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

Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the Literaturedehydration, and extreme temperatures. We reviewed the available clinical literature to capturecontemporary findings, strategies, and recommendations relevant to these concerns.Although the overall body of research literature remains limited, when taken together it providescompelling evidence that altitude exposure itself is a risk factor for some degree of potentiallypermanent neurological damage as evident on MRI. Although such damage might not later be clinicallyobservable as functional impairment at sea level, it represents the effects of processes consistent withthose which underlie secondary brain injury after TBI. As such, altitude-related neurological changessuggest that TBI patients may be relatively more vulnerable to secondary brain injuries at high altitude.Whether by exacerbation of underlying pathophysiological processes or by cumulative effect, TBIrelatedsequelae are probably worsened to some degree by exposure to high altitude and resultinghypoxia.This reinforces the importance of rapid evacuation and descent with careful attention to mitigatingother sources of physiologic stress. Military medical air crews are highly experienced in trauma casualtycare and management, but sometimes are forced to perform under very demanding and sometimesunexpected circumstances. To avoid complications, minimize secondary injury and promote goodoutcome, it is especially critical that TBI patients avoid exposure to hypoxia, hypotension, andhyperthermia in the immediate aftermath of injury. There is a pressing need for additional research andinstructive case reports to document risks, benefits, interventions and outcomes associated withmilitary aeromedical transport of TBI casualties.Based on our review, there is little question that hypoxia itself – whether as the result of high altitude ortraumatic injury processes – is a strong predictor of poor outcome in TBI. Studies included in this reviewidentified clear adverse effects of hypoxia on morbidity, disability, neuropsychological/cognitivefunction, daily life functional status and morbidity among TBI patients. Taken together, they underscorethat a single episode of hypoxia is potentially dangerous and should be avoided by treatment withsupplemental oxygen. However, it is important to note that hypocapnia and hyperoxemia are alsopotentially dangerous to TBI patients. Recent findings indicate that while careful airway managementand controlled oxygenation are important, TBI patients should not be hyperventilated in the pre-hospitalsetting unless there are clear signs and symptoms of brain herniation due to elevated ICP.With rare exception, clinical studies show that elevated ICP (> 20 mmHg) and hypotension (< 90 mmHg)also play a critical role in determining outcome from brain injury. Both events reduce cerebral bloodflow, leading to hypoperfusion and ischemia. Therefore, CPP (MAP minus ICP) may be the mostinformative variable for study. Ischemic brain damage can occur if CPP falls below 70 mmHg and CPPless than 60 mmHg is associated with poor outcome. Additional research is needed to determinewhether the incidence or impact of these alterations might vary by TBI severity level. We found onestudy (Manley et al., 2001) indicating a potential correlation between hypotension and brain traumaseverity. Our search on these variables revealed no clinical studies involving mild TBI (mTBI) patientcohorts.Hypotension can be provoked or aggravated by dehydration, which progresses faster at higher altitudes.Dehydration can compromise the body’s ability to compensate for injury-related fluid loss. In one study,low fluid balance (< 594 mL) was found to be an even more powerful independent predictor of poor TBIoutcome than ICP (Clifton et al., 2002). Fluid resuscitation and management is thus important not onlyto prevent hypotension itself, but also to correct for potentially dangerous blood sodium abnormalities,September 14, 2010 24