TRAUMATIC BRAIN INJURY (A VALADKA, SECTION EDITOR)
Osmotic Therapy in Traumatic Brain Injury
Shankar P. Gopinath
Published online: 7 March 2018
Springer International Publishing AG, part of Springer Nature 2018
Purpose of Review The goal of this paper is to review hyperosmolar therapy in patients with intracranial hypertension after
traumatic brain injury (TBI).
Recent Findings Recent studies that have compared hypertonic saline and mannitol for intracranial hypertension after TBI show
greater intracranial pressure (ICP) control with hypertonic saline. However, these studies are limited by substantial variation in
methodology, and the results fail to show improved neurological outcomes.
Summary Although mannitol is the traditional hyperosmolar agent recommended for intracranial hypertension, there is increas-
ing evidence for the safety and efficacy of hypertonic saline. Data from prior studies suggest that short-term differences in ICP
control between hypertonic saline and mannitol appear to be insufficient to independently affect mortality or neurological
outcome after severe TBI. A sufficiently powered, multicenter, randomized controlled trial focusing on hypertonic saline and
mannitol in severe TBI patients is necessary to determine whether a particular hyperosmolar agent independently contributes to a
superior neurological outcome.
Keywords Hyperosmolar therapy
traumatic brain injury
The management of intracranial hypertension is a major
component of the critical care management of patients
with moderate and severe traumatic brain injury (TBI).
A variety of therapeutic options is available to treat intra-
cranial hypertension, and in many patients more than one
approach is adopted. Osmotic therapy is one of the tools
available to treat intracranial hypertension and will be the
focus of the present chapter.
In coordination with other interventions, osmotic therapy is
considered a reliable and effective option for patients with ce-
rebral edema. Although osmotic therapy is used commonly in
the critical care management of TBI, the most recent Brain
Trauma Foundation guidelines acknowledge that more high-
quality data are required before recommending a particular
hyperosmolar agent . The two major osmotic agents used
in TBI are mannitol and hypertonic saline. In the present chap-
ter, we review the rationale for osmotic therapy, mechanism of
actions of hyperosmolar agents, recent studies on osmotic ther-
apy for TBI, and current recommendations for osmotic therapy.
Rationale for Use of Hyperosmolar Therapy
Increased intracranial pressure (ICP) due to cerebral edema is a
critical problem after TBI. Cerebral edema after TBI is a result
of a combination of vasogenic and cytotoxic edema .
Vasogenic edema arises due to disruption of the blood-brain
barrier (BBB) and diffusion of water into the intercellular
spaces. Cytotoxic edema is attributable to direct cellular injury
and intracellular edema. Progressive diffuse and focal cerebral
edema can cause focal neurological impairment as well as me-
chanical compression of intracranial structures. In patients with
TBI and diffuse cerebral edema, persistently high ICP can com-
promise cerebral perfusion, particularly in the presence of im-
paired autoregulation, and cause hypoperfusion and ischemia of
the brain. Reducing cerebral edema and ICP, therefore, is an
important component of TBI treatment.
This article is part of the Topical Collection on Traumatic Brain Injury
* Shankar P. Gopinath
Department of Neurosurgery, Baylor College of Medicine, 7200
Cambridge, Suite 9A, MS: BCM650, Houston, TX 77030, USA
Current Trauma Reports (2018) 4:121–126