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Anaes TopicsNeuromuscular blockade & reversal

Anaes · Neuromuscular blockade & reversal

Suxamethonium

Also known as Succinylcholine · Sux · Depolarising neuromuscular blocker · RSI muscle relaxant · Diacetylcholine

Suxamethonium (succinylcholine, sux) is the ONLY depolarising neuromuscular blocker in clinical use — taught as two acetylcholine molecules joined back-to-back (di-acetylcholine ester), it activates the postsynaptic nicotinic (muscle) receptor to produce fasciculation then a sustained depolarisation with phase I block and flaccid paralysis. Taught onset/duration (fastest onset 30 to 60 seconds, shortest duration 5 to 10 minutes) keep it the rapid-sequence induction agent of choice for the full-stomach or aspiration-risk patient; contemporary RSI practice still favours sux (70.5% of MPOG RSI cases, though falling 85.4 to 37.3% over 2015 to 2022) with no mortality/hypoxia/pulmonary/AKI difference versus rocuronium (Marcus 2026), and an ED TriNetX cohort found sux associated with lower 60-day mortality (30.1 versus 33.4%, RR 0.901) and MI (10.5 versus 11.9%, RR 0.888) than rocuronium with etomidate backbone and no first-pass data (O'Connell 2026). It is hydrolysed by plasma butyrylcholinesterase (not synaptic acetylcholinesterase), so deficiency — genetic or acquired — produces prolonged apnoea lasting hours (Snak de Souza 2026 systematic review, 30 studies and 290 patients; Abbasi 2026 single-case illustration). Repeated boluses convert the block toward a phase II (desensitisation) pattern. Exam-critical harms: severe hyperkalaemia from upregulated extrajunctional receptors — avoid sux after 24 hours post-burn by expert consensus (Puxty 2026 scoping review, 19 studies, all low quality), with the longer taught window and potassium numbers carried as teaching; malignant hyperthermia — sux is a trigger alongside volatiles (Fang 2026 two-case RYR1 report); bradycardia; raised intraocular pressure (open-eye contraindication); raised intracranial/intragastric pressure; myalgia; masseter spasm; anaphylaxis. The sux-sparing RSI alternative is rocuronium with sugammadex reversal (formulary dosing; mivacurium-versus-sux bronchoscopy data are protocol-only with no results, Zhang 2026).

high8 referencesUpdated 26 July 202612 min readVerification in progress

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Red flags

  • Suxamethonium can cause life-threatening HYPERKALAEMIA in patients with upregulated extrajunctional acetylcholine receptors — it is contraindicated after burns (beyond 24 hours and up to about 2 years), denervation or spinal-cord injury, prolonged immobility, crush injury and severe critical illness; a sudden perioperative cardiac arrest in these patients is hyperkalaemia until proven otherwise.
  • Suxamethonium is a POTENT trigger of malignant hyperthermia — never give it to a known or suspected MH-susceptible patient; masseter spasm after a sux dose may be the first sign.
  • Suxamethonium raises intraocular pressure and is CONTRAINDICATED in the open-eye/globe injury (risk of expulsion of globe contents).
  • In butyrylcholinesterase (pseudocholinesterase) deficiency — genetic or acquired (liver disease, pregnancy, organophosphates) — suxamethonium causes PROLONGED APNOEA lasting hours; manage with sedation and mechanical ventilation, not neostigmine.
  • Neostigmine (an anticholinesterase) AUGMENTS and prolongs a phase I (depolarising) block — NEVER use it to reverse a suxamethonium block.
  • Repeated doses or large total doses (above about 4 to 6 mg per kg) convert the block to a phase II (desensitisation) block resembling a non-depolariser, with slow recovery.
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Practise this topic8 MCQs with explanations

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ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • Suxamethonium can cause life-threatening HYPERKALAEMIA in patients with upregulated extrajunctional acetylcholine receptors — it is contraindicated after burns (beyond 24 hours and up to about 2 years), denervation or spinal-cord injury, prolonged immobility, crush injury and severe critical illness; a sudden perioperative cardiac arrest in these patients is hyperkalaemia until proven otherwise.
  • Suxamethonium is a POTENT trigger of malignant hyperthermia — never give it to a known or suspected MH-susceptible patient; masseter spasm after a sux dose may be the first sign.
  • Suxamethonium raises intraocular pressure and is CONTRAINDICATED in the open-eye/globe injury (risk of expulsion of globe contents).
  • In butyrylcholinesterase (pseudocholinesterase) deficiency — genetic or acquired (liver disease, pregnancy, organophosphates) — suxamethonium causes PROLONGED APNOEA lasting hours; manage with sedation and mechanical ventilation, not neostigmine.
  • Neostigmine (an anticholinesterase) AUGMENTS and prolongs a phase I (depolarising) block — NEVER use it to reverse a suxamethonium block.
  • Repeated doses or large total doses (above about 4 to 6 mg per kg) convert the block to a phase II (desensitisation) block resembling a non-depolariser, with slow recovery.
The one-line answer

Suxamethonium is the only depolarising neuromuscular blocker in clinical use — taught as two acetylcholine molecules joined back-to-back that activate the nicotinic receptor, producing fasciculation then flaccid paralysis. Its taught onset (30 to 60 seconds) and duration (5 to 10 minutes) — textbook numbers no single study owns — keep it the rapid-sequence induction agent of choice; contemporary support is practice-level (sux still the commonest RSI relaxant in MPOG abdominal-surgery practice at 70.5%, though use is falling) [6] and outcome-level (ED TriNetX RSI with etomidate: sux lower 60-day mortality 30.1 versus 33.4%, RR 0.901, and MI 10.5 versus 11.9%, RR 0.888; no onset, first-pass, or dosing data in that study) [2]. Its adverse-effect list — hyperkalaemia, malignant hyperthermia, prolonged apnoea — is the single highest-yield list in neuromuscular pharmacology.[1]

Meet the patient

A fasted patient with a small-bowel obstruction needs an emergency laparotomy. She is at high aspiration risk, so you plan a rapid sequence induction. The relaxant you reach for is suxamethonium — because you need to be intubating within a minute of induction, and you need her breathing back if the airway turns difficult.[2][6]

The decision every sux dose rests on is threefold: is she a patient in whom sux is safe (no upregulated receptors, no MH susceptibility), does she need the fast in-fast out only sux gives, and have you excluded the contraindications that can kill her? Sux rewards a clean history and punishes a casual one.[2][7]

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References8ShowHide
  1. [1]Martyn JA, Richtsfeld M Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms Anesthesiology, 2006.PMID 16394702
  2. [2]O'Connell DH, et al. Outcomes of Succinylcholine and Rocuronium for Rapid Sequence Intubation in the Emergency Department West J Emerg Med, 2026.PMID 42258841
  3. [3]Snak de Souza CD, Ibarra Moreno CA, Riazi S, Hopkins PM Genotype-phenotype relationships in butyrylcholinesterase deficiency: a systematic review Br J Anaesth, 2026.PMID 42120224
  4. [4]Abbasi H, Rauf A, Moore D Prolonged Neuromuscular Paralysis Following Succinylcholine Induction Leading to a Trans-Kambin Oblique Lateral Lumbar Interbody Fusion (OLLIF) Procedure Performed Without Neuromonitoring Cureus, 2026.PMID 42037893
  5. [5]Fang Y, Mei W, Bi J Considerations for diverse RYR1 variants in malignant hyperthermia susceptible patients: a report of two cases BMC Anesthesiol, 2026.PMID 42271251
  6. [6]Marcus SG, et al. Rapid Sequence Induction Practices and Outcomes in Abdominal Surgery Patients: A Multicenter Observational Cohort Study Anesthesiology, 2026.PMID 42257652
  7. [7]Puxty KA, et al. Cardiac arrest in adult patients following burn injury: a scoping review with expert recommendations on management Scand J Trauma Resusc Emerg Med, 2026.PMID 41507944
  8. [8]Zhang X, Xu Y, Li J, Xi Y, Xu Z, Liang P Effect and safety of mivacurium chloride and succinylcholine for bronchoscopy: study protocol for a single-center, randomized, non-inferiority, and positive-controlled clinical trial Trials, 2026.PMID 41566470

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