Suxamethonium Aponea

Pathophysiology

• Suxamethonium (succinylcholine) is a depolarising neuromuscular blocking agent

• Normally metabolised by plasma cholinesterase (pseudocholinesterase/butyrylcholinesterase)

• Suxamethonium aponea occurs due to:

  • Deficiency in plasma cholinesterase quantity or quality

  • Most commonly caused by genetic variants leading to atypical cholinesterase

  • Results in prolonged paralysis (hours instead of minutes)

Clinical Presentation

• Unexpected prolonged paralysis after succinylcholine administration

• Failure to resume spontaneous respiration after short surgical procedures

• Continued flaccid paralysis beyond expected duration (>10-15 minutes)

• Patient remains conscious but unable to move, breathe, or communicate

• Vital signs typically stable (if ventilation maintained)

• Anxiety and psychological distress once sedation wears off

At-Risk Populations

• Genetic variants (autosomal recessive inheritance pattern):

  • Homozygous atypical gene (1:3,000 patients)

  • Heterozygous atypical gene (1:25 patients)

• Family history of prolonged paralysis after anaesthesia

• Certain ethnic populations with higher prevalence of atypical genes

• Patients with:

  • Liver disease (decreased cholinesterase production)

  • Malnutrition

  • Pregnancy (particularly third trimester)

  • Burns (acute phase)

  • Uraemia/renal failure

  • Certain medications:

    • Organophosphates

    • Echothiophate eye drops

    • Cyclophosphamide

    • Metoclopramide

    • Oral contraceptives

    • Certain MAO inhibitors

Diagnosis

• Clinical suspicion based on unexpectedly prolonged paralysis

• Timing: paralysis persisting >15-30 minutes after succinylcholine

• Exclusion of other causes of prolonged paralysis:

  • Residual non-depolarising blockade

  • Respiratory centre depression

  • Electrolyte abnormalities

  • Hypothermia

  • Acid-base disturbances

Neuromuscular Transmission (NMT) Monitoring Findings

• Characteristic pattern:

  • No fade on train-of-four (TOF) stimulation

  • No post-tetanic facilitation

  • All four twitches equally suppressed

  • Gradual recovery of all twitches simultaneously

• Differs from non-depolarising blockade (which shows fade)

• Very slow recovery of twitch height over hours

Management

• Immediate measures:

  • Continue mechanical ventilation

  • Maintain sedation/anesthesia until recovery

  • Reassure patient if awake

  • Inform surgical team

• Supportive care:

  • Maintain normothermia

  • Monitor ventilation and oxygenation

  • Provide adequate sedation and analgesia

  • Consider transfer and ICU admission for prolonged cases

• No specific antidote/reversal agent available

• Fresh frozen plasma (FFP) may be considered in severe cases (provides functional cholinesterase)

• Avoid repeated doses of succinylcholine

Recovery and Follow-up

• Continue ventilation until full recovery of neuromuscular function

• Monitor with NMT until TOF ratio >0.9

• Document in medical records as significant anaesthetic complication

• Refer patient for testing to confirm diagnosis

• Genetic counselling for patient and family

• Medical alert bracelet recommended

• Inform patient about implications for future anaesthetics

Testing for Cholinesterase Deficiency

• Dibucaine number:

  • Measures inhibition of enzyme by dibucaine

  • Normal: 70-80% inhibition

  • Heterozygous: 40-60% inhibition

  • Homozygous atypical: 10-30% inhibition

• Fluoride number:

  • Similar test using sodium fluoride

  • Helps differentiate variants

• Plasma cholinesterase activity level

• Genetic testing for butyrylcholinesterase gene mutations

• Testing should be delayed 6-8 weeks after event (acute phase may have falsely low levels)

• First-degree relatives should be tested

Future Anesthetic Considerations

• Avoid succinylcholine in confirmed cases

• Use non-depolarizing neuromuscular blockers if needed

• Consider alternative airway management techniques

• Always have NMT monitoring available