Abstract
Hypernatremia invariably denotes hyperosmolarity and, at least transiently, causes cellular dehydratation. Because of blood brain barrier properties, cerebral tissue volume is modified by acute changes in osmolarity. An acute hyperosmolarity (by intravenous sodium or mannitol) temporally decreases intracranial pressure. This treatment is thus useful in critical situations, allowing time for diagnosis and, if possible, other treatment. But in cases of sustained hypernatremia, cellular dehydratation is rapidly counterbalanced by an increase in cellular osmolarity. For the brain, it has been shown that cerebral volume is restored in a few hours during prolonged hypernatremia. Moreover, the plasmatic osmotic load induces an increase in diuresis and natriuresis. A tight control is then necessary to prevent hypovolemia and electrolytes disorders. Teams using this treatment should undertake controlled randomized studies to ascertain any beneficial effect that cannot be explained by physiology.
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