Traumatic Brain Injury and Effects of Altitude - Human Performance ...

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Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the LiteratureFigure 2. Events and processes underlying primary and secondary brain injurySecondary brain damage can also be induced by breakdown of the blood-brain barrier (BBB) 2 , which inturn leads to edema, neuroinflammation and increased ICP (Goodman, 2009). As ICP increases, reducedcerebral perfusion leads to ischemia.Consequently, it is crucial to avoid conditions and circumstances that can aggravate primary brain injury,accelerate secondary injury processes, or introduce additional sources of physiologic stress that maydirectly or indirectly compromise brain health and function. The most commonly reported causes ofsecondary injury are hypoxia and/or hypotension, which are estimated to occur in 30-50% of headinjuredpatients before they reach the hospital (Chestnut et al., 1993; Ghajar, 2000). TBI patients whoexperience hypoxia or hypotension in the pre-hospital setting are at substantially greater risk of death ordisability due to secondary brain injury (Chestnut et al., 1993; Chi et al., 2006; Ghajar, 2000). Becausehigh altitude is often associated with hypoxic conditions, it is reasonable to consider that exposure toaltitude may aggravate or increase the risk of secondary brain injury. Although the processes underlyingbrain response to altitude exposure are not yet fully understood, the effects of altitude exposure onneurologically healthy individuals are well-documented.2 The BBB normally prevents certain blood proteins and water from entering the cerebral space. Dysfunction of the BBB canoccur as the result of physical disruption, hypertension, and/or the release pass through of destructive compounds that canbind to glutamate and kainate receptors and initiate excitotoxic events, including free radical release and neuronal apoptosis ornecrosis, excitatory neurotransmitters and free radicals. When the BBB breaks down, water enters the brain and causes edema,which can spread quickly and bring about a dangerous increase in ICP.September 14, 2010 8
Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the LiteratureClinical Parameters of TBI at AltitudeNeurons respond to oxygen deprivation in the order of milliseconds. Because the brain is the mostoxygen-dependent organ in the body, it is the first organ to be affected by reduced oxygen delivery athigh altitude. The concentration of oxygen in air is constant at 20.9% up to about 12, 000 meters, but asone ascends in altitude, barometric pressure decreases and causes a reduction in the partial pressure 3 ofoxygen. This is referred to as hypobaric hypoxia. At 5500 meters (about 18,000 feet) above sea level, thepartial pressure of oxygen is reduced to about half its value at sea level; at 8800 meters (about 29,000feet) it is reduced to a third of its sea level value.When the body is subjected to hypobaric hypoxia, less oxygen can move from the airspace of the lungsinto the blood. Low arterial PO 2 causes vasodilation in the brain (Borgstrom et al., 1975), which alterscerebral blood flow. The precise underlying mechanisms and processes 4 of altitude-related changes inthe brain are not yet fully understood, but the results are similar to the events that trigger secondaryinjury cascades following TBI. These include cerebral edema, increased ICP, compromised perfusion,ischemic injury, and apoptosis 5 . Therefore, individuals who sustain TBI at high altitude, or who must betransported at high altitude, are placed at additional risk for secondary hypoxic tissue injury. Thispresents a unique challenge for those who provide acute medical care and transport.High-altitude illness refers to a spectrum of syndromes that can develop in otherwise healthy individualsshortly after ascent to high (1500-3500 meters), very high (3500-5500 meters) or extreme (above 5500meters) altitudes. Neurological effects vary widely among individuals. Symptoms such as headache andaltered night vision can develop in some individuals at as little as 1500 meters (approximately 5000feet), which is the altitude equivalent inside a pressurized commercial aircraft. In general, though,neurological effects are more likely to occur at altitudes above 2500 meters (approximately 8000 feet).Prevention of altitude illness depends on slow ascent, prompt recognition of signs and symptoms,supplementary oxygen and descent to lower altitude to avoid worsening effects.Three altitude-related syndromes have been identified: acute mountain sickness; high altitude cerebraledema; and high altitude pulmonary cerebral edema. Acute mountain sickness (AMS) involves a varietyof non-specific symptoms such as headache, fatigue, dizziness, nausea, vomiting, and/or sleepdisturbance. Typically, one or more of these symptoms develop 6-12 hours after arrival at altitude; theyare easily confused with effects of exhaustion, migraine, dehydration or hypothermia. Some individualsexperience discomfort and/or AMS at as low as 2400 meters (8000 feet) (Muhm et al., 2007). Withoutthe benefit of supplemental oxygen, AMS affects about half (53%) of those who trek (walk) to heights of4000 - 5000 meters (13, 000-16, 000 feet; Hackett et al., 1976; Verdy & Judge, 2006). Rapid ascentdramatically increases the risk of developing altitude-related high-altitude illness (Hackett et al., 1976),3 In a gas mixture (in this case, air), partial pressure of oxygen refers to the pressure it would have if it occupied the samevolume, alone, at the same temperature.4 A detailed analysis of the cellular basis and pathophysiological mechanisms underlying these and related effects is beyond thescope of this report; these have been discussed at length by other authors (Bailey et al., 2009; Basnyat & Murdoch, 2003;Finnoff, 2008; Goodman et al., 2009; Kushi et al., 2003; Schmidt et al., 2005; Wilson et al., 2009).5 Apoptosis is a type of programmed cell death involving a series of biochemical events which lead to the death of cells. Theprocesses associated with apoptosis do not damage the organism. By contrast, necrosis is a form of traumatic cell death thatresults from acute cellular injury.September 14, 2010 9
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