Over the past 15 years, more than 330,000 US soldiers have suffered a traumatic brain injury (TBI). It is one of the leading causes of death and disability connected to the country’s recent conflicts in Afghanistan and Iraq. Many of these patients were evacuated by air from these countries to Europe and the US for further treatment.

In general, these patients were flown quickly to hospitals outside the battle zone, where more extensive treatment was available. But now a new study by researchers at the University of Maryland School of Medicine has found evidence that such air evacuations may pose a significant added risk, potentially causing more damage to already injured brains. The study is the first to suggest that air evacuation may be hazardous for TBI patients.

“This research shows that exposure to reduced barometric pressure, as occurs on military planes used for evacuation, substantially worsens neurological function and increases brain cell loss after experimental TBI – even when oxygen levels are kept in the normal range. It suggests that we need to carefully re-evaluate the cost-benefit of air transport in the first days after injury,” said lead researcher Dr Alan Faden, the David S Brown professor in trauma in the departments of anaesthesiology, anatomy & neurobiology, neurology, and neurosurgery, and director, Shock, Trauma and Anaesthesiology Research Centre (STAR) as well as the National Study Centre for Trauma and Emergency Medical Services.

Faden and his colleagues tested rats that were subjected to TBI, using a model that simulates key aspects of human brain injury. Animals were exposed to six hours of lowered air pressure, known as hypobaria, at levels that simulated conditions during transport; control animals were exposed to normal pressure. All the animals received extra oxygen to restore normal oxygen concentrations in the blood. In another study, animals received oxygen, either as in the first study or at much higher 100% concentration, which is often used during military air evacuations. On its own, low air pressure worsened long-term cognitive function and increased chronic brain inflammation and brain tissue loss. Pure oxygen further worsened outcomes.

Faden and his colleagues believe the findings raise concerns about the increased use of relatively early air evacuation, and suggest that this potential risk should be weighed against the benefits of improved care after evacuation. It may be necessary, he says, to change the current policy for TBI patients and delaying air evacuation in many cases.

In an accompanying editorial, Dr Patrick Kochanek, a leading expert on TBI and trauma care at the University of Pittsburgh, called the findings “highly novel and eye-opening,” and said that they could have “impactful clinical relevance for the field of traumatic brain injury in both military and civilian applications.”

Faden and colleagues believe that one of the mechanisms by which hypobaria worsens TBI is by increasing persistent brain inflammation after injury. They are currently examining how this process occurs and have tested treatments that can reduce the risks of air evacuation. Early results are promising. Scientists suspect that breathing pure oxygen could worsen TBI by increasing production of dangerous free radicals in the brain. After brain injury, these free radicals flood the site of injury, and pure oxygen may further boost these levels.

Several recent studies from trauma centres, including from the R Adams Cowley Shock Trauma Centre at the University of Maryland Medical Centre, have found evidence that using 100% oxygen in trauma patients may be counter-productive. The research was funded by the US Air Force.

Abstract
Aeromedical evacuation, an important component in the care of many traumatic brain injury patients, particularly in war zones, exposes them to prolonged periods of hypobaria. The effects of such exposure on pathophysiological changes and outcome following traumatic brain injury are largely unexplored. The objective of this study was to investigate whether prolonged hypobaria in rats subjected to traumatic brain injury alters behavioral and histological outcomes. Adult male Sprague-Dawley rats were subjected to fluid percussion induced injury at 1.5-1.9 atmospheres of pressure. The effects of hypobaric exposure (6 hour duration; equivalent to 0.75 atmospheres) at 6, 24, and 72 hours, or 7 days after TBI were evaluated with regard to sensorimotor, cognitive and histological changes. Additional groups were evaluated to determine the effects of two hypobaric exposures after traumatic brain injury, representing primary simulated aeromedical evacuation (6 hour duration at 24 hours after injury) and secondary evacuation (10 hour duration at 72 hours after injury), as well as the effects of 100% inspired oxygen concentrations (hyperoxia) during simulated evacuation. Hypobaric exposure up to 7 days following injury significantly worsened cognitive deficits, hippocampal neuronal cell loss and microglial/astrocyte activation in comparison to injured controls not exposed to hypobaria. Hyperoxia during hypobaric exposure, or two exposures to prolonged hypobaric conditions further exacerbated spatial memory deficits. These findings indicate that exposure to prolonged hypobaria up to 7 days after traumatic brain injury, even while maintaining physiological oxygen concentration, worsens long-term cognitive function and neuroinflammation. Multiple exposures or use of 100% oxygen further exacerbates these pathophysiological effects.

University of Maryland School of Medicine material
Journal of Neurotrauma abstract

FROM: http://www.medicalbrief.co.za/archives/air-evacuation-may-further-harm-tbi-patients/