01Purpose and principlesWhat the treatment does and how it fits into care.
Initial treatment has two goals: stop additional thrombus formation and deliver the patient to a team able to restore flow before tissue becomes unsalvageable. Anticoagulation does not reperfuse an occluded artery. It reduces propagation and further embolisation while the vascular service selects thrombectomy, thrombolysis, endovascular treatment, bypass, primary amputation or palliation according to viability, anatomy and patient factors.
The current UK SmPC for heparin sodium 5,000 IU/mL includes acute peripheral arterial occlusion. For adults it specifies a 5,000 IU intravenous loading dose followed by a continuous intravenous infusion of 1,000–2,000 IU/hour, with laboratory monitoring beginning 4–6 hours after initiation and adjustment to an APTT 1.5–2.5 times the midpoint of the normal or control range. Hospitals use product-specific preparation and assay-calibrated UFH nomograms, so the prescription must name the formulation, dose, route and monitoring plan.
Heparin must not become a checkbox that delays referral or ignores contraindications. Active bleeding and a history compatible with immune HIT are particularly consequential. If UFH is unsafe, contact vascular surgery immediately and obtain haematology or thrombosis advice for a non-heparin alternative selected for renal function, planned operation and local availability. Do not substitute low-molecular-weight heparin automatically in immune HIT.
Imaging supports treatment only when the timeline is safe. A viable or marginally threatened limb can usually undergo rapid anatomical imaging, whereas new weakness makes the limb immediately threatened. The vascular clinician should decide whether direct transfer to theatre, a hybrid suite or an interventional unit is faster than local imaging. A Rutherford III limb requires experienced confirmation because attempted reperfusion of necrotic muscle can cause severe hyperkalaemia, acidosis and renal injury.
Key points
- Contact the on-call vascular service immediately, map sensory and motor loss, and treat any weakness or sensory loss beyond the toes as an immediately threatened Rutherford IIb limb.
- Give intravenous unfractionated heparin promptly unless active major bleeding, a critical bleeding site or current or previous immune HIT contraindicates it; seek urgent vascular and haematology advice for an alternative.
- Do not let CTA, duplex, ABPI, blood results or transfer administration delay emergency revascularisation; profound anaesthesia, paralysis and absent arterial plus venous signals require senior confirmation of irreversible Rutherford III.
- Provide titrated analgesia, intravenous access, fluids when clinically indicated, nil-by-mouth status and correction of major physiological derangement in parallel.
- Use the current UK heparin SmPC regimen and the hospital UFH infusion nomogram rather than guessing preparation or assay targets.
- Draw full blood count, coagulation, renal profile, electrolytes, CK and group-and-save without postponing vascular contact or heparin when safe.
- Document onset, Rutherford features, anticoagulation time, contraindication screen, referral acceptance, destination and imaging decision.
- Continue serial neurovascular examination during every wait or transfer because deterioration changes the urgency and intervention window.
02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.
No weakness with no sensory loss or numbness confined to the toes indicates a marginally threatened limb that remains salvageable if treated promptly.
Sensory loss beyond the toes, rest pain and especially mild to moderate motor weakness indicate immediate threat requiring emergency revascularisation.
Profound anaesthesia, paralysis or rigor, absent capillary refill and absent arterial and venous Doppler signals indicate likely irreversible damage.
Active clinically important haemorrhage, suspected intracranial bleeding or a recent operation at a critical bleeding site makes routine heparin unsafe and needs senior discussion.
Previous immune heparin-induced thrombocytopenia or new thrombosis with an unexplained platelet fall requires avoidance of heparin and urgent specialist anticoagulant selection.
Shock, arrhythmia, acidosis, hyperkalaemia, oliguria or bilateral ischaemia increases immediate mortality risk and requires resuscitation alongside vascular decision-making.
Increasing analgesia requirement, spreading numbness or new weakness while awaiting transport must be reported directly to the accepting vascular clinician rather than merely documented.
03Assessment before treatmentTests and checks that guide safe selection.
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 sensory, motor and Doppler assessmentFirst step - Why
- Grade limb viability and determine how much diagnostic delay is permissible.
- Interpretation and limitations
- Toe-only sensory loss without weakness is IIa; broader loss or any weakness is IIb; profound anaesthesia and paralysis with absent arterial and venous signals suggests III. Repeat during waits.
- 02
Full blood count including platelets - Why
- Identify anaemia, thrombocytopenia and a baseline for anticoagulation and intervention.
- Interpretation and limitations
- A low or rapidly falling platelet count plus recent heparin exposure raises HIT. The result can change anticoagulant choice, but sampling must occur without delaying emergency vascular contact.
- 03
Coagulation screen and baseline APTT - Why
- Establish haemostatic context and provide a baseline before UFH titration.
- Interpretation and limitations
- A prolonged baseline APTT may make standard titration unreliable and should prompt specialist interpretation or an alternative assay. A normal result does not remove bleeding risk.
- 04
Renal profile, electrolytes and acid-base status - Why
- Guide contrast, fluids, alternative anticoagulants and management of ischaemic muscle injury.
- Interpretation and limitations
- Hyperkalaemia or acidosis can become rapidly life-threatening, especially after reperfusion. Renal dysfunction affects contrast planning and many non-heparin anticoagulants, but not the referral urgency.
- 05
Creatine kinase and urinalysis - Why
- Assess muscle injury and myoglobin release before and after reperfusion.
- Interpretation and limitations
- Marked CK elevation or dark urine supports substantial muscle injury and renal risk. Normal early values cannot demonstrate viability or justify delay when neurological deficit is present.
- 06
CT angiography or immediate procedural angiography - Why
- Map anatomy for endovascular or open revascularisation when time allows.
- Interpretation and limitations
- Choose the fastest study that meaningfully guides treatment. In IIb disease, imaging is appropriate only if it does not delay emergency reperfusion; obvious III may proceed to senior amputation planning.
04Treatment approachPreparation, options, escalation and aftercare.
01Immediate ALI pathwayAnticoagulate and connect to definitive careFirst stepDefinitiveAcute pain, coldness, pulse or Doppler loss, paraesthesia or weakness creates suspected acute limb ischaemia.+
- 1Call the on-call vascular service immediately, state symptom onset and Rutherford sensory, motor and Doppler findings, and agree destination before routine investigations create delay.
- 2Give titrated analgesia, establish intravenous access, screen rapidly for active bleeding and previous immune HIT, then give the licensed intravenous UFH regimen when safe.
- 3Keep the patient nil by mouth, support circulation with intravenous fluid when indicated, draw baseline bloods and correct dangerous hyperkalaemia or acidosis in parallel.
- 4Arrange CTA, duplex or direct procedural imaging only through the vascular plan; new motor deficit makes emergency reperfusion the priority.
- 5Repeat and communicate examination changes through transfer, documenting heparin dose, infusion, monitoring and any reason it was withheld.
02Heparin contraindicatedEscalate for a non-heparin planEscalationActive major bleeding, a critical bleeding site or current or previous immune HIT makes routine UFH unsafe.+
- 1Do not delay vascular referral while looking for a substitute; state the exact contraindication and last heparin exposure to the receiving team.
- 2For suspected or confirmed immune HIT, avoid UFH and LMWH and obtain urgent haematology advice on a locally available non-heparin anticoagulant.
- 3AlternativeMatch any alternative to renal and hepatic function, planned procedure, monitoring capability and reversibility, with a named senior prescriber.
- 4If bleeding is active, resuscitate and control the source while vascular specialists balance thrombosis, haemorrhage and limb viability.
03Immediately threatened limbPrevent imaging delay in Rutherford IIbSensory loss extends beyond the toes or any ischaemic motor weakness is present.+
- 1Tell the accepting vascular clinician that neurological deficit is present and give the latest time-stamped examination rather than saying only “cold leg”.
- 2Transfer directly to the location capable of emergency revascularisation when remote imaging would add delay without changing the plan.
- 3Continue heparin when safe, analgesia and physiological monitoring while preparing for open, endovascular or hybrid reperfusion.
- 4Watch for worsening paralysis, acidosis and hyperkalaemia, which may alter salvageability and peri-operative risk.
04Likely irreversible limbConfirm before avoiding reperfusionProfound anaesthesia, paralysis or rigor and absent arterial and venous signals indicate Rutherford III.+
- 1AlternativeObtain immediate senior vascular assessment to confirm irreversibility and identify any discordant feature or alternative diagnosis.
- 2Avoid automatic revascularisation of established necrotic tissue because reperfusion can release lethal potassium, acid and myoglobin.
- 3Plan primary amputation or comfort-focused care according to physiology, comorbidity, goals and multidisciplinary judgement.
05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.
Unfractionated heparin
For adult acute peripheral arterial occlusion, give 5,000 IU intravenously, then infuse 1,000–2,000 IU/hour; check APTT 4–6 hours after initiation and adjust to 1.5–2.5 times the midpoint of normal or control using the local nomogram.Do not use during active bleeding or in current or previous heparin-associated thrombocytopenia and seek urgent specialist advice after major trauma or recent brain, spinal or eye surgery. Confirm the exact 5,000 IU/mL product and infusion dilution, baseline platelets and coagulation; older adults or advanced renal or hepatic disease may need dose reduction and closer bleeding review.
06Complications, monitoring and follow-upAdverse effects, response and longer-term review.
- Use the hospital UFH nomogram for timed APTT or anti-Xa sampling, infusion adjustment and response to unexpectedly high or low results.
- Repeat haemoglobin, platelets and clinical bleeding assessment; stop heparin and evaluate urgently if immune HIT or significant haemorrhage is suspected.
- Check plasma potassium before treatment in people at risk and during prolonged therapy, because heparin-associated hypoaldosteronism can cause hyperkalaemia.
- Repeat sensory and motor examination and Doppler signals during referral, imaging and transfer, immediately reporting any deterioration.
- Follow potassium, pH, renal function, CK, urine output and ECG after prolonged ischaemia or reperfusion.
- After intervention, document restored perfusion and monitor for re-occlusion, distal embolisation, bleeding and compartment syndrome.
07Special situationsVariants, exceptions and circumstances that change the usual approach.
Heparin is temporising
It limits further clot formation but does not reopen a blocked artery; a threatened limb still needs a definitive reperfusion decision.
The prescription must be complete
Write product strength, loading dose, infusion dose and solution, assay, sampling time, adjustment pathway and responsible team rather than “start heparin”.
HIT can present as thrombosis
Immune HIT may cause new arterial thrombosis before thrombocytopenia is obvious, particularly after heparin exposure within the preceding weeks.
Imaging has conditional value
Good anatomy is useful, but its value becomes negative if obtaining it postpones treatment of an immediately threatened limb.
Communication is clinical treatment
A time-stamped statement of motor power, sensory extent and Doppler signals helps the vascular team choose direct transfer and prepare theatre resources.
Irreversibility changes the goal
When Rutherford III is confirmed, avoiding futile reperfusion can prevent systemic toxicity and redirect care to primary amputation or symptom control.
08Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for CT angiography or blood results before making the first vascular telephone call.
- 02
Writing only “heparin infusion” without a loading dose, strength, rate, assay target or monitoring time.
- 03
Giving LMWH automatically to a patient with previous immune HIT because it is a different preparation.
- 04
Treating pain relief as evidence that limb perfusion or neurological function has improved.
- 05
Using a bleeding contraindication to justify delaying specialist referral instead of seeking an alternative plan.
- 06
Failing to repeat toe and ankle power during transfer after an initially marginal examination.