Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Identify a suddenly threatened limb, grade viability and start time-critical anticoagulation and vascular treatment without avoidable imaging delay.
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.
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.
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.
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.
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.
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.
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.
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.
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.
No sensory or motor loss; arterial and venous Doppler signals are audible. Urgent assessment is still required, but the limb is not immediately threatened.
Minimal sensory loss, usually toes, with no motor deficit; salvageable if treated promptly.
Sensory loss beyond the toes and rest pain, with mild or moderate weakness; arterial Doppler usually absent and urgent revascularisation is mandatory.
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.
Abrupt onset, atrial fibrillation, recent myocardial infarction, valve disease, known intracardiac thrombus, aneurysm or a normal contralateral limb.
Prior claudication/rest pain, previous bypass/stent, diffuse pulse loss, smoking, diabetes or known PAD; onset may be less dramatic because of collaterals.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Motor deficit is the key bedside sign of an immediately threatened Rutherford IIb limb.
Record both arterial and venous signals; a palpable pulse elsewhere does not exclude a distal threatened territory.
Anticoagulation limits propagation but does not replace embolectomy, thrombectomy, thrombolysis or bypass when the limb is threatened.
Biomarkers may lag and guidelines advise against using CK/myoglobin alone to decide salvage versus amputation.
Compartment syndrome, hyperkalaemia and acidosis can follow a technically successful procedure.
Waiting for CTA before calling vascular surgery in a limb with sensory or motor deficit.
Failing to document motor power and sensation, making deterioration impossible to recognise.
Treating a normal or modest CK as evidence that the limb is safe.
Assuming heparin alone will salvage a Rutherford IIb limb.
Missing compartment syndrome and metabolic collapse after reperfusion.
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A patient develops sudden left-foot pain. The foot is cool with absent arterial Doppler, reduced sensation beyond the toes and new weak ankle movement. What is the priority?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
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.
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.