Succinylcholine – You Gotta Know It
One of the pharmacologic agents I like to cover in depth with medical students is succinylcholine. It has a unique metabolism. Among anaphylactic reactions, it’s a common culprit. It’s an IV agent associated with malignant hyperthermia. And when you call us for a stat intubation, we’re finding reasons NOT to use it.
Succinylcholine (“sux”) is composed of two acetylcholine molecules linked together and binds the post-synaptic neuromuscular junction (NMJ) end plate causing depolarization. Initially, this depolarizing effect stimulates muscle contraction which we can see as diffuse fasciculations. Unlike acetylcholine which is rapidly hydrolyzed by acetylcholinesterase, sux remains in the NMJ causing continued depolarization and profound muscular relaxation as calcium is slowly moved back into the sarcoplasmic reticulum. This phase 1 block explains why we see fasciculations (contractions) followed by relaxation.
With higher doses of sux (typically > 4 mg/kg), continuous binding to the acetylcholine receptors causes an ongoing influx of sodium and efflux of potassium. The sodium-potassium ATPase’s activity is upregulated bringing ion concentrations back towards their resting states. The receptor no longer responds appropriately to acetylcholine, and the NMJ blockade is prolonged. This phase 2 block has features similar to non-depolarizing blockers (ie, rocuronium, vecuronium) such as a fade with train-of-four peripheral nerve stimulation. If a phase 2 block develops, supportive care is often the best management until the block wears off.
Okay, enough about the details. Why is this topic important? Because healthcare providers will call anesthesia for stat intubations, and we need to look for contraindications to sux.
- Known familial or prior history of malignant hyperthermia
- Known hypersensitivity reactions
- Skeletal muscle myopathies
- Acute burn injury, extensive denervation injury, and upper motor neuron injury
- Severe hyperkalemia
A standard induction dose of sux will raise one’s potassium by 0.5 mEq. This usually is insignificant… unless you’re already hyperkalemic and have evidence of end-organ involvement (EKG with peaked T waves and/or widened QRS complexes… think about ESRD patients). In fact, cardiac arrest minutes after sux administration is due to hyperkalemia until proven otherwise and should be treated accordingly with hyperventilation, bicarbonate, glucose/insulin, albuterol, etc.
Burn and denervation injuries cause an upregulation of NMJ acetylcholine receptors, so giving these patients a dose of sux will result in the depolarization of a LOT more receptors and subsequent release of MORE potassium. Not a good idea.
Regardless of your speciality, it’s good to know the contraindications of succinylcholine for those rare instances in which someone needs to give it!