Generalized tonic-clonic seizures are a recognized cause of rhabdomyolysis and may be complicated by acute kidney injury, particularly when muscle injury is severe or prolonged. We describe the case of a 53-year-old man who presented following a witnessed generalized seizure and collapse, with subsequent development of severe rhabdomyolysis and stage three acute kidney injury. Initial assessment focused on neurological and infectious causes of altered consciousness, including neuroimaging and cerebrospinal fluid analysis, which did not demonstrate an acute intracranial or central nervous system infectious process. During admission, renal function progressively deteriorated, accompanied by electrolyte abnormalities. Serial biochemical testing later revealed a marked rise in creatine kinase, peaking at greater than 89,000 international units per liter, confirming severe rhabdomyolysis. Extensive investigations excluded alternative causes of renal impairment, including autoimmune, vasculitic, obstructive, and glomerular pathology. The patient was managed with aggressive intravenous fluid resuscitation, electrolyte correction, and supportive care, resulting in gradual improvement in renal function and down-trending creatine kinase levels without the need for renal replacement therapy. This case highlights the evolving nature of seizure-associated rhabdomyolysis and its potential to cause significant acute kidney injury. It emphasizes the importance of considering rhabdomyolysis in patients presenting after generalized seizures and supports early measurement and monitoring of creatine kinase to guide timely management and reduce the risk of renal complications.
Alsherbeeny et al. (Sun,) studied this question.