Dr. Lee Woodson writes:
“Cardiac arrest in burned patients after succinylcholine administration was first reported in 1958. Animal and human studies consistently demonstrate an association of increased numbers of skeletal muscle acetylcholine receptors with resistance to non-depolarizing muscle relaxants and increased sensitivity to succinylcholine. In addition, the distribution of the new receptors is altered. Nicotinic receptors are normally restricted to the neuromuscular synaptic cleft but in these disease states new receptors are distributed across the surface of the skeletal muscle membrane. The new receptors are also a distinctly different isoform (α7AChR) that has been referred to as an immature, extrajunctional, or fetal receptor. The immature receptors are more easily depolarized by succinylcholine and their ion channel stays open longer. The immature receptors are also strongly and persistently depolarized by the metabolite of acetylcholine and succinylcholine, choline. It has been suggested that the hyperkalemic response to succinylcholine after burn or denervation injury results when potassium is released from receptor-associated ion channels across the entire muscle cell membrane, rather than just the junctional receptors. Depolarization persists because the channels stay open longer and the breakdown product of succinylcholine, choline, is also a strong agonist for the immature receptors.
Proliferation of acetylcholine receptors across the muscle membrane has been used to explain both resistance to non-depolarizing muscle relaxants and the exaggerated hyperkalemic response to succinylcholine.”
Herndon, David N. "Anesthesia for Burned Patients." Total Burn Care. Fourth ed. Edinburgh: Saunders Elsevier, 2012. 184-85. Print.