Treating reactions and nerve abscesses preserves function.

Reactions in Leprosy

During or after treatment, patients may develop immunologically-mediated reactions that are a major cause of sudden nerve damage. Type 1 (reversal) reactions cause acute inflammation of skin lesions and nerves with the risk of rapid loss of nerve function, while Type 2 reactions (erythema nodosum leprosum) produce crops of tender skin nodules with fever and systemic upset. Both are treated urgently — typically with corticosteroids — because prompt control of the neuritis prevents the permanent paralysis and deformity that would otherwise follow, which is why nerve function is monitored throughout treatment.

Classification & Diagnosis

Leprosy is classified across a spectrum from tuberculoid (few, well-defined anaesthetic skin patches with early nerve involvement, in patients with good immunity) to lepromatous (widespread skin and nerve disease with abundant bacilli in poor-immunity hosts), with borderline forms between. The diagnosis rests on the clinical triad of anaesthetic skin lesions, thickened peripheral nerves and demonstration of acid-fast bacilli (slit-skin smear), and recognising it early — before fixed deformity develops — is the single most effective way to prevent disability.

Deformity is due to nerve damage, and is preventable by early treatment.

• Chronic M. Leprae infection of peripheral nerves & skin; major cause of hand/foot deformity in endemic areas.
• Thickened nerves at cool sites: ulnar (claw hand), common peroneal (foot drop), facial (lagophthalmos).
• Loss of protective sensation → trophic ulcers, injury, digit resorption (preventable).
• WHO multi-drug therapy (rifampicin/dapsone/clofazimine) cures infection & halts nerve damage.
• Protect anaesthetic parts; physiotherapy/splints; tendon transfers & deformity correction; treat reactions promptly.