Orthopaedics

Definition & Indications

An amputation is the surgical removal of part or all of a limb. Although it is often seen as a failure of treatment, a well-performed amputation is a reconstructive procedure that relieves suffering and restores function with a prosthesis. The indications are classically remembered as the ‘three Ds’ — Dead (dead limb: critical ischaemia/gangrene, e.g. peripheral vascular disease, diabetes), Dangerous (a limb threatening life: spreading sepsis/gas gangrene, malignancy, crush with rhabdomyolysis), and Damn nuisance (a useless, painful or deformed limb worse than no limb: intractable pain, gross deformity, non-functional paralysis).

Levels & Types

Amputations are described by level (e.g. below-knee, above-knee, Syme’s at the ankle, trans-metatarsal; below- or above-elbow). The level is chosen to remove all diseased/non-viable tissue while preserving the longest, most functional stump that will heal and take a prosthesis. A below-knee amputation (preserving the knee) gives far better function and energy-efficient walking than an above-knee amputation, so the knee is saved whenever possible. Amputations may be provisional (guillotine) in infected/emergency cases (leaving the wound open, closed later) or definitive with primary shaping and closure.

Principles of a Good Stump

A good stump is the key to successful prosthetic use. Principles: adequate length with a well-padded, non-adherent scar placed away from pressure areas; myoplasty/myodesis (securing opposing muscles over the bone end) for a stable, powered, cylindrical stump; sectioning nerves cleanly under tension so they retract (to keep the inevitable neuroma away from pressure); secure haemostasis; and appropriate bone shaping (bevelling). Postoperative oedema control, stump shaping and early rehabilitation prepare the stump for a prosthesis.

Complications

Early: haematoma, wound infection, skin-flap or stump necrosis (especially in ischaemic limbs), and reactionary haemorrhage. Late: a painful or symptomatic neuroma, phantom limb sensation and phantom limb pain, stump ulceration (from a poorly fitting prosthesis), flexion contractures of the joint above (prevented by positioning and physiotherapy), and psychological adjustment problems.

Rehabilitation

Amputation is only the first step; rehabilitation determines the outcome. A multidisciplinary team manages pain, conditions and shapes the stump, provides a prosthesis and gait training, and supports psychological adjustment and return to work and daily life. Early involvement of physiotherapy and prosthetics optimises independence.

Special Situation — the Ischaemic Limb

In amputations for peripheral vascular disease and diabetes — the commonest indication in adults — the guiding principle is a conflict between amputating low enough to preserve function and high enough to reach tissue with a blood supply that will heal. Level selection is aided by clinical assessment of skin perfusion and, where needed, vascular studies. These patients are often elderly with multiple comorbidities, so perioperative optimisation, meticulous handling of ischaemic tissue and diabetic control are as important as the operation itself for a stump that heals.

• Amputation is reconstructive; indications = 3 Ds: Dead, Dangerous, Damn nuisance.
• Choose the level to remove disease yet keep the longest functional stump that heals.
• Save the knee (below-knee walks far more efficiently than above-knee).
• Good stump: length, padded mobile scar, myoplasty, nerves cut under tension, shaped bone.
• Complications: neuroma, phantom pain, stump ulcer, flexion contracture; rehab is key.

Definition

Scoliosis is a lateral curvature of the spine with vertebral rotation (a three-dimensional deformity), defined by a Cobb angle > 10°. A structural scoliosis is a fixed curve with vertebral rotation that does not correct on bending, whereas a non-structural (postural) scoliosis is a flexible curve secondary to another cause (leg-length discrepancy, pain/spasm) that corrects on removing the cause.

Classification / Causes

The commonest form is idiopathic scoliosis (adolescent idiopathic scoliosis being the most frequent, typically in adolescent girls). Other causes: congenital (vertebral anomalies — hemivertebra, failure of segmentation), neuromuscular (cerebral palsy, poliomyelitis, muscular dystrophy — a long C-shaped collapsing curve), and syndromic/other (neurofibromatosis, Marfan’s).

Clinical Features & Assessment

Often a painless deformity noticed as asymmetry — uneven shoulders or waist, a prominent scapula, or a rib hump on the forward-bending (Adam’s) test (the rotation makes the ribs prominent on the convex side). Assess for leg-length discrepancy (to exclude postural curves) and for neurological signs (which suggest an underlying cord/neuromuscular cause). Curve magnitude is measured as the Cobb angle on a standing radiograph.

Management

Treatment depends on the cause, curve magnitude and skeletal maturity (remaining growth). Small curves (< ~20–25°) are observed with serial radiographs. Moderate curves (~25–40–45°) in a still-growing child are treated with a brace to prevent progression. Large or progressive curves (> ~45–50°) are treated by surgical correction and instrumented spinal fusion. Congenital and neuromuscular curves are managed according to their cause. Untreated large curves can impair cardiorespiratory function.

Complications of Untreated Curves

A large, progressive scoliosis is not merely cosmetic: severe thoracic curves reduce the volume of the chest and can cause restrictive lung disease and, ultimately, cardiorespiratory compromise, while the deformity itself causes back pain, a poor body image and difficulty with seating (particularly in neuromuscular curves). Neuromuscular and congenital curves tend to progress even after skeletal maturity, which is why they are monitored and treated on their own criteria rather than those used for idiopathic curves.

• Lateral curvature + rotation of the spine; Cobb angle > 10°; structural vs postural.
• Commonest = adolescent idiopathic; also congenital, neuromuscular, syndromic.
• Rib hump on Adam’s forward-bend test; Cobb angle measures severity.
• Observe small curves; brace moderate curves in growing child; fuse large/progressive curves.
• Progression greatest during the growth spurt — monitor immature spines closely.

Definition

Poliomyelitis is a viral infection (poliovirus, an enterovirus) that attacks the anterior horn cells of the spinal cord, producing a pure lower-motor-neuron, flaccid paralysis — without sensory loss. Though now rare where vaccination is widespread, its late orthopaedic sequelae remain important, especially in regions where the disease was endemic. The disease has an acute stage, a stage of recovery, and a residual (chronic) stage of paralysis and deformity, which is the orthopaedic concern.

Pathology & Features

Destruction of anterior horn cells causes asymmetrical flaccid paralysis with wasting; because only the motor cells are affected, sensation is preserved. Muscle imbalance across joints (some muscles paralysed, their antagonists acting unopposed), together with growth, leads to fixed deformities (e.g. equinus, flail joints, scoliosis), joint instability, shortening of the limb (growth retardation), and trophic/vasomotor changes.

Principles of Management

Management differs by stage. In the acute stage, care is supportive (rest, respiratory support, positioning to prevent deformity). In the convalescent stage, physiotherapy maintains range and strengthens recovering muscles, with splints to prevent deformity. The residual stage is where reconstructive orthopaedic surgery is used to improve function.

Reconstructive Surgery in the Residual Stage

The aims are to correct deformity, stabilise flail joints, balance muscle power and equalise limb length. Procedures include soft-tissue release of contractures, tendon transfers (to rebalance a joint by re-routing a working muscle), arthrodesis (to stabilise a flail or unstable joint, e.g. the foot or shoulder), osteotomy to correct bony deformity, and leg-length equalisation. Calipers/orthoses support flail limbs for walking. Treatment is individualised and planned around the pattern of working and paralysed muscles.

Assessing the Patient for Surgery

Planning reconstruction in the residual stage depends on a meticulous muscle chart that grades the power of every muscle across each affected joint, because the whole strategy is to use the working muscles to compensate for the paralysed ones. The surgeon assesses which deformities are flexible or fixed, whether joints are stable or flail, and the degree of limb-length discrepancy, then sequences procedures logically — first correcting fixed deformity and stabilising the skeleton, then rebalancing muscle power by transfer, and finally equalising length.

Post-Polio Syndrome

Decades after the original illness, some survivors develop post-polio syndrome — new weakness, fatigue and pain in previously affected (and sometimes apparently unaffected) muscles, thought to result from the gradual failure of the enlarged motor units that had compensated for the original cell loss. It is managed supportively with energy conservation, appropriate orthoses and graded activity, and it is important to recognise so that new weakness in a polio survivor is not mistakenly attributed to a fresh neurological disease.

• Poliovirus destroys anterior horn cells → pure LMN flaccid, asymmetrical paralysis, sensation intact.
• Residual stage: fixed deformities, flail/unstable joints, limb shortening.
• Acute → supportive; convalescent → physiotherapy/splints to prevent deformity.
• Residual reconstructive surgery: soft-tissue release, tendon transfer, arthrodesis, osteotomy, limb equalisation.
• Only transfer muscles with adequate power, across a corrected, stable joint; orthoses support flail limbs.

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.

• 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.

Definition

Volkmann’s ischaemic contracture is the end-result of untreated acute compartment syndrome of the forearm — the ischaemic necrosis, and subsequent fibrosis and shortening, of the forearm flexor muscles, producing a fixed flexion (claw) deformity of the wrist and fingers. It is a preventable catastrophe: the tragedy is that timely recognition and fasciotomy of the compartment syndrome would have avoided it.

Cause & Pathology

The classic setting is a supracondylar fracture of the humerus in a child (injuring or compressing the brachial artery), a tight plaster, or forearm crush — causing raised compartment pressure and muscle ischaemia. The deep flexors (flexor digitorum profundus and flexor pollicis longus) are most affected; ischaemic muscle is replaced by inelastic fibrous tissue that contracts, and the adjacent nerves (median, ulnar) are also damaged, adding paralysis and sensory loss.

Clinical Features

The established contracture shows a flexed, pronated forearm with a flexed wrist and clawed fingers; extending the wrist increases the finger flexion and flexing the wrist allows the fingers to extend a little (the Volkmann sign, reflecting the shortened muscles crossing both joints). There is often accompanying nerve deficit (median/ulnar) with wasting and sensory loss.

Management

Prevention is paramount: prompt reduction of the fracture, avoidance of tight casts/full flexion, vigilance for compartment syndrome, and emergency fasciotomy if it develops. Once the contracture is established, treatment is difficult and aims to improve function: physiotherapy and splinting for mild cases; and surgery for established deformity — excision of dead muscle, release/lengthening of contracted muscles (or a muscle-slide procedure), tendon transfers to restore movement, nerve decompression/reconstruction, and corrective procedures. Results are limited, underscoring the value of prevention.

Relation to Compartment Syndrome

Volkmann’s contracture is best understood as the tragic end-point of a missed compartment syndrome of the forearm, and it is worth stating the prevention explicitly: after a supracondylar fracture the limb is watched for the earliest ischaemic signs, tight circular dressings and extreme elbow flexion are avoided, perfusion is restored, and any established compartment syndrome is decompressed by emergency fasciotomy within hours. Everything about the condition argues for vigilance, because once the muscles have infarcted and fibrosed the deformity and disability are permanent and only partly correctable.

• End-result of untreated forearm compartment syndrome: ischaemic fibrosis of flexor muscles → claw hand.
• Classic cause: supracondylar humeral fracture (child), tight cast, crush; deep flexors (FDP/FPL) worst.
• Fixed flexed/pronated forearm, flexed wrist, clawed fingers + median/ulnar nerve deficit.
• Prevention is everything: watch for pain on passive finger extension; emergency fasciotomy.
• Established contracture: muscle excision/slide, tendon transfers, nerve reconstruction — limited results.