EMS providers often encounter patients who have become victims of environmental emergencies. Even in urban areas, patients may suffer from heat- or cold-related illnesses. In more remote areas, altitude illness, undersea illness, and decompression sickness may be encountered. Electrical injuries from both lightning and electrical sources may be seen. EMS workers need to understand how to stabilize these illnesses and injuries, while remaining safe.
Understand the pathophysiology, diagnosis, and management of hypothermia, frostbite, nonfreezing cold injury, and other cold-related injuries.
Understand the pathophysiology, diagnosis, and management of heat stroke, heat exhaustion, and other heat-related injuries.
Understand altitude-related illness, including AMS, HACE, HAPE.
Understand the pathophysiology and treatment of undersea-related illnesses. Understand the diagnosis and management of electrical injuries.
Understand the pathophysiology of electrical injuries.
Understand that standard triage decisions may be reversed in the case of electrical injuries.
Appreciate possible risks to the rescuer in electrical injuries.
Understand the pathophysiology of decompression sickness.
Understand barotrauma injuries
Be familiar with treatment of diving and undersea injuries.
Heat transfer occurs through radiation, conduction, convection, and evaporation. Each of these mechanisms serves to transfer heat to and from the body. In homeostasis, these mechanisms of energy diffuse heat generated through the body’s metabolic processes. Conduction is the transfer of heat between objects in direct contact. The amount of energy lost by a body in contact with another object depends on several factors, including the amount of the body in contact with the object, the conductivity of the objects, and the difference in temperature between the two objects. Conduction is a major cause of profound heat loss among victims who have fallen into cold water, for example. Convection is the transfer of heat caused by the movement of molecules of gas of liquid near the body. Convection explains why wind can exacerbate cold temperatures (the wind chill index). Radiation refers to the transfer of electromagnetic radiation between objects, in this case between humans and the environment. Evaporative heat loss takes place when water changes state, from liquid to gas. Heat loss increases with sweating.1
Certain populations are more at risk for accidental hypothermia than others. Patients at either end of the human age spectrum are particularly at risk for hypothermia.
In the elderly, both metabolic and behavioral factors contribute to a propensity for rapid development of hypothermia in cold conditions.2 In infants, increased surface area and absence of behavioral adaptations to cold exposure contribute to a high risk of hypothermia, even in ambient conditions.
Next, ingestion of certain medications places patients at risk for hypothermic illness. Medications can either interfere with thermogenesis or promote heat loss through various processes, including vasodilatation. Sedatives and psychotropic medications, including barbiturates, benzodiazepines, phenothiazines, lithium, and tricyclic antidepressants can all cause hypothermia.
Rescuers need to be vigilant for hypothermia in select populations: trauma patients, in particular, are vulnerable to hypothermia both as a consequence of their underlying injuries and hypovolemia. This is by virtue of the fact that they may have spent time in cold environments following their injuries, and as an iatrogenic consequence of standard trauma exposure and resuscitation practices.
Hypothermia is generally defined as a core body temperature of 35°C or less, and is often categorized as being either primary or secondary in origin.3 Primary hypothermia occurs when individuals are exposed to ambient conditions that exceed their ability to thermoregulate. This is distinct from secondary hypothermia, which occurs in patients with specific endocrine, neurologic, or metabolic conditions such as sepsis and cerebral lesions.4 Primary (or accidental) hypothermia will be primarily discussed in this chapter.
Mammals maintain a careful equilibrium between heat loss and heat production. In humans, thermoregulation occurs via a complex sensory and transmission framework consisting of temperature sensitive sensors in the cutaneous tissues, the spinothalamic tract, the thalamus, and the hypothalamus.5 The body can conserve and generate heat as a response using the autonomic, circulatory, and endocrine systems to stimulate thermogenesis. Hypothermia develops when cooling losses exceed the body’s ability to maintain warmth.
Hypothermia has effects on all organ systems, but particularly the central nervous system, cardiac, renal, and hemostatic systems. Effects on the CNS are particularly pronounced: Cold depresses the central nervous system and amnesia, dysarthria, poor decision making, and delirium can be seen at even modestly decreased core body temperatures.6 The cardiac system is similarly affected by cold. Cardiac output is affected by an impaired cardiac conduction system and by impaired myocardial contractility.7 Dysrhythmias in moderate to severe hypothermia are common, and potentially lethal. Classically, tachycardia followed by bradycardia is described in cases of progressive hypothermia. Cold causes disruptions in the cardiac cycle, with prolongations of conduction time and electrocardiac intervals. These disruptions, combined with disruptions in transmembrane myocyte potentials, can incite multiple dysrhythmias, including reentrant tachycardias, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.8 One ECG finding, the J (or Osborn) wave, is classically described in hypothermia.9 This wave is classically seen on an ECG at the junction of the QRS complex and the ST segment.
The renal system responds to hypothermia by increasing diuresis, sometimes considerably. This “cold diuresis” effect is primarily caused by a relative central hypervolemia due to peripheral vasoconstriction, and leads to ongoing diuresis even in the face of relative dehydration.10
The hemostatic system is significantly affected by cold. Both coagulopathy and hypercoagulability can be seen in hypothermic patients. Coagulopathy can be caused by inhibitions in the coagulation cascade, thrombocytopenia, and platelet dysfunction.11
Patients with hypothermia may be affected to varied degrees: Some, with severe hypothermia, may present in cardiac arrest. In these cases, determining whether hypothermia or some other medical/trauma etiology is responsible for the arrest may be difficult. Patients may be unconscious with pulses, and others may be conscious but have significantly diminished mentation. Patients with mild illness may present with or without shivering and may appear clinically intoxicated—confused, inattentive, and displaying slurred speech. Protective behaviors, such as heat-seeking efforts, may be ignored. It is important to be alert to the potential for hypothermic injury in patients otherwise suspected of being impaired by drugs of abuse.
The decision to begin resuscitation can be difficult in patients found pulseless in cold conditions. In the absence of obviously lethal trauma, resuscitative attempts should as a rule be initiated, and continued until normothermia is achieved. There have been multiple case reports of patients successfully resuscitated even after prolonged periods of cardiac arrest.12,13 Prehospital treatment for hypothermic patients not in cardiac arrest should be initiated as per Box 47-1.14 Attention must be paid to ensuring that all traumatic injuries and medical comorbidities are assessed and managed, in addition to treatment of hypothermia. Aggressive attention should be paid to airway management: There is no reliable data to suggest that intubation induces lethal arrhythmias. Similarly, standard cardiac resuscitation efforts should be initiated.15
Box 47-1 Prehospital Management of Hypothermia
Assess vital signs. Be aware that some patients may have significant bradycardia and present minimal cardiac output, adequate to support diminished metabolic demand. Endotracheal intubation and other airway maneuvers should be initiated as medically indicated.
Minimize further hypothermia by drying and insulating the patient: Remove wet clothing and wrap the patient in dry blankets.
Correct dehydration: Most patients with moderate to severe hypothermia benefit from a fluid challenge to correct dehydration. Warmed fluids should be used.
Initiate active rewarming to the torso. Hot water bottles or heated bags of IV fluid can be placed in the patient’s axillae and groin. It is in practice difficult to provide a meaningful amount of rewarming to patients in the EMS setting.
Begin gentle transport to a receiving facility. Avoid rough handling of the patient, which may initiate cardiac arrhythmias.
Prior to the initiation of rewarming, patients must have their temperatures measured accurately. The most accurate readings are taken from esophageal monitors (in the intubated patient) although rectal thermometers, while less accurate than esophageal probes, may be the best available option. Oral, external auditory, and bladder thermometers are unreliable instruments to measure true core body temperature.16 The appropriate method of rewarming should be selected based on the severity of patient symptoms. Rewarming efforts can be divided into three categories: passive external, active external, and active internal methods.17
Passive external rewarming refers to efforts to protect and insulate patients from heat loss, in order to facilitate native thermogenesis. Such efforts are best reserved for cases of hypothermia in a selected population of younger, healthier patients.
In contrast, active rewarming refers to the transfer of heat from a source, to an affected patient. Active rewarming can be either external (heat applied to the external surface of the skin) or internal (invasive techniques designed to rewarm the blood and organs) as noted in Box 47-2. Active rewarming is required for patients with moderate to severe hypothermia and those with complicating comorbidities, such as age or metabolic complicating factors. Most active warming in the EMS environment will be active external warming, using heated bags of IV fluid, or water bottles placed in the groin and axilla. Other options include warm air convection devices modified for use with portable power systems. The decision to pursue invasive cooling should be made with consideration for the degree of hemodynamic instability as well as the extent of hypothermia.3 During all attempts at rewarming, attention should be paid to the possibility of afterdrop—the ongoing cooling of the core caused by relocation of cold peripheral blood into the relatively warmer core.18 In dehydrated and significantly hypothermic patients, this translocation of cold can be life threatening. Afterdrop seems to be minimized by directing warming efforts to the torso, and by avoiding use of cold extremities until the core temperature is stabilized.
Box 47-2 Active Rewarming Methods Commonly Used in EMS
Active external warming techniques
External heaters
Water bottles and warmed bags of IV fluids in groin/axilla
Circulated hot air
Immersion in warm water
Active internal methods (usually employed at receiving facilities)
IV infusions of warmed fluids
GI lavage via NG tube or rectal tube
Thoracic lavage via thoracostomy tube/peritoneal lavage via peritoneal incision
Hemodialysis
Extracorporeal blood rewarming
Cardiopulmonary bypass
Frostbite refers to tissue injury and destruction caused by freezing. Frostnip, in contrast, is a mild temporary form of cold-induced injury and is also known as first-degree frostbite. These injuries are distinct from nonfreezing cold injuries such as trench foot, discussed separately. While frostbite remains a concern for outdoor enthusiasts, it is not uncommonly encountered in urban populations, particularly in the homeless. Second-degree frostbite refers to superficial frostbite where third- and fourth-degree refers to deeper injuries.
Physiologic factors related to dermal circulation are the key to frostbite. Skin contains a complex system of capillaries with richly innervated arteriovenous connections. Cutaneous vascular tone is controlled by both direct local and systemic sympathetic vasoconstrictor fibers. In cold conditions, vasoconstriction occurs, predisposing subsequent local freezing injury. Frostbite injury begins with extracellular ice crystal formation, followed by intracellular ice formation, cellular dehydration, dysfunction, and subsequent death. Evidence has shown that frostbite and burn injuries share similar patterns of endothelial damage, edema, and inflammatory mediator release.
Frostbite has traditionally been categorized, like burns, by severity—although new classification schemes have more recently been proposed to better reflect prognosis. First-degree injury is typified by white or yellow skin accompanied by localized erythema and numbness. Superficial blisters are seen in second-degree injury, and deeper, blood filled blisters are seen in third-degree injury. Fourth-degree injury involves the deeper tissues, including muscle and bone. Regardless of the ultimate degree of severity, frostbite generally presents with a cold, initially numb, edematous affected area. Pain subsequently develops with rewarming. The extent of eventual tissue loss is poorly correlated to the affected area’s clinical appearance. Several weeks are needed to determine the ultimate extent of any tissue loss.19
Field treatment of frostbite depends, to a great extent, on circumstances. The most important factor when making the decision to initiate the thawing of a frostbitten area is the likelihood of refreezing. Patients with short transport times should have wet clothing removed from the frostbitten area, but thawing efforts should generally be left for hospital staff to initiate. Patients with very long transport times, particularly in the aeromedical setting, may benefit from rewarming efforts so long as refreezing of the affected area can be prevented. Once in the ED, rapid rewarming, best done by immersing the affected area in a water bath at 104°F-108°F, is recommended. Analgesia and indicated tetanus prophylaxis are mandatory. Most literature promotes the use of inflammatory cascade inhibitors, such as aspirin and ibuprofen, to control thrombosis and tissue loss.20
Most small emergency departments can manage the initial treatment of severe frostbite. Once rewarming efforts have been initiated, subsequent management, including transfer for treatment and rehabilitation in specialized trauma units should be considered. Admission for all but the most trivial frostbite should be considered given the significant functional loss that can accompany this injury.
Mild hypothermia can be managed at most emergency departments. With severe hypothermia, transport to a center capable of initiating active internal warming should be considered. In such a case, the benefits of advanced-level ED care need to be weighed against the risks of prolonged ambulance transport.
Trench foot describes tissue damage caused by cold temperatures above freezing. Unlike frostbite, these injuries do not involve cellular freezing. Often an underdiagnosed injury, trench foot, like its cousin immersion foot, is caused by prolonged exposure to wet, cold conditions. Classically this condition has been described in soldiers who wear wet boots for prolonged periods, but has also been described in shipwreck survivors and in the homeless.21 Trench foot is primarily caused by profound vasoconstriction and sympathetic response caused by prolonged cold exposure and decreased blood flow to the affected extremities. Endothelial damage and capillary leakage result. Eventual amputation is a possible outcome.
Like frostbite, trench foot presents with pallor, edema, and loss of sensation. Because of the profound vasoconstrictive nature of this injury, decreased capillary refill, and severe pain remain hallmarks. Like frostbite, trench foot can result in significant tissue damage and long-term loss of function.22
The primary goal of therapy for trench foot is the preservation of viable tissue. Rapid rewarming is thought to result in a sharp increase in tissue oxygen consumption. For this reason, rapid rewarming is avoided. Little recent data concerning optimum management of this condition are available: Best evidence suggests that affected extremities should be kept dry and slightly cooler than room temperature to reduce distal metabolic demand.23,24
When exposed to high temperatures, the body will attempt to dissipate excess heat through a range of thermoregulatory mechanisms. When the capacity of these mechanisms is overcome, heat-related illness occurs. Body heat is generated via basal metabolism, by exertion, and via exposure to the sun, hot objects, and warm ambient temperatures.25 Excessive heat is toxic to cells and causes the release of inflammatory proteins. High temperatures denature proteins, interrupt cellular processes, and cause cell death.26,27 The term heat-related illnesses refers to a range of conditions, including heat exhaustion, heat cramps, and both classic and exertional heat strokes.
Humans are able to regulate their core temperatures via autonomic processes which modify the rates of heat production (shivering and changes to basal metabolism) and by heat loss (sweating and vasoconstriction/dilatation). Behavioral modification also serves a role in controlling temperature. When thermoregulatory mechanisms can no longer compensate for excessive heating, heat illness develops. Depending on the degree and duration of heat exposure, illness along a continuum of severity may occur.
Heat transfer, as in cases of hypothermia, can only occur via four processes: radiation, convection, evaporation, and conduction. At cool temperatures, radiation accounts for the bulk of heat loss. Evaporation is the second most important means of heat transfer. Conduction (the transfer of heat from the skin to the air) is relatively inefficient although convection, caused by the movement of air over the skin surface, improves this process.28 At higher temperatures, the body can no longer radiate heat to the environment and evaporation becomes increasingly important for heat transfer. As humidity increases, evaporative heat loss decreases. For this reason, a combination of high temperature and high humidity can overcome the two main physiologic mechanisms that the body uses to dissipate heat.
Age extremes are a well-appreciated risk factor for the development of heat-related illness. The elderly are more susceptible to heat stroke because of decreased sweating ability and decreased cardiovascular capacity to distribute blood flow to the skin.29 In children, basal metabolic rate is higher than that of adults.
Medications can contribute to the development of heat-related illness by either increasing the amount of basal heat production (thyroid hormone, amphetamines, tricyclics) or by decreasing the effectiveness of heat loss mechanisms (most anticholinergics and antihistamines).30
Clearly, exposure to warm, humid climates places individuals at risk for heat-related illness. Certain populations, including professional and amateur athletes, military members, and outdoor enthusiasts are at risk for developing heat illness due to their exposure to the warm climates. Many members of these groups are often unwilling to modify their activities to suit warm ambient conditions.31
Patients with certain preexisting conditions are at risk for developing heat illness. Patients with endocrine abnormalities, illnesses causing dehydration, fatigue, sleep deprivation, and cardiovascular disease all have decreased abilities to respond to heat stress. The presence of obesity and lack of physical conditioning also contribute to the risk.
Heat exhaustion occurs when salt, free water, or both is depleted through exposure to hot conditions. Patients with heat exhaustion may present with headache, nausea, malaise, and dizziness.32 Their temperature may be normal or slightly elevated, but, unlike heat stroke, there are no central nervous system symptoms.
Heat stroke represents the most severe manifestation of heat-related illness. It is a life-threatening emergency with high mortality if not promptly treated. Heat stroke can be divided into two categories, which differ by affected population and by presentation: These are classic and exertional heat strokes. Both forms present with hyperthermia (>40°C) and altered mental status and both are caused by heat leading to edema and destruction of tissue.33,34
Classic heat stroke is often seen in older adults and the chronically ill during heat waves. It often occurs in the form of epidemics. Compared to exertional heat stroke, classic heat stroke often occurs over days and is notable for its significant abnormalities in fluids and electrolytes.34 In contrast, exertional heat stroke usually occurs when excess heat generated by muscular exercise exceeds the body’s ability to disperse it. This form of heat stroke is commonly seen in athletes and in the young. Soldiers, particularly those at the beginning of training, are at high risk for this condition.
Both forms may present with prodromal dizziness, weakness, confusion. CNS symptoms seen in heat stroke include irritability, confusion, hallucinations, seizures, and coma.
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