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A Rare and Underrecognized Critical Care Entity, Cerebral Salt Wasting FREE TO VIEW

Anita Rajagopal, MD; John Lucia, MD
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St Vincent Medical Center, Department of Internal Medicine, Indianapolis, IN

Chest. 2014;145(3_MeetingAbstracts):156A. doi:10.1378/chest.1714057
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SESSION TITLE: Critical Care Case Report Posters

SESSION TYPE: Case Report Poster

PRESENTED ON: Sunday, March 23, 2014 at 01:15 PM - 02:15 PM

INTRODUCTION: First described in 1950, cerebral salt wasting syndrome (CSW) is defined by development of extracellular volume depletion due to renal sodium transport abnormality in patients with intracranial disease and normal adrenal and thyroid function [1]. The entity has been controversial and its existence debatable.

CASE PRESENTATION: A 61-year-old female, with a history of hypertension, presented with headaches, unresponsiveness, and left facial droop. Exam noted she followed commands, was orientated to self, and GCS 13. CTA head revealed basilar aneurysm with subarachnoid hemorrhage. After coiling, she was admitted to ICU. Day 6 she was hypotensive (bp107/63) with clinical signs of volume depletion. She made 15L of urine, repleted with 9L LR over 24hrs, serum Na 136, urine Na 99, and urine osmolality 247. The next day, lab work revealed similar findings (Table 1). This volume loss was clearly salt wasting as indicated by the high urine sodium. The subsequent rise in urine osmolality shows appropriate ADH response to volume depletion. SIADH was ruled out given that serum sodium was in normal range and there were clear signs of volume depletion present.

DISCUSSION: Existence of CSW was questioned after identification of SIADH in 1957 [2]. For years, CSW was considered either an element of SIADH or simply nonexistent. Both conditions have been reported in the setting of cranial conditions. The rarity and previous cynicism of CSW has led to misdiagnosis. Differentiation between these two conditions is imperative due to distinct treatment; volume replacement versus water restriction.

CONCLUSIONS: This case illustrates the need for CSW recognition as a separate entity from SIADH. Failure to make this distinction in a patient with hyponatremia who has cranial conditions could lead to unbefitting and dangerous therapy with water restriction resulting in fatal outcomes.

Reference #1: Peters JP, et al. A salt-wasting syndrome associated with cerebral disease. Trans Assc Am Phys. 1950, 63:57-64

Reference #2: Schwartz WB, et al. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med 1957 Oct 23(4):529-42

DISCLOSURE: The following authors have nothing to disclose: Anita Rajagopal, John Lucia

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