J Neurosurg 55:938-941, 1981 Hyponatremia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) PAUL B. NELSON, M.D., SAID M. SEIF, PH.D., JOSEPH C. MAROON, M.D., AND ALAN G. ROBINSON, M.D. Departments of Neurosurgery and Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania ~/ Patients with intracranial disorders are prone to develop hyponatremia with inability to prevent the loss of sodium in their urine. This was originally referred to as "cerebral salt wasting," but more recently is thought to be secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Blood volume determinations were made in 12 unselected neurosurgical patients with intracranial disease who fulfilled the laboratory criteria for SIADH. Ten of the 12 patients had significant decreases in their red blood cell mass, plasma volume, and total blood volume. The finding of a decreased blood volume in patients who fulfill the laboratory criteria for SIADH is better explained by the original concepts of cerebral salt wasting than by SIADH. The primary defect may be the inability of the kidney to conserve sodium. KEY WORDS 9 hyponatremia 9 natriuresis 9 antidiuretic hormone 9 SIADH 9 inappropriate secretion of antidiuretic hormone syndrome 9 cerebral salt wasting p ATIENTSwith intracranial disorders are prone to develop hyponatremia with inability to prevent the loss of sodium in their urine. 1,3,5,6,17,20 The hyponatremia is frequently associated with a worsen- ing in the patient's neurological condition,a,3,5 The problem was referred to in the early 1950's as "cere- bral salt wasting.''3,~7,2~ The syndrome was defined as the inability to prevent salt loss in the urine despite depressed concentrations of sodium in the serum. These early investigators concentrated on renal loss of salt as the primary defect. They thought that the central nervous system influenced the kidney's ability to reabsorb sodium in the proximal tubule. The ther- apeutic implications were that progressive salt deple- tion may lead to peripheral vascular collapse and may jeopardize recovery from the primary illness. The early investigators treated these patients with salt replacement in excess of the amount lost in the urine. The administration of glucocorticoids and mineralo- corticoids did not reverse the syndrome. The approach to hyponatremia associated with na- triuresis changed in 1957 when Schwartz, eta/., 19 defined the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). In their original pa- per, they described two patients with bronchogenic carcinoma who had hyponatremia and persistent loss of sodium in their urine. Extracellular volume was measured in one patient and found to be expanded. The syndrome improved with fluid restriction. Since similar findings had been seen in experimental con- ditions where hyponatremia resulted when normal individuals were given antidiuretic hormone (ADH) and water, 13 Schwartz, et aL,19 concluded that sus- tained inappropriate secretion of ADH was probably the cause of the abnormal laboratory findings in their patients. No direct determinations of ADH were made. Laboratory criteria to make the diagnosis of SIADH became a low serum sodium level, a low serum osmolality, a high urinary sodium, and a uri- nary osmolality that was inappropriately concentrated as compared to the serum osmolality. The diagnosis assumed normal renal and adrenal function and that the patients were not taking diuretics. Since 1957, it has generally become accepted that patients with intracranial disorders who exhibit hy- ponatremia with excessive loss of sodium in their urine have SIADH. This syndrome has been re- ported to be the probable cause of hyponatremia 938 J. Neurosurg. / Volume 55 / December, 1981