Clinical Case Scenario
A 32- year-old male with a history of alcohol abuse was admitted for increased aggressive behaviour and subsequent decreased responsiveness. Due to agitation in ED he received haloperidol (5mg) and lorazepam (2.5 mg).
Vital signs revealed a blood pressure - 133/106 mmHg, HR -108 beats /min, RR-15 breaths per minute, and temperature of 37.1°C.
Initial laboratory results revealed a white blood cell count of 12.2/mm3, ALT - 65 U/l, AST - 76 U/l, a glucose level of 231 mg/dl. Urine toxicology was unremarkable.
He was diagnosed to have acute alcohol intoxication with impending withdrawal, and admitted in the ICU due to agitation. He received thiamine, and was started on dexmedetomidine infusion together with IV lorazepam. On day 3 of admission, patient developed polyuria and produced a total output of 4.6 litres in 24 hours. Urine osmolality was 270 mOsm/kg and the serum sodium went up to 145 mmol/L from 136 mmol/L. CT brain revealed no intracranial pathology. The sedatives were discontinued for assessment of his neurological status. On day 5 polyuria resolved and sodium level remained stable.
What is the likely mechanism for the transient polyuria in this patient?
