Orthopaedics

Definition & Importance

A peripheral nerve injury is damage to a nerve trunk that interrupts motor, sensory and autonomic conduction to the part it supplies. Nerves are commonly injured by laceration, traction, compression, ischaemia or as a complication of fractures and dislocations. Because a divided nerve regenerates slowly and imperfectly, early recognition and appropriate management are vital to preserve limb function.

Classification (Seddon & Sunderland)

Seddon described three grades. Neurapraxia — a temporary conduction block (e.g. from pressure) with the axon intact; full recovery is expected in days to weeks. Axonotmesis — the axon is disrupted but the endoneurial sheath is intact; Wallerian degeneration occurs distally but the axon can regrow along the preserved tube (~1 mm/day). Neurotmesis — complete division of the nerve (axon and sheath); spontaneous useful recovery is not possible and surgical repair is required. The Sunderland classification refines this into five degrees by the layer disrupted.

Degeneration & Regeneration

After division, the distal segment undergoes Wallerian degeneration — the axon and myelin break down and are cleared by macrophages, leaving the endoneurial tubes (Schwann-cell columns). The proximal stump then sprouts axons that, if the tubes are intact and aligned, grow distally at about 1 mm per day to re-innervate the target. If the tubes are disrupted (neurotmesis) the sprouts may form a disorganised neuroma rather than reaching the end organ.

Clinical Features

There is motor loss (weakness/paralysis and, later, wasting of the supplied muscles), sensory loss in the nerve’s autonomous zone, autonomic changes (dry, warm then cold skin, loss of sweating) and loss of reflexes. A Tinel’s sign (tingling on percussion over the regenerating nerve front) that advances distally over time indicates recovery.

Investigations & Management

Nerve conduction studies and EMG (performed after ~3 weeks) localise and grade the lesion and monitor recovery; imaging (ultrasound/MRI) may show the nerve and any compressing lesion. Management depends on the type and cause. Closed injuries that are likely neurapraxia or axonotmesis are managed expectantly with splintage, physiotherapy to prevent contractures, and monitoring for recovery (advancing Tinel’s, EMG). A clean-cut (sharp) division is treated by primary microsurgical repair; a contaminated or ragged wound is repaired secondarily once healed. A gap is bridged with a nerve graft (e.g. sural nerve). Late/irrecoverable palsies are treated by tendon transfers to restore function.

• Seddon: neurapraxia (block, recovers), axonotmesis (axon lost/sheath intact, regrows), neurotmesis (division, repair).
• Wallerian degeneration distally; regeneration ~1 mm/day if tubes intact; neuroma if not.
• Motor, sensory, autonomic loss; advancing Tinel’s sign signals recovery.
• NCS/EMG at ~3 weeks localise and monitor; closed likely neurapraxia/axonotmesis → observe.
• Sharp division → primary repair; gap → nerve graft; irrecoverable → tendon transfer.

Definition & Anatomy

The brachial plexus is the network of nerves (roots C5–T1) that supplies the upper limb, organised into roots → trunks → divisions → cords → branches. Brachial plexus injuries usually follow high-energy traction (motorcycle accidents forcing the head and shoulder apart), birth injury, penetrating trauma or traction during surgery, and cause varying patterns of upper-limb paralysis and sensory loss.

Patterns of Injury

Upper plexus (Erb’s, C5–C6) — from widening of the head–shoulder angle; the arm hangs in the ‘waiter’s tip’ position (adducted, internally rotated, extended elbow, pronated), the hand being spared. Lower plexus (Klumpke’s, C8–T1) — from forced abduction of the arm; affects the intrinsic hand muscles (claw hand) and may show a Horner’s syndrome. Total (whole plexus) palsy gives a flail, anaesthetic limb.

Clinical Assessment & Investigations

A careful neurological examination maps the level and completeness of the lesion (motor power, sensation, reflexes, Horner’s sign). Nerve conduction studies/EMG (after a few weeks) and MRI / CT myelography assess root avulsion versus rupture. Associated vascular and bony injuries are excluded.

Management

Many obstetric and traction (neurapraxic) injuries recover spontaneously and are managed with physiotherapy to maintain a supple limb while awaiting recovery. Surgery is considered when there is no recovery within the expected window: options include nerve repair, nerve grafting and nerve transfers (neurotisation) for suitable lesions, and later reconstructive procedures (tendon/muscle transfers, arthrodesis, free muscle transfer) to restore key functions such as elbow flexion. Realistic goals and rehabilitation are essential.

Complications & Prognosis

The prognosis depends chiefly on the level and type of injury: neurapraxic and postganglionic lesions may recover well, whereas preganglionic root avulsions have a poor outlook and denervated muscle that is not re-innervated within roughly 18–24 months becomes irreversibly fibrotic. Complications include a flail, insensate limb, disabling neuropathic pain (particularly with avulsions), joint contractures, and — in the anaesthetic hand — unnoticed injuries and trophic changes. Realistic goal-setting, pain management and sustained rehabilitation are as important as the reconstructive surgery.

• Roots C5–T1 → trunks → divisions → cords → branches; injured by traction.
• Erb’s (C5–C6): waiter’s tip, hand spared. Klumpke’s (C8–T1): claw hand ± Horner’s.
• Preganglionic avulsion (Horner’s, winged scapula) = poor prognosis, not directly repairable.
• MRI/CT myelography + EMG distinguish avulsion from rupture.
• Physiotherapy while awaiting recovery; nerve grafts/transfers then reconstruction if no recovery.

Definition

Carpal tunnel syndrome (CTS) is the commonest entrapment neuropathy, caused by compression of the median nerve as it passes through the carpal tunnel at the wrist — the space bounded by the carpal bones and roofed by the flexor retinaculum (transverse carpal ligament). Anything that reduces the volume of the tunnel or increases its contents raises the pressure on the nerve.

Causes & Risk Factors

Often idiopathic, but recognised associations include pregnancy, hypothyroidism, rheumatoid arthritis, diabetes, acromegaly, obesity, repetitive wrist use, and local causes (fractures, ganglia, tenosynovitis). It is commoner in middle-aged women.

Clinical Features

Tingling, numbness and pain in the median nerve distribution (thumb, index, middle and radial half of the ring finger), classically worse at night and relieved by shaking the hand. Advanced disease causes weakness and wasting of the thenar muscles (abductor pollicis brevis) and clumsiness. Tinel’s sign (tapping over the nerve) and Phalen’s test (sustained wrist flexion) reproduce the symptoms.

Investigations

The diagnosis is largely clinical; nerve conduction studies confirm and grade median nerve slowing at the wrist and are useful before surgery or in atypical cases. Investigate for underlying causes (thyroid function, glucose) where indicated.

Management

Conservative treatment suits mild/intermittent symptoms: night wrist splints (in neutral), activity modification, treatment of any underlying cause, and corticosteroid injection into the carpal tunnel. Surgical decompression — division of the flexor retinaculum (‘carpal tunnel release’, open or endoscopic) — is indicated for persistent or severe symptoms or when there is thenar wasting / motor loss, and gives reliable relief.

Complications & Differential Diagnosis

Untreated or severe carpal tunnel syndrome leads to permanent thenar wasting and weakness of opposition, with incomplete recovery even after decompression, so timely surgery in the presence of motor signs matters. The main differentials are a cervical radiculopathy (C6/C7), a more proximal median-nerve entrapment (pronator syndrome), and a generalised peripheral neuropathy — distinguished by the distribution of symptoms, associated neck or systemic features, and nerve conduction studies. Surgical complications of release include incomplete division, scar tenderness (‘pillar pain’) and, rarely, injury to the palmar cutaneous or recurrent motor branch.

• Commonest entrapment neuropathy: median nerve compressed under the flexor retinaculum.
• Associations: idiopathic, pregnancy, hypothyroidism, RA, diabetes, repetitive use.
• Night tingling in thumb–radial ring finger (spares little finger); thenar wasting late.
• Tinel’s & Phalen’s reproduce symptoms; NCS confirm.
• Splint/steroid injection for mild; carpal tunnel release for severe or thenar wasting.

Definition & Importance

Hand infections are common and potentially serious: the hand’s tightly compartmentalised anatomy allows infection to spread rapidly along fascial planes and tendon sheaths, and delay or inadequate treatment can cause tendon necrosis, stiffness and permanent loss of function. Most follow a penetrating injury; the usual organism is Staphylococcus aureus.

Specific Infections

Paronychia — infection of the nail fold, the commonest hand infection; acute (usually staphylococcal) or chronic (often candidal, in those with wet hands). Felon — infection of the closed pulp space of the finger-tip; the fibrous septa create a compartment, so pus produces intense throbbing pain and can cause pressure necrosis of the skin and underlying bone. Acute suppurative flexor tenosynovitis — infection within a flexor tendon sheath, a surgical emergency.

Management

General principles are elevation, rest/splintage, analgesia and appropriate antibiotics against Staph. aureus, with early surgical drainage of any abscess (‘where there is pus, let it out’). A superficial paronychia may resolve with antibiotics or simple drainage of the nail fold; a felon and deep-space infections require incision and drainage; flexor tenosynovitis requires emergency sheath drainage and irrigation. After control of infection, early mobilisation and hand therapy restore movement and prevent stiffness.

Anatomy of Spread

The functional anatomy explains why hand infections are dangerous. The pulp of the finger-tip is divided by fibrous septa into a closed compartment, so a felon behaves like an abscess under pressure and can strangle the blood supply to the tip. The flexor tendons run in synovial sheaths that, in the little finger and thumb, communicate with the ulnar and radial bursae of the palm and can allow infection to track across the wrist (a ‘horseshoe abscess’). The deep palmar (thenar and mid-palmar) spaces are potential spaces where pus can collect and point dorsally. Understanding these planes guides where to look for spread and where to drain.

Prevention & Prognosis

Because outcome depends heavily on early treatment, the principles are prompt cleaning and appropriate care of every hand wound, tetanus prophylaxis, and a low threshold for exploring a wound that overlies a tendon sheath or joint. Human and animal bite wounds deserve particular respect — they are heavily contaminated (e.g. Pasteurella, Eikenella), should not be closed primarily, and need antibiotics and often surgical toilet. With early recognition and drainage most hand infections resolve fully; delay is the enemy of function.

• Rapid spread along sheaths/spaces → stiffness & loss of function; usually Staph. aureus.
• Paronychia (nail fold), felon (pulp space compartment), web-space, deep-palmar-space infections.
• Flexor tenosynovitis = emergency; Kanavel signs (flexed finger, fusiform swelling, sheath tenderness, pain on extension).
• Elevation, antibiotics, and early drainage of pus; emergency sheath drainage for tenosynovitis.
• Follow with hand therapy to prevent stiffness.