Suxamethonium โ the Lethal Hyperkalaemia
Why suxamethonium kills the healing burns patient
Burn injury โ up-regulation & spread of extrajunctional (immature, fetal-type) ACh receptorsReceptors proliferate across the whole muscle membrane, not just the motor end-plate
Suxamethonium depolarises this vast receptor fieldMassive efflux of Kโบ from muscle into the circulation
Acute severe hyperkalaemia โ peaked T-waves โ VT/VF / cardiac arrest
The rule (Dr. Tanya's note)
Avoid suxamethonium after ~24โ48 hours from the burn, up to ~1โ2 years (until the burn is fully healed and the receptor population normalises). In the first 24 hours the receptor up-regulation has not yet developed, so suxamethonium is still considered safe if truly needed for a rapid-sequence induction. The safest habit for the healing/contracted patient is a rocuronium modified-RSI instead.
Resistance to Non-Depolarising Relaxants
๐ผ Bigger doses, shorter effect
- The same receptor up-regulation that makes suxamethonium dangerous makes the patient resistant to non-depolarising relaxants โ more receptors must be occupied to achieve block.
- Add altered pharmacokinetics: hypermetabolism โ โ clearance; a larger volume of distribution.
- Result: dose requirements may be substantially increased and duration shortened โ titrate to neuromuscular (TOF) monitoring rather than to a weight-based dose.
The Hypermetabolic Patient & Drug Binding
Protein binding shifts
- โ Albumin (protein loss/catabolism) โ โ free fraction of acidic, albumin-bound drugs (e.g. diazepam, phenytoin) โ exaggerated effect
- โ ฮฑโ-acid glycoprotein โ โ binding of basic drugs (e.g. some local anaesthetics, opioids) โ โ free fraction
Practical consequences
- High opioid requirement & tolerance from chronic pain/repeated exposure โ plan multimodal analgesia
- Hyperdynamic circulation โ faster onset of IV agents but โ clearance
- Ketamine is a useful, cardiostable, analgesic induction/maintenance agent in these patients