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 37.1Β°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.
Wrong Answer: β Option A - Osmotic diuresis due to hyperglycaemia A glucose concentration of 231 mg/dL is unlikely to explain 4.6 L/day of polyuria by itself. Osmotic diuresis occurs when an excess of non-reabsorbed solute, such as glucose, remains in the renal tubules and increases urinary water loss. In significant glucosuria, urine osmolality is generally increased. Here, the urine is relatively dilute at 270 mOsm/kg despite rising serum sodium, favouring impaired ADH-mediated water conservation rather than primary osmotic diuresis.
Right Answer: β B. Dexmedetomidine-induced transient central diabetes insipidus. Explanation Dexmedetomidine is a highly selective central Ξ±β-adrenergic agonist commonly used for ICU sedation. Although hypotension and bradycardia are its best-recognised adverse effects, rare cases of marked polyuria resembling diabetes insipidus have been reported. The proposed mechanism involves central Ξ±β-adrenergic effects on noradrenergic pathways, including pathways involving the locus coeruleus and hypothalamic nuclei that regulate arginine vasopressin (ADH) release. Suppression of ADH secretion can impair renal water conservation and produce a transient central DI-like picture. In this patient, the combination of polyuria, a rise in serum sodium from 136 to 145 mmol/L, and urine osmolality of only 270 mOsm/kg indicates impaired urinary concentration. The close temporal association with dexmedetomidine exposure and resolution after discontinuation strongly supports a transient dexmedetomidine-associated central DI-like syndrome.
Wrong Answer: β Option C - Beer potomania Beer potomania results from excessive beer intake combined with very low dietary solute intake. The reduced solute load limits the kidney's ability to excrete free water and typically produces hypotonic hyponatraemia. Although brisk diuresis may occur after restoration of solute intake, this patient did not present with hyponatraemia and instead developed a rise in serum sodium.
Wrong Answer: β Option D - Alcohol-induced nephrogenic diabetes insipidus Alcohol can suppress ADH secretion and contribute to increased urine output, but this is a central effect rather than nephrogenic DI. Nephrogenic DI is characterised by renal resistance to ADH. The patient's clinical course is more consistent with a transient central mechanism related to dexmedetomidine, especially because the polyuria resolved after discontinuation of the drug.
