Hypertonic fluids are a solution known to have heightened concentrations of certain electrolytes. These fluids are believed to help decline intracranial pressure. According to a recent study, out-of-hospital administration of hypertonic fluids after a severe traumatic brain injury (TBI) doesn’t improve patient outcomes. Apparently, traumatic brain injury (TBI) is the leading cause of death among individuals going through blunt trauma, and survivors generally suffer from severe disability.
Experts presume that primary injury to the brain is caused at the time of impact, but subsequently reduced cerebral blood flow can trigger a secondary brain injury. Hypertonic fluids are assumed to restore cerebral perfusion with decreased cerebral edema. These fluids seemingly benefit in resuscitation of patients with severe TBI. Investigations have claimed that early administration of hypertonic fluids to patients with severe TBI enhances survival. Yet, no large definitive trials have been reported till date and the effects on neurologic outcome are not known.
Authors comment, “Current therapy following severe TBI is focused on minimizing secondary injury by supporting systemic perfusion (blood flow) and reducing intracranial pressure (ICP). Intravenous fluid resuscitation currently begins in the out-of-hospital setting; however, therapy for management of cerebral edema (swelling) is often delayed until after hospital arrival.”
A study was commenced for determining whether administration of hypertonic fluids as early as possible i.e., after severe TBI in patients without hemorrhagic shock, would result in improved 6-month neurologic outcomes. The randomized, placebo-controlled clinical trial encompassed 114 North American emergency medical services agencies within the Resuscitation Outcomes Consortium. Initiated between May 2006 and May 2009, the investigations began on patients aged 15 years or older with blunt trauma and a prehospital Glasgow Coma Scale score which failed to meet the criteria of shock from blood loss known as hypovolemia. This system was employed for evaluating the degree of brain impairment.
Scientists add, “There were no statistically significant differences in distribution of GOSE category or Disability Rating Score by treatment group. Survival at 28 days was 74.3 percent with hypertonic saline/dextran, 75.7 percent with hypertonic saline, and 75.1 percent with normal saline. In summary, in this randomized controlled trial, we were unable to demonstrate any improvement in 6-month neurologic outcome or survival for trauma patients with presumed severe TBI without evidence of hypovolemic shock, who received a single bolus [large dose] of hypertonic fluids compared with normal saline in the out-of-hospital setting. While this does not preclude a benefit from such treatment were it administered differently, at present there appears to be no compelling reason to adopt a practice of hypertonic fluid resuscitation for TBI in the out-of-hospital setting.”
Study subjects were provided with hypertonic saline/dextran which is a water-soluble polymer of glucose hypertonic saline, or normal saline. Eileen M. Bulger, M.D., of Harborview Medical Center, University of Washington, Seattle, and colleagues noted neurologic outcome with the Extended Glasgow Outcome Scale (GOSE) after six months. No major variations appeared in characteristics of the patients at the beginning of the study, injury severity scores, and out-of-hospital care provided between treatment groups.
From the total volunteers, complete 6-month neurologic outcome data of 1,087 from 1,282 treated patients forming 85 percent was available. No difference in proportions of patients with severe TBI was registered in the 6-month neurologic outcome among groups. GOSE score of 4 or less was for severe disability, vegetative state, or death. While hypertonic saline/dextran receiving group reported 53.7 percent, hypertonic saline group displayed 51.5 percent. And when 54.3 percent was shown by hypertonic saline group, 51.5 percent was noted by normal saline group.
The study was published in the October 6 issue of JAMA.