CLASS

Non-depolarising neuromuscular blocker

PRESENTATION

Clear colourless solution.

Formulations

2ml vial; 100mg, 50mg/ml

INDICATIONS & DOSING

Paralysis; endotracheal intubation, surgical immobility, management of laryngospasm, modification of response to ECT

Adult; 1.5mg/kg IV, 3mg/kg IM
Paediatric; 2mg/kg IV, 4mg/kg IM
Neonate; 3mg/kg IV, 6mg/kg IM

PRACTICALITIES

Administration

Administered as neat solution followed by an IV flush
Care to prevent accidental storage of neuromuscular blocker within the IV set following administration; may result in subsequent undesired paralysis and respiratory arrest

Incompatibilities

Alkaline solutions; thiopentone

Practice tips

Suxamethonium degrades slowly at room temperature and is usually refrigerated
Dose according to total body weight in obesity
Onset is obvious clinically by the onset of muscle fasciculations
Rapid onset particularly useful in achieving the aims of a rapid sequence induction
A short duration of action and significant side-effect profile makes suxamethonium a less desirable choice for the provision of surgical immobility; subsequent administration of a non-depolarising neuromuscular blockade is usually required if surgical immobility is desired
Faster onset/offset in paediatric population and high cardiac output states
Intramuscular onset; sublingual < deltoid < thigh
Slower offset with hypothermia, acidaemia, hyperkalaemia, hypocalcaemia, hypermagnesaemia
Attempts at reversal of paralysis with neostigmine may lead to paradoxical prolongation of paralysis
Repeated exposure or high doses (>4mg/kg) can lead to ‘phase II block’ with prolongation of clinical effect and a clinical profile similar to non-depolarising neuromuscular blockade

PHARMACOKINETICS

Onset

IV; ~60 seconds
IM; 1-3 minutes

Duration of action (in the absence of abnormal plasmacholinesterase variants)

IV; ~5-10 minutes
IM; 10-30 minutes

Metabolism

Metabolised extensively by plasmacholinesterases to succinylmonocholine (weak activity) and subsequently succinic acid and choline (inactive)

Elimination

<10% renally eliminated

MECHANISM

Non-competitive activation of acetylcholine receptors at the neuromuscular junction allows an influx of cations with subsequent depolarisation and activation of voltage-gated sodium channels.

Suxamethonium remains bound to the receptor, preventing repolarisation and subsequent depolarisation/neuromuscular transmission. Sarcoplasmic calcium concentration is restored to baseline, leading to an end of muscle contraction and a flaccid paralysis.

DESIRED CLINICAL EFFECTS

Airway

Relaxation of vocal cords; facilitation of endotracheal intubation, ablation of airway reflexes including laryngospasm

Respiratory

Improved chest-wall compliance
Improved ventilator synchrony
Prevention of coughing (and associated rises in ICP)

Musculoskeletal

Flaccid paralysis; surgical immobility, prevention of ECT-related injury, prevention of shivering (oxygen consumption)

OTHER CLINICAL EFFECTS, ADVERSE EFFECTS & TOXICITIES

Respiratory

Respiratory arrest
Residual paralysis; micro-aspiration, pneumonia, respiratory failure

Cardiovascular

Bradycardia secondary to agonism of muscarinic Ach receptors; more prevalent with repeat dosing and in the paediatric population
Malignant ventricular arrhythmias secondary to hyperkalaemia in susceptible patients (see below)

Musculoskeletal

Fasciculations
Myalgia; particularly noticeable with early mobilisation post-paralysis
Masseter spasm; particularly in the paediatric population

Neurological

Awareness under anaesthesia
A transient rise in ICP and IOP due to widespread muscle contraction

Electrolytes

A transient rise in serum potassium of 0.2-0.4mmol/L in normal patients, exaggerated in susceptible patient groups (see below)

Immune

Anaphylaxis
Histamine-release; hypotension

Other

Malignant hyperthermia; trigger
Anaesthesia Induced Rhabdomyolysis (AIR); trigger (see below)

CONSIDERATIONS

Precautions

Malignant hyperthermia susceptible patients; potent trigger
Congenital plasmacholinesterase deficiency; prolongation of paralysis (‘sux apnoea’, particularly with atypical plasmacholinesterase homozygotes)
Acquired plasmacholinesterase deficiency; prolongation of paralysis in pregnancy, renal/hepatic disease, cardiac failure, hypothyroidism, burns, malignancy, specific drugs (see below)
Hyperkalaemia; additive hyperkalaemia with risk of malignant ventricular arrhythmias
Patients with upregulated immature ACh receptors (burns from 24 hours to 18 months after injury, stroke/spinal cord trauma from 7 days to 6 months after injury, denervating/degenerative neuromuscular disease, prolonged immobilisation); massive potassium efflux with risk of malignant ventricular arrhythmias (risk correlates with severity/extent)
Muscle trauma; massive potassium efflux with risk of malignant ventricular arrhythmias (risk correlates with extent of muscle involvement)
Anaesthesia induced rhabodmysis (AIR) susceptible patients – muscular dystrophies with an absence of dystrophin (particularly Duchenne’s muscular dystrophy); rhabdomyolysis with massive potassium efflux and risk of malignant ventricular arrhythmias
Sepsis (particularly abdominal); risk of hyperkalaemia (variable evidence)
Myotonias; provocation of prolonged and painful muscle spasm, including temperomandibular spasm and intubation difficulty
Neuromuscular disease – myasthenia gravis, Lambert-Eaton syndrome; resistance to paralysis
Raised intracranial pressure; rises in ICP may result in herniation of cerebral contents
Raised intraocular pressure/acute narrow angle glaucoma; rises in IOP may result in optic ischaemia
Penetrating eye injury; rises in IOP may result in expulsion of orbital contents

Obstetric

ADEC category A

Drug interactions

Inhibitors of plasma cholinesterase – neostigmine, lignocaine, cytotoxics, lithium, ketamine, pancuronium, OCP, cytotoxics; prolonged paralysis
Digoxin; enhanced effect, potentially leading to ventricular excitation

REFERENCES

Drug information has been compiled from multiple sources including

Drugs in Anaesthesia and Intensive Care (Scarth & Smith)
Micromedex (IBM)
BJA Education (Oxford Academic)
Pharmacology for Anaesthesia and Intensive Care (Cambridge)
Australian Prescriber (NPS MedicineWise)

DRUGS

SUXAMETHONIUM