High antidiuretic hormone levels and hyponatremia in children with gastroenteritis

Nonosmotic antidiuretic hormone (ADH) activity can cause severe hyponatremia during involuntary fluid administration. We looked for evidence of this before and during intravenous (IV) fluid administration in children treated for gastroenteritis.

In this prospective observational study, plasma ADH, electrolytes, osmolality, and glucose were measured in 52 subjects before (T0) and 4 hours after (T4) starting 0.45% saline + 2.5% dextrose and subsequently when indicated. Hormonal markers of stress were measured at T0. Urine samples were collected to measure electrolytes and osmolality.

The nonosmotic stimuli of ADH secretion that we identified were vomiting (50 of 52), dehydration (median: 5%; range: 3-8%), hypoglycemia (2 of 52), and raised hormonal markers of stress (mean +/- SD: cortisol, 1094 +/- 589 nmol/L; reverse triiodothyronine, 792 +/- 293 pmol/L). At T0, half the children were hyponatremic (plasma sodium concentration of < 135 mmol/L; n = 27). The median plasma ADH concentration at T0 was significantly elevated (median: 7.4 pg/mL; range: < 1.9-85.6 pg/mL). ADH was high in both hyponatremic and normonatremic children and remained high at T4 in 33 of the 52 children, 22 of whom were concurrently hyponatremic. At T4, mean plasma sodium concentration was unchanged in the hyponatremic children but was 2.6 mmol/L (+/-2.0) lower in those who were initially normonatremic. Urine tonicity was high compared with 0.45% saline in 16 of 19 children at baseline and in 20 of 37 children after 3 to 12 hours of IV fluids.

Nonosmotic stimuli of ADH secretion are frequent in children with gastroenteritis. Their persistence during IV-fluid administration predisposes to dilutional hyponatremia. The use of hypotonic saline for deficit replacement needs to be reassessed.