SIADH and disorders of water balance — formative SAQs

SAQ 1 (10)

A 4-year-old girl is admitted with severe community-acquired pneumonia and started on intravenous maintenance fluids. On day 2 she becomes drowsy and has a brief generalised seizure. Serum sodium is 120 mmol/L, serum osmolality 248 mOsm/kg, urine osmolality 480 mOsm/kg, and urine sodium 62 mmol/L. She is well perfused with no oedema and normal capillary refill. She is not on diuretics, and cortisol and thyroid function are normal. [8][12]

1. State the diagnosis, and explain how the biochemistry and volume status confirm it. (3) [8][12]
2. Give the immediate emergency management, including the drug, dose, route, and the correction target. (4) [7][3]
3. Outline the definitive management once she is stable, and the single most important safety limit. (3) [10][12]

Model answer

Diagnosis. This is SIADH causing acute symptomatic hyponatraemia (hyponatraemic encephalopathy). The biochemistry is diagnostic: a low serum sodium (120 mmol/L) with a low serum osmolality (248 mOsm/kg) confirms a true hypotonic hyponatraemia, and the inappropriately concentrated urine (480 mOsm/kg) with a high urine sodium (62 mmol/L) shows ADH is acting when the low osmolality should have switched it off. She is clinically euvolaemic (no dehydration, no oedema), off diuretics, with normal cortisol and thyroid function, so the endocrine mimics are excluded and SIADH is confirmed. The pneumonia is the ADH trigger. [8][12]

Emergency management. She has a seizure from hyponatraemic encephalopathy, so give intravenous hypertonic 3% saline, about 2 mL/kg (commonly capped near 100 mL) over 10 to 15 minutes, repeated if she continues to seize. The target is to raise the serum sodium by only 4 to 6 mmol/L — enough to reverse the cerebral oedema and stop the fit — and then stop the rapid correction. Manage the airway and seizure as for any seizing child and get senior and intensive care help. Check the sodium every 2 to 4 hours during active correction. [7][3]

Definitive management and safety limit. Once she is out of danger, treat the SIADH with fluid restriction (below insensible plus urinary losses), switch any hypotonic fluid to isotonic fluid, and treat the pneumonia, because SIADH resolves when its trigger resolves. The single most important safety limit is the correction rate: the total sodium rise must not exceed 8 mmol/L in 24 hours, because faster correction of a hyponatraemia of uncertain duration risks osmotic demyelination syndrome. If she overshoots, re-lower the sodium with 5% dextrose and desmopressin. [10][12]

SAQ 2 (10)

A 9-year-old boy is 6 days post resection of a large posterior fossa tumour. He develops hyponatraemia (serum sodium 126 mmol/L) with a urine sodium of 90 mmol/L and a high urine output of 4 mL/kg/h. He has lost 1.4 kg since surgery, is tachycardic with a capillary refill of 3 seconds, and his fluid balance chart shows a negative balance. [9][3]

1. What are the two main differential diagnoses, and which is most likely here? Justify your answer. (4) [9][3]
2. Explain why the urine sodium cannot distinguish them, and what does. (3) [9][12]
3. State the correct management, and the specific harm of the wrong treatment. (3) [9][3]

Model answer

Differentials. The two diagnoses to weigh are SIADH and cerebral salt wasting, because both occur in the neurosurgical child and both produce a low sodium with a high urine sodium. The most likely diagnosis here is cerebral salt wasting: he is clinically volume depleted (weight loss of 1.4 kg, tachycardia, prolonged capillary refill), he has a high urine output (4 mL/kg/h), and his fluid balance is negative — a picture of primary renal salt and water loss, not water retention. In SIADH he would be euvolaemic with a neutral or positive balance. [9][3]

Why urine sodium cannot distinguish them. Both SIADH and cerebral salt wasting have a high urine sodium (over 30 mmol/L), because in SIADH the kidney excretes the sodium it is given, and in salt wasting the kidney is actively dumping sodium. The urine sodium is therefore high in both and cannot separate them. The discriminator is volume status, supported by the urine output trend, the daily weight, and the fluid balance chart: the salt-waster is dry and running a negative balance, the SIADH child is euvolaemic. [9][12]

Management and the harm of getting it wrong. The correct treatment for cerebral salt wasting is salt and volume replacement — isotonic fluid and sodium to replace the ongoing renal losses — which is the opposite of SIADH management. The specific harm of the wrong treatment is that fluid restriction (the correct SIADH treatment) worsens cerebral salt wasting, deepening the volume depletion and the hyponatraemia and risking hypovolaemic shock and, in a brain-injured child, cerebral ischaemia. This is why establishing volume status before restricting fluid is essential. [9][3]