Sevoflurane

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An event is serious (based on the ICH definition) when the patient outcome is:

• * death

• * life-threatening

• * hospitalisation

• * disability

• * congenital anomaly

• * other medically important event

In a case series, two patients (a man aged 48-years and a woman aged 68-years) were described, who developed nephrogenic diabetes insipidus (NDI) while receiving sedative therapy with sevoflurane [route and dosage not stated; duration of treatment to reaction onset not clearly stated].

Patient-1: A 48-year-old man with no significant medical history, was admitted to ICU with COVID-19 infection related acute respiratory distress syndrome (ARDS). He required mechanical ventilation. After 48 hours of deep sedation and neuromuscular paralysis, he was started on IV sedation with propofol, midazolam and remifentanil due to the requirement of continued ventilatory support and increased agitation. After 2−3 days, due to persistent agitation, sevoflurane was started for sedation using ventilators of the operating theatre along with continuous end tidal gas monitoring. After 6−8 days of sevoflurane administration, a gradual increase in his urine output was noted along with increase in plasma sodium and plasma osmolality without glycosuria indicating a diagnosis of diabetes insipidus. After a significant decrease was noted in his creatine clearance, development of acute kidney injury was considered. Therefore, his treatment was started with desmopressin, but no improvement was noted; hence, a diagnosis of NDI was confirmed, and sevoflurane therapy was stopped. Despite discontinuation of sevoflurane, persistent polyuria with hypernatremia was observed. To compensate for the renal loss, he received Ringer's lactate along with free water through the nasogastric tube, parenteral nutrition and FreAmine to compensate for the extrarenal fluid loss. Additionally, a combination of an unspecified thiazide and potassium sparing diuretic were started for three days along with indomethacin for reduction of the urine output. Gradual improvement was noted in his condition in the following days.

Patient-2: A 68-year-old woman with no significant medical history, was admitted to ICU with COVID-19 infection related acute respiratory distress syndrome (ARDS). She required mechanical ventilation. After 48 hours of deep sedation and neuromuscular paralysis, she was started on IV sedation with propofol, midazolam and remifentanil due to the requirement of continued ventilatory support and increased agitation. After 2−3 days, due to persistent agitation, sevoflurane was started for sedation using ventilators of the operating theatre along with continuous end tidal gas monitoring. After 6−8 days of sevoflurane administration, a gradual increase in her urine output was noted along with increase in plasma sodium and plasma osmolality without glycosuria indicating a diagnosis of diabetes insipidus. After a significant decrease was noted in her creatine clearance, development of acute kidney injury was considered. Therefore, her treatment was started with desmopressin, but no improvement was noted; hence, a diagnosis of NDI was confirmed, and sevoflurane therapy was stopped. Despite discontinuation of sevoflurane, persistent polyuria with hypernatremia was observed. To compensate for the renal loss, she received Ringer's lactate along with free water through the nasogastric tube, parenteral nutrition and FreAmine to compensate for the extrarenal fluid loss. Additionally, the combination of an unspecified thiazide and potassium sparing diuretic were started for three days along with indomethacin for reduction of the urine output. Gradual improvement was noted in her condition in the subsequent days.