01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Ischaemic muscle loses ATP, membrane pump function and cellular integrity. Potassium and phosphate leave cells, anaerobic metabolism generates acid, and damaged myocytes release creatine kinase and myoglobin. When arterial flow returns, these products enter the systemic circulation. The resulting reperfusion syndrome can cause hyperkalaemic arrhythmia, metabolic acidosis, vasodilation, myocardial depression, acute lung injury and shock even when the artery is technically patent.
Local reperfusion is equally dangerous. Endothelial injury and reactive oxygen species increase capillary permeability, so an apparently successful revascularisation may produce marked oedema within closed fascial compartments. Microvascular perfusion can then fall despite palpable distal pulses. Prolonged or severe ischaemia, a large muscle mass, crush injury and delayed presentation increase the risk, but clinical surveillance remains necessary after any threatened-limb reconstruction.
Management anticipates release before the clamp, catheter or thrombectomy device restores flow. High-risk patients need monitoring, immediate access to hyperkalaemia treatment, renal and critical-care support, and a fasciotomy plan. Treatment separates membrane protection, intracellular potassium shift and body removal. Calcium addresses electrical toxicity only; insulin–glucose and salbutamol redistribute potassium, while renal excretion, binders or dialysis achieve clearance.
Key points
- 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.
- UKKA treatment uses 10 units soluble insulin with 25 g glucose and adds 10% glucose at 50 mL/hour for five hours when pretreatment glucose is below 7 mmol/L.
- Repeat potassium at least 1, 2, 4, 6 and 24 hours after treatment, because intracellular shift is temporary and damaged muscle may continue releasing potassium.
- Reperfusion also increases capillary leak and muscle oedema; palpable pulses do not exclude a post-revascularisation compartment syndrome.
- Severe refractory hyperkalaemia, oliguria, acidosis or continuing tissue breakdown requires early renal and critical-care planning for dialysis.
- Do not use aggressive unmeasured fluid loading as a substitute for haemodynamic assessment; resuscitation must account for heart, kidney and compartment consequences.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Prolonged limb ischaemia
Extended severe arterial occlusion injures a large muscle mass, allowing intracellular potassium, acid and myoglobin to accumulate before flow returns.
Crush and tissue necrosis
Direct myocyte disruption compounds arterial ischaemia and creates continuing potassium and pigment release after technically successful revascularisation.
Impaired renal clearance
Chronic kidney disease, acute tubular injury, shock or oliguria prevents clearance of the potassium and acid delivered during reperfusion.
Compartment oedema
Endothelial leak after restored flow expands muscle inside closed fascia, producing secondary microvascular ischaemia despite arterial patency.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Energy failure
Oxygen deprivation stops oxidative phosphorylation, depletes ATP and disables membrane ion pumps, causing intracellular sodium and calcium accumulation and cell swelling.
- 2Cellular contents escape
Membrane injury releases potassium, phosphate, myoglobin and enzymes while anaerobic metabolism produces hydrogen ions and lactate within the ischaemic bed.
- 3Washout becomes systemic
Restored arterial flow carries accumulated metabolites into the central circulation, destabilising myocardial conduction and vascular tone within minutes.
- 4Inflammation increases leak
Reactive oxygen species, complement and neutrophil activation damage endothelium, increasing capillary permeability, interstitial oedema and local compartment pressure.
- 5Kidney injury amplifies toxicity
Shock and myoglobin injure renal tubules, reducing potassium and acid elimination and converting transient washout into persistent or recurrent systemic danger.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
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.
05InvestigationsWhat to request, why it matters and how to interpret it.
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
Continuous ECG and twelve-lead ECGFirst step - Why
- Detect evolving potassium-mediated conduction toxicity before cardiac arrest occurs.
- Interpretation and limitations
- Treat compatible changes immediately; a normal tracing does not exclude severe or rapidly rising hyperkalaemia and must not replace serial biochemical measurement.
- 02
Urgent blood gas and laboratory potassium - Why
- Measure potassium and acid-base disturbance at the time of clinical deterioration.
- Interpretation and limitations
- Use rapidly available blood gas to guide emergency action, confirm through the laboratory when feasible, and repeat because reperfusion release and shift treatments change values quickly.
- 03
Creatine kinase and renal profile - Why
- Estimate muscle injury and detect loss of potassium and myoglobin clearance.
- Interpretation and limitations
- Rising CK, creatinine, phosphate and persistent acidosis with oliguria indicate continuing systemic danger; CK magnitude alone does not determine when to treat hyperkalaemia.
- 04
Hourly urine output and urinalysis - Why
- Track renal perfusion and identify pigmenturia from myoglobin release.
- Interpretation and limitations
- Dark haem-positive urine with few red cells supports myoglobinuria; falling urine output despite resuscitation requires renal and critical-care escalation.
- 05
Serial compartment examination - Why
- Detect local oedema causing recurrent tissue ischaemia after macroscopic flow returns.
- Interpretation and limitations
- Trend pain, passive stretch, tension and named nerve function; palpable pulses remain compatible with compartment syndrome and do not safely clear the limb.
- 06
Compartment pressure when examination is equivocal - Why
- Support a surgical decision in an obtunded or diagnostically uncertain patient.
- Interpretation and limitations
- Measure all suspected compartments with concurrent diastolic pressure; do not delay fasciotomy for pressures when the clinical diagnosis is already clear.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Re-occlusion
Recurrent pain, coldness and lost Doppler signals suggest renewed macrovascular obstruction rather than isolated metabolic reperfusion injury, though both can coexist.
Haemorrhagic shock
Hypotension after thrombolysis or surgery may arise from access, operative or occult bleeding and requires haemoglobin and focused source assessment.
Myocardial ischaemia
Arrhythmia and shock may reflect acute coronary disease, but immediate potassium and ECG evaluation is essential after reperfusing a large ischaemic muscle bed.
Sepsis
Vasodilatory shock and acidosis from infection can resemble systemic reperfusion, particularly in a necrotic or infected foot, and warrants parallel evaluation.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Worked casePrepare for high-risk reperfusionFirst stepA patient with prolonged Rutherford IIb leg ischaemia is moving to urgent thrombectomy and flow restoration.+
- 1Inputs: document ischaemia duration, involved muscle mass, neurological deficit, baseline ECG, potassium, blood gas, creatinine, CK and urine output.
- 2Reasoning: recognise that prolonged severe muscle ischaemia predicts potassium and acid washout plus oedema when flow returns, even if baseline potassium is normal.
- 3Action: alert anaesthesia, vascular, critical-care and renal teams, ensure hyperkalaemia medicines and continuous ECG are ready, and decide the fasciotomy strategy.
- 4Result: restore flow with haemodynamic control, sample early after reperfusion and treat electrical or biochemical toxicity immediately rather than awaiting a later routine panel.
- 5Verification: confirm stable ECG, falling potassium and lactate, adequate urine output, soft compartments and preserved serial motor and sensory function.
02Emergency treatmentProtect, shift and remove potassiumPotassium is at least 6.5 mmol/L, is rising rapidly, or the ECG shows compatible toxicity after reperfusion.+
- 1Give the UKKA-recommended intravenous calcium salt and dose immediately for toxic ECG changes, then reassess the ECG because membrane protection is temporary.
- 2Give 10 units soluble insulin with 25 g glucose, adding the five-hour 10% glucose infusion when pretreatment glucose is below 7 mmol/L.
- 3Add nebulised salbutamol under the acute algorithm when appropriate, never as sole therapy for severe hyperkalaemia, and stop all exogenous potassium.
- 4DefinitiveContact renal and critical care early for refractory hyperkalaemia, oliguria, severe acidosis or continuing muscle necrosis and prepare definitive dialysis when indicated.
03Local complicationDetect compartment syndrome earlyThe reperfused limb develops increasing pain, swelling, analgesic requirement, passive-stretch pain or neurological change.+
- 1Remove or split external constriction, correct systemic hypotension and obtain immediate senior vascular and surgical assessment with a timed repeat examination.
- 2Proceed to urgent complete fasciotomy when the clinical diagnosis is clear; use compartment pressures only when findings are incomplete or equivocal.
- 3Leave wounds open at the index operation, reassess muscle viability and continue systemic potassium, acid-base, CK and renal monitoring after decompression.
04Ongoing carePrevent rebound organ injuryInitial ECG and potassium improve after treatment but damaged muscle or impaired renal clearance remains.+
- 1Repeat potassium at 1, 2, 4, 6 and 24 hours and continue glucose monitoring for six hours after insulin, extending both for repeat treatment.
- 2Use clinically assessed fluids to maintain perfusion and urine output without causing pulmonary oedema or worsening tissue swelling, seeking renal advice early.
- 3Reassess tissue viability, vascular patency and compartment status and remove non-viable sources when systemic toxicity continues despite medical treatment.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Intravenous calcium salts
Give 10 mL calcium chloride 10% intravenously over 5 minutes in cardiac arrest or peri-arrest; for all other patients with hyperkalaemic ECG signs, give 30 mL calcium gluconate 10% intravenously over 10 minutes.Confirm salt and concentration because elemental calcium differs; use a secure intravenous line and monitor for extravasation. Calcium does not lower potassium, its protection is temporary, and calcium gluconate use for severe hyperkalaemia follows the national algorithm and current product authorisation.
Soluble insulin with glucose
Give 10 units soluble insulin with 25 g glucose intravenously; if pretreatment glucose is below 7 mmol/L, add 10% glucose at 50 mL/hour for five hours under UKKA guidance.Check glucose before dosing and at 0, 30, 60, 90, 120, 180, 240, 300 and 360 minutes. Renal failure, low body weight, non-diabetes and repeat dosing increase delayed hypoglycaemia risk.
Nebulised salbutamol
Give 10–20 mg nebulised salbutamol as adjunctive therapy for moderate or severe acute hyperkalaemia under the UKKA hospital algorithm.Never use as monotherapy in severe disease. Response is variable and may be reduced by non-selective beta-blockers; monitor tachycardia, tremor, myocardial ischaemia and glucose.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Malignant arrhythmia
Rapid potassium and acid release can produce bradycardia, broad-complex tachyarrhythmia, ventricular fibrillation or asystole during or shortly after flow restoration.
Acute kidney injury
Myoglobin, hypoperfusion and inflammation damage renal tubules, causing oliguria, worsening acidosis, potassium retention and possible dialysis dependence.
Compartment syndrome
Reperfusion oedema raises pressure within closed fascia, causing renewed muscle and nerve ischaemia that may require immediate complete decompression.
Multiorgan failure
Severe inflammatory and metabolic release can cause shock, lung injury, coagulopathy and progressive organ dysfunction despite technically successful arterial reconstruction.
Limb loss
Irreversible initial injury, recurrent occlusion, compartment necrosis or uncontrolled systemic toxicity may still require amputation after attempted salvage.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Use continuous cardiac monitoring through the high-risk reperfusion period and obtain repeat twelve-lead ECGs after calcium or any rhythm change.
- Measure potassium at least 1, 2, 4, 6 and 24 hours after acute treatment, with more frequent checks during rapid release or recurrent electrical toxicity.
- After insulin–glucose, check blood glucose at baseline, 30, 60, 90 and 120 minutes, then hourly through six hours and longer after repeat doses.
- Trend blood gas, lactate, bicarbonate, creatinine, CK, phosphate, calcium and hourly urine output until tissue release and renal risk are clearly resolving.
- Repeat named motor, sensory, Doppler, temperature, swelling and passive-stretch findings because post-revascularisation compartment syndrome can evolve after an initially successful result.
- Track fluid input, haemodynamics, oxygenation and weight where possible so renal perfusion treatment does not create pulmonary oedema or conceal shock.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Normal baseline can mislead
Potassium may be acceptable before revascularisation because toxic intracellular contents have not yet washed into the central circulation.
Calcium buys time
An improved ECG after calcium shows membrane stabilisation, not potassium clearance, and deterioration can recur within the ongoing release phase.
Shift is temporary
Insulin and salbutamol redistribute potassium but do not remove it, so damaged muscle and renal failure create predictable rebound risk.
Pulses miss capillaries
A patent reconstructed artery and palpable foot pulse can coexist with dangerously low microvascular flow inside a swollen compartment.
Source control matters
Persistently necrotic muscle can continue releasing potassium and myoglobin; repeated medical treatment cannot make dead tissue viable.
Fluids need physiology
Rhabdomyolysis often requires resuscitation, but urine targets and fluid rate must reflect cardiac reserve, pulmonary status and actual renal response.
11Common pitfallsFrequent interpretation and management errors.
- 01
Declaring the operation successful because the artery is open while ignoring ECG change, acidosis, oliguria or compartment swelling.
- 02
Giving intravenous calcium as the only hyperkalaemia treatment and failing to arrange intracellular shift and definitive potassium removal.
- 03
Stopping glucose surveillance after one normal early result despite delayed hypoglycaemia risk after insulin in renal failure.
- 04
Checking potassium once after treatment and missing rebound from ongoing muscle necrosis or poor renal excretion.
- 05
Using a palpable pulse to exclude compartment syndrome in a tense painful reperfused limb.
- 06
Waiting for CK to peak before treating a toxic ECG or arranging renal support for oliguria and refractory acidosis.