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 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
Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the LiteratureAll of the hypoxia studies identified and included for this review involved patients with moderate and/orsevere TBI. None included patients with mild TBI, and none found reported differential effects ofhypoxia based on level of TBI severity.Our search captured six recent studies of hypoxia as a risk factor in TBI outcome (Appendix: Table 4). Ofthese, four retrospective studies and one prospective study found a strong association between hypoxiaand TBI outcome. Three identified a significant relationship between hypoxic episodes and patientmorbidity, disability and/or mortality (Chi et al., 2006; Davis et al., 2009; Jiang et al., 2002), while tworeported an association between hypoxia and functional outcome. Ariza et al. (2004) observed arelationship between pre-hospital hypoxia and prefrontal outcome, evinced by impaired attention,reaction time, mental flexibility, fluency and verbal memory. Chang et al. (2009) found that thefrequency and duration of brain tissue hypoxia in the intensive care setting was related to subsequentpoor functional outcome as assessed in various domains such as personal care, home management,social integration, work/school activity, ambulation and executive functioning.While Manley’s (2001) prospective study found no relationship between hypoxia and TBI outcome, theauthors identified several limitations of this study to include data recording artifact from the datacollection environment.Of particular relevance to this review is the observation that both hypoxemia and hyperoxemia(increased arterial blood oxygen saturation) are potentially dangerous to patients with TBI (Davis et al.,2009). This is consistent with contemporary practice that cautions against aggressive hyperventilationduring acute phases of severe TBI and pre-hospital care (Bullock & Povlishock, 2007). Hyperventilationcan cause hypocapnia -- a reduction in the arterial pressure of carbon dioxide (PaCO 2 ) – which leads tovasoconstriction in the brain. This restricts circulation and oxygenation, which in turn exacerbatesischemia and hypoxia. Hyperventilation can be effective to reduce ICP in some patients (Letarte, 1999).However, its use is recommended only in patients with clear signs and symptoms of brain herniation andoxygen delivery should be monitored. Prophylactic hyperventilation (PaCO2 of 25 mm HG or less) is notrecommended for severe TBI patients, and should be avoided during the first 24 hours post-injury whenCBF may be critically reduced (Bullock & Povlishock, 2007).Papadimos (2008) proposes that inhaled nitrous oxide (INO) may be an effective intervention to supportoxygenation while reducing the risk of inflammation and intracranial pressure, especially in patients whohave TBI in combination with acute respiratory distress. Rodent studies show results from this techniquewith potential translational value, as have at least two clinical case reports (Papadimos et al., 2009;Vavilala et al., 2001).INTRA-CRANIAL PRESSURE/BLOOD PRESSUREAlterations in blood pressure and oxygenation that could normally be tolerated well by the uninjuredbrain are potentially damaging to the injured brain. Secondary ischemic damage is more common inpatients who have sustained hypoxia, hypotension, or elevated ICP. It is also more common and severein more severe TBI and is found in the majority of patients who die of head injury (Chan et al., 1992;Graham et al., 1989; Marion et al., 1991).September 14, 2010 17
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