Acute limb ischaemia

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

ALI commonly results from cardiac embolism, in-situ thrombosis of atherosclerotic disease, thrombosed aneurysm, graft/stent occlusion or arterial injury. Sudden severe symptoms in a previously asymptomatic limb favour embolism; preceding claudication and collateral vessels favour thrombosis, but management is governed first by viability.

Examine both limbs and document capillary refill, temperature, colour, pulses, continuous-wave Doppler signals, sensation and motor power. Serial examinations matter because a viable limb can deteriorate while tests or transfer are arranged.

Treatment may be surgical embolectomy/bypass, catheter-directed thrombolysis, aspiration/mechanical thrombectomy or a hybrid approach. An insensate, paralysed, rigorously fixed Rutherford III limb is generally not salvageable; attempted reperfusion may cause fatal systemic injury.

Key points

ALI is a sudden fall in limb perfusion, usually within 14 days, that threatens tissue viability.
The six Ps—pain, pallor, pulselessness, perishing cold, paraesthesia and paralysis—describe the syndrome, but an incomplete set does not exclude it.
Neurological deficit drives urgency: paraesthesia and especially motor weakness indicate a threatened limb.
Rutherford I is viable, IIa marginally threatened, IIb immediately threatened and III irreversible.
Call vascular surgery before waiting for routine tests; a IIb limb requires immediate revascularisation planning.
Give IV unfractionated heparin promptly unless active bleeding, previous heparin-induced thrombocytopenia or another major contraindication exists.
CTA is usual first-line anatomical imaging when it will guide treatment, but imaging must not delay revascularisation of an immediately threatened limb.
After reperfusion, actively look for compartment syndrome, hyperkalaemia, acidosis, acute kidney injury and recurrent ischaemia.

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

Cardiac or proximal embolism

Atrial fibrillation, recent myocardial infarction, valve disease, intracardiac thrombus or an aneurysm can release embolic material. Abrupt severe symptoms in a previously asymptomatic limb and a normal opposite limb support this mechanism.

In-situ arterial thrombosis

A diseased peripheral artery can thrombose over an atherosclerotic stenosis. Previous claudication, rest pain, smoking, diabetes and diffuse pulse loss suggest underlying disease, sometimes with a less dramatic onset because collaterals exist.

Graft, stent or aneurysm thrombosis

Previous bypasses and stents may occlude, while a thrombosed peripheral aneurysm can block both the main channel and distal runoff. Prior vascular history and imaging help define this anatomy.

Arterial injury

Trauma or an arterial procedure may disrupt the intima, thrombose the vessel or create local compression. A close temporal relation, wound or access-site abnormality supports an iatrogenic or traumatic cause.

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

1
Abrupt arterial obstruction
Embolus, thrombus or injury suddenly reduces flow beyond the blockage. The severity depends on lesion location, completeness and whether pre-existing collateral channels can sustain the distal tissues.
2
Distal microcirculatory failure
Reduced inflow produces pallor, cooling, pain and loss of an arterial Doppler signal. Continued oxygen deprivation impairs peripheral nerves, causing paraesthesia before progressing to motor weakness.
3
Irreversible tissue injury
Prolonged severe ischaemia causes muscle and nerve necrosis, profound anaesthesia and paralysis or rigor. At this stage, attempted reperfusion may release a dangerous systemic load without salvaging the limb.
4
Reperfusion injury
Restored flow carries potassium, acid and muscle breakdown products into the circulation and increases tissue swelling. Metabolic instability, acute kidney injury and compartment syndrome may follow an otherwise successful procedure.

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

Rutherford I—viable

No sensory or motor loss; arterial and venous Doppler signals are audible. Urgent assessment is still required, but the limb is not immediately threatened.

Rutherford IIa—marginally threatenedRed flag

Minimal sensory loss, usually toes, with no motor deficit; salvageable if treated promptly.

Rutherford IIb—immediately threatenedRed flag

Sensory loss beyond the toes and rest pain, with mild or moderate weakness; arterial Doppler usually absent and urgent revascularisation is mandatory.

Rutherford III—irreversibleRed flag

Profound anaesthesia, paralysis/rigor and absent arterial and venous Doppler signals suggest non-viable tissue; urgent senior decision about primary amputation or palliation is required.

Embolic clues

Abrupt onset, atrial fibrillation, recent myocardial infarction, valve disease, known intracardiac thrombus, aneurysm or a normal contralateral limb.

Thrombotic clues

Prior claudication/rest pain, previous bypass/stent, diffuse pulse loss, smoking, diabetes or known PAD; onset may be less dramatic because of collaterals.

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
Immediate serial neurovascular examination with hand-held DopplerFirst step
Why
Grade limb viability and detect deterioration.
Interpretation and limitations
Motor deficit or spreading sensory loss indicates Rutherford IIb and must accelerate revascularisation; absent venous as well as arterial signals supports Rutherford III.
02
CT angiography with runoff
Why
Locate occlusion and plan open, endovascular or hybrid treatment.
Interpretation and limitations
Preferred first-line anatomical imaging when it does not delay treatment; shows inflow, lesion length, distal runoff, aneurysm and prior grafts.
03
FBC, U&E/eGFR, glucose, coagulation screen, group-and-save
Why
Prepare for anticoagulation/procedure and identify anaemia, renal impairment, diabetes or coagulopathy.
Interpretation and limitations
Correct material abnormalities in parallel; do not wait for results before vascular contact or heparin when it is clearly safe to start.
04
Blood gas, lactate, potassium and CK
Why
Assess systemic ischaemia/reperfusion risk and establish baselines.
Interpretation and limitations
Marked abnormalities signal severity and peri-operative risk, but CK/myoglobin must not be used alone to deny revascularisation.
05
ECG, telemetry and echocardiography when stable
Why
Find atrial fibrillation or a cardiac embolic source and guide recurrence prevention.
Interpretation and limitations
This follows immediate limb salvage priorities; a normal ECG does not exclude paroxysmal AF.

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

Deep-vein thrombosis

Venous thrombosis usually produces swelling, warmth and venous tenderness rather than a cold pale limb with absent arterial Doppler signals. Massive venous obstruction can produce painful cyanotic swelling and may also threaten perfusion, so it requires urgent specialist assessment.

Acute compartment syndrome

Severe pain out of proportion, pain on passive stretch and a tense compartment favour compartment syndrome. Arterial pulses may remain present until late, so pulse presence alone does not exclude it.

Peripheral nerve or spinal disease

Radiculopathy or acute neuropathy can cause pain, sensory loss and weakness, but the limb generally remains warm with preserved colour, capillary refill and arterial Doppler signals.

Ruptured popliteal cyst

A ruptured cyst produces sudden calf pain and swelling that may mimic thrombosis. Preserved arterial perfusion and ultrasound evidence of a fluid collection support this diagnosis and argue against an immediately threatened arterial limb.

Peripheral vasospasm

Vasospasm tends to cause episodic, often symmetrical distal colour change with recovery on warming and preserved proximal signals. Persistent neurological loss or an absent arterial Doppler signal argues for occlusion.

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

01first minutesSuspected ALIFirst stepSudden limb pain/coldness, pulse loss, sensory change or weakness.

1First: assess ABCs, note exact onset, examine both limbs and document Doppler, sensation and motor power; give analgesia and keep the patient nil by mouth.
2Next: contact the on-call vascular specialist immediately and arrange transfer to a centre offering open and endovascular treatment.
3Next: give IV unfractionated heparin unless contraindicated; provide IV access, cautious hydration and oxygen only when hypoxaemic.
4EscalationEscalation: repeat the limb examination during every delay or transfer and report any new sensory or motor deficit at once.

02threatened limbRutherford IIa or IIbSensory loss with or without motor weakness but a potentially salvageable limb.

1First: IIb with weakness goes directly to immediate revascularisation planning; do not wait for non-essential imaging.
2Next: obtain CTA when the vascular team judges it will guide treatment without harmful delay.
3Next: choose surgical embolectomy/bypass, catheter-based thrombectomy/thrombolysis or a hybrid approach according to cause, severity, duration and bleeding risk.
4EscalationEscalation: monitor in a high-acuity setting for reperfusion injury and compartment syndrome; fasciotomy is urgent when compartment syndrome develops.

03non-viableRutherford IIIProfound anaesthesia, paralysis/rigor and absent arterial and venous Doppler signals.

1First: obtain immediate senior vascular confirmation and assess the whole patient, goals and likelihood of systemic harm from reperfusion.
2Next: do not undertake routine thrombolysis or blind reperfusion of established irreversible ischaemia.
3Next: plan primary amputation when appropriate, or symptom-focused care if surgery is not consistent with prognosis or preferences.
4EscalationEscalation: treat shock, hyperkalaemia, acidosis, renal injury and sepsis in parallel.

04aftercarePrevent recurrence after salvageSuccessful revascularisation or stabilisation.

1First: reassess limb perfusion, wounds, renal function, potassium and muscle compartments.
2Next: investigate embolic source, graft/stent failure, aneurysm and underlying PAD.
3Next: use long-term anticoagulation after an AF/intracardiac-thrombus embolus; use antiplatelet and lipid therapy for atherosclerotic disease as indicated.
4EscalationEscalation: urgent re-imaging/re-intervention for recurrent pain, pulse loss, falling Doppler signal or new neurology.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Immediate anticoagulation to limit clot propagation while awaiting revascularisation.

Unfractionated heparin

5,000 units IV bolus, or 70–100 units/kg IV, followed by an IV infusion adjusted to APTT or ACT response.

Do not give with active major bleeding or previous immune HIT; review recent surgery, intracranial bleeding risk and baseline platelets/coagulation. A non-heparin anticoagulant needs specialist/haematology input if HIT is suspected.

Severe ischaemic pain while definitive treatment is arranged.

Morphine

One licensed injection regimen uses 2.5–10 mg IV, injected slowly over 4–5 minutes; select the lowest effective dose and titrate any further dosing to response in a monitored setting.

Reduce dose in older/frail people and use particular caution in renal or hepatic impairment; monitor consciousness, respiratory rate, oxygenation and BP. Analgesia must not postpone repeated neurological examination.

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

Limb necrosis and amputation

Persistent ischaemia destroys muscle, skin and nerve, eventually making the limb non-viable. Profound anaesthesia, paralysis or rigor suggest advanced, potentially irreversible injury requiring an urgent senior salvage decision.

Compartment syndrome

Reperfusion increases capillary leak and muscle swelling within fixed fascial spaces. Rising pressure then impairs the newly restored circulation, causing recurrent pain, neurological loss and further tissue damage.

Hyperkalaemia and acidosis

Ischaemic muscle accumulates potassium and acid, which enter the circulation after reperfusion. Severe abnormalities can destabilise cardiac conduction and contribute to peri-procedural circulatory collapse.

Rhabdomyolysis and kidney injury

Necrotic muscle releases creatine kinase and myoglobin, while shock reduces renal perfusion. The combination can cause acute kidney injury, particularly after a large ischaemic territory is reperfused.

Recurrent embolism or thrombosis

An unrecognised or untreated cardiac embolic source, diseased graft or underlying peripheral arterial disease can lead to repeat occlusion in the treated or another vascular territory.

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

Repeat and time-stamp sensation, motor power, temperature, capillary refill and arterial/venous Doppler findings.
During UFH, monitor APTT/ACT to the treatment protocol plus platelets, haemoglobin and bleeding.
After reperfusion, monitor limb swelling/tenseness, pain on passive stretch and neurological function for compartment syndrome.
Trend potassium, acid-base status, lactate, CK, creatinine/eGFR and urine output for reperfusion injury.
Before discharge, document the embolic/thrombotic cause, long-term antithrombotic plan, smoking/lipid management and vascular follow-up.

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

Weakness changes the clock

Motor deficit is the key bedside sign of an immediately threatened Rutherford IIb limb.

Doppler is more than pulse hunting

Record both arterial and venous signals; a palpable pulse elsewhere does not exclude a distal threatened territory.

Heparin is a bridge, not reperfusion

Anticoagulation limits propagation but does not replace embolectomy, thrombectomy, thrombolysis or bypass when the limb is threatened.

A normal CK cannot reassure

Biomarkers may lag and guidelines advise against using CK/myoglobin alone to decide salvage versus amputation.

Reperfusion creates a second emergency

Compartment syndrome, hyperkalaemia and acidosis can follow a technically successful procedure.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for CTA before calling vascular surgery in a limb with sensory or motor deficit.
02
Failing to document motor power and sensation, making deterioration impossible to recognise.
03
Treating a normal or modest CK as evidence that the limb is safe.
04
Assuming heparin alone will salvage a Rutherford IIb limb.
05
Missing compartment syndrome and metabolic collapse after reperfusion.