Selected Topics: ToxicologySuccinylcholine-induced Hyperkalemia in a Patient with Multiple Sclerosis
Introduction
Patients frequently present to the emergency department (ED) in need of prompt airway management. Expertise in this procedure, along with an intricate knowledge of the pharmacologic agents utilized to perform a rapid sequence intubation (RSI), is one of the defining features of the emergency physician (1). Succinylcholine, a depolarizing neuromuscular blocking agent, has long been the preferred paralytic for use in RSI 2, 3. Most of the contraindications to succinylcholine utilization relate to the potential to induce hyperkalemia, which can occur as a result of receptor upregulation in advanced neuromuscular disorders, including spinal cord injury and muscular dystrophy 3, 4, 5, 6, 7. Multiple sclerosis is a debilitating, immune-mediated disease characterized by demyelination, axonal damage, and ultimately, scar formation in the central nervous system 8, 9. Although hyperkalemia after the administration of succinylcholine to a patient with multiple sclerosis is frequently discussed, documented cases in the literature are rare 3, 9, 10.
Section snippets
Case Report
A 38-year-old right-hand-dominant woman presented to the ED for increasing lower extremity weakness and shortness of breath. Two years before this admission, the patient developed lower extremity weakness, and was diagnosed with multiple sclerosis. She was treated with steroids, with resolution of symptoms. Several months later, she developed left-sided weakness and again was treated with steroids, although after this second exacerbation, she developed some residual weakness involving the left
Discussion
Succinylcholine, or diacetylcholine (Figure 2), is the only depolarizing neuromuscular blocker currently approved for use in the United States. By binding to the two alpha subunits on the nicotinic receptor, a conformational change ensues and the channel opens, thereby permitting the influx of calcium and sodium, and the efflux of potassium 3, 11, 12. Because succinylcholine is not degraded by acetylcholinesterase, it remains bound to the receptor longer than acetylcholine itself would,
Conclusion
Succinylcholine-induced hyperkalemia is well described with various neuromuscular disorders. Although not widely reported with multiple sclerosis, a case of a 38-year-old woman with life-threatening hyperkalemia after the administration of a depolarizing neuromuscular blocking agent is presented.
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