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 Literaturefluid loss after injury. Whether hypotonic (due to loss of electrolytes), hypertonic (due to loss of water)or isotonic (due to loss of water and electrolytes), dehydration can interfere with central nervous systemfunction.Fluid management is thus an important and challenging aspect of TBI patient care. Although fluidrestriction has traditionally prevailed as the clinical protocol for preventing edema after brain injury(Shenkin et al., 1976), this practice is not supported by experimental findings (Gaab et al., 1979; Morseet al., 1985). Today, effective fluid balance management is widely accepted as a cornerstone formaintaining adequate blood pressure; in turn, optimal fluid management may help to reduce secondarybrain injury by reducing ICP and improving cerebral blood flow (Badjatia et al., 2008; Shackford et al.,1992).Fluid resuscitation and management may also be important to correct for electrolyte derangements thatcan compromise TBI patient status and outcome. 11 For example, TBI-related injury and/or secondaryeffects are often associated with blood sodium imbalance. Hyponatremia (low blood sodium, < 135mEq/L) is common after TBI, causing water retention by an increased volume of extracellular fluid. Thismay indicate TBI-related pituitary dysfunction and related anti-diuretic hormone (ADH/vasopressin)abnormality. If not treated, hyponatremia can cause confusion, convulsions, stupor, or even coma.However, it is likewise important to prevent blood sodium excess. Hypernatremia (elevated bloodsodium, > 145 mEq/L) can also occur after TBI and is equally important to monitor and treat. Earlysymptoms of hypernatremia are often subtle, including lethargy, weakness, and irritability. In severeform, hypernatremia can also cause seizures and coma.We identified just two studies that specifically addressed the effects of fluid volume on TBI outcome(Appendix: Table 6). An analysis of data from the National Acute Brain Injury Study of 392 severe TBIpatients found that low fluid balance (< - 594 mL) was an independent predictor of poor TBI outcome,and was an even more powerful a predictor than ICP (> 25 mmHg) (Clifton et al., 2002). Although theexact basis for this relationship was not clear, the authors’ analyses indicated that the low fluid balanceeffect was not related to ICP, MAP or CPP. The study emphasized the need for careful attention to TBIpatient fluid balance, noting that some of the most severely affected patients did not receive adequatefluid replacement.The importance of effective fluid management is reinforced by the finding that even a mildderangement of electrolyte balance (sodium disorder) can have potentially serious implications forpatients with severe TBI. In the immediate aftermath of TBI, mild hypernatremia (Na > 145 mmol/l) wasindependently associated with a higher risk of mortality (Maggiore et al., 2009). Hypernatremiaoccurred in more than half of the 130 severe TBI patients in this study and was due to TBI-relatedcentral diabetes insipidus in a subset of them.There are several treatment options available for fluid resuscitation/management. Mannitol (a sugaralcohol solution) is generally safe, effective, and has been commonly used to reduce ICP, and improveCPP and cerebral oxygenation. However, mannitol has several known limitations including the possibilitythat it may cause hypotension in already hypovolemic (dehydrated) patients. An alternative approachinvolves the use of hypertonic saline (Schmoker et al., 1991), which has been well-supported by the11 A detailed review of underlying mechanisms is beyond the scope of this review, and can be found elsewhere (Rhoney et al.,2006).September 14, 2010 20
Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the Literatureclinical literature for use in TBI patients (Anderson et al., 1997; Gemma et al., 1996; Oddo et al., 2009;Sandhu et al., 2004; Soreide & Deakin, 2005). Very recent evidence suggests that pre-hospital treatmentof severe TBI patients with hypertonic saline solution can serve to attenuate cell inflammatory processesand edema associated with secondary brain injury (Rhind et al., 2010). The Institute of Medicine hasrecommended hypertonic saline as the fluid treatment of choice for combat and civilian casualties(Committee on Fluid Resuscitation for Combat Casualties, 1999). Hypertonic saline administration is nowalso recommended as optimal for fluid resuscitation on the battlefield under current Guidelines for theField Management of Combat-related Head Trauma (Knuth et al., 2005) and has also been specified asappropriate for use in the treatment of TBI patients in mountain rescue settings (Sumann et al., 2009).White et al. (2006) present an informative review of hypertonic saline treatment effects, benefits andpotential complications.TEMPERATURENormal human body temperature is (37 °C or 98.6 °F) is maintained by the preoptic hypothalamus.When this area of the brain detects a change in body temperature, it triggers the autonomic nervoussystem to respond accordingly to provide for cooling (sweat production) or warming (shivering). If thisresponse is not adequate to correct for heat loss or production, thermal injury can occur withneurological manifestations. Temperature-related changes in the brain can affect secondary injuryrelated processes including oxygen requirements, inflammation, ischemia and edema (Mcilvoy, 2005).Hyperthermia (elevated core body temperature, 37.5-38.3 °C or 100-101 °F) causes an increase in brainmetabolism and reduces cerebral blood flow, probably as the result of cerebral vasoconstriction due tohyperventilation (hypocapnia). Early symptoms include confusion, altered affect and impaired workperformance. Hyperthermia may be associated with altered brain wave activity consistent with reducedarousal (Nielsen et al., 2001). If core body temperature is not reduced, the individual may experiencecoordination problems, seizures and coma. Numerous experimental animal studies show thathyperthermia can exacerbate the secondary processes and effects associated with brain injury (Busto etal., 1987, 1989; Dietrich, 1992; Dietrich et al., 1990; Minamisawa et al., 1990). Whether due toenvironmental factors, infection or hypothalamic dysfunction, hyperthermia is a common problem in TBIpatients. Incidence has been reported as high as 68% within 72 hours of injury (Albrecht et al., 1998).Hyperthermia early after TBI has been associated with lower GCS, diffuse axonal injury, cerebral edemaand hypotension (Cairns & Andrews, 2002). Badjatia (2009) has written a detailed and informativereview of the pathophysiology and clinical care considerations in TBI with hyperthermia.Hypothermia is marked by a core body temperature at or below 35 °C (95 °F). In addition to obviousenvironmental risk factors such as cold and wind, other risk factors for hypothermia include highaltitude, fatigue, hypoxia, dehydration, trauma, hypopituitarism 12 , and central nervous systemdysfunction (Imray & Oakley, 2005). Even mild hypothermia can affect cognitive functions includingmemory, learning and reasoning. These impairments are likely due to direct effects of cold on the brainitself (Coleshaw et al., 1983; Shurtleff et al., 1994). Moderate hypothermia (28-32 °C or 82.5-89.5 °F) isassociated with progressively reduced consciousness, decreased blood pressure, heart rate andmetabolism. With severe hypothermia (< 28 °C or 82.4 °F), the affected individual usually becomesunresponsive with cardiac arrhythmias. Brain wave activity declines and cerebral autoregulation andpupillary dilation stop at core body temperatures below 26 °C (78.8 °F).12 Hypopituitarism is the abnormal reduced secretion of hormones produced by the pituitary gland.September 14, 2010 21
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