• Michiel G.H. Betjes.
• Division of Nephrology and Hypertension, Department of Internal Medicine, University Hospital Rotterdam, Dijkzigt, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands
• Eur. J. Intern. Med. 2002 Feb 1; 13 (1): 9-14.

AbstractHyponatremia in acute brain disease is a common occurrence, especially after an aneurysmal subarachnoid hemorrhage. Originally, excessive natriuresis, called cerebral salt wasting, and later the syndrome of inappropriate antidiuretic hormone secretion (SIADH), were considered to be the causes of hyponatremia. In recent years, it has become clear that most of these patients are volume-depleted and have a negative sodium balance, consistent with the original description of cerebral salt wasting. Elevated plasma concentrations of atrial or brain natriuretic peptide have been identified as the putative natriuretic factor. Hyponatremia and volume depletion may aggravate neurological symptoms, and timely treatment with adequate replacement of water and NaCl is essential. The use of fludrocortisone to increase sodium reabsorption by the renal tubules may be an alternative approach.

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