Abstract

Electrolyte imbalances are common among patients with traumatic brain injury (TBI). Cerebral salt wasting (CSW) is an electrolyte imbalance characterized by hyponatremia and hypovolemia. Differentiating the syndrome of inappropriate antidiuretic hormone and CSW remains difficult and the pathophysiological mechanisms underlying CSW are unclear. Our intent was to review the literature on CSW within the TBI population, in order to report the incidence and timing of CSW after TBI, examine outcomes, and summarize the biochemical changes in patients who developed CSW. We searched MEDLINE through 2014, hand-reviewed citations, and searched abstracts from the American Association for the Surgery of Trauma (2003–2014). Publications were included if they were conducted within a TBI population, presented original data, and diagnosed CSW. Publications were excluded if they were review articles, discussed hyponatremia but did not differentiate the etiology causing hyponatremia, or presented cases with chronic disease. Fifteen of the 47 publications reviewed met the selection criteria; nine (60 %) were case reports, five (33 %) were prospective and 1 (7 %) was a retrospective study. Incidence of CSW varied between 0.8 - 34.6 %. The populations studied were heterogeneous and the criteria used to define hyponatremia and CSW varied. Though believed to play a role in the development of CSW, increased levels of natriuretic peptides in patients diagnosed with CSW were not consistently reported. These findings reinforce the elusiveness of the CSW diagnosis and the need for strict and consistent diagnostic criteria.Electronic supplementary materialThe online version of this article (doi:10.1186/s13049-015-0180-5) contains supplementary material, which is available to authorized users.

Highlights

  • Brain injury or illness, including traumatic brain injury (TBI), is frequently associated with perturbations in water balance including hyponatremia [1]

  • TBI is associated with hyponatremia, cerebral salt wasting (CSW) has rarely been studied in the TBI population, and much of the literature consists of case reports, reviews and small cohort studies that focus on incidence, etiology, and biochemical changes

  • We recorded levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), antidiuretic hormone (ADH), aldosterone, cortisol, adrenocorticotropic hormone (ACTH), and plasma renin activity in order to summarize biochemical changes that are potentially part of the pathophysiological pathway leading to CSW

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Summary

Introduction

Brain injury or illness, including traumatic brain injury (TBI), is frequently associated with perturbations in water balance including hyponatremia [1]. CSW is complex and poorly understood; it can be confused with SIADH and. CSW is most frequently studied in patients with aneurysmal subarachnoid hemorrhage (aSAH) [5]. This population experiences a high incidence of hyponatremia, observed in up to 57 % of patients [9]. TBI is associated with hyponatremia, CSW has rarely been studied in the TBI population, and much of the literature consists of case reports, reviews and small cohort studies that focus on incidence, etiology, and biochemical changes. Little information is available on outcomes in patients with CSW after TBI

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