Hand Examination and Clinical Localisation

Hand examination is common in trauma clinics, emergency departments, fracture clinics, rheumatology, nerve clinics and elective hand practice. It is high-value because a careful clinical examination often identifies the injured structure before imaging or electrodiagnostic testing.

The settings. The examination is asked for in a small number of recurring situations:

• laceration with possible tendon, nerve or vessel injury
• finger deformity after trauma
• post-fracture stiffness or tendon rupture
• carpal tunnel, cubital tunnel or peripheral nerve compression
• ulnar or radial nerve palsy
• rheumatoid or inflammatory hand deformity
• Dupuytren disease, trigger finger and tendon imbalance
• infection, compartment syndrome or complex regional pain

The aim. The hand has many structures in a small space, and a vague statement such as "weak grip" is not enough. The aim is to localise the weakness to a tendon, muscle, nerve level, joint, skin, pain generator or vascular problem. Pain, swelling, tendon rupture, joint dislocation, compartment syndrome, infection and poor cooperation can all look like weakness, so localisation requires pattern recognition plus a comparison of active and passive motion.

Three linked systems. Hand movement comes from the extrinsic tendons, the intrinsic muscles and the nerves that drive them. The extrinsic flexors and extensors cross the wrist and fingers from the forearm. The intrinsics, the thenar and hypothenar muscles, lumbricals and interossei, control pinch, MCP flexion, IP extension and fine balance, and the median, ulnar and radial nerve branches provide motor control and sensory feedback.

The same sign from different levels. The same visible problem can arise from different levels. Thumb weakness can be APB weakness from median nerve compression, FPL weakness from AIN palsy, EPL rupture after distal radius fracture, pain inhibition from CMC arthritis or stiffness after immobilisation.

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Active against passive. Active motion tests the whole muscle-tendon-nerve unit, and passive motion tests the joint and the soft tissues around it. Compare the two, and the opposite hand, before naming a rupture or a palsy; the table below is the logic that follows.

Clinical signs in the hand arise from predictable failure patterns, and knowing the mechanism prevents misdiagnosis.

Tendon discontinuity. Active movement is lost across one joint while passive motion is preserved: an FDP laceration causing absent DIP flexion. Prove it by isolating that tendon and checking the wound level. A rupture is a mechanical failure and will not recover with nerve observation.

Nerve denervation. Weakness follows a nerve distribution, often with sensory or autonomic change: an ulnar palsy causing FDI wasting and pinch weakness. Map the motor and sensory pattern, then localise the level. A nerve palsy can recover, need decompression, need repair or need tendon transfer depending on level, cause and time course.

Joint or capsular restriction. Active and passive motion are both limited: a PIP contracture after injury. Assess passive end feel and radiographs. Joint stiffness becomes harder to reverse with time, especially in the PIP joint.

Pain inhibition. Apparent weakness without a consistent anatomical pattern: an acute fracture, infection or CRPS. Control the pain, identify the driver and repeat focused testing. Pain-limited motion can hide a tendon or nerve injury; reassess once pain is controlled but do not delay urgent referral.

Mechanical imbalance. A characteristic deformity from tendon, ligament or intrinsic imbalance: boutonniere, swan neck or ulnar claw. Match the posture to the disrupted stabiliser.

Position and exposure. Sit opposite the patient with both hands and forearms exposed. The hands should rest on a table so the cascade, resting posture, sweat pattern, scars, wasting and deformity can be compared side to side.

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History. Ask the questions that localise. The mechanism may be a sharp laceration, crush, fall, bite, closed rupture, gradual compression or inflammatory disease, and its timing separates an acute tendon or nerve injury from a delayed rupture, chronic compression or progressive deformity. For a wound, record location, depth and contamination, and ask specifically about glass, bite, machinery, farm or water exposure.

The symptoms worth asking for by name are pain, numbness, paraesthesia, weakness, triggering, locking, cold intolerance and colour change. Function means writing, buttons, pinch, grip, tools, keyboard, sport, musical instrument and work demands. Previous pathology changes the interpretation: distal radius fracture, rheumatoid disease, diabetes, cervical radiculopathy, previous tendon repair, carpal tunnel release or nerve injury.

Inspection. Look before touching:

• resting finger cascade
• rotational deformity or scissoring
• wounds in relation to tendon and nerve zones
• swelling, bruising, erythema, drainage or bite marks
• thenar, hypothenar and first dorsal interosseous wasting
• trophic skin changes, sweating asymmetry or dry skin
• nail-bed injury, mallet posture, boutonniere posture or swan-neck posture
• Dupuytren nodules, cords and contracture
• rheumatoid MCP ulnar drift, Z-thumb and tendon imbalance

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Flexor tendons

Isolate every tendon. The finger may still flex weakly through adjacent tendons, lumbricals or tenodesis, so a composite grip can look intact over a divided tendon and isolated testing is essential. A clean volar laceration over the finger with loss of isolated tendon function is a tendon injury until proven otherwise.

Examine before the block. Flexor tendon injury should be assessed before local anaesthetic blocks eliminate useful motor testing.

Extensor tendons

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Core motor tests

Core sensory tests

Localisation patterns

Median nerve. Carpal tunnel causes thenar weakness and radial digit symptoms. AIN palsy takes FPL and FDP to the index, and a proximal median lesion adds forearm pronation and flexor involvement.

Ulnar nerve. Low ulnar lesions affect the intrinsics more than FDP; high ulnar lesions add FCU and FDP weakness in the ring and little fingers. Dorsal ulnar sensory sparing suggests a lesion distal to the dorsal cutaneous branch.

The ulnar paradox. Expect the deformity to run backwards. The claw comes from unopposed FDP flexing the ulnar two fingers against paralysed intrinsics, so it needs a working FDP. A high lesion denervates FDP to ring and little as well, and the claw is therefore less marked: the more proximal, more damaging injury looks tidier, and a striking claw points to a lesion at the wrist, not the elbow. Reduced clawing as a high lesion recovers is also expected rather than reassuring, because FDP reinnervates first.

Radial nerve and PIN. High radial nerve palsy affects wrist, finger and thumb extension and may have sensory loss. PIN palsy is motor only and commonly affects finger and thumb extension more than wrist extension.

Watch the direction the wrist extends, not just whether it does. ECRL is supplied above the PIN and survives, while ECU does not, so a PIN palsy typically extends the wrist into radial deviation. Wrist extension that is present but deviates radially, with no sensory loss, is a PIN lesion; wrist drop with dorsal first web numbness is a lesion above the PIN branch.

Joint assessment explains stiffness, deformity and instability.

Range and end feel. Measure MCP, PIP and DIP active and passive range, and separate an extension lag from a fixed flexion contracture. Check whether motion improves when adjacent joints are positioned differently. Compare a soft end feel, a hard bony block and pain-limited movement.

Deformity localisation

Intrinsic or extrinsic tightness. When PIP flexion is limited, decide whether the block is intrinsic muscle tightness, extrinsic (extensor or capsular) tightness or PIP joint contracture; the Bunnell-Littler test does this. With the MCP held in extension, which tightens the intrinsics, assess passive PIP flexion, then flex the MCP, relaxing the intrinsics, and reassess. If PIP flexion improves with the MCP flexed, the limitation is intrinsic tightness; if it stays equally limited in both positions, the problem is PIP joint or capsular contracture; if it is worse with the MCP flexed, suspect extrinsic extensor tightness.

The DIP equivalent. The Haines-Zancolli (oblique retinacular ligament) test asks the same question one joint further on: passive DIP flexion that is limited with the PIP extended but free with the PIP flexed indicates a tight oblique retinacular ligament (Landsmeer) rather than a DIP joint contracture. These tests separate therapy from intrinsic release from capsulotomy.

Function. Assess real tasks: key, pulp and tripod pinch; power, hook and writing grip; opening a jar or using tools if relevant; and occupation-specific or sport-specific function.

The hand is intolerant of missed vascular injury. A pink finger can still have a single digital artery injury; urgency depends on perfusion, contamination, nerve injury and associated structural damage.

Vascular assessment. Check capillary refill and colour, temperature compared with adjacent digits, and the radial and ulnar pulses. Add digital Allen testing when digital artery injury is suspected, a Doppler signal when clinical perfusion is uncertain, and the pulse oximetry waveform on the injured digit if available.

Sensory assessment. Light touch and pinprick are the screen. Static two-point discrimination is used for digital nerve injury and Semmes-Weinstein monofilament testing when quantifying sensory threshold. Compare with the opposite hand and adjacent digits, and document before local anaesthetic, exploration or repair.

Choose the test knowingly. Reproducibility of static two-point discrimination and Semmes-Weinstein monofilaments is poor for both, and the monofilament is the more reliable of the two (see the sensibility card in the Evidence Base). Record the method used and interpret the number with the motor findings, not on its own.

Clinical examination decides what imaging or tests are needed.

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The single most useful skill in hand examination is separating causes that produce the same surface appearance. Loss of active movement, weak grip and an abnormal posture each have several explanations, and the differentials carry very different urgencies.

The examination should lead to a decision, not just a diagnosis. Three decisions follow from it: whether the patient needs to be seen urgently, what is done safely at first contact, and which planned pathway the non-urgent problem enters.

Complications often come from missed localisation rather than from the examination itself.

Hand and wrist trauma is one of the highest-volume presentations in any emergency or orthopaedic service worldwide, and the clinical examination is the universal first step regardless of resource setting.

Global epidemiology

• Hand and wrist injuries account for a large share of all emergency department trauma presentations across high-, middle- and low-income settings, with lacerations, fractures and tendon injuries predominating in working-age adults.
• Occupational and machinery-related mechanisms are over-represented in industrial and agricultural economies, while falls and sport dominate in many high-income settings.
• Flexor and extensor tendon, digital nerve and vascular injuries cluster in young working adults, making accurate first-contact examination economically as well as clinically important.

Side-by-side guidance

Registry and practice variation

• Distal radius fracture fixation is tracked in arthroplasty and trauma registries and large series; flexor and extensor tendon rupture (especially FPL and EPL) is a recognised complication of volar plating, which is why specific thumb-tendon testing belongs in every post-fixation review.
• In well-resourced settings, ultrasound, MRI and electrodiagnostics are readily available adjuncts after the clinical examination.
• In limited-resource settings, the structured clinical examination carries even greater weight because imaging and electrodiagnostics may be delayed or unavailable; the same look-feel-move-test-function sequence still localises the lesion and triages urgency.

Hand examination feels objective, but several widely taught manoeuvres are weaker than candidates assume. Knowing the limits is a hallmark of consultant-level reasoning.