HYPOTONIC HYPONATREMIA - THERAPEUTICS AND CONTROVERSIES

Inappropriatly slow or excessive correction of severe (< 115 mEq/l) hy ponatremia could induce a high morbidity and mortality rate. In acute (< 48 hr) hponatremia, there is an increased risk for death and perman ent brain damage due to grand mal seizure and respiratory arrest. Inde ed, if correction is delayed, the ability of brain to adapt to hyponat remia by limiting the amount of brain swelling is not sufficient and b rain stem herniation occurs. Menstruant women are particularly likely to experience these complications. In chronic (> 48 hr) hyponatremia, the extrusion of intracerebral osmolytes decreases the brain size whic h returns to an almost normal volume. In this situation, an excessive correction (> 15-20 mEq/l/24 h) will lead to brain dehydration and bra in demyelination also called ''central pontine myelinolysis'' or ''osm otic demyelination syndrome'' (ODS) could develop. Asymptomatic patien ts with chronic hyponatremia are particularly at risk to develop brain demyelination, therefore, they must be corrected cautiously with freq uent monitoring of the natremia and with a magnitude of correction not exceeding 15 mEq/l/24 h. The different therapeutic approach regarding to the origin of the hyponatremia are considered.