Acute psychosis with convulsive episodes following total thyroidectomy induced by concurrent hypothyroidism and hypocalcemia: a case report.

backgroundTotal thyroidectomy is a common surgical procedure, with postoperative anxiety and depression being recognized complications. However, the development of acute psychosis is a rare and severe manifestation. The etiology of such presentations is often complex, involving metabolic derangements that directly impact central nervous system function. We report a case of severe psychosis with convulsive features precipitated by the synergistic effects of two distinct postoperative complications: iatrogenic hypothyroidism and hypoparathyroidism-induced hypocalcemia. The unique monthly cyclical pattern of symptoms followed by postictal somnolence highlights a novel clinical presentation. CASE PRESENTATION: A 59-year-old Arab male with no prior psychiatric history underwent a total thyroidectomy for a large goiter causing airway compression. One month postoperatively, he presented with a dramatic onset of severe agitation, confusion, bizarre behaviors, and convulsive episodes. These episodes were uniquely cyclical, occurring monthly and followed by prolonged periods of sleep and amnesia. Laboratory investigations confirmed the presence of two concurrent metabolic insults: severe hypothyroidism, evidenced by a markedly elevated thyroid-stimulating hormone (TSH) level, and significant hypocalcemia secondary to iatrogenic hypoparathyroidism. A diagnosis of Psychotic Disorder Due to Another Medical Condition was made. The patient was managed with a multidisciplinary approach, including thyroid hormone replacement, calcium and vitamin D supplementation, and a short-term regimen of antipsychotic medications (olanzapine and aripiprazole) for acute behavioral control. His symptoms resolved completely within two months, and he returned to his premorbid level of functioning.

conclusionsThis case illustrates a "perfect storm" scenario where concurrent hypothyroidism and hypocalcemia created a state of profound neuropsychiatric decompensation. The hypothyroidism likely contributed to cerebral metabolic depression and neurotransmitter dysregulation, while the hypocalcemia induced a state of neuronal hyperexcitability, precipitating the convulsive episodes. The distinct cyclical pattern of psychosis with convulsions and postictal features suggests a potential epileptiform process masquerading as pure psychosis. This report underscores the absolute necessity for vigilant postoperative monitoring of both thyroid function and calcium homeostasis following total thyroidectomy. A high index of suspicion for these dual metabolic insults is critical for prompt diagnosis and effective, multidisciplinary management to prevent severe morbidity.