Suxamethonium

How to use it safely (practical clinical structure)

Confirm indication and consider alternatives
- Rapid sequence induction (RSI) where very rapid onset and short duration are required
- Short procedures requiring brief paralysis (less common now)
- Rescue paralysis for laryngospasm (with airway manoeuvres/CPAP first)
- Consider rocuronium + sugammadex as alternative if contraindications present
Screen for contraindications and high-risk states
- Risk of dangerous hyperkalaemia: major burns (>24–48 h after injury), crush injury, severe denervation/UMN/LMN lesions, prolonged immobility/ICU-acquired weakness, motor neurone disease, Guillain–Barré, muscular dystrophies
- Known/suspected malignant hyperthermia susceptibility
- History of suxamethonium apnoea or known pseudocholinesterase deficiency
- Open globe injury / penetrating eye trauma (relative; avoid if possible)
Dose and administration
- IV intubating dose: 1–1.5 mg/kg (often 1 mg/kg; higher end for RSI/obesity/if delayed onset unacceptable)
- IM (if no IV access): ~3–4 mg/kg (onset slower, duration longer)
- Onset ~30–60 s; clinical duration ~5–10 min (varies with dose and cholinesterase activity)
Monitoring and expected neuromuscular pattern
- Fasciculations then flaccid paralysis; TOF shows no fade in phase I block
- If prolonged infusion/repeated doses: may convert to phase II block with fade and post-tetanic facilitation
If prolonged paralysis occurs
- Provide sedation/analgesia and ventilatory support; exclude other causes (hypothermia, electrolyte disturbance, drug error)
- Consider pseudocholinesterase deficiency: send plasma cholinesterase activity and dibucaine number (and fluoride number if available)
- Avoid empiric anticholinesterase reversal in phase I block (may prolong); in established phase II block, reversal may be possible but is unpredictable—seek senior help

Class, structure, and presentation

Depolarising NMBD; essentially two acetylcholine molecules linked together
Quaternary ammonium compound → highly ionised, poor lipid solubility, does not cross BBB/placenta significantly (small amounts may cross placenta but clinically limited due to rapid hydrolysis)
Usually supplied as suxamethonium chloride solution; commonly stored refrigerated (local practice) due to stability considerations

Mechanism of action (NMJ)

Agonist at nicotinic ACh receptors at the neuromuscular junction → persistent end-plate depolarisation → inactivation of voltage-gated Na+ channels → flaccid paralysis
Phase I block: depolarising block with fasciculations; TOF: reduced amplitude without fade; post-tetanic facilitation absent; not reversed by neostigmine (may prolong)
Phase II block (with large/repeated doses/infusion): desensitisation/repolarisation with receptor dysfunction; resembles non-depolarising block (fade on TOF); may respond to anticholinesterase variably

Pharmacokinetics

Rapid onset due to high potency at NMJ and rapid delivery to effect site
Very short duration because it is rapidly hydrolysed in plasma by pseudocholinesterase (butyrylcholinesterase) to succinylmonocholine + choline; only a small fraction reaches NMJ
Elimination half-life is short; duration is determined by redistribution and metabolism; prolonged block occurs when pseudocholinesterase activity is reduced or atypical
Factors reducing pseudocholinesterase activity: pregnancy (esp. late), liver disease, malnutrition, burns (acute phase), chronic illness, organophosphate exposure, some drugs (e.g., anticholinesterases), genetic variants

Pharmacodynamics and clinical effects

Neuromuscular: fasciculations (can cause myalgia), then paralysis; excellent intubating conditions rapidly
Cardiovascular: bradycardia (esp. children, repeated doses), dysrhythmias; due to muscarinic stimulation and nicotinic ganglionic effects
Autonomic: may cause tachycardia/hypertension (ganglionic stimulation) or bradycardia (muscarinic), overall variable
Respiratory: no direct bronchospasm typical, but histamine release can occur; ensure adequate anaesthesia to avoid laryngospasm/bronchospasm from airway stimulation

Adverse effects (high-yield)

Hyperkalaemia: typically rises ~0.5 mmol/L in healthy patients; can be life-threatening in upregulated extrajunctional ACh receptor states (burns, denervation, prolonged immobility, neuromuscular disease)
- Timing in burns: risk increases after ~24–48 h and may persist for months; avoid after this window unless compelling reason and expert decision
Malignant hyperthermia trigger (with volatile agents); treat with dantrolene and supportive measures
Bradycardia/asystole (esp. children, second dose within minutes, or with halothane historically); consider atropine prophylaxis in children depending on local practice
Raised intraocular pressure (IOP): transient rise (peaks within minutes) due to extraocular muscle fasciculation and choroidal vascular effects; avoid in open globe injury
Raised intragastric pressure: also increases lower oesophageal sphincter tone; net aspiration risk not clearly increased but RSI principles still apply
Raised intracranial pressure: transient rise reported; clinically relevant mainly if poor intracranial compliance—ensure adequate induction/ventilation and consider alternative if concern
Myalgia (post-op muscle pains) due to fasciculations; more common in ambulatory patients
Masseter muscle spasm: may occur; can be an early sign of MH (especially with volatile exposure) but can also be isolated—treat as potential MH until assessed
Anaphylaxis: NMBDs are common causes; suxamethonium has relatively higher anaphylaxis risk among NMBDs in many series; manage per anaphylaxis algorithm and refer for investigation
Prolonged apnoea/paralysis: atypical or deficient pseudocholinesterase; management is ventilation + sedation until recovery

Contraindications and cautions (exam list)

Absolute/strong: previous suxamethonium apnoea or known pseudocholinesterase deficiency; MH susceptibility; high-risk hyperkalaemia states (burns >48 h, denervation, neuromuscular disease, prolonged immobility, severe trauma/crush)
Relative: open globe injury; severe hyperkalaemia; severe rhabdomyolysis risk; significant bradyarrhythmia risk without mitigation
Paediatrics: avoid routine use for elective intubation; reserved for emergency airway/laryngospasm due to risk of occult myopathy-associated hyperkalaemic arrest

Drug interactions

Anticholinesterases (neostigmine, pyridostigmine) inhibit plasma cholinesterase → prolong suxamethonium action
Organophosphates irreversibly inhibit cholinesterase → markedly prolonged block
Non-depolarising NMBDs: small “defasciculating” dose may reduce fasciculations/myalgia but can worsen intubating conditions unless sux dose increased; not routinely recommended
Volatile agents potentiate NM blockade and are MH co-triggers

Pseudocholinesterase deficiency (high-yield viva)

Butyrylcholinesterase (pseudocholinesterase) is produced in liver and present in plasma; metabolises suxamethonium and ester local anaesthetics (e.g., chloroprocaine, tetracaine) and some other ester drugs
Clinical clue: unexpectedly prolonged paralysis/apnoea after suxamethonium (and sometimes after mivacurium)
Dibucaine number: dibucaine inhibits normal enzyme strongly; lower numbers indicate atypical enzyme
- Typical values: normal ~80; heterozygote ~50–70; homozygous atypical ~20 (approximate ranges used in viva)
Management: ventilate and sedate until recovery; document clearly, inform patient, provide alert letter/bracelet advice; refer for formal testing and family screening where appropriate
Fresh frozen plasma has been used historically to provide enzyme but is rarely indicated; supportive care is usually safest

Comparison with rocuronium (RSI decision-making)

Suxamethonium: fastest onset and shortest duration; but more contraindications and adverse effects (hyperkalaemia, MH, anaphylaxis, bradycardia, myalgia)
Rocuronium: comparable onset at higher dose (e.g., 1.0–1.2 mg/kg) with longer duration; can be rapidly reversed with sugammadex (availability/cost/logistics apply)

Describe the mechanism of action of suxamethonium and explain phase I vs phase II block.

Key is depolarising agonism at the NMJ and how monitoring differs between phases.

Suxamethonium is a nicotinic ACh receptor agonist at the NMJ → persistent end-plate depolarisation → voltage-gated Na+ channel inactivation → paralysis
Phase I block: depolarising; fasciculations then flaccid paralysis; TOF shows reduced twitch height with no fade; post-tetanic facilitation absent; anticholinesterases do not reverse and may prolong
Phase II block: after repeated doses/infusion; receptor desensitisation and altered ion channel function; TOF fade and post-tetanic facilitation may appear; may respond variably to anticholinesterases

Why is suxamethonium short acting despite being a potent NMBD?

Duration is limited by rapid plasma hydrolysis; only a small fraction reaches the NMJ.

Rapid hydrolysis by plasma pseudocholinesterase to succinylmonocholine + choline
Only a small proportion reaches the NMJ before being metabolised; recovery occurs as drug diffuses away and is cleared
Reduced enzyme activity or atypical enzyme → prolonged block

List the major adverse effects of suxamethonium and give mechanisms where relevant.

Examiners expect hyperkalaemia, MH, bradycardia, raised IOP, myalgia, anaphylaxis, prolonged apnoea.

Hyperkalaemia: K+ efflux during depolarisation; exaggerated with upregulated extrajunctional receptors (burns, denervation, prolonged immobility, neuromuscular disease)
Malignant hyperthermia trigger (with volatile agents)
Bradycardia/dysrhythmias: muscarinic effects (esp. children, repeated doses) and autonomic ganglionic effects
Raised IOP (transient) due to extraocular muscle fasciculation and ocular haemodynamic changes
Myalgia due to fasciculations (more common in ambulatory patients)
Anaphylaxis (NMBD class effect; suxamethonium relatively higher risk in many datasets)
Prolonged apnoea in pseudocholinesterase deficiency or inhibition (organophosphates/anticholinesterases)

A patient remains apnoeic and paralysed 30 minutes after suxamethonium. How do you manage this and what tests do you request?

This is a classic FRCA scenario: manage first, then investigate.

Immediate management: maintain airway, ventilate, and provide adequate sedation/analgesia; monitor TOF and clinical signs; check temperature, electrolytes, acid-base, and exclude drug error
Consider pseudocholinesterase deficiency/inhibition; send plasma cholinesterase activity and dibucaine number (± fluoride number depending on lab)
Avoid routine neostigmine in phase I block (may prolong); if evidence of phase II block, reversal may be attempted cautiously with expert input but is unpredictable
Communicate and document: explain to patient post-op, provide written warning, refer for anaesthetic allergy/enzymology clinic as appropriate; advise family screening if genetic deficiency confirmed

Explain the dibucaine number and give typical values for normal, heterozygous atypical, and homozygous atypical pseudocholinesterase.

Dibucaine inhibits normal pseudocholinesterase strongly; atypical enzyme is inhibited less.

Dibucaine number = % inhibition of pseudocholinesterase activity by dibucaine under standard conditions
Normal: ~80
Heterozygous atypical: ~50–70
Homozygous atypical: ~20

Why is suxamethonium contraindicated in major burns and when does the risk begin?

The key concept is receptor upregulation leading to massive K+ release.

Burns cause upregulation of extrajunctional ACh receptors and increased receptor sensitivity → suxamethonium triggers widespread depolarisation → large K+ efflux → ventricular arrhythmias/cardiac arrest
Risk increases after ~24–48 hours post-burn and can persist for months (often quoted up to 1–2 years depending on ongoing denervation/immobility and burn severity)

Discuss suxamethonium in children: when would you use it and what is the key safety concern?

Modern practice avoids routine elective use in children.

Use mainly for emergency airway control (e.g., laryngospasm, full stomach emergency RSI) when rapid onset/offset is valuable and contraindications excluded
Key concern: occult myopathy (e.g., undiagnosed Duchenne muscular dystrophy) → severe hyperkalaemia and cardiac arrest after suxamethonium
Also bradycardia risk is higher; consider antimuscarinic prophylaxis depending on age and local policy

What are the effects of suxamethonium on intraocular pressure and how does this influence management of eye trauma?

Examiners want the direction, timing, and clinical implication.

Transient rise in IOP after administration (peaks within minutes) due to extraocular muscle fasciculation and ocular haemodynamic changes
Avoid in open globe injury/penetrating eye trauma where extrusion risk exists; choose alternative RSI strategy (e.g., rocuronium) and optimise intubation conditions

How does suxamethonium affect serum potassium in a healthy adult and why can this become dangerous?

Quantify the normal rise and explain the pathological amplification.

Typical K+ rise in healthy adults is about 0.5 mmol/L (variable)
Dangerous hyperkalaemia occurs when extrajunctional ACh receptors are upregulated (burns, denervation, prolonged immobility, neuromuscular disease) leading to exaggerated K+ efflux during depolarisation

A patient develops masseter spasm after suxamethonium during induction. What are your concerns and immediate actions?

Treat as possible MH until proven otherwise, and manage the airway safely.

Concern: may be an early sign of malignant hyperthermia (especially if volatile agent used); also can make laryngoscopy difficult
Actions: call for help; stop volatile agents; switch to TIVA; assess for other MH signs (ETCO2 rise, tachycardia, rigidity, hyperthermia, acidosis); prepare dantrolene and MH protocol if suspicion persists
Airway: oxygenate/ventilate; consider alternative intubation strategy; avoid further triggers; monitor closely and consider ICU/HDU admission and CK/ABG monitoring

Compare suxamethonium with rocuronium for RSI, including reversal options.

Frame around onset, duration, contraindications, and reversal.

Suxamethonium: onset ~30–60 s; duration ~5–10 min; more adverse effects/contraindications (hyperkalaemia states, MH, bradycardia, myalgia, anaphylaxis, raised IOP)
Rocuronium: onset can be similar at 1.0–1.2 mg/kg; longer duration; fewer specific contraindications; can be reversed rapidly with sugammadex (if available)
Decision depends on patient factors (K+ risk, MH risk, airway difficulty, aspiration risk), local availability of sugammadex, and need for rapid return of spontaneous ventilation