Abstract

Hypernatremia results from a deficit of total body water in relation to the total body's sodium stores. This is caused by two main mechanisms: 1) net water depletion exceeding sodium losses or 2) increased sodium gain exceeding water gain. Net water depletion occurs when increased water loss exceeds sodium loss, either due to extrarenal losses (increased evaporative water losses, hypernatremic dehydration caused by diarrhea) or to renal losses (central and nephrogenic diabetes insipidus, intrinsic renal disease). Insufficient water intake occurs with neonatal hypernatremic dehydration secondary to lactation failure, essential hypernatremia or osmoreceptor dysfunction. Increased sodium gain can be caused by iatrogenic hypernatremia, administration of concentrated infant formula, deliberate abusive water restriction and deliberate or non-accidental salt poisoning. Hypernatremia results in a movement of water across cell membranes from the intracellular to the extracellular space, resulting in cellular dehydration, which, in cells of the central nervous system results in brain shrinkage leading to tearing of cerebral blood vessels and neurological complications. As a protective mechanism, idiogenic osmoles accumulate inside the brain cells to help them retain water intracellularly. However this may lead to cerebral edema during rapid rehydration as these idiogenic osmoles attract water inside the neurons. As the appropriate management of hypernatremia invariably depends on the underlying mechanism and cause, a methodical history taking and clinical examination, with the judicious use of laboratory tests will lead to a precise etiological diagnosis to enable appropriate and timely therapy.

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