fludrocortisone-acetate and Brain-Diseases

In the neurocritical care setting, hyponatremia is the commonest electrolyte disorder, which is associated with significant morbimortality. Cerebral salt wasting and syndrome of inappropriate antidiuretic hormone have been classically described as the 2 most frequent entities responsible of hyponatremia in neurocritical care patients. Nevertheless, to distinguish between both syndromes is usually difficult and useless as volume status is difficult to be determined, underlying pathophysiological mechanisms are still not fully understood, fluid restriction is usually contraindicated in these patients, and the first option in the therapeutic strategy is always the same: 3% hypertonic saline solution. Therefore, we definitively agree with the current concept of "cerebral salt wasting", which means that whatever is the etiology of hyponatremia, initially in neurocritical care patients the treatment will be the same: hypertonic saline solution.

Topics: Antidiuretic Hormone Receptor Antagonists; Brain Diseases; Brain Injuries, Traumatic; Brain Ischemia; Cerebrovascular Circulation; Combined Modality Therapy; Critical Illness; Early Diagnosis; Fludrocortisone; Humans; Hyponatremia; Inappropriate ADH Syndrome; Myelinolysis, Central Pontine; Natriuresis; Neurosurgical Procedures; Postoperative Complications; Saline Solution, Hypertonic; Subarachnoid Hemorrhage; Vasoconstriction

Cerebral salt wasting syndrome (CSWS) in patients with aneurysmal subarachnoid hemorrhage (SAH) is considered to correlate with delayed ischemic neurological deficits (DIND) induced by cerebral vasospasm; however, its exact mechanism is still not well-known. The purpose of the present study is to evaluate the relationship between hyponatremia caused by CSWS and the increase of the urinary sodium excretion in early phase following SAH. Fifty-four patients with SAH were divided into 2 groups, normonatremia group and hyponatremia group which suffered hyponatremia after SAH. The hyponatremia group comprise 14 patients (26%) in whom the hyponatremia developed of the SAH. In this group, the serum level of sodium significantly decreased 7 days after SAH and then gradually normalised. Further, excretion of sodium in the urine tended to increase 3 days after SAH and significantly increased 7 days after SAH. In conclusion, the increased urinary sodium excretion in the early phase of SAH would serve as a predictive factor for CSWS after SAH. We consider that it is important to start sodium and fluid supplementation and inhibit natriuresis by fludrocortisone acetate administration before hyponatremia occurs in order to prevention delayed ischemic neurological deficits in SAH patients.

Topics: Adult; Aged; Aged, 80 and over; alpha-Macroglobulins; Biomarkers; Brain Diseases; Early Diagnosis; Female; Fludrocortisone; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Sodium; Subarachnoid Hemorrhage

Topics: Brain Diseases; Demyelinating Diseases; Drug Therapy, Combination; Female; Fludrocortisone; Humans; Magnetic Resonance Spectroscopy; Middle Aged; Pons; Thyroxine