Acute limb ischaemia with a motor deficit
A 79-year-old woman with permanent atrial fibrillation, hypertension, and a 40-pack-year smoking history presents 7 hours after sudden onset of severe left leg pain. She is on apixaban 5 mg twice daily; the last dose was 10 hours ago. The left leg is pale from mid-thigh, cold below the knee, with reduced sensation over the dorsum of the foot and weakness of ankle dorsiflexion. Capillary refill is 4 seconds. The femoral pulse is present, but popliteal and pedal pulses are absent; handheld Doppler detects a faint signal over the posterior tibial artery. The right leg has a normal pulse examination. Creatinine is 124 µmol/L, potassium 4.1 mmol/L, creatine kinase 900 U/L, and lactate 3.1 mmol/L. There is no groin swelling or pulsatile mass. The vascular theatre is available, but the on-call interventional radiologist suggests catheter-directed thrombolysis.
1. Classify the limb and outline the first hour of management.
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This is Rutherford class IIb acute limb ischaemia: sudden onset, rest pain, sensory loss beyond the toes, and a motor deficit (weak ankle dorsiflexion), with a faint but audible Doppler signal. The limb is immediately threatened and requires urgent revascularisation, not observation.
In the first hour I would:
- Give IV unfractionated heparin after checking the platelet count, unless there is a contraindication. A bolus of 80 U/kg followed by infusion is reasonable; low-molecular-weight heparin is an alternative but harder to titrate in renal impairment.
- Give analgesia and keep the leg dependent and warm, without direct heat.
- Take blood for full blood count, coagulation, renal function, potassium, creatine kinase, and group and save.
- Request an ECG and involve cardiology because of atrial fibrillation.
- Call the vascular surgeon and book theatre immediately. Do not wait for CT angiography if the clinical diagnosis is clear; duplex ultrasound or on-table angiography can define the anatomy.
- Consent for embolectomy, possible bypass, and fasciotomy.
The presence of a motor deficit is the key discriminator: it makes this a surgical emergency rather than a candidate for prolonged thrombolysis.
2. The radiologist proposes catheter-directed thrombolysis. How do you respond?
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I would decline catheter-directed thrombolysis as the primary strategy. Thrombolysis has a role in Rutherford I or selected IIa limbs when immediate surgery is unavailable and the limb is not immediately threatened. In IIb there is a motor deficit and the limb is immediately threatened; the priority is rapid restoration of flow, and thrombolysis takes hours, may fail, and carries a significant bleeding risk. She has also taken apixaban within the last 10 hours, which increases the risk of haemorrhage, including intracranial bleeding.
The safer plan is surgical revascularisation, usually femoral embolectomy with intraoperative completion angiography, or bypass if the artery is diseased. The vascular surgeon may still use on-table thrombolysis as an adjunct if there is distal thrombus, but not as a delay strategy. If theatre were unavailable and transfer would cause further delay, thrombolysis could be considered as a last resort, but here theatre is available. The radiologist’s suggestion should be discussed with the vascular surgeon, and the decision documented.
3. What will you monitor after revascularisation and when would you perform fasciotomy?
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After revascularisation I would monitor for reperfusion injury and compartment syndrome. This includes hourly urine output and urine colour, serum potassium, creatinine, creatine kinase, bicarbonate, and lactate. Hyperkalaemia, myoglobinuria, metabolic acidosis, and acute kidney injury can develop within hours. I would give IV fluids to maintain urine output, treat hyperkalaemia promptly, and monitor cardiac rhythm. The leg should be examined regularly for pain out of proportion, tense compartments, and worsening neurology.
Fasciotomy is indicated for clinical compartment syndrome or when compartment pressure measurements show a delta pressure of less than 30 mmHg, not routinely for every revascularisation. Because she is heparinised, bleeding after fasciotomy can be significant; the decision must weigh the risk of muscle necrosis against bleeding. I would also monitor for re-occlusion, bleeding, haematoma, and cardiac arrhythmia. If the limb remains non-viable despite revascularisation, amputation may be necessary; this should be discussed honestly with the patient and family.