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EV0385

Life-threatening hypernatremia revealing hypoactive catatonia in schizophrenia: rapid improvement with lorazepam

LIFE-THREATENING HYPERNATREMIA REVEALING HYPOACTIVE CATATONIA IN SCHIZOPHRENIA: RAPID REVERSAL WITH LORAZEPAM

Hypoactive catatonia associated with reduced oral intake in schizophrenia can lead to life-threatening hypernatremia and can be rapidly reversed with lorazepam.

The aim of this study is to highlight that recognition of hypoactive catatonia in schizophrenia may be delayed when it is mistaken for negative symptoms or psychotic deterioration, and that catatonia-related reductions in oral intake may contribute to severe, life-threatening electrolyte disturbances. In this case report, a 67-year-old man with a 20-year history of schizophrenia was admitted to an internal medicine unit with marked hypernatremia (serum sodium 157 mmol/L), and a psychiatric consultation was requested because of behavioral changes and reduced oral intake; catatonia severity was assessed using the Bush-Francis Catatonia Rating Scale (BFCRS). The patient had discontinued his medication in the preceding weeks, and his presentation was initially interpreted as a psychotic exacerbation; his antipsychotic dose was increased, but there was no improvement. On examination, the patient was alert but mute, uncooperative, resistant to care, and refusing oral intake, with marked negativism and posturing; preserved alertness and the absence of fluctuation made delirium unlikely, while the absence of rigidity, autonomic instability, and supportive laboratory findings made neuroleptic malignant syndrome unlikely. A lorazepam challenge produced marked clinical improvement within 2 hours, and maintenance treatment at 4 mg/day rapidly restored communication and oral intake, with the BFCRS score decreasing from 13 to 5. During concurrent medical treatment, serum sodium decreased from 157 mmol/L to 144 mmol/L within 24 hours, with no neurological complications attributable to sodium correction. The authors emphasize that hypoactive catatonia should be considered in patients with schizophrenia who present with mutism, negativism, posturing, reduced oral intake, and electrolyte imbalance, particularly when presumed psychotic deterioration does not respond to an increase in antipsychotic dosage. The clinical course suggests that catatonia-related reductions in oral intake contributed to hypernatremia and that hypernatremia may, in turn, have exacerbated the catatonic state, indicating a potentially bidirectional relationship; early recognition and prompt lorazepam treatment may prevent serious medical complications.

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