Use of Salt-Water Solution to Improve Symptoms in Concussion
Use of Salt-Water Solution to Improve Symptoms in Concussion
The purpose of this study is to find out if 3% hypertonic saline (salt-water solution) given
 in a vein improves the headache that may be caused by a concussion. 3% hypertonic saline may
 also improve some of the other symptoms that may be caused by concussion (for example:
 confusion, nausea, vomiting).

 This research is being done because there have been previous experience which suggests that
 3% hypertonic saline has been beneficial in the treatment of children with more severe brain
 injury.
A concussion is formally described as a clinical syndrome characterized by immediate and
 transient changes in brain function including alteration of mental status and level of
 consciousness, resulting from mechanical force or trauma. Despite its prevalence, its
 pathophysiology remains a mystery as does its spectrum of clinical presentation.

 A concussion, sometimes described as a mild traumatic brain injury (TBI), can often present
 with initial loss of consciousness, change in behavior, confusion, amnesia, or aphasia which
 all result in a Glasgow Coma Scale (GCS) that is less than normal. As the time from the
 initial injury lengthens, these symptoms can progressively worsen and new symptoms such as
 vomiting and headaches can also develop. Usually, there is no evidence of a significant
 intracranial injury by computed tomography (CT) imaging and these symptoms often improve with
 a gradual progression towards a normal neurologic baseline; in fact, the risk of complication
 in this population is very rare. The time for this improvement varies greatly and can occur
 over a period ranging from hours to days. During this transient time, the patient is often
 very uncomfortable due to persistent headaches, inability to tolerate oral intake due to
 nausea and/or vomiting, confusion, and episodes of amnesia. In some instances, the combative
 behavior of the patient can be difficult to tolerate both by the family and the medical
 staff.

 Just as the symptoms caused by a concussion vary greatly in presentation and duration, so do
 the theories behind the pathophysiology of mild TBI. The transient loss of cerebral function
 after a head injury was formally differentiated from severe head injury for the first time by
 the Persian physician Rhazes in 900 AD and has since caused much speculation and varying
 clinical descriptions throughout history. It took another 500 years before a "commotion" or
 shaking of the brain was theorized to be responsible for clinical signs. Presently, the exact
 cause of concussive symptoms continue to remain an enigma; a major question however, is
 whether a concussion is due to a lesser degree of diffuse structural change seen in severe
 traumatic brain injury, or if it is in fact a mechanism caused by reversible functional
 changes of the neurons and axons.

 Animal models have demonstrated altered metabolic profiles of the brain tissue which resolves
 within hours of initial insult. Other animal models have demonstrated a change in the
 integrity of the microvascular endothelium after TBI. It can be hypothesized that there are
 areas of "microcontusion" and pericontusional edema that maybe responsible for alterations in
 brain chemistry which may ultimately lead to the clinical symptoms associated with mild TBI.
 Multiple other studies have theorized that the direct and indirect effects of trauma on
 cerebral vasculature may lead to a vasoconstrictive phenomenon that may be responsible for
 postconcussive symptoms.

 Currently, the management of patients with mild traumatic brain injuries includes observation
 and symptomatic therapies including analgesia without obscuring a neurologic exam
 (acetaminophen) and antiemetic measures (ondansetron). While many patients are often
 discharged home after initial evaluation in the Emergency Department, some are admitted to
 the hospital for supportive care. The symptoms may resolve in a period of hours to days.

 There has been substantial retrospective data and limited prospective data in children which
 suggests that hypertonic saline (HTS) can improve the control of intracranial pressure (ICP)
 in patients with acute brain injury. In 1992, a report published by the Journal of
 Neurosurgical Anesthesiology indicated that HTS reduced elevated ICP in children after head
 injury. This study looked at a single intravenous bolus of HTS in comparison to the same
 volume of normal saline and demonstrated a clear difference. Subsequently, it was
 demonstrated that HTS appears to be efficacious in controlling ICP. In a retrospective chart
 review, 68 children with closed head injury were cared for using a standardized protocol and
 the intravenous infusion of 3% HTS in quantities designed to drive the serum sodium to levels
 that would reduce the ICP to less than 20 mmHg. Of the patients in who HTS was used, only 3
 patients (4%) died of uncontrolled ICP. Of note, there were no adverse effects of
 super-physiologic hyperosmolarity such as renal failure, pulmonary edema, or central pontine
 demyelination.

 The use of 3% hypertonic saline in traumatic brain injury has recently been investigated by
 many centers and is now included as first tier therapy in the management of decreasing
 intracranial pressure (ICP) secondary to severe traumatic brain injury in the pediatric
 population. Its mechanism in ICP reduction lies in its favorable rheologic and osmolar
 gradient effects; it concomitantly augments intravascular volume and increase mean arterial
 pressure to provide optimum cerebral perfusion pressure. Again, multiple studies have shown
 the direct effect of HTS in lowering ICP along with its safety in a pediatric population. HTS
 has also been used to treat altered mental status in diabetic ketoacidosis.

 Many of the symptoms associated with mild traumatic brain injury may be due to mild
 elevations in intracranial pressure, minimal cerebral edema, and/or vasospasm of the cerebral
 vasculature. Hypertonic saline may be instrumental in improving the symptoms of concussion by
 addressing the commonly suspected mechanisms responsible for these symptoms. By reducing mild
 cerebral edema and/or improving cerebral perfusion pressure, cerebral vasospasm may be
 overcome by reversal or by improved flow; thus, 3% HTS may allow favorable treatment of
 postconcussive symptoms.
Inclusion Criteria:

 -  Greater than or equal to 6 years of age

 -  Admitted for observation of closed head injury

 -  GCS greater than or equal to 13

 -  Presence of headache

 -  CT scan showing no brain injury or only a small contusion (an area of low attenuation
 less than 10 mm or a punctuate area of high attenuation with surrounding edema less
 than 5mm). CT evidence of high or mixed attenuation would be consistent with a
 hemorrhagic lesion and therefore not qualify to participate in the study. Evidence of
 skull fractures and cephalohematomas on CT would not exclude the patient from the
 study.

 Exclusion Criteria:

 -  Age less than 6

 -  GCS less than 13

 -  Radiographic evidence of extra-axial blood or subarachnoid blood

 -  Possible or witnessed posttraumatic seizure

 -  Developmental delay/ mental retardation

 -  Underlying cardiac or renal pathology

 -  Suspected and/or documented use of alcohol and/or illicit substances

 -  Medication history which includes administration of acetaminophen within 4 hours prior
 to enrollment or chronic anticoagulant use (ie: Coumadin, Aspirin

 -  Associated injuries requiring the use of narcotics for analgesia (ie: long bone
 injuries, deep laceration repair)

 -  Intubation

 -  Non-English speaking

 -  No parental consent