Rare neurologic sequelae: A case report of toxic metabolic encephalopathy caused by carbamazepine-induced hypovolemic hyponatremia

Abstract

Metabolic or secondary encephalopathies originate from non-cerebral organ system failures, often with multifactorial origins. Toxic-metabolic encephalopathy (TME) results from acute cerebral dysfunction due to metabolic disruptions, including drug effects. TME leads to altered consciousness, from delirium to coma, necessitating intensive care and mechanical ventilation. This study delves into TME, a reversible brain pathology triggered by extracerebral factors, notably drug-induced disturbances. Clinical presentation involves nonspecific altered consciousness, sometimes with asterixis or myoclonus. Carbamazepine (CBZ), a common antiepileptic medication, is linked to hyponatremia, defined by serum sodium levels below 135 mmol/l. The complexity of AED-induced hyponatremia is explored through a comprehensive patient analysis, revealing an array of symptoms including altered mentality, seizures, respiratory distress, and even coma or death. The case study dissects a patient's experience with toxic-metabolic encephalopathy secondary to CBZ-induced hypovolemic hyponatremia. This underscores the need for vigilant monitoring and management of adverse drug reactions, spotlighting the intricate interplay of drug-induced metabolic encephalopathies within clinical practice. The study reinforces the importance of awareness and tailored management strategies to enhance treatment outcomes for individuals with epilepsy.