Suxamethonium !

Depolarising muscle relaxant with onset in under a minute and an effect of a few minutes, for rapid intubation. It can cause severe hyperkalaemia.

Updated 2026-11-01

Class: Neuromuscular blockers
Receptor: Muscle nicotinic acetylcholine receptor (motor end plate)
ATC code: M03AB01
WHO Model List of Essential Medicines

Also called: Succinylcholine

Muscle nicotinic acetylcholine receptor (motor end plate)Suxamethonium

The figure shows succinylcholine bound to the muscle-type nicotinic receptor of the Torpedo ray (Tetronarce), the classic model of the human receptor; it occupies the acetylcholine site.

Target in 3D: Muscle nicotinic acetylcholine receptor (motor end plate). PDB structure 8F6Z (RCSB PDB, public domain). View the structure at RCSB PDB

Mechanism of action

Suxamethonium is two acetylcholine molecules joined together. It binds the nicotinic receptor of the motor end plate and activates it: the end plate depolarises and fasciculations appear. Because synaptic acetylcholinesterase does not break it down, the end plate stays depolarised, nearby sodium channels stay inactivated and the muscle cannot respond: flaccid paralysis (phase I block). The effect ends when plasma cholinesterase (butyrylcholinesterase) hydrolyses it outside the synapse.

Activates the nicotinic receptor like acetylcholine
The end plate depolarises: fasciculations
Depolarisation persists and the muscle stops responding
Plasma cholinesterase hydrolyses it and ends the effect

Pharmacokinetics

Metabolism: Rapid hydrolysis by plasma cholinesterase to succinylmonocholine and then to succinic acid and choline.
Elimination: A small fraction is excreted unchanged in urine.
Onset and duration: Paralysis in under a minute intravenously; a single dose lasts about 4 to 6 minutes.

Indications

Rapid sequence intubation (full stomach, emergency)
Brief relaxation in surgery or mechanical ventilation; intramuscular when there is no venous access

Adverse effects

Common

Fasciculations and postoperative muscle pain
Bradycardia, especially in children or with a second dose
Raised intraocular, intragastric and intracranial pressure
Hypersalivation
Masseter (jaw) rigidity

Contraindications

Known or suspected susceptibility to malignant hyperthermia
Skeletal muscle myopathies
After the acute phase of major burns, multiple trauma, extensive denervation or upper motor neuron injury
Hypersensitivity to suxamethonium

Key interactions

Halogenated anaesthetics: Together they raise the risk of malignant hyperthermia and arrhythmias.
Cholinesterase inhibitors (neostigmine, organophosphates): Prolong the block: neostigmine does not reverse it.
Drugs that lower plasma cholinesterase (oral contraceptives, glucocorticoids, some MAOIs): Longer block.
Magnesium, lithium, some non-penicillin antibiotics, lidocaine, beta-blockers: Enhance the block.
Digoxin: Higher risk of arrhythmias from hyperkalaemia.

What is monitored

Continuous ECG: peaked T waves as an early sign of hyperkalaemia
Temperature and end-tidal CO2 (malignant hyperthermia)
Serum potassium when at risk
Peripheral nerve stimulator (train-of-four)
Ventilation until full recovery

Administration and safety

Paralysing agent: store apart with a warning label and confirm the product before use.
Keep refrigerated; out of the fridge it loses potency over time.
Only with ventilation and airway equipment ready and the patient already unconscious, except in an extreme emergency.
Keep dantrolene available wherever suxamethonium or halogenated agents are used.

Nursing care

Before: ask about personal or family history of malignant hyperthermia, prolonged apnoea after anaesthesia, myopathies and recent burns or spinal cord injuries.
During: watch ECG, end-tidal CO2, temperature and jaw rigidity.
If a healthy child has a sudden cardiac arrest after suxamethonium, treat at once as hyperkalaemia.
After: tell the patient that muscle aches are common and pass.

Pregnancy and breastfeeding

Often used for caesarean sections; plasma cholinesterase falls in pregnancy and the block can last longer.

Test yourself

Think of the answer, then tap the question to see it.

Why can suxamethonium kill an apparently healthy child with undiagnosed Duchenne muscular dystrophy?

It triggers acute rhabdomyolysis with hyperkalaemia and cardiac arrest minutes after the dose.

Which enzyme ends the effect of suxamethonium, and what happens when it is lacking?

Plasma cholinesterase (butyrylcholinesterase); with deficient BCHE variants, paralysis and apnoea are prolonged and ventilation is needed until the drug is cleared.

What initial treatment does malignant hyperthermia during anaesthesia need?

Stop suxamethonium and halogenated agents, give intravenous dantrolene and 100% oxygen, cool the patient and correct acidosis and hyperkalaemia.

Why does neostigmine not reverse the phase I block of suxamethonium?

Because that block is not competitive: the end plate is already depolarised and more acetylcholine does not restore it; neostigmine only antagonises competitive blockers.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: DailyMed - SUCCINYLCHOLINE CHLORIDE injection, solution (DailyMed (U.S. National Library of Medicine), 2026); Malignant hyperthermia: MedlinePlus Genetics (MedlinePlus (U.S. National Library of Medicine), 2026); Pseudocholinesterase deficiency: MedlinePlus Genetics (MedlinePlus (U.S. National Library of Medicine), 2026); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026).

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Representative model, for educational purposes only.