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SUXAMETHONIUM

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)

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