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- dose of 1 mg/kg IV or 2 mg/kg IM produces intubating conditions within 0.7-1 min
- apnoea lasts approx 5 mins with complete recovery of hand muscle paralysis taking another 5 mins
- paralysis may be maintained using further boluses of 0.25-0.5 mg/kg or continuous infusion
- tachyphylaxis common and phase II block develops. May occur after as little as 2-5 mg/kg


- catalysed by plasma cholinesterase
- ester links broken
- plasma cholinesterase usually present in plasma in sufficient concentration to give half-life of approximately 4 mins

Adverse effects

- malignant hyperpyrexia
- hyperkalaemia: due to shift from inside cells. Normal rise of order of 0.7 mmol/l but in some patients rise may be considerably greater (up to 5 mmol/l). Following patients particularly susceptible:

  • patients with severe burns
  • patients with extensive muscle damage
  • paraplegic patients
  • patients with peripheral neuropathy

Susceptibility develops gradually becoming a clinical problem approx a week after injury
- bradycardia: especially in children given repeated doses
- myalgia: more common in young ambulant women. Develops day after receiving suxamethonium. Occurs in up to 50% of patients. Can be abolished by pre-treating with non-depolarising relaxant but this necessitates an increase in dose of suxamethonium
- rise in ICP and IOP. Latter > former. Transient.
- anaphylactoid reactions
- contractures in patients with myotonia


Potentiated by:

- ecothiopate: anti-cholinesterase
- propanidid: partially depolarizes cell membrane in end-plate area
- anti-cholinesterase: intense muscarinic activity of neostigmine and pyridostigmine makes them unsuitable for use in prolonging suxamethonium action
- tacrine: anti-cholinesterase activity with relatively little muscarinic activity. Has been used quite widely to potentiate and prolong activity of suxamethonium. Atropine 0.3 mg will block what little muscarinic activity it does have. Associated with less muscle pain than repeated doses of suxamethonium

Antagonized by:

- gallamine and other non-depolarising relaxants

Abnormalities of suxamethonium metabolism

- dibucaine number and fluoride number are measures of the activity of plasma cholinesterase
- dibucaine number is the percentage inhibition of cholinesterase by 10-5 molar dibucaine
- "fluoride number" is the percentage inhibition by 5x10-5 molar sodium fluoride
- suxamethonium metabolism is normal in 94% of the population. These people have normal genotypes E1uE1u with normal enzyme activity and DN of 75-85
- 3 abnormal genes exist:

  • E1A (atypical) homozygotes comprise 0.03% of the population
  • E1F (fluoride resistant) homozygotes 0.003%
  • E1S (silent) homozygotes 0.001%

- normal serum cholinesterase approx. 80 units/ml

Abnormal plasma cholinesterase

Atypical cholinesterase.

- Mendelian recessive
- homozygotes have 1-2 hr apnoea during which phase II block develops. DN 16-25.
- heterozygotes (1/25 of population) have little or no disturbance (DN 50-65), with apnoeas of up to 10 min.

Fluoride-resistant cholinesterase

- clinically the same as atypical form except apnoea in homozygotes lasts about 1 hr.


All possible combinations of heterozygotes exist with apnoeas around 10 min. (1/25 of population)

Plasma cholinesterase deficiency


- hydrolysis of suxamethonium proceeds at rate of only 5% per hour.
- due to silent gene E1S
- homozygotes have 1-2 hours apnoea, during which phase II block develops
- heterozygotes have normal DN and FN but only half the normal plasma cholinesterase activity.


      Disease states

- cardiac failure
- hepatic failure
- uraemia
- trophoblastic disease
- myxoedema
- hypoproteinaemia due to malnutrition
- obesity
- hyperpyrexia
- organophosphorus poisoning


- plasmaphoresis
- drugs: cyclophosphamide, ecothiopate, procainamide, quinidine, phenothiazines, ketamine, trimetaphan, pancuronium, propanidid, metrifonate

Plasma cholinesterase antagonism

- by anticholinesterases and tacrine

Plasma cholinesterase excess

- result is shortening of the duration of the action of sux.
- acquired: obesity, toxic goitre, nephrosis, depression, psoriasis, alcoholism
- congenital: C5 variant.

Differential diagnosis of prolonged apnoea after suxamethonium

- atypical cholinesterase
- dehydration and electrolyte imbalance leading to the early development of phase II block
- low plasma cholinesterase level. This seldom causes prolonged apnoea if 50mg is not exceeded. This dose is adequate for most patients requiring single injection. Unlikely to be the cause of apnoea lasting > 20-30 min, if cholinesterase level > 25 units/ml.
- overdose of suxamethonium; ie > 1g by infusion
- central depression of respiratory centre by narcotic analgesic or anaesthetic
- hypocapnia
- hypercapnia poisoning respiratory centre
- reflex laryngeal apnoea due to the presence of a tracheal tube. Removal of the tube or deflation of the cuff leads to restoration of spontaneous breathing.
- acute rise of intracranial pressure
- moribundity: some gravely ill patients only breathe again with difficulty once they become apnoeic.
- metabolic acidosis


- use peripheral nerve stimulator to distinguish between central depression and neuromuscular block
- check Pco2 and cholinesterase level
- cholinesterase abnormality: IPPV and sedation until block wears off, blood for cholinesterase analysis. Infuse plasma or cholase to correct deficiency. Screen near relatives and issue with warning cards or bracelets.
- avoid suxamethonium in known or suspected suxamethonium sensitive patients. In documented heterozygotes it can be given, if specifically indicated, in very small test doses eg 0.05-0.1 mg/kg, when it produces a normal response.

© Charles Gomersall December 1999


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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