Use of 3% Hypertonic Saline to Improve Clinical Symptoms in Concussed Patients

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.