Figure 121

Cerebral adaptation to hyponatremia. A, Decreases in extracellular osmolality cause movement of water (H2O) into the cells, increasing intracellular volume and thus causing tissue edema. This cellular edema within the fixed confines of the cranium causes increased intracranial pressure, leading to neurologic symptoms. To prevent this from happening, mechanisms geared toward volume regulation come into operation, to prevent cerebral edema from developing in the vast majority of patients with hyponatremia.

After induction of extracellular fluid hypo-osmolality, H2O moves into the brain in response to osmotic gradients, producing cerebral edema (middle panel, 1). However, within 1 to 3 hours, a decrease in cerebral extracellular volume occurs by movement of fluid into the cerebrospinal fluid, which is then shunted back into the systemic circulation. This happens very promptly and is evident by the loss of extracellular and intracellular solutes (sodium and chloride ions) as early as 30 minutes after the onset of hyponatremia. As H2O losses accompany the losses of brain solute (middle panel, 2), the expanded brain volume decreases back toward normal (middle panel, 33) [15]. B, Relative decreases in individual osmolytes during adaptation to chronic hyponatremia. Thereafter, if hyponatremia persists, other organic osmolytes such as phosphocreatine, myoinositol, and amino acids like glutamine, and taurine are lost. The loss of these solutes markedly decreases cerebral swelling. Patients who have had a slower onset of hyponatremia (over 72 to 96 hours or longer), the risk for osmotic demyelination rises if hyponatremia is corrected too rapidly [18,19]. Na+—sodium; K+—potassium; Cl-—chloride.

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