Suxamethonium

Why this drug is interesting

Suxamethonium is two acetylcholine molecules joined together. It binds the nicotinic receptor and activates it, producing the fasciculation that precedes paralysis — and then, because it is not broken down by acetylcholinesterase at the junction, it stays bound and holds the motor end plate depolarised. A depolarised end plate cannot depolarise again, and the muscle is paralysed.

That mechanism gives it the fastest onset and shortest duration of any available paralytic, and it also generates every one of its serious adverse effects. The potassium efflux, the malignant hyperthermia trigger, the myalgia, the rise in intraocular and intragastric pressure — all follow from the fact that this drug switches the receptor on rather than blocking it.

Dosing

• 1 mg/kg IV to achieve endotracheal intubation
• "This dose will usually produce muscular relaxation in about 30 to 60 seconds and has a duration of action of about 2 to 6 minutes."¹
• "Larger doses will produce more prolonged muscular relaxation, but doubling the dose does not necessarily double the duration of relaxation."¹
• Supplementary doses of 50–100% of the initial dose at 5–10 minute intervals will maintain relaxation — though repeated dosing risks phase II block and bradycardia
• The total dose should not exceed 500 mg

Renal and hepatic impairment

The label permits a normal single dose in renal insufficiency in the absence of hyperkalaemia, but states that "multiples or larger doses may cause clinically significant rises in serum potassium and should not be used."¹ Termination of action depends on plasma cholinesterase, synthesised in the liver — levels fall in liver disease, but except in severe hepatic failure this is rarely clinically significant.

Contraindications — read this list against your patient

The acquired hyperkalaemia risks

Beyond the labelled contraindications, suxamethonium causes an exaggerated potassium release where acetylcholine receptors have proliferated across the muscle membrane — up-regulation — or where muscle is being destroyed. The receptor spread takes days to develop, which is why the timing matters:

• Burns and major trauma — the label puts the period of greatest hyperkalaemia risk at about 5 to 70 days after injury, "and may be further prolonged if there is delayed healing due to persistent infection"
• Denervation — spinal cord injury, stroke, critical illness neuromyopathy; the label gives the risk window as within the first 6 months
• Prolonged immobility or ICU stay
• Crush injury and rhabdomyolysis
• Severe sepsis — the label relates the hyperkalaemia potential to "the severity and duration of infection", with no anatomical restriction

Malignant hyperthermia

Suxamethonium is a trigger, along with the volatile anaesthetic agents. The label states that if the condition occurs unexpectedly, "all anaesthetic agents known to be associated with its development including Suxamethonium must be discontinued straight away. Full supportive measures must be employed immediately. Intravenous dantrolene sodium is indicated in the treatment of malignant hyperthermia."¹

Dantrolene is the specific treatment; it takes time to reconstitute and requires many vials, which is why departments that stock it rehearse the process. Know whether yours does.

Suxamethonium apnoea

Suxamethonium is hydrolysed by plasma (pseudo)cholinesterase. Patients with inherited atypical variants of this enzyme — or with acquired deficiency from liver disease, pregnancy, malnutrition or certain drugs — metabolise it slowly, and the expected 2–6 minutes becomes hours.

• The patient remains paralysed and apnoeic long after the block should have resolved
• Management is entirely supportive: continue ventilation and, critically, ensure the patient is adequately sedated
• The block resolves spontaneously as the drug is eventually metabolised
• Refer for cholinesterase testing and genotyping afterwards, and tell the patient and their family — this is inherited, and it is the sort of information that prevents the same event happening to a relative

Other adverse effects

• Myalgia — common, sometimes severe, worse in young muscular patients and in those who mobilise soon afterwards
• Raised intraocular pressure — current label text, not history: suxamethonium "causes a slight transient rise in intra-ocular pressure and is therefore not recommended in the presence of open eye injuries, or where an increase in intra-ocular pressure is undesirable, unless the potential benefit outweighs the potential risk to the eye." In practice airway safety usually outweighs the eye, but the label frames this as a benefit-risk judgement rather than a myth
• Raised intragastric pressure — offset by a concurrent rise in lower oesophageal sphincter tone
• Raised intracranial pressure — transient and of doubtful clinical significance in most patients
• Bradycardia and asystole, particularly in children and with repeat dosing
• Anaphylaxis — neuromuscular blockers are a leading cause of perioperative anaphylaxis
• Phase II (desensitisation) block with large or repeated doses

Suxamethonium paralyses the respiratory muscles as completely as any other, and — like rocuronium — has no effect whatever on consciousness. Facilities for intubation and ventilation must be immediately available before it is given.

Critical appraisal

1. Its decline in emergency practice is about information, not pharmacology. Suxamethonium remains an excellent drug in a patient whose history you know. Emergency airway management is defined by not knowing the history — and the contraindications cluster in exactly the population that needs emergency intubation.
2. "It wears off" was always a weaker safety net than it appeared. The relaxant wearing off in a patient still deeply anaesthetised by the induction agent does not produce a patient who breathes. That reasoning kept suxamethonium in favour for longer than the evidence supported.
3. The penetrating eye injury teaching deserves re-examination. It is repeated confidently and rests on limited evidence; most current airway guidance would prioritise securing the airway over a theoretical rise in intraocular pressure. Trainees are often taught the aphorism without the uncertainty.
4. Suxamethonium apnoea is a communication failure as often as a pharmacological one. The event itself is manageable. What is repeatedly done badly is telling the patient afterwards, in terms they can pass on to their relatives and to future anaesthetists.
5. It still has a place. Where a genuinely short duration of paralysis is wanted, and the contraindications can be confidently excluded, its onset and offset remain unmatched.

References

1. 1
   Suxamethonium Chloride 50mg/ml Solution for Injection/Infusion — Summary of Product Characteristics, Martindale Pharma. electronic Medicines Compendium. Sections 4.2–4.4, 4.8. Verified 24 Aug 2026. Compare ADVANZ Pharma, emc.
2. 2
   Glycopyrronium Bromide 200 micrograms/ml Solution for Injection — Summary of Product Characteristics. electronic Medicines Compendium. Licensed to attenuate or prevent bradycardia associated with suxamethonium.
3. 3
   Association of Anaesthetists. Quick Reference Handbook — malignant hyperthermia. anaesthetists.org/qrh
4. 4
   Royal College of Anaesthetists and Difficult Airway Society. NAP4: Major complications of airway management in the United Kingdom. nationalauditprojects.org.uk
5. 5
   Suxamethonium chloride — dosing and safety monograph. BNF, NICE. bnf.nice.org.uk