Pathophysiology and treatment of cerebral edema in traumatic brain injury

Authors

Ruchira M. Jha, Department of Critical Care Medicine, And Safar Center for Resuscitation Research, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Department of Neurology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Department of Neurosurgery, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Clinical and Translational Science Institute, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States.Follow
Patrick M. Kochanek, Department of Critical Care Medicine, And Safar Center for Resuscitation Research, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Clinical and Translational Science Institute, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Department of Anesthesiology, University of Pittsburgh, Pittsburgh, PA, United States.
J Marc Simard, Department of Neurosurgery, School of Medicine, University of Maryland, Baltimore, MD, United States; Department of Pathology, School of Medicine, University of Maryland, Baltimore, MD, United States; Department of Physiology, School of Medicine, University of Maryland, Baltimore, MD, United States. Electronic address: msimard@som.umaryland.edu.

Document Type

Article

Abstract

Cerebral edema (CE) and resultant intracranial hypertension are associated with unfavorable prognosis in traumatic brain injury (TBI). CE is a leading cause of in-hospital mortality, occurring in >60% of patients with mass lesions, and ∼15% of those with normal initial computed tomography scans. After treatment of mass lesions in severe TBI, an important focus of acute neurocritical care is evaluating and managing the secondary injury process of CE and resultant intracranial hypertension. This review focuses on a contemporary understanding of various pathophysiologic pathways contributing to CE, with a subsequent description of potential targeted therapies. There is a discussion of identified cellular/cytotoxic contributors to CE, as well as mechanisms that influence blood-brain-barrier (BBB) disruption/vasogenic edema, with the caveat that this distinction may be somewhat artificial since molecular processes contributing to these pathways are interrelated. While an exhaustive discussion of all pathways with putative contributions to CE is beyond the scope of this review, the roles of some key contributors are highlighted, and references are provided for further details. Potential future molecular targets for treating CE are presented based on pathophysiologic mechanisms. We thus aim to provide a translational synopsis of present and future strategies targeting CE after TBI in the context of a paradigm shift towards precision medicine. This article is part of the Special Issue entitled "Novel Treatments for Traumatic Brain Injury".

Medical Subject Headings

Animals; Brain Edema (etiology, physiopathology, therapy); Brain Injuries, Traumatic (complications, physiopathology, therapy); Humans; Neuroprotective Agents (pharmacology, therapeutic use)

Publication Date

2-1-2019

Publication Title

Neuropharmacology

E-ISSN

1873-7064

Volume

145

Issue

Pt B

First Page

230

Last Page

246

PubMed ID

30086289

Digital Object Identifier (DOI)

10.1016/j.neuropharm.2018.08.004

Recommended Citation

Jha, Ruchira M.; Kochanek, Patrick M.; and Simard, J Marc, "Pathophysiology and treatment of cerebral edema in traumatic brain injury" (2019). Neurology. 1355.
https://scholar.barrowneuro.org/neurology/1355