Synopsis
Recognise and treat the local and systemic metabolic consequences that can follow restoration of blood flow to an ischaemic limb.
- Restoring flow to severely ischaemic muscle can wash potassium, acid, myoglobin and inflammatory mediators into the circulation, causing arrhythmia, shock and kidney injury.
- Obtain continuous ECG monitoring and serial potassium, blood gas, creatinine, creatine kinase and urine-output measurements before and after high-risk reperfusion.
- Give intravenous calcium immediately for hyperkalaemic ECG toxicity; calcium protects the myocardium but does not lower the serum potassium concentration.
Key red flags
Peaked T waves, PR prolongation, absent P waves, QRS widening, bradycardia or ventricular arrhythmia after reperfusion requires immediate hyperkalaemia treatment.
Rapidly increasing compartment swelling, passive-stretch pain or new neurological loss despite restored pulses indicates compartment syndrome and needs emergency fasciotomy assessment.
Oliguria, dark urine, severe acidosis or rapidly rising creatine kinase indicates rhabdomyolysis with acute kidney injury and likely rebound potassium.
Peaked T waves, PR prolongation, disappearing P waves, broad QRS, bradycardia or ventricular arrhythmia after reperfusion demands immediate calcium.
Sudden hypotension, acidosis and rising potassium immediately after clamp release or thrombectomy suggests systemic release from an ischaemic muscle bed.
Swollen painful muscle, dark urine, rising creatine kinase and phosphate with falling calcium indicates extensive myocyte injury and renal risk.
Oliguria, increasing creatinine and persistent acidosis reduce potassium clearance and predict rebound after temporary intracellular shifting treatment.
Escalating pain, passive-stretch pain, tense swelling or new sensory and motor deficit after flow restoration indicates compartment syndrome.
Persistent fixed mottling, muscle rigor, profound anaesthesia or worsening systemic toxicity may show that flow restoration has not rescued dead tissue.
Investigation priorities
Detect evolving potassium-mediated conduction toxicity before cardiac arrest occurs.
Management branches
A patient with prolonged Rutherford IIb leg ischaemia is moving to urgent thrombectomy and flow restoration.
- Inputs: document ischaemia duration, involved muscle mass, neurological deficit, baseline ECG, potassium, blood gas, creatinine, CK and urine output.
- Reasoning: recognise that prolonged severe muscle ischaemia predicts potassium and acid washout plus oedema when flow returns, even if baseline potassium is normal.