Objectives: To review the literature on the use of hypertonic saline (HS) in treating cerebral edema and intracranial hypertension.
Data sources: Review of scientific and clinical literature retrieved from a computerized MEDLINE search from January 1965 through November 1999.
Study selection: Pertinent literature is referenced, including clinical and laboratory investigations, to demonstrate principles and efficacy of treatment with HS in patients with intracranial space-occupying pathology.
Data extraction: The literature was reviewed to summarize the mechanisms of action, efficacy, adverse effects, systemic effects, and comparisons with standard treatments in both clinical and laboratory settings.
Data synthesis: HS has an osmotic effect on the brain because of its high tonicity and ability to effectively remain outside the bloodbrain barrier. Numerous animal studies have suggested that fluid resuscitation with HS bolus after hemorrhagic shock prevents the intracranial pressure (ICP) increase that follows resuscitation with standard fluids. There may be a minimal benefit in restoring cerebral blood flow, which is thought to be mitigated through local effects of HS on cerebral microvasculature. In animal models with cerebral injury, the maximum benefit is observed in animals with focal injury associated with vasogenic edema (cryogenic injury). The ICP reduction is seen for < or =2 hrs and may be maintained for longer periods by using a continuous infusion of HS. The ICP reduction is thought to be caused by a reduction in water content in areas of the brain with intact blood-brain barrier such as the nonlesioned hemisphere and cerebellum. Most comparisons with mannitol suggest almost equal efficacy in reducing ICP, but there is a suggestion that mannitol may have a longer duration of action. Human studies published to date reporting on the use of HS in treating cerebral edema and elevated ICP include case reports, case series, and small controlled trials. Results from studies directly comparing HS with standard treatment in regard to safety and efficacy are inconclusive. However, the low frequency of side effects and a definite reduction of ICP observed with use of HS in these studies are very promising. Systemic effects include transient volume expansion, natriuresis, hemodilution, immunomodulation, and improved pulmonary gas exchange. Adverse effects include electrolyte abnormalities, cardiac failure, bleeding diathesis, and phlebitis. Although unproven, a potential for central pontine myelinolysis and rebound intracranial hypertension exists with uncontrolled administration.
Conclusions: HS demonstrates a favorable effect on both systemic hemodynamics and intracranial pressure in both laboratory and clinical settings. Preliminary evidence supports the need for controlled clinical trials evaluating its use as resuscitative fluid in brain-injured patients with hemorrhagic shock, as therapy for intracranial hypertension resistant to standard therapy, as firstline therapy for intracranial hypertension in certain intracranial pathologies, as small volume fluid resuscitation during spinal shock, and as maintenance intravenous fluid in neurocritical care units.