INTRODUCTION AND EPIDEMIOLOGY
Head trauma is an important cause of morbidity and mortality in children. Over 750,000 children and adolescents with head injuries present annually to EDs in the United States, double that of a decade ago. The highest incidence is in the 0- to 4-year age group.1 Annual estimates of pediatric sports-related concussion in the United States range from 1.1 to 1.9 million.2 Although the majority of concussions are not seen in healthcare settings, an estimated 378,000 patients were seen as outpatient visits, 150,000 presented to the ED, and 5000 were admitted to hospitals annually in the United States alone.2
Concussion, minor head injury, and mild traumatic brain injury historically have had different definitions in medical literature. Typically, minor head injury is defined by Glasgow Coma Scale (GCS) score of 14 or 15 at the time of presentation to the ED. At a major conference of concussion specialists in Berlin in 2016, a consensus definition of concussion was derived: traumatic brain injury induced by biomechanical forces.3
Concussion may be caused by a direct blow to the head, face, neck, or elsewhere on the body, with an impulsive force transmitted to the head. It typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously. However, in some cases, signs and symptoms evolve over a number of minutes to hours.
Concussion may result in neuropathologic changes, but the acute clinical signs and symptoms reflect a functional disturbance rather than gross structural injury, and as such, no abnormality is seen on standard structural neuroimaging studies.
Blunt head trauma in children often causes diffuse rather than focal injuries. A relatively larger calvarium and weaker cervical musculature in children impair protective mechanisms. The brain rotates around its center of gravity, resulting in diffuse axonal injury and possible subdural hemorrhage. Acceleration and deceleration forces initiate a neurochemical cascade that results in neuronal membrane disruption and axonal stretching.4
The acute phase of injury is characterized by an increase in cerebral cellular energy demand coupled with insufficient energy substrate delivery resulting in a metabolic crisis. This metabolic mismatch leads to alterations in neuronal depolarization, ion transport, glycolysis, mitochondrial function, and neurotransmitter release. Global and regional cerebral blood flow is reduced. Stretching of axons due to mechanical forces results in indiscriminate release of neurotransmitters and calcium influx and potassium efflux, resulting in widespread depolarization. Cells respond by activating ion pumps in an attempt to restore the normal membrane potential, which accelerates glycolysis and contributes to a state of hypermetabolism. Intracellular magnesium levels appear to diminish and may remain suppressed for several days. Magnesium is essential for generation of adenosine triphosphate, initiation of protein synthesis, and maintenance of cellular membrane potential. High intracellular calcium levels combined with stretch injury can cause destruction of microtubules within axons. The effect of this ...