Neurovascular compromise after fracture or reduction

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Create a reproducible baseline before sedation or manipulation whenever physiology allows. Record limb colour, temperature, capillary refill, wound bleeding and pulse strength compared with the other side, adding handheld Doppler signals. Test named motor actions against gravity where safe and small autonomous sensory zones, not a vague global feel. Document pain limitations and pre-existing neuropathy. A written or electronic diagram makes later change visible across handovers.

Match anatomy to the injury. Shoulder dislocation threatens axillary nerve sensation over the regimental-badge area and deltoid contraction. Humeral shaft injury threatens radial wrist and finger extension and first-dorsal-web-space sensation. Elbow or forearm injury needs median thumb opposition or index flexion, anterior interosseous pinch, ulnar finger abduction and radial extension testing. Around the knee, document common fibular dorsiflexion and first-web sensation, tibial plantarflexion and sole sensation and popliteal-to-foot perfusion.

Arterial examination drives immediate action. Control external bleeding with direct pressure, packing or a distal tourniquet, not blind clamps. A pulseless deformed limb is urgently realigned and splinted. Repeat pulse comparison, Doppler and perfusion with the time. If the injured pulse does not feel the same as the contralateral side after these steps, current BOASt treats arterial injury as suspected until CT angiography demonstrates otherwise. Normal capillary refill alone cannot clear an intimal lesion.

Hard vascular findings and instability shorten the pathway. Uncontrolled bleeding and a persistently ischaemic limb need simultaneous resuscitation and consultant-led orthopaedic plus vascular or plastic operation. CT angiography is recommended when arterial injury is suspected and should be obtained concurrently with suitable whole-body CT, but not at the cost of delayed haemorrhage control. There is no safe ischaemic time; BOASt expects emergency revascularisation to commence within one hour of arrival.

The operative sequence restores flow quickly and protects the repair. A temporary shunt is recommended when it provides the fastest reperfusion. Current BOASt then advises rapid skeletal reduction and stabilisation immediately after reperfusion and before definitive arterial reconstruction. Use repair or interposition graft when feasible, consider fasciotomy after every revascularisation and document a senior decision not to decompress. Postoperatively, reassess under staff trained to detect a threatened limb and consider single antiplatelet therapy only after bleeding-risk assessment.

Nerve deficits have their own clock. BOASt requires examination after any injection, manipulation or cast and before and after relevant surgery. A dislocation with deficit is reduced immediately; an unstable fracture is reduced and provisionally stabilised as soon as safe. For a new deficit, remove pressure and gently reposition. Seek immediate advice for a nerve visibly injured during surgery or a persistent new postoperative deficit, and advice within twenty-four hours for penetrating deficit or nerve injury not otherwise requiring fracture operation.

Do not misclassify compartment syndrome as isolated neuropraxia. Escalating pain, passive-stretch pain and tense swelling with present pulses needs compartment assessment and may require immediate decompression. After reperfusion, monitor potassium, acid-base state, CK, renal function and compartments because swelling can worsen. Long-term review assesses graft patency, fracture healing, motor recovery, protective sensation, neuropathic pain and function, with splinting, tendon transfer or nerve reconstruction considered through the specialist pathway.

Key points

Record what each named nerve and artery does, not the phrase neurovascularly intact: test individual motor actions, autonomous sensory areas, pulse quality, Doppler, temperature and capillary refill.
Examine at first opportunity and again after analgesic injection, manipulation, reduction, splintage, casting, before and after surgery and whenever pain, swelling or function changes.
Control haemorrhage immediately with direct pressure, wound packing or the most distal effective tourniquet; do not use blind clamping inside the wound.
Urgently realign and splint a deformed pulseless limb and repeat the timed arterial examination. Persistent pulse inequality means suspected arterial injury until shown otherwise.
CT angiography is recommended for suspected arterial injury and should run with whole-body CT when appropriate, but uncontrolled bleeding or a persistently ischaemic limb must not wait for imaging.
Current BOASt expects emergency revascularisation to commence within one hour of hospital arrival; use a temporary vascular shunt when it restores flow fastest, then achieve rapid skeletal stability before definitive repair.
For a new nerve deficit, release circumferential bandages and plaster fully to skin and gently reposition. Persistent postoperative deficit requires immediate specialist contact.
Seek peripheral-nerve advice within 24 hours for penetrating injury with deficit or a nerve injury without planned fracture surgery, and before fixation when a deficit accompanies the fracture.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Displacement and traction

Fracture fragments or dislocation stretch, kink or compress adjacent arteries and nerves, especially around the knee, elbow, shoulder and ankle.

Direct laceration

Sharp bone, penetrating trauma or operative instruments can partially or completely divide a vessel or nerve while the skin opening remains small.

Intimal and thrombotic injury

Blunt traction can tear the arterial intima, creating delayed thrombosis despite an initially warm limb and palpable or Doppler-detected flow.

External or implant compression

Tight casts, swelling, malpositioned screws, plates, sutures or haematoma can create a new postoperative or post-reduction deficit.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Macrovascular ischaemia
Occlusion or transection stops tissue inflow, causing energy failure, acidosis and progressive muscle and nerve necrosis with no reliably safe ischaemic duration.
2
Collateral masking
Collateral circulation may maintain warmth or a distal pulse despite a significant lesion, so asymmetry and mechanism remain important after reduction.
3
Nerve conduction block
Compression and traction can cause transient neurapraxia, while axonal disruption or division produces slower, incomplete recovery and muscle denervation.
4
Compartment microischaemia
Raised fascial pressure can compromise nerve and muscle capillaries while large-vessel pulses persist, producing a different but concurrent surgical emergency.
5
Reperfusion toxicity
Returning flow washes potassium, myoglobin and acids systemically and drives capillary leak, risking arrhythmia, renal injury and renewed compartment pressure.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Hard arterial signs

Active haemorrhage, expanding pulsatile haematoma, bruit or thrill and distal ischaemia indicate a confirmed emergency that should bypass avoidable diagnostic delay.

Soft arterial signs

Pulse asymmetry, concerning trajectory, stable haematoma or isolated nerve deficit raises suspicion and usually prompts CT angiography after urgent alignment.

Intimal injury pattern

Initially preserved flow followed by pulse loss, coolness or worsening pain after blunt traction suggests delayed thrombosis rather than simple spasm.

Neuropraxic pattern

Motor and sensory loss immediately after traction that improves after reduction and pressure release suggests conduction block but still requires serial documentation.

Nerve laceration pattern

A penetrating wound with complete deficit, observed discontinuity or no recovery after alignment needs early specialist nerve advice and planned exploration.

Post-reduction deterioration

A new deficit after manipulation can reflect cast pressure, altered fragment position, entrapment, compartment syndrome or iatrogenic injury and is never routine.

Red flags requiring action

Active haemorrhage, expanding pulsatile haematoma, bruit or thrill, a cold pale pulseless limb or rapidly progressive neurological loss requires immediate operative haemorrhage control or revascularisation rather than delayed diagnostic observation.
A deformed pulseless limb must be realigned and splinted urgently; failure of pulses and perfusion to normalise makes arterial injury presumptive until CT angiography or surgery proves otherwise.
New severe pain, passive-stretch pain, tension, paraesthesia or weakness with preserved pulses may be compartment syndrome and needs the separate immediate decompression pathway.
A new nerve deficit after reduction, casting or surgery requires release of bandages and plaster to skin, gentle repositioning and immediate specialist contact if it persists; documentation of the previous examination is critical.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line timed clinical examinationFirst stepFirst line
Why
Establish arterial and named-nerve status before and after every intervention.
Interpretation and limitations
Record comparison, modality, examiner, time and limiting pain; repeated examination detects change that one normal entry cannot exclude.
02
Handheld Doppler
Why
Confirm and compare arterial signals when pulses are difficult to palpate.
Interpretation and limitations
A signal does not prove normal flow or exclude intimal injury; waveform quality and side-to-side difference inform escalation.
03
CT angiography
Why
Locate suspected occlusion, intimal flap, extravasation or transection for operative planning.
Interpretation and limitations
Recommended after realignment when suspicion persists and physiology permits; combine with whole-body CT but bypass when haemorrhage or ischaemia demands operation.
04
Pressure and compartment assessment
Why
Identify microvascular ischaemia coexisting with intact larger arteries.
Interpretation and limitations
Use hourly clinical examination and concurrent pressure measurement when incomplete; a delta pressure below 30 mmHg signals increased risk.
05
Fracture and joint radiographs
Why
Define displacement, dislocation and implant or fragment relationships to neurovascular structures.
Interpretation and limitations
Obtain orthogonal whole-segment views after emergency alignment when possible; imaging must not delay reduction of a dysvascular deformity.
06
Electrodiagnostic studies
Why
Localise and grade persistent axonal nerve injury during follow-up.
Interpretation and limitations
They are rarely useful in the first emergency hours; time them through the nerve service alongside serial clinical recovery and imaging.
07
Ultrasound or MRI neurography
Why
Assess selected nerve continuity, entrapment or postoperative compression.
Interpretation and limitations
Use for a defined specialist question after urgent reduction, vascular and compartment threats are controlled, not as a prerequisite for referral.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute compartment syndrome

Disproportionate pain and passive-stretch pain with preserved pulses suggests microvascular compartment compromise, although both conditions can coexist.

Pain-limited movement

Severe fracture pain can suppress effort without true nerve loss, but sensory change or failure after analgesia and realignment requires escalation.

Pre-existing neuropathy

Diabetes, radiculopathy or previous nerve injury can alter baseline sensation and power, making collateral history and contralateral comparison essential.

Central neurological injury

Spinal cord, plexus or brain injury can cause broader deficits that do not map to the single peripheral nerve adjacent to a fracture.

Venous obstruction

Marked swelling and cyanosis from venous injury impairs outflow and tissue pressure but usually differs from the cold pale pattern of arterial inflow failure.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01DysvascularRealign and restore flowFirst stepA fractured or dislocated limb is pulseless, cold, poorly perfused or actively bleeding.

1Resuscitate and control haemorrhage with pressure, packing or a distal tourniquet while documenting timed arterial and nerve findings.
2Urgently realign and splint the deformity, repeat comparison and activate consultant orthopaedic and vascular or plastic care.
3Use CT angiography concurrently with trauma CT when suspected injury remains and perfusion permits, without delaying operative control.
4DefinitiveCommence revascularisation within one hour of arrival, using a temporary shunt for rapid flow and stabilising bone before definitive repair.

02New nerve deficitRemove reversible pressureWeakness or sensory loss appears after injury, injection, reduction, cast application or surgery.

1Repeat a nerve-specific examination and compare with the immediately preceding timed entry rather than relying on a global label.
2Release bandages and plaster to skin, inspect swelling and compartments and gently reposition or reduce an associated dislocation.
3Seek immediate nerve-pathway advice if a postoperative deficit persists or nerve damage is seen, and within 24 hours for penetrating deficit.
4Document nerve relation to fixation at surgery and provide splintage, skin protection and a planned recovery or reconstruction review.

03After repairProtect reperfusion and recoveryDefinitiveArterial flow has returned or a nerve injury has entered definitive surveillance.

1Monitor pulses, Doppler, perfusion, motor and sensation frequently in a staffed setting and respond immediately to recurrent change.
2Consider fasciotomy after revascularisation and track ECG, potassium, CK, renal function and urine output for reperfusion injury.
3Assess bleeding before specialist single-antiplatelet therapy and communicate the exact graft, fixation and thrombosis plan.
4Follow graft patency, fracture union, nerve regeneration, contracture, pain and meaningful limb function through the responsible surgical teams.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Irreversible limb ischaemia

Delayed reperfusion causes muscle necrosis, fixed mottling, nerve loss, infection, systemic toxicity and primary or secondary amputation.

Compartment syndrome

Reperfusion oedema and bleeding raise fascial pressure, requiring deliberate fasciotomy consideration even after technically successful arterial repair.

Permanent peripheral nerve deficit

Missed laceration, entrapment or prolonged compression leaves weakness, sensory loss, neuropathic pain, deformity and loss of protective sensation.

Repair thrombosis or bleeding

A graft or arterial repair can occlude, leak or embolise, so recurrent pain, pulse change or swelling needs immediate reassessment.

Functional and psychological loss

Even a viable limb may retain chronic pain, poor motor control and occupational limitation requiring rehabilitation and adjustment support.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat and timestamp pulse comparison, Doppler, colour, temperature and capillary refill after reduction, splintage, imaging, fixation, vascular repair and every clinical change.
Record individual nerve motor and sensory modalities at the same transition points, including pain or sedation limitations and the relation to implants.
After revascularisation, provide frequent trained limb observations and escalate recurrent pain, signal loss, coolness, swelling or neurological deterioration immediately.
Trend ECG, potassium, acid-base state, CK, creatinine and urine output after prolonged ischaemia or crush and reassess compartments repeatedly.
Review wound, graft or repair, fracture alignment and union and any antiplatelet or anticoagulant plan against bleeding and planned procedures.
Track motor grade, sensory protection, neuropathic pain, joint range, splint needs, gait or hand use and work goals during nerve recovery.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Compare the other side

An injured pulse that feels weaker than its counterpart remains suspicious even when both are technically palpable.

A Doppler signal is not clearance

Collateral or transmitted flow can produce a signal distal to a significant lesion, so mechanism and asymmetry still matter.

Documentation changes causation

A precise pre-reduction baseline distinguishes traumatic nerve injury from entrapment, cast compression or an iatrogenic postoperative change.

Flow precedes definitive elegance

A temporary shunt can save ischaemic time before skeletal stabilisation and formal reconstruction in a complex limb.

Pulses and compartments answer different questions

Large-artery patency does not measure capillary perfusion inside a pressurised fascial space.

Skin protection is nerve care

Loss of sensation creates unnoticed pressure and thermal injury, requiring splints, footwear and education while recovery is awaited.

11Common pitfallsFrequent interpretation and management errors.

01
Recording only neurovascularly intact rather than named pulses, Doppler, motor actions and autonomous sensory territories.
02
Waiting for radiographs or CT before realigning a pulseless deformed limb.
03
Using return of a weak pulse after reduction as proof that no intimal arterial injury remains.
04
Ignoring a new nerve deficit as expected neurapraxia without releasing pressure, checking compartments and comparing prior findings.
05
Delaying revascularisation for definitive fracture fixation rather than using rapid shunting and an agreed operative sequence.
06
Failing to consider fasciotomy, metabolic reperfusion injury and repair thrombosis after arterial flow returns.