Injuries due to ultraviolet radiation exposure The defining environmental features at high altitude are the decline in barometric pressure and the subsequent decrease in the ambient partial pressure of oxygen, important changes that set in motion an array of physiologic responses. Some of these responses reflect effective acclimatization while others predispose to the various forms of acute and chronic altitude illness described in the preceding chapters. As noted in Chapter 2, however, there are multiple other environmental changes that occur with ascent including decreased temperature, decreased humidity, and increased solar radiation. In conjunction with the increase in physical activity that often takes place with mountain travel, these environmental changes have the potential to cause a variety of other medical problems in the absence of appropriate preventive measures, including hypothermia, frostbite and nonfreezing cold injury, heat-related illness, and injuries related to excess ultraviolet radiation. This chapter describes each of these entities in greater detail, with particular emphasis on their pathophysiology and risk factors, clinical presentation, strategies for prevention and treatment, and expected outcomes. People traveling to the mountains are at risk for accidental hypothermia, an unintentional drop in core temperature ≤35°C resulting from an imbalance between heat production and heat loss. This is a primary form of hypothermia, as opposed to the secondary hypothermia that can develop due to underlying medical conditions, such as hypothyroidism, severe dermatologic disorders, or diabetic ketoacidosis (Brown et al. 2012). While often associated with exposure to subfreezing temperatures, hypothermia can develop with ambient temperatures >0°C, at any time of the year, and in any climate provided certain environmental factors, such as exposure to wind and rain, and behavioral factors are in place (Dow et al. 2019). Exposure to cold elicits several characteristic behavioral and physiologic responses, including peripheral vasoconstriction and shivering. The former redirects warm blood to the core of the body, including the brain, while the latter increases metabolic heat production up to five times as high as baseline depending on the temperature and wind conditions (Iampietro et al. 1960) as a means to counteract heat loss. Shivering ceases, however, once the individual’s glycogen stores are exhausted or the core temperature falls below a particular threshold, typically <32°C (Dow et al. 2019; Paal et al. 2016). Once this shivering fatigue occurs, tissue oxygen consumption declines significantly, which may be protective against permanent hypoxic neurologic injury when severe hypothermia is complicated by cardiac arrest. Cold also causes diuresis, likely as a result of changes in blood pressure and renal blood flow due to redistribution of fluid and alterations in the arginine-vasopressin system (Broman et al. 1998; Sun 2006). Hypothermia does not develop simply as a result of exposure to cold temperatures and, instead, occurs when there is an imbalance between heat production, on the one hand, and heat loss, on the other. As noted earlier, this can occur regardless of the climate or time of year. Heat production is increased above basal levels as a result of physical activity or shivering, both of which can be sustained as long as the individual maintains nutritional intake and adequate energy stores. The ability to raise energy production in response to cold stress is impaired at both extremes of age. In general, humans lose heat by one of several different mechanisms (Figure 27.1), including: (1) Conduction: The transfer of heat through direct contact between the skin and another colder object; (2) Convection: The transfer of heat by movement of air or water over the skin surface; (3) Evaporation: The loss of heat through conversion of sweat or airway mucosal moisture from the liquid to the gaseous phase; and (4) Radiation: The transfer of energy by electromagnetic waves. While radiation accounts for the majority of heat loss under normal conditions, the other mechanisms play an increasing role in the wilderness setting and, depending on the circumstances of travel, increase the risk of hypothermia. For example, conductive losses increase by lying on snow or cold ground and, to a greater extent, during immersion in cold water. Evaporative losses increase with heavy exercise and convective losses increase in windy conditions. Importantly, the balance of these factors can change over time, thereby altering the risk for hypothermia. For example, an individual may be traveling in subfreezing, windy conditions but maintain core temperature due to ongoing physical activity, even while sweating significantly under outer garments. Once they stop for a break, energy production declines and may now be outweighed by conductive losses through wet clothing and convective losses due to the ongoing windy conditions if they are not able to take adequate shelter. Any injury that leads to immobilization or impaired consciousness, particularly traumatic brain injury, further increases the cooling rate, thereby increasing risk of hypothermia. Figure 27.1Mechanisms of heat dissipation. (A) Conduction: The transfer of heat through direct contact between the skin and another cooler object; (B) Convection: The transfer of heat by air or water moving over the skin surface; (C) Evaporation: The loss of heat through conversion of sweat from the liquid to the gaseous phase; and (D) Radiation: The transfer of energy by electromagnetic waves. Beyond these key factors, impaired central and peripheral responses to cold can also increase the risk of hypothermia (Danzl and Huecker 2017). This is more typically a problem with comorbid medical conditions that predispose to secondary hypothermia in an urban setting but can be seen in the mountains in the setting of alcohol or drug ingestion or if a traveler was taking medications known to affect centrally mediated thermoregulation or vasoconstriction, such as certain medications used in psychiatric illness (Young 1996). Other traveler-specific factors that may affect the rate of cooling include the amount of insulating subcutaneous fat, as well as the body surface-to-mass ratio (Paal et al. 2016). The clinical manifestations of hypothermia fall into three general categories. As mentioned earlier, shivering serves to increase metabolic activity and heat production. Shivering ceases when energy reserves are exhausted and/or the core temperature falls below a certain threshold. While 30–32°C is often cited as the temperature range below which shivering ceases, the actual threshold varies between individuals and may be as low as 28–30°C (Dow et al. 2019; Paal et al. 2016). It is important to note that individuals may often shiver in the absence of reduced core temperature; as such, it can be used as an early warning of cold exposure. A decline in cerebral activity starts when the core temperature falls below 33–34°C. This manifests initially as apathy, confusion, irritability, and lethargy but progresses to somnolence and, later, coma as core temperature falls further. Cold-induced hyperventilation may also occur and lead to cerebral vasoconstriction secondary to hypocapnia. As core temperature falls below 30°C, bradycardia develops and cardiac output falls, which together with cold-induced diuresis, may lead to hypotension. Cardiac conduction abnormalities also occur and manifest in mild cases as premature atrial and ventricular contractions or atrial fibrillation. Once core temperature falls below 28°C, susceptibility to ventricular fibrillation increases significantly, particularly in response to acidosis, hypoxia, or movement. As suggested in these descriptions, the particular findings in a given patient will vary as a function of the core temperature. Because the findings tend to manifest in a relatively predictable manner as temperature falls, exam findings can be used to estimate the severity of hypothermia even in the absence of a suitable means to measure temperature, as often is the case in the field environment. This is the basis for the Swiss hypothermia classification system (Durrer et al. 2003) used by rescuers in the field as opposed to the standard temperature-based classification system used in the hospital setting (Dow et al. 2019; Zafren and Giesbrecht 2014) (Table 27.1). It should be noted, however, that because of the interindividual variability in clinical responses, the Swiss system provides only an approximation, rather than exact measure, of core temperature (Paal et al. 2016). Standard classification Grade Core temperature Clinical features Mild 32–35°C Thermoregulatory shivering control intact Moderate 28–32°C Shivering ceases; rewarming only possible with exogenous heat; decreasing level of consciousness Severe <28°C Most patients are unconscious; high risk of asystole or ventricular fibrillation Swiss classification Grade Clinical features Estimated core temperature* HT I Clear consciousness with shivering 32–35°C HT II Impaired consciousness; may or may not be shivering 28–32°C HT III Unconscious; vital signs present 24–28°C HT IV Apparent death; vital signs absent Variable * Note: The estimated core temperature in the Swiss classification is only an approximation given the interindividual variability in responses to cold. Source: Standard classification: Danzl and Huecker (2017); Swiss classification: Durrer et al. (2003). In the most severe cases, usually with temperature <24°C, patients may appear moribund, have no detectable vital signs, and even lack corneal and pupillary reflexes. In the absence of obvious signs of death, however, such as lethal trauma or avalanche burial >60 minutes with an obstructed airway (Truhlar et al. 2015; Van Tilburg et al. 2017), the patient should not be considered dead, as successful warming and resuscitation have been described in a patient who appeared lifeless with core temperature as low as 13.7°C (Gilbert et al. 2000). Prevention of hypothermia relies on behavioral modifications on the part of the traveler. Individuals traveling in the mountains must be aware that hypothermia does not require subfreezing ambient temperature and be vigilant about regulating their clothing, physical activity, shelter and fluid, and nutritional intake in response to changes in ambient conditions including temperature, wind, and precipitation. Avoiding travel in adverse ambient conditions (heavy rain, cold temperatures, high winds) is the optimal strategy but may not always be feasible. When engaging in physical activity, travelers should be prepared to remove layers of clothing as they become warm in order to prevent sweating, which can contribute to heat loss when activity ceases, particularly in windy conditions. Fluid intake should be maintained as a means to preserve intravascular volume while ongoing nutritional intake is important to maintain energy reserves to not only support physical activity, but also support ongoing shivering if core temperature begins to fall. The appropriate management strategy depends on the setting in which treatment is delivered. These strategies are described in detail in recent consensus guidelines and reviews on this topic (Brown et al. 2012; Dow et al. 2019; Paal et al. 2016; Truhlar et al. 2015) and are summarized next. Once hypothermia is identified, the primary goal is to prevent further heat loss. This can be done by insulating the affected individual from the cold ground, getting them into a shelter such as a tent, mountain hut, or lodge, and replacing wet clothing with dry layers. If the latter is not feasible, a vapor barrier can be created to protect against convective and evaporative losses using a plastic sheet, tarp, or garbage bag. Once such measures are instituted, efforts can be made to begin rewarming the patient. Unlike in the hospital, options are limited to external rewarming measures and may include interventions such as application of large heat packs or warm water bottles to the axillae, chest, and back with an appropriate barrier between the skin and heat source to prevent burns (Dow et al. 2019). Body-to-body rewarming may increase patient comfort but does not increase temperature beyond shivering alone (Giesbrecht et al. 1994). Carbohydrate-rich food and warm, carbohydrate-containing fluids should be administered to those not at risk for aspiration. Rather than increasing temperature, these measures provide calories to support ongoing shivering and heat production. Patients should be maintained in the supine or seated position with limited physical activity in the early stages of rewarming to prevent complications of rescue collapse and after drop, described later. Care should always be taken to avoid jostling severely hypothermic patients to decrease the risk of ventricular fibrillation (Dow et al. 2019). For patients with severe hypothermia found in cardiac arrest in the field, CPR can be delayed or only given intermittently until hospital arrival, but only if technical or safety issues prevent performance of continuous CPR (Dow et al. 2019). In-hospital treatment may include a combination of passive rewarming, active external rewarming, and core rewarming depending on the degree of hypothermia (Table 27.2). Extracorporeal life support (ECLS) is becoming the standard of care for patients with core temperature <24°C in cardiac arrest or <28°C with refractory circulatory instability, but it is not available at all medical centers. In the field, patients with Swiss stage IV hypothermia in cardiac arrest or those in Swiss stage III with refractory cardiac instability can be targeted for transfer to an ECLS-capable facility, if feasible. Pending initiation of ECLS, CPR should be initiated in patients with cardiac arrest in the presence of asystole or nonperfusing rhythms (ventricular tachycardia, ventricular fibrillation), but withheld in cases of organized cardiac rhythms unless there is other evidence (e.g., echocardiography) of lack of cardiac activity (Dow et al. 2019). While there is no temperature cut-off for withholding CPR or ECLS, resuscitation should not be attempted in avalanche victims buried ≥60 minutes with an obstructed airway (Dow et al. 2019) or those with a serum potassium >12 mmol/L upon arrival (>8 mmol/L if buried in an avalanche) (Truhlar et al. 2015). Defibrillation should be attempted one to three times for patients with ventricular fibrillation or pulseless ventricular tachycardia, but further defibrillation attempts should be held until the core temperature has risen by 1–2°C or to ≥30°C (Dow et al. 2019; Truhlar et al. 2015). Termination of resuscitative efforts, including ECLS, should be considered if patients do not have return of spontaneous circulation with a core temperature 32–35°C or higher (Brown et al. 2012; Paal et al. 2016). Passive external Change out of wet clothing Place in sleeping bag Protect from wind Remove from cold environment Active external Electric blankets and heating pads Forced circulated hot air Garments that circulate warm water (plumbed garments) Hot water bottles in axillae, groin, against torso Radiant heat (e.g., heat lamps) Warm water immersion Core Cardiopulmonary bypass Extracorporeal blood rewarming (venoarterial or venovenous) Heated, humidified air via ventilator circuit Heated intravenous solutions Hemodialysis Warm water lavage (colonic, gastric, mediastinal, peritoneal, thoracic) Care should be taken to avoid two complications that can develop during evacuation and rewarming. Refers to a continued drop in core temperature that occurs after a patient has been removed from the cold due to redistribution of cold blood from the periphery to the core as a result of factors that increase peripheral blood flow, such as early initiation of exercise during rewarming or use of surface rewarming techniques (Danzl and Huecker 2017; Paal et al. 2016). The risk of this can be minimized by limiting exercise following rescue (Dow et al. 2019), but others have argued that awake and alert patients should be allowed to mobilize if this will facilitate evacuation (Paal et al. 2016). Refers to cardiac arrest that occurs as a result of extrication and/or transport of a severely hypothermic patient. It is thought to occur due to circulatory collapse stemming from two factors: (1) hypovolemia due to cold-induced diuresis and decreased venous return with assumption of the upright position and (2) cardiac arrhythmias that are easily triggered by excessive movement due to the irritability of the hypothermic myocardium. To avoid this problem, care should be taken to avoid jostling patients with any movement, transport in the horizontal position to maintain venous return, and limit invasive procedures when feasible (Dow et al. 2019; Paal et al. 2016). Beyond these hypothermia-specific entities, patients are at risk for a variety of other problems, including pulmonary edema and infection, rhabdomyolysis, acute kidney injury, electrolyte abnormalities, disseminated intravascular coagulation, and seizures (Debaty et al. 2015; van der Ploeg et al. 2010). Outcomes from hypothermia vary depending on a variety of factors including the antecedent events (e.g., trauma, avalanche), medical comorbidities of the patient, performance of the rescue team, proximity of and rewarming techniques used by the treating hospital, complications experienced during recovery, and, most importantly, whether the patient experienced hypoxia (e.g., due to asphyxiation) or developed cardiac arrest before cooling (Locher et al. 1991; Paal et al. 2016). Survival is excellent and approaches 100% in those individuals with primary hypothermia who do not suffer cardiac arrest (Kornberger et al. 1999), but is reduced to about 40% in those who experience cardiac arrest and are resuscitated with ECLS (Pasquier et al. 2018; Saczkowski et al. 2018). Cardiac arrest due to rescue collapse is associated with better outcomes than unwitnessed arrest (Debaty et al. 2015). Although some neurologic deficits may be present immediately following rewarming, full recovery is possible in patients rewarmed after cardiac arrest with or without ECLS provided cooling was not preceded by hypoxia or trauma and the patient had no significant comorbidities (Ruttmann et al. 2007; Saczkowski et al. 2018; Walpoth et al. 1997). Frostbite is a localized form of environmental injury resulting from the freezing of tissue. Unlike in hypo- and hyperthermia, where severe cases can be associated with increased risk of mortality, the main concern in frostbite is localized loss of tissue and associated function. It can occur in any environment associated with subfreezing temperatures, but risk increases significantly with travel to the mountains due to a combination of the decrease in temperature and hypobaric hypoxia that occur with ascent. Frostbite develops when tissue temperature falls below its freezing point due to a localized imbalance between heat production and heat loss. Depending on the rate at which the local tissue temperature falls, ice crystals form in either the intra- or extracellular space. The former occurs with rapid cooling while the latter predominates when cooling occurs more slowly. Crystal formation indirectly injures cells through a combination of cellular dehydration and shrinkage, electrolyte derangements, and denaturation of lipid-protein complexes. Once thawing occurs, further tissue injury results from an adverse cycle of events, including microvascular thrombosis, ischemia-reperfusion injury, and release of inflammatory mediators and free radicals, which subsequently cause destruction of the microcirculation, leading to progressive tissue ischemia and infarction (Freer et al. 2017; Handford et al. 2017; Murphy et al. 2000). The risk of frostbite is increased by factors that either decrease tissue perfusion and oxygenation, increase the rate of heat loss, or impair decision making necessary to protect from adverse conditions (Table 27.3). Several features of the mountain environment are particularly important in this regard. As noted above, as one ascends to higher elevation, temperature falls (1°C for every 150 m gain in elevation) while acute hypobaric hypoxia decreases arterial oxygen content, particularly at extreme elevations. The effect of altitude can be appreciated from a study by Hashmi et al. (1998) in which they examined data from 1500 cases of frostbite seen at a tertiary medical facility and noted a steep increase in incidence with travel above 5200 m. People traveling in the mountains are also often exposed to high winds. While cold temperatures alone are problematic, it is the combination of cold and high wind speed that markedly increases the rate of heat loss and, therefore, the risk of frostbite (Wilson and Goldman 1970). Finally, many mountain travelers develop frostbite as a result of touching metal objects, such as crampons, ice axes, or fuel bottles with their bare hands. Such contact causes conductive heat loss, particularly if the skin is cold or damp at the time of contact, and causes frostbite even with short contact times (Geng et al. 2006). Decreased tissue perfusion and oxygenation Constrictive clothing Diabetes mellitus Hypovolemia Peripheral vascular disease Shock Tobacco smoking Decreased heat generation/Increased heat loss Decreased ambient temperature Immobility Increased winds Contact with objects or liquids with high thermal conductivity (metal, liquid) Wet skin Impaired decision-making/Apathy Alcohol or another drug intoxication Psychiatric illness Moderate to severe hypothermia Severe fatigue The most frequently affected areas include the ears, nose, cheeks, fingers, and toes. The symptoms and signs of injury to these areas vary depending on the phase of the illness. Individuals initially report that the injured part is cold and numb and may note difficulty moving an affected extremity or digit due to numbness and decreased flexibility of the freezing tissue. Prior to warming, the area is insensate, but once thawing occurs, individuals develop pain that is throbbing, burning, or electric in nature and can persist for long periods following the freezing event. Before rewarming, the affected area may be white, yellow-gray, or cyanotic, with a hard, waxy texture. Once rewarming occurs, individuals develop hyperemia and, within several hours, edema. Clear or hemorrhagic blisters and bullae may also be seen depending on the severity of the injury (Figure 27.2), with the former conveying a better prognosis than the latter. Depending on the severity of the injury, the injured area may later develop a dry, black eschar and eventually mummify in a clearly demarcated pattern over a period of weeks (Freer et al. 2017; Orr and Fainer 1952). Figure 27.2Clinical findings in frostbite. Clear and hemorrhagic blisters on the fingers of both hands in a climber who developed frostbite while trying to climb Ama Dablam (elevation 6812 m) in November. (Images provided by Andrew M. Luks.) The full extent of injury can be difficult to assess in the field and before rewarming, as varying injury severity can be seen in individuals exposed to similar conditions (Knize et al. 1969). A variety of classification schemes have been used to grade the severity of injury and estimate the degree of tissue loss that may result. One of the earlier and more common schemes relies on clinical and imaging findings and classifies frostbite as first, second, third, or fourth degree depending on the depth of injury (Table 27.4). A simplified version of this scheme that is now more commonly used and more suitable for field use relies on exam findings before or after rewarming and divides injuries into superficial and deep categories. Superficial corresponds to first- and second-degree injury in the standard classification, while deep corresponds to third- and fourth-degree injury. Because of difficulties predicting the extent of amputation necessary in severe cases with these classification systems (Handford et al. 2017), an alternative system (Cauchy et al. 2001) was created and has been more widely adopted in recent years that grades frostbite of the hands and feet on a scale from 1 to 4 based on the appearance immediately after thawing and the results of a radioisotope scan (Table 27.4). Portable ultrasound and soft-tissue cyanosis have also been proposed as methods that can be used in an austere environment to assess perfusion and the risk of amputation and guide early management rather than waiting for a bone scan (Cauchy et al. 2016). Two-tier classification Four-tier classification Clinical features Superficial First Numbness; erythema; may develop a white or yellow, firm, raised plaque; mild edema; no tissue infarction Second Clear or milky fluid-containing blisters with surrounding erythema Deep Third Hemorrhagic blisters indicative of deeper injury involving the reticular dermis Fourth Injury extends through dermis to subcutaneous tissues; necrosis extending to muscle and level of bone Cauchy classification system Variable Grade 1 Grade 2 Grade 3 Grade 4 Extent of initial lesion after rapid rewarming Absence of initial lesion On distal phalanx On intermediary and proximal phalanx On carpal/tarsal area Bone scan at day 2 Useless Hypofixation of radiotracer uptake area Absence of radiotracer uptake area on the digit Absence of radiotracer uptake area on the carpal/tarsal area Blisters at day 2 None Clear Hemorrhagic; located on digit Hemorrhagic; located over carpal/tarsal area As with hypothermia, prevention of frostbite is a function of behavioral modification and individual and/or group decisions. The primary preventive measures, which are described in detail elsewhere (Freer et al. 2017; McIntosh et al. 2019), fall within three general categories. Individuals must be vigilant about maintaining core temperature and covering exposed skin to prevent peripheral vasoconstriction. Adequate fluid intake helps maintain intravascular volume status while ongoing nutritional intake generates heat through metabolism and provides energy to support shivering and physical activity. Constrictive clothing and, in particular, extra pairs of socks or tight fitting footwear should be avoided. Supplemental oxygen should be strongly considered when climbing above 7500 m in elevation. Exercise not only generates heat but also enhances cold-induced vasodilation, which maintains tissue perfusion (Dobnikar et al. 2009). Chemical heat packs can be added to gloves and footwear but care must be taken to avoid direct contact with skin and restricting space within footwear. Individuals should adjust their clothing layers and change socks as needed to avoid perspiration, as wet skin increases the risk of heat loss, while touching metal or handling fuel with bare hands should be avoided to minimize rapid conductive heat loss. Alcohol consumption impairs the behavioral responses necessary to prevent frostbite and should also be avoided. Individuals should pay close attention to weather forecasts and avoid travel in extreme weather with low temperatures and/or high winds. When such travel is necessary, exposed skin should be covered with clothing, gloves, hats, balaclavas, and goggles. Emollients are commonly used with the intention of preventing frostbite but have not been shown to be effective and may even increase risk (De Buck 2017; Lehmuskallio 2000). Beyond these factors, care should be taken to avoid excess fatigue, hypothermia, alcohol consumption, or any other factor that impairs concentration or promotes apathy, as these problems may limit one’s ability to institute the necessary preventive measures. Individuals must also be able to recognize frostnip—a rapidly reversible superficial injury in which ice crystals form on the skin rather than in the tissue—because it serves as a warning that conditions favorable for frostbite are present and more aggressive protective measures are necessary. The approach to treatment, which is described in detail in multiple other resources (Freer et al. 2017; McIntosh et al. 2019; Zafren and Giesbrecht 2014), varies based on whether the individual is still in the field or has accessed a hospital. Beyond the immediate priorities of getting out of the elements, removing wet and/or constrictive clothing, and rewarming those who also have hypothermia, a critical decision is whether to thaw the involved tissue. Unless refreezing can be prevented, the extremity should be left frozen, as repetitive freeze-thaw cycles worsen frostbite injury. However, when transport to definitive care is anticipated to take more than one to two hours, the extremity will likely thaw spontaneously, in which case, extreme care is warranted to prevent refreezing in transport or while waiting for evacuation (Freer et al. 2017). Affected extremities should be padded and splinted for protection, while ibuprofen or aspirin should be administered to block inflammatory processes that may contribute to ongoing injury. Rubbing of the affected area should be avoided and blisters left intact. Boots can be removed but if it is anticipated that the individual will need to evacuate on foot, they should be left in place, as the boot may be impossible to put back on once swelling occurs during thawing and the unprotected foot may be susceptible to refreezing or further injury. Oxygen is often administered at elevations >4000 m to maintain a saturation >90% (McIntosh et al. 2019; Syme and Commission 2002; Zafren and Giesbrecht 2014). In addition to rapid rewarming of the affected area in circulating water warmed to 37–39°C (Freer et al. 2017), a variety of measures are typically instituted after transport to definitive care, including administration of ibuprofen, parenteral pain control, and, if indicated by standard guidelines, tetanus prophylaxis (McIntosh et al. 2019). Administration of thrombolytics is also considered in cases of deep injury to counteract microvascular thrombosis (Bruen et al. 2007; Gonzaga et al. 2016; Twomey et al. 2005), as is the administration of the prostacyclin analog, iloprost, that promotes vasodilation and potentially prevents platelet aggregation and microvascular occlusion (Cauchy et al. 2011) without the risk of hemorrhage associated with thrombolytics. The combined use of tPA and iloprost may improve outcome in severe cases (Lindford et al. 2017). Whether to give prophylactic antibiotics remains an area of debate, with no clear evidence supporting their use (Handford et al. 2017; McIntosh et al. 2019). In addition to these pharmacologic interventions, imaging studies including angiography, bone scanning, magnetic resonance angiography, and vascular ultrasound are used to fully assess the extent of injury and guide further management (Handford et al. 2017). The approach to ongoing care is beyond the scope of this chapter and is described elsewhere (Freer et al. 2017; Handford et al. 2017; McIntosh et al. 2019). A variety of other cold-related problems can affect travelers to high altitude. Two of them are considered briefly below, while a full discussion of these and other cold-related entities including cold urticaria, cryoglobulinemia, and pernio can be found elsewhere (Imray et al. 2017). First recognized in the setting of prolonged military campaigns, such as Napoleon’s ill-fated Russia campaign in 1812 and the stalemate on the western front in World War I, nonfreezing cold injury (NFCI) develops from prolonged exposure to wet, cold conditions. With improvements in modern outdoor clothing and footwear, this entity, which is often referred to as trench foot or immersion foot, is seen much less frequently among mountain travelers but can still occur if individuals are forced to walk in cold, wet conditions for long periods without adequate opportunities to dry their feet, socks, and footwear. The duration of exposure necessary to provoke NFCI is unclear. In the first phase of injury during ongoing cold exposure, individuals develop loss of sensation and proprioception in the affected extremity, which takes on a pale yellow-white or mottled appearance, usually without blistering (Ungley et al. 2003). During and after rewarming, the affected extremity remains cold and numb with a mottled, pale blue appearance as blood flow increases. This is followed within several hours by a hyperemic phase lasting days to weeks in which the extremity is painful, hyperalgesic, hot, erythematous, and edematous with bounding pulses (Ungley et al. 2003; Webster et al. 1942). Once this resolves, the extremity may look normal, except in rare cases where tissue necrosis occurred, but the individual may have increased cold sensitivity, hyperhidrosis, and chronic pain, perhaps on a permanent basis (Imray et al. 2017). Muscle atrophy and paralysis may also occur due to peripheral nerve injury (Ungley et al. 2003). When identified in the prehyperemic stage, the extremity should be elevated and rewarmed more slowly than in cases of frostbite to limit pain, edema, and metabolic demands in the healing skin. Physical therapy should be initiated to prevent or reverse atrophy. Nonsteroidal anti-inflammatory agents and opiates are often used for pain relief but are typically not effective, in which case agents targeting neuropathic pain, such as gabapentin and amitriptyline may be tried (Imray et al. 2009). A more detailed description of the clinical presentation and management can be found elsewhere (Imray et al. 2017; Imray et al. 2011). A disorder of abnormal vasomotor control, Raynaud’s phenomenon can occur as an isolated problem (primary Raynaud’s phenomenon), or in association with collagen vascular diseases such as systemic lupus erythematosus or scleroderma (secondary Raynaud’s phenomenon) (LeRoy and Medsger 1992). The characteristic feature of the disorder is recurrent episodes of pallor or cyanosis of the distal extremities due to vasospasm and limitations in arterial blood flow in response to cold, moisture, stress, or vibration (Figure 27.3). These color changes are typically bilateral, usually accompanied by pain, numbness, and burning sensations, and often followed by reactive hyperemia as blood flow returns to the digits (Wigley 2002). Figure 27.3Clearly demarcated areas of pallor typical of an acute attack of Raynaud’s phenomenon. (Image provided by Andrew M. Luks.) Because cold is one of the primary triggers for Raynaud’s phenomenon, mountain travel and the associated exposure to colder ambient temperatures may predispose to these episodes and potentially exacerbate the risk of frostbite. Despite these theoretical concerns, little is known about the extent to which high altitude exposure affects individuals with this problem. To examine this question, Luks et al. (2009) surveyed 142 people with Raynaud’s phenomenon, most of whom had primary disease, who travel to altitudes >2440 m during the winter and summer months. Respondents reported spending between five and seven days per month above 2440 m and engaging in a wide variety of activities, including winter sports such as skiing. There was marked heterogeneity in the respondents’ perceptions of the frequency, duration, and severity of attacks at high altitude compared to their home elevation, but the data suggested that by using a variety of preventive and treatment strategies, these individuals tolerated travel to this environment and were able to continue their mountain activities. Whether Raynaud’s episodes increase the risk of frostbite was not clear from this study. Fifteen percent of respondents reported a history of frostbite at high altitude, but there was no control group to determine if this rate is increased relative to the general population exposed to similar conditions. In another study that did not include altitude as a variable, Ervasti et al. (2004) found an odds ratio for frostbite among Finnish military recruits with cold-provoked white-finger (CPWF) syndrome, another name for Raynaud’s phenomenon, of 2.05 (95% CI 1.72–2.44). However, this odds ratio applied to all degrees of frostbite severity. When focused more specifically on deep frostbite, defined as frostbite accompanied by blisters, ulcers, or gangrene, the risk was only increased in those who smoked or were exposed to vibration. On cursory examination, given that temperature declines with increasing elevation, exposure to high altitude would not appear to be associated with a risk of heat illness. In reality, however, high altitude travelers are at risk for a variety of heat-related problems, particularly when engaged in heavy exertion, especially when wearing insulative clothing that reduces heat loss. Many of the major mountain ranges and noteworthy peaks, such as Kilimanjaro, are at lower latitudes where average temperatures are higher than at greater latitudes. While nighttime temperatures may be quite low, marked rises often occur during the daytime on sunny days, particularly in cirques or valleys or when wind is minimal. Sun exposure also increases significantly with increasing altitude, especially with travel on snow-covered terrain, further increasing radiation-based heat gain. Finally, much mountain travel is associated with physical activity, which increases heat generation and the risk of dehydration, factors which contribute to heat-related illness. Exercise or exposure to hot ambient conditions elicits a series of physiologic responses mediated by an integrated system of sensors, effectors, and the hypothalamus to minimize the rise in core temperature (Leon and Kenefick 2017). The most important of these are diversion of blood flow from the core to the periphery and sweating. Diversion of blood flow relies on intact cardiac function to increase and maintain perfusion and splanchnic vasoconstriction and peripheral vasodilation mediated by the autonomic nervous system. This is further aided by arteriovenous anastomoses that increase the amount of blood that can be directed toward particular organs (Leon and Kenefick 2017). Sweating promotes heat loss through evaporation, with the amount of loss being a function of the density, secretion rate, and activation threshold of an individual’s sweat glands, the type of clothing being worn, and the water vapor pressure gradient between the skin and the surrounding environment. Under more arid conditions, evaporation readily contributes to heat loss because there is a sufficient water vapor pressure difference between the sweat on the skin and the surrounding environment. Ascent to high altitude makes for efficient heat loss through evaporation due to the decrease in humidity that occurs at higher elevations. Other important responses occur at the cellular level, including acute phase responses involving cytokines, endothelial cells, leukocytes, and epithelial cells protect against cellular thermal injury and increased expression of heat shock proteins that protect cell proteins against heat and other stresses (Bouchama and Knochel 2002; Leon and Bouchama 2015). There are multiple clinical problems that fall under the heading of heat illness. Although they are typically described as distinct entities, they are more appropriately characterized as falling along a continuum from mild to very severe disease (Leon and Kenefick 2017; Lipman et al. 2019). Of the entities described here, the first three are usually associated with normal core temperature at presentation while the latter two are marked by the presence of hyperthermia. Transient muscle spasms that occur during or immediately following exercise in warm conditions. Benign, self-limited, lower extremity edema resulting from cutaneous vasodilation, with subsequent increased hydrostatic pressure in the lower extremities and leakage of fluid from the vascular to the interstitial space. A benign, transient loss of consciousness with rapid return to normal function. Often seen with prolonged standing or following cessation of exercise, it is thought to result from a decrease in venous return due to cutaneous vasodilation and pooling of blood in the lower extremities. An inability to continue activity resulting from insufficient cardiac output due to heat stress and intravascular volume depletion. Affected individuals are typically febrile and manifest a variety of symptoms including tachycardia, hypotension, fatigue, nausea, vomiting, diaphoresis, cramps, and lightheadedness or syncope. Importantly, individuals with this entity lack central nervous system manifestations and evidence of end-organ injury. If not recognized and treated appropriately, heat exhaustion can progress to heat stroke (Bouchama and Knochel 2002; Leon and Kenefick 2017). A life-threatening, multisystem form of heat illness defined by the presence of a core temperature >40°C in conjunction with central nervous system abnormalities such as irritability, confusion, seizures, impaired consciousness, and coma (Bouchama and Knochel 2002). Resulting from either passive exposure to hot conditions (classic heat stroke) or strenuous physical activity (exertional heat stroke), it can come on rapidly or over a period of hours to days depending on the clinical circumstances. In addition to central nervous system injury, affected individuals may develop other forms of end-organ dysfunction, including acute liver and kidney injury, acute respiratory distress syndrome, rhabdomyolysis, intestinal ischemia, and disseminated intravascular coagulation (Bouchama and Knochel 2002; Leon and Kenefick 2017). In addition to these commonly cited entities, another clinical problem that can be seen with prolonged exertion in hot environments is exercise-associated hyponatremia. This dilutional form of hyponatremia develops as a result of free water consumption in excess of that necessary to replace losses due to sweating or water excretion from the urinary or respiratory tracts. Inappropriate secretion of arginine vasopressin often contributes to this problem in some cases by preventing renal excretion of excess water (Hew-Butler et al. 2015; Rogers and Hew-Butler 2009). It is common for this problem to develop during endurance events in which participants exercise for long periods of time while consuming large volumes of water, sports drinks, or other hypotonic fluids with insufficient salt intake (Almond et al. 2005; Hew-Butler et al. 2015). As with hypothermia, core temperature increases when there is an imbalance between heat generation and heat dissipation. Importantly, the roles of several of the key factors in this balance—evaporation, conduction, convection, and radiation—are different in hot climates compared to cooler ones. Under normal or cold temperatures, conduction, convection, and radiation all lead to heat dissipation because the temperature gradient favors loss of heat from the body. Under hot conditions, however, the ambient temperature, wind, and contacting surface may be warm enough that the gradient is reversed and these factors subsequently contribute to heat gain along with basal metabolism and physical activity. The utility of evaporation is markedly diminished in humid conditions due to a decrease in the water vapor pressure gradient. As noted above, the body relies on multiple processes to maintain normal temperature in the face of increased heat generation. In certain cases, however, particularly once core temperature crosses a critical level, these processes go awry and cause progression to heat stroke (Bouchama and Knochel 2002; Leon and Kenefick 2017). In addition to an exaggerated acute phase response and altered expression of heat shock proteins, one factor that is thought to play a key role in this transition is hypoperfusion of the gastrointestinal tract, which increases mucosal permeability and predisposes to translocation of endotoxin from the gut to the systemic circulation (Lambert et al. 2002; Shapiro et al. 1986). The risk of this situation is increased in the setting of hypovolemia and/or impaired cardiac function. Endotoxemia subsequently magnifies the inflammatory response, leading to endothelial injury and microvascular thrombosis, impaired thermoregulation, hypotension, and end-organ injury. A more detailed discussion of these pathophysiologic processes can be found in several extensive reviews on the topic (Bouchama and Knochel 2002; Leon and Bouchama 2015). The risk factors for the more severe forms of heat illness can be divided into four broad categories of problems that either impair heat dissipation or increase heat generation (Leon and Kenefick 2017). Beyond temperature, other factors that affect risk include the humidity, which affects the water vapor pressure gradient for evaporative heat loss, wind speed, and degree of sun exposure. These variables are incorporated into two separate measures of heat stress that can be used to guide activity levels in hot environments, the heat index, and the wetbulb globe temperature. The former takes into account temperature and humidity while the latter factors in temperature, humidity, wind speed, sun angle, and cloud cover (National Oceanic and Atmospheric Administration [NOAA]). Chronic medical conditions, such as heart failure, diabetes mellitus, and skin disorders (e.g., burns, miliaria rubra), can impair heat dissipation and, subsequently, increase the risk of classic heat stroke while recent acute febrile illnesses have been implicated in the development of exertional heat illness (Carter et al. 2007; Keren et al. 1981), perhaps due to alterations in hydration status or transient changes in thermoregulation (Leon and Kenefick 2017). Certain medications impair heat loss by, for example, limiting cardiac output (beta-blockers), decreasing intravascular volume (diuretics), or blocking peripheral vasodilation (alpha-adrenergics), while many illicit drugs (cocaine and methamphetamine) increase heat production. Some individual-level risk factors such as age, body habitus, and prior heat illness are not readily modifiable. Thermoregulation is impaired at the extremes of age while overweight individuals with large body mass to surface area ratios have difficulty with heat dissipation. Perhaps not surprising, infants and young children also lack important behavioral responses to heat stress. Other variables such as cardiovascular fitness, degree of heat acclimatization, hydration status, use of protective clothing and equipment that prevent heat dissipation, and activity plan can be addressed with either several weeks of advanced planning or decisions at the time of the planned endeavor in the hot environment. Despite these well known risk factors, many cases develop in individuals who lack clear risk factors (Stacey et al. 2015), making it challenging to identify those prone to exertional heat stroke. Effective prevention is a function of actions taken both before and during physical activity in a hot environment. When it is known well in advance that physical activity will be required in a hot environment, individuals can engage in a program of heat acclimation. Ten to 14 days of exercise lasting more than one hour in hot conditions leads to a series of durable adaptations including plasma volume expansion, increased cutaneous blood flow, increased sweat output, and lower sweat threshold, all of which promote heat dissipation and facilitate exercise in hot climates (Armstrong and Maresh 1991; Pryor et al. 2015; Weller et al. 2007). Shorter programs are also effective but have less durability of response (Garrett et al. 2009), while increased cardiopulmonary fitness alone can also have a durable protective effect (Cheung and McLellan 1998; Lipman et al. 2019; Pandolf et al. 1977). In the period immediately preceding the planned activity, individuals should monitor the weather forecast and, in particular take note of the heat index or the less readily available wetbulb globe temperature index, as a means to assess the risk of heat illness and modify the intensity, timing, and duration of the planned activity accordingly. Individuals exercising in warm environments should ensure euhydration prior to exercise and maintain adequate fluid and electrolyte intake during the activity. Individuals should avoid forced overhydration, which can increase the risk of exercise-induced hyponatremia, and instead drink to thirst. They should limit use of medications known to impair thermoregulatory responses, such as beta-blockers, tricyclic antidepressants, or neuroleptic agents, among others (Lipman et al. 2019) and avoid use of clothing that limits heat dissipation. Layers of clothing can be added or removed based on perceived changes in warmth. Finally, they should set aside time for breaks, ideally in the shade, as a means to limit heat generation. Treatment for the mild forms of heat illness is described in Table 27.5. For the more severe problems, heat exhaustion and exertional heat stroke, treatment varies based on where care is being delivered. Illness Treatment Heat cramps Oral isotonic fluid administration Heat edema Compression stockings Leg elevation Heat syncope Oral isotonic fluid administration Passive cooling measures Remove from heat source Source: Lipman et al. 2019
Introduction
Hypothermia
Physiologic responses to cold
Mechanisms and risk factors for hypothermia
Heat Production
Heat Loss
Clinical features
Shivering
Central Nervous System Manifestations
Cardiac Manifestations
Prevention
Treatment
Field Treatment
Hospital Treatment
Complications of Rewarming
Afterdrop
Rescue Collapse
Outcomes
Frostbite
Pathophysiology
Risk factors
Clinical presentation
Classification systems
Prevention
Maintain Extremity Perfusion and Oxygen Delivery
Maintain Balance Between Heat Generation and Heat Loss
Protect from the Cold
Treatment
Field Treatment
Hospital Treatment
Other Cold-Related Problems
Nonfreezing cold injury (NFCI)
Raynaud’s phenomenon
Heat-Related Illness
Physiologic responses to heat
Clinical syndromes
Heat Cramps
Heat Edema
Heat Syncope
Heat Exhaustion
Heat Stroke
Mechanisms for heat-related illness
Risk factors for heat exhaustion and heat stroke
Environmental Factors
Acute and Chronic Medical Illness
Medications and Drugs
Individual Factors
Prevention
Before the Planned Activity
During the Planned Activity
Treatment
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