Malignant hyperthermia

What it is

Malignant hyperthermia is a pharmacogenetic disorder of skeletal muscle, usually inherited in an autosomal dominant way, most often through a variant of the ryanodine receptor gene (RYR1) and less often of CACNA1S or STAC3. In a susceptible person, the volatile anaesthetic agents and suxamethonium trigger an uncontrolled release of calcium from the sarcoplasmic reticulum. The muscle contracts and burns energy without stopping: it produces carbon dioxide, heat and lactate, consumes oxygen and ATP, and finally breaks down, releasing potassium, myoglobin and creatine kinase. The earliest clue is usually a rise in end-tidal carbon dioxide that does not fall when ventilation is increased, together with unexplained tachycardia; masseter or generalised rigidity may appear, and the rise in temperature is often a late sign. Untreated, the crisis leads to severe mixed acidosis, hyperkalaemia, arrhythmias, kidney injury, disseminated intravascular coagulation and death. Treatment is a team effort: stop the triggers, hyperventilate with pure oxygen, give dantrolene, the only specific antidote, cool the patient, correct potassium and acid, and monitor in intensive care because the crisis can return. Afterwards the patient and family need referral for diagnostic testing, and every future anaesthetic must be trigger-free.

How to recognise it

• End-tidal CO2 rises steadily and does not fall with higher minute ventilation; the soda lime may be exhausted quickly and feel hot.
• Unexplained tachycardia, arrhythmias and unstable blood pressure.
• Masseter spasm after suxamethonium, or generalised muscle rigidity despite full relaxation.
• Blood gas shows a mixed respiratory and metabolic acidosis; potassium and creatine kinase rise; urine turns dark from myoglobin.
• Temperature rises fast, but often only after the other signs.

Why it happens

• A variant ryanodine receptor (or its partner proteins) lets calcium leak out of the sarcoplasmic reticulum when exposed to a trigger.
• Persistent calcium keeps actin and myosin cycling: the muscle consumes ATP and oxygen and produces CO2, lactate and heat.
• When energy runs out, muscle cells break down (rhabdomyolysis), releasing potassium, myoglobin and creatine kinase into the blood.
• Some inherited myopathies, such as central core disease, carry the same susceptibility.

What to do at once

1. Declare suspected malignant hyperthermia and call for help and the MH kit — treatment needs many hands, and dantrolene takes time to prepare.
2. Stop all volatile agents and suxamethonium and switch to intravenous anaesthesia — removing the trigger stops further calcium release.
3. Hyperventilate with high-flow pure oxygen and fit activated charcoal filters — this clears CO2 and the vapour left in the circuit.
4. Give dantrolene intravenously without delay and repeat until CO2 and heart rate settle — it blocks calcium release and is the only antidote.
5. Cool actively if hot: cold intravenous fluids, ice packs and cold lavage, stopping near normal temperature — avoids overshoot into hypothermia.
6. Treat hyperkalaemia with calcium, insulin with glucose, and bicarbonate for severe acidosis — high potassium causes lethal arrhythmias.
7. Treat arrhythmias with standard drugs, avoiding calcium channel blockers — combined with dantrolene they can cause hyperkalaemia and collapse.
8. Send blood gases, potassium, CK, myoglobin and clotting; catheterise and keep urine flowing — myoglobin damages the kidneys.
9. Finish or stop surgery as soon as possible and arrange intensive care — the crisis can recur during the following day.

Malignant hyperthermia and the syndromes that can look like it

Costly mistakes

• Waiting for fever before thinking of malignant hyperthermia: rising CO2 and tachycardia come first.
• Blaming light anaesthesia or a failing absorber and simply increasing the volatile agent.
• Delaying dantrolene, or giving too little because preparation is slow; assign people to mix it.
• Giving a calcium channel blocker for arrhythmias while dantrolene is running.
• Discharging the patient early or forgetting to warn relatives and future anaesthetists.

Next step

• Monitor in intensive care for at least 24 hours: end-tidal CO2, temperature, potassium, creatine kinase and urine output; repeat dantrolene if signs return.
• Watch for rhabdomyolysis, acute kidney injury, compartment syndrome and disseminated intravascular coagulation.
• Call a senior anaesthetist at once and contact the regional malignant hyperthermia advice line or reference centre if one exists.
• Explain the event to the patient and family; refer for contracture testing on a muscle biopsy or genetic testing, and test relatives.
• Record a clear alert in the notes and give the patient a written warning; future anaesthetics use a prepared machine and no triggers.
• Debrief the team, report the event and replace the dantrolene stock.

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Elsewhere in DurgiPedia

• Skeletal muscle excitation–contraction coupling
• Body temperature regulation
• Hyperkalaemia and other electrolyte changes
• Arterial blood gas: worked cases for the station

Connections

← All of anaesthesia

Educational content; it does not replace supervised training, your institution's protocols or the anaesthetist's or intensivist's decision. It contains no doses and no ventilator or infusion settings.

Sources: Malignant Hyperthermia (StatPearls (NCBI Bookshelf), 2026).

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