Polyuria after head injury: interpreting a water-deprivation test
A 24-year-old man is admitted after a motorcycle accident with a minor head injury. He recovers, but 3 months later he complains of passing 8–10 L of dilute urine a day and drinking constantly. He is not on diuretics and has no diabetes mellitus: fasting glucose 5.2 mmol/L, HbA1c 5.4%. Serum sodium 146 mmol/L, plasma osmolality 296 mOsm/kg, urine osmolality 85 mOsm/kg; creatinine and calcium are normal. A water-deprivation test is performed: after 8 hours, body weight has fallen by 3%, plasma osmolality rises to 306 mOsm/kg, and urine osmolality rises only to 300 mOsm/kg. He is then given desmopressin (DDAVP); 2 hours later urine osmolality is 650 mOsm/kg. MRI shows loss of the normal posterior pituitary bright spot. The ward resident suggests restricting fluids to 1 L/day to 'restore ADH', and starting a thiazide.
1. Interpret the water-deprivation test and give the diagnosis. Why does the desmopressin response distinguish central from nephrogenic diabetes insipidus?
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The starting plasma osmolality is high (296) with a dilute urine (85), so ADH is either not secreted or not acting. During water deprivation, a normal person concentrates urine to >800 mOsm/kg and plasma osmolality stays near 290–295; here urine reaches only 300 while plasma rises to 306 and weight falls 3%, which is the safety limit. That confirms diabetes insipidus and excludes primary polydipsia, in which urine would concentrate during deprivation.
Desmopressin, a V2 agonist, raises urine osmolality to 650, showing that the collecting ducts respond and the kidneys can concentrate; the defect is lack of endogenous ADH. In nephrogenic DI, the collecting ducts are resistant, so urine osmolality rises little or not at all after desmopressin. The head injury and loss of the posterior pituitary bright spot support central DI, probably from stalk or posterior pituitary damage. The absence of hypercalcaemia and normal creatinine remove two other causes of nephrogenic DI. The 3% weight-loss endpoint was reached, so the test should not have been continued further.
2. Critically evaluate the resident's plan of fluid restriction plus a thiazide. What is appropriate management?
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Fluid restriction is the wrong treatment for central DI. The patient cannot concentrate urine, so restricting fluid will not 'restore ADH'; it will produce rapid hypernatraemia, because he is losing several litres of dilute urine plus insensible water. In a patient with intact thirst and access to water, serum sodium is only 146; with restriction, sodium can climb dangerously and cause seizures. Fluid restriction is used in primary polydipsia, not central DI. Thiazides are used in nephrogenic DI, where mild volume depletion increases proximal sodium and water reabsorption and reduces urine volume; they are not first-line in central DI.
The appropriate treatment is desmopressin, titrated to reduce urine output and thirst, with free access to water and monitoring of sodium. Warn about water intoxication if he drinks excessively while on desmopressin. After head trauma, also test anterior pituitary function (morning cortisol, thyroid function, IGF-1, testosterone) because stalk injury can cause multiple deficiencies; untreated cortisol deficiency can be dangerous. Endocrine follow-up and a medical alert card are appropriate.
3. Why is serum sodium only mildly elevated despite 8–10 L of urine output? What would happen if water access were lost?
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Serum sodium concentration depends on total body water relative to sodium, not on urine volume alone. If he drinks enough to match his urinary and insensible losses, sodium stays near normal even though turnover is huge; his value of 146 is at the upper limit, suggesting slight negative water balance. The dilute urine (85 mOsm/kg) means he is losing free water, so without intake his serum sodium would rise quickly.
A rough calculation: 8 L of urine at 85 mOsm/kg contains about 680 mOsm, while obligate solute excretion might be about 600–900 mOsm/day; the urine is dilute, so most of that 8 L is free water. Free-water clearance is approximately (1 − 85/296) × 8 L, or about 5.7 L/day. If he lost that much without replacement, serum sodium would rise by far more than a few mmol/L and he would become hypernatraemic, with brain shrinkage, confusion, seizures and risk of vascular rupture. This is why access to water is a safety issue and why desmopressin, not fluid restriction, is used. In hospital, if he is nil by mouth, give appropriate hypotonic fluid and monitor sodium frequently.