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# 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](https://durgical.com/en/pharmacology/classes/neuromuscular-blockers/)
- Receptor: Muscle nicotinic acetylcholine receptor (motor end plate)
- ATC code: M03AB01
- WHO Model List of Essential Medicines

## ⚠ High-alert medication

An error with this medicine can cause serious harm: double checks and protocols are used.

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](https://www.rcsb.org/structure/8F6Z) · Drag to rotate · pinch to zoom

## 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

### Serious (rare, important)

- Hyperkalaemia with arrhythmias and cardiac arrest
- Hyperkalaemic rhabdomyolysis and cardiac arrest in children with undiagnosed myopathy (for example, Duchenne)
- Malignant hyperthermia
- Anaphylaxis
- Prolonged apnoea with plasma cholinesterase deficiency
- Phase II block with repeated doses

## 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.

## Memory aid

SUX = Sudden, Ultra-short, eXcess potassium: fast, brief and dangerous in burns, denervation and children with myopathy.

## 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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## Related drugs

- [Rocuronium](https://durgical.com/en/pharmacology/rocuronium/)
- [Sevoflurane](https://durgical.com/en/pharmacology/sevoflurane/)
- [Calcium gluconate](https://durgical.com/en/pharmacology/calcium-gluconate/)

[← Back to the class: Neuromuscular blockers](https://durgical.com/en/pharmacology/classes/neuromuscular-blockers/)

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](https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=30f58922-3c74-4813-ace0-fcd2024acd09) (DailyMed (U.S. National Library of Medicine), 2026); [Malignant hyperthermia: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/malignant-hyperthermia/) (MedlinePlus (U.S. National Library of Medicine), 2026); [Pseudocholinesterase deficiency: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/pseudocholinesterase-deficiency/) (MedlinePlus (U.S. National Library of Medicine), 2026); [ATCDDD - ATC/DDD Index](https://atcddd.fhi.no/atc_ddd_index/?code=M03AB01) (WHO Collaborating Centre for Drug Statistics Methodology, 2026).

## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake

Representative model, for educational purposes only.

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