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Hyponatraemia is common in inpatients and this includes newborns in neonatal intensive care units. Surveys from around the world suggest that up to a third of very low birthweight infants are hyponatraemic in the first week after birth and between 25 and 65% thereafter (unpublished data).1 2
Key points
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A low serum sodium implies absolute or relative water excess, but total body sodium may be reduced, normal or increased
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Extracellular volume contraction, weight loss, or inadequate weight gain suggests primary sodium depletion
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Extracellular volume expansion, weight gain, or failure to lose weight after birth, suggests a defect in water excretion
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Consider renal failure (oliguria, high plasma creatinine, and high fractional sodium excretion) or ADH driven water retention
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Both an increase in osmolality or a fall in central arterial blood pressure will stimulate the physiological release of ADH
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A reduced effective central arterial pressure may be difficult to recognise
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The newborn in intensive care is at risk of reduced blood volume, obstructed central venous return due to high intrathoracic pressures, and poor myocardial performance
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A diagnosis of SIADH should only be made if the urine is not maximally dilute and there is continuing urinary sodium loss despite hyponatraemia, normovolaemia, and normal renal, adrenal, cardiac and thyroid function
Sodium and water balance
How much is known about the causes of hyponatraemia in the newborn? Sodium is the principal electrolyte of extracellular fluid. The normal serum concentration in adults ranges from 132–144 mmol/l. A low serum sodium concentration reflects either an excess of water or primary sodium depletion. Water retention may occur with an increased, normal, or reduced total body sodium content. Elucidation of the cause of hyponatraemia first requires consideration of the regulation of sodium and water balance in the newborn. After birth, extracellular fluid volume contracts, and this is accompanied by net negative sodium …