Succinylcholine (SCh) is a depolarizing neuromuscular-blocking agent, which produce sustained opening of the nicotinic cholinergic receptor channel. Under normal conditions, post-junctional membrane depolarization results in leakage of potassium that produces an increase of 0.5 – 1.0 mEq/L in serum K+ concentration. When SCh depolarizes muscle that has been traumatized (crush injury) or denervated (upper motor neuron lesion) enough K+ may leak from cells to produce systemic hyperkalemia and cardiac arrest. This susceptibility to hyperkalemia is thought to be caused by proliferation of junctional and extrajunctional cholinergic receptors.
Patient population at risk for SCh-induced hyperkalemia include patients with upper motor neuron lesions resulting from stroke, brain or spinal cord tumors, other intracerebral or spinal cord masses, closed head injury, or encephalitis and also other disease processes like unhealed third-degree burns, severe intra-abdominal infections, severe metabolic acidosis with hypovolemia, crush injuries, and prolonged nondepolarizing muscle blockade or immobility. Life-threatening potassium release is not reliably prevented by pretreatment with a nondepolarizing agent. The subsequent cardiac arrest can prove to be refractory to routine cardiopulmonary resuscitation, requiring Calcium,, insulin, glucose, bicarbonate, epinephrine, cation-exchange resin, dantrolene, and even cardiopulmonary bypass to reduce metabolic acidosis and serum potassium levels. The risk of hyperkalemia appears to peak 7-10 days after the injury, but the exact time of onset and the duration of the risk period vary.