The Effects of Hyperbaric Oxygen on Non-acute Traumatic Brain Injury

Overview

Traumatic brain injury (TBI) continues to be a major cause of death and disability throughout the world. The reduced cerebral blood flow secondary to the direct trauma-induced damage deregulates cerebral metabolism and depletes energy stores within the brain. Diffusion barriers to the cellular delivery of oxygen develop and persist. Besides, TBI often leads to intracranial hypertension, which in turn exacerbates diffusion disorders, further reducing cerebral oxygenation, and deteriorates the injury. By increasing the partial pressure of oxygen in blood, reducing intracranial pressure and cerebral edema, Hyperbaric oxygen therapy (HBO2) has been used in early treatment of TBI. However, due to the different severity of TBI, the clinical situation of early insult is complex and unpredictable, ordinarily there was a time delay between TBI and onset of HBO2 treatment averaging more than 2 weeks, especially in patients with severe TBI. Whether the delayed intervention is still effective is controversial.

Traumatic brain injury (TBI) continues to be a major cause of death and disability throughout the world. The pathophysiological processes which occur post-TBI are complex and have not been fully elucidated. Penetrating injury, mechanical stress, cceleration-deceleration injury, and shear forces provide the direct trauma-induced damage. Subsequently, the reduced cerebral blood flow deregulates cerebral metabolism and depletes energy stores within the brain. Diffusion barriers to the cellular delivery of oxygen develop and persist. Besides, TBI often leads to intracranial hypertension, which in turn exacerbates diffusion disorders, further reducing cerebral oxygenation, and deteriorates the injury. Ischemia has been implicated as a major cause of secondary brain injury and death following severe brain injury. Hyperbaric oxygen therapy (HBO2) has been used in early treatment of TBI. Studies have shown that increased tissue oxygen delivery is capable of driving an increase in oxygen utilization, leading to improved cerebral aerobic metabolism. By increasing the partial pressure of oxygen in blood, HBO2 increases cerebral oxygen saturation. In addition, HBO2 has been shown in both experimental and clinical studies to reduce intracranial pressure and cerebral edema after severe TBI. HBO2 has been shown to decrease mortality rates and improve functional outcome in severely brain-injured patients. However, due to the different severity of TBI, the clinical situation of early insult is complex and diverse, and a considerable number of patients in the acute stage was accompanied by unstable intracranial hemorrhage, hemodynamic instability, ventilator assisted ventilation and other unpredictable conditions, therefore, ordinarily there was a time delay between TBI and onset of HBO2 treatment averaging more than 2 weeks, especially in patients with severe TBI. Whether the delayed intervention is still effective is controversial.