Central diabetes insipidus after brain injury — FFICM MCQ

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HardRenal and MetabolicCentral diabetes insipidus after brain injuryFFICM

A 39-year-old woman with catastrophic traumatic brain injury produces 550 ml/hour of dilute urine. Sodium rises from 144 to 158 mmol/L over 8 hours, serum osmolality is high and urine osmolality is low. Glucose is 6.1 mmol/L and there has been no mannitol for 24 hours. What is the most likely diagnosis?

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Correct answer: A — Central diabetes insipidus

The correct answer is A, central diabetes insipidus. Catastrophic traumatic brain injury can disrupt hypothalamic-pituitary ADH secretion, producing large volumes of dilute urine (over 500 ml/hour), rising serum sodium and osmolality, and inappropriately low urine osmolality, exactly the pattern described. This combination of polyuria with a hyperosmolar, hypernatraemic serum and dilute urine (low urine osmolality relative to plasma) is the classic biochemical signature of cranial DI following loss of posterior pituitary ADH release. Normal glucose (6.1 mmol/L) excludes an osmotic diuretic cause, and the absence of mannitol for 24 hours removes another osmotic diuresis explanation, leaving ADH deficiency as the mechanism. This is a well recognised endocrine complication of severe TBI and brainstem herniation, directly relevant to donor optimisation care. Why the other options are wrong: E. Osmotic diuresis from hyperglycaemia: glucose is normal at 6.1 mmol/L, so there is no glycosuria or osmotic solute load to drive polyuria. B. Cerebral salt wasting: this causes natriuresis with hyponatraemia and volume depletion, the opposite sodium trend to the rising sodium seen here. C. Syndrome of inappropriate antidiuresis: SIAD causes water retention, hyponatraemia and concentrated (high osmolality) urine, not dilute urine with hypernatraemia. D. Acute tubular necrosis recovery phase: the post-ATN diuretic phase produces polyuria but typically with isosmotic or only mildly dilute urine and no primary defect in ADH secretion; there is no history here of preceding renal injury or oliguric phase. Key point: Polyuria with rising serum sodium/osmolality but low urine osmolality after catastrophic brain injury, with normal glucose, points to central diabetes insipidus from ADH deficiency.

Reference: NHS Blood and Transplant, ODT Clinical: Donor Optimisation, 'Pathophysiological consequences of brain-stem death' section (diabetes insipidus as immediate endocrine consequence of hypothalamic failure), https://www.odt.nhs.uk/deceased-donation/best-practice-guidance/donor-optimisation/