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

Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the Literaturereported in the retrospective study by Donovan et al. (2008) had intracranial air volumes above 14 ml atthe time of air transport. Using a computer model to simulate the pressure effects of expandingintracranial air, Andersson et al. (2003) consider worst case results of intracranial air volume increaseduring aeromedical transport. Based on their theoretical modeling, the authors conclude thatintracranial air volume will increase by 30% at a maximum cabin altitude of 8000 feet and that resultingICP depends on initial air volume and the rate of cabin pressure change. They considered that for anintracranial air volume of 30 ml, ICP could increase by approximately 11 mmHg, which is potentially highenough to impair a patient’s clinical condition.HYPOXIAAlthough the concentration of oxygen in the air remains constant up to the limits of the troposphere,atmospheric pressure decreases exponentially with altitude. This causes a reduction in the partialpressure of oxygen, which in turn causes tissue hypoxia. Normal brain tissue oxygen pressure (P0 2 ) isbetween 20 and 40 mmHg. When brain tissue P0 2 falls to 15 mmHg or below, it is considered hypoxic(Kiening, 1996).When brain cells are deprived of oxygen, this initiates a cascade of damaging biochemical andphysiologic events. A dramatic increase in excitatory neurotransmitters (e.g., glutamate, aspartate)causes a massive, unregulated influx of calcium which in turn triggers the release of enzymes. Affectedneurons begin to catabolize themselves to maintain energy and activity. An accumulation of catabolicwaste products such as lactic acid causes irreversible damage to neurons, eventually resulting in celldeath. This contributes to secondary brain injury, and to the worsening of outcome in patients withmoderate and severe TBI (Chestnut et al., 1993; Miller et al., 1978; Schreiber, et al., 2002; Stocchetti etal., 1996).To prevent secondary damage by hypoxia, TBI patients (GCS < 14) at high altitude should be treated withsupplemental oxygen 7 . Grissom (2006) recommends oxygen treatment of combat casualties at highaltitude under the following circumstances:SpO 2 < 90% at altitudes up to 10, 000 feet; SpO 2 < 85% at 12, 000 feet; and SpO 2 < 80% at 14,000 feetInjuries associated with impaired oxygenation including blunt or penetrating chest trauma, orneck or facial trauma associated with airway obstructionUnconscious patientTraumatic brain injury with a Glasgow Coma Scale score < 13Hemorrhagic shock as identified by systolic blood pressure less than 90 mmHg or heart rategreater than systolic blood pressureOxygen treatment should be titrated to achieve an SpO 2 > 90% or applied empirically by highflowface mask when SpO 2 is not available or obtainable because of decreased peripheralperfusion7 Oxygen treatment also provides the additional benefit of reducing ICP and increasing CPP.September 14, 2010 16