SIADH and disorders of water balance

The organising principle is water, not salt. Serum sodium is a ratio of sodium to water, so a low sodium usually means the body is holding on to free water it should be excreting. The gatekeeper of that free water is antidiuretic hormone (ADH, also called arginine vasopressin), released from the posterior pituitary when the hypothalamic osmoreceptors sense a rising osmolality. When ADH is switched on inappropriately, the kidney reabsorbs water it should be losing, the urine stays concentrated, and the serum dilutes. Read every hyponatraemia through the question "why is this child not excreting free water?" and the diagnosis follows. ^{[3] [8]}

This page covers the full breadth of paediatric water-balance disorders on the low-sodium side: the ADH axis, the volume-status approach to hyponatraemia, SIADH and its causes, the crucial distinction from cerebral salt wasting, hospital-acquired hyponatraemia from hypotonic fluids, acute management with hypertonic saline, chronic management with fluid restriction and urea, and the sodium correction rate that governs the risk of osmotic demyelination. It deliberately stops at the water-losing disorders: diabetes insipidus and the polyuria-polydipsia workup are owned by their own leaf and only cross-referenced here. ^{[1] [8]}

Overview & Definition

Hyponatraemia is a serum sodium below 135 mmol per litre, and it is the commonest electrolyte disturbance in hospitalised children. ^[4] Severity is graded by the number and by the symptoms: mild is roughly 130 to 134, moderate 125 to 129, and profound under 125 mmol per litre, but the sodium value alone never dictates urgency — a child who is seizing at 128 is a bigger emergency than a well child at 118. ^{[1] [2]}

SIADH is the syndrome of inappropriate antidiuretic hormone secretion, more precisely called the syndrome of inappropriate antidiuresis. It is euvolaemic hypotonic hyponatraemia caused by ADH acting when the low osmolality should have switched it off. The kidney cannot dilute the urine, free water is retained, and the serum sodium falls even though total body sodium is close to normal. ^{[8] [12]}

The two numbers that anchor the whole topic are chronicity and rate. Acute hyponatraemia (developed over under 48 hours) causes cerebral oedema because the brain has not had time to adapt, so it presents with encephalopathy and tolerates faster correction. Chronic hyponatraemia (over 48 hours or unknown duration) is far more dangerous to correct, because the adapted brain is vulnerable to osmotic demyelination if the sodium rises too fast. Assume any hyponatraemia of unknown duration is chronic. ^{[3] [10]}

References12ShowHide

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2. [2]Verbalis JG; Goldsmith SR; Greenberg A; et al Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med, 2013.PMID 24074529
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9. [9]Bettinelli A; Longoni L; Tammaro F; et al Renal salt-wasting syndrome in children with intracranial disorders. Pediatr Nephrol, 2012.PMID 22237777
10. [10]Sterns RH Adverse Consequences of Overly-Rapid Correction of Hyponatremia. Front Horm Res, 2019.PMID 32097948
11. [11]Huang EA; Feldman BJ; Schwartz ID; et al Oral urea for the treatment of chronic syndrome of inappropriate antidiuresis in children. J Pediatr, 2006.PMID 16423613
12. [12]Hoorn EJ; Zietse R Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines. J Am Soc Nephrol, 2017.PMID 28174217