Environmental Injuries: Hypothermia, Frostbite, Heat Illness, and Altitude Illness

Brian V. Reamy

HYPOTHERMIA

Epidemiology

Individuals younger than 2 years of age and older than 60 years of age are most at risk.
Increasing homelessness and sports activities in inclement environments have contributed to an increased incidence of hypothermia in the past decade.
Risk factors include the use of intoxicants, psychiatric illness, medical illnesses, sleep deprivation, dehydration, malnutrition, and trauma. Impaired judgment resulting from psychiatric illness or the use of ethanol is the most common predisposing factor (8).

Pathophysiology

The body combats the fall in core temperature through shivering thermogenesis and increased gluconeogenesis. When the core temperature drops below 35°C, the victim becomes poikilothermic and cools to the ambient temperature.
Central nervous system (CNS) function is directly depressed by the cold. The electroencephalogram (EEG) becomes abnormal below at temperature of 33.5°C (92.5°F) and silent at 19°C (66°F) (4).
Initial reflex tachypnea continues until core temperature falls below 30°C (86°F). Failure of brainstem control of respiratory drive and the freezing of the thoracic musculature eventually lead to a cessation of breathing.
Cold triggers peripheral vasoconstriction and tachycardia.
Below 34°C (93°F), bradycardia, hypotension, decreased cardiac output, and a lengthening of cardiac electrical conduction ensue. A J-wave (Osborn hypothermic hump) may be noted at the QRS-ST junction. The myocardium becomes increasingly irritable, and spontaneous atrial and ventricular dysrhythmias can occur (4).
Below 28°C (82°F), ventricular fibrillation can develop with minor stimuli, such as removing a patient’s wet clothing or ambulance transport.

Clinical Features

Nonspecific symptoms and signs predominate and mimic the effects of mild dementia or ethanol intoxication. The CNS effects of cold lead to impaired memory and judgment, slurred speech, and decreased alertness. Paradoxic bradycardia and hypoventilation occur despite hypotension. Multiple cardiac dysrhythmias develop as the core temperature falls. A cold-induced ileus, abdominal spasm, and rigidity can mimic an acute abdomen.

Diagnosis

An accurate core temperature is crucial and is ideally obtained with a rectal thermistor probe. At a minimum, a rectal temperature obtained with a thermometer scaled for hypothermia is required. Oral and ear temperatures are grossly inaccurate. A core temperature above 35°C can rapidly exclude hypothermia.
Hypothermia is classified as mild, moderate, or severe based on the core temperature (Table 42.1).
Common laboratory findings include a falsely elevated hematocrit caused by dehydration, a low leukocyte count caused by sequestration, hyperamylasemia resulting from pancreatic injury, an aberrant coagulation profile, hypokalemia, and hypoglycemia caused by glycogen depletion. Below 30°C, insulin is rendered inactive, and a paradoxic hyperglycemia can ensue.

Treatment

Field treatment should focus on gentle handling of the victim, so as to not cause cardiac dysrhythmias. Wet clothing should
be removed and dry clothing or a blanket applied. Massage of cold-injured limbs should be avoided; it can damage fragile, frozen parts and trigger dysrhythmias. Traumatic injuries to the spine or limbs should be stabilized.

Table 42.1 Hypothermia Severity and Treatment

Temperature	Clinical Features	Treatment
Mild
35°C/95°F	Maximum shivering	Passive external
33°C/91°F	Ataxia, apathy, tachypnea	Rewarming Passive external Warming
Moderate
32°C/90°F	Stupor, shivering stops	Active core rewarming (± active external rewarming)
Severe
28°C/82°F	Decreased ventricular fibrillation threshold, hypoventilation	Active core rewarming
14°C/57°F	Lowest adult accidental hypothermia survival	Active core rewarming
9°C/48°F	Lowest therapeutic survival	Active core rewarming

An airway should be maintained and cardiac monitoring begun if available. If the skin is frozen, needle electrodes should be used or can be fashioned by passing a 20-gauge needle through an electrode pad into the frozen skin. If the patient is alert, warm, noncaffeinated beverages can be provided. Fluid resuscitation with intravenous (IV) 5% dextrose in normal saline (D5NS) should be started. Lactated Ringer’s should be avoided because of problems with the metabolism of lactate by a cold-injured liver.
Emergency room treatment should focus on rewarming of the patient. Defibrillation is generally limited to 1 counter-shock until the core temperature is raised above 30°C (86°F) (level of evidence [LOE] B, nonrandomized clinical trials; Emergency Cardiovascular Care Guidelines of the American Heart Association [AHA], 2010) (3). It may also be reasonable to perform defibrillation attempts concurrent with rewarming regardless of core temperature (Class IIb, LOE C, AHA advanced cardiac life support [ACLS] guidelines, 2010) (3). Medications may be less effective with severe hypothermia, but it is not unreasonable to consider use of vasopressors according to standard ACLS algorithms (Class IIb, LOE C, AHA ACLS guidelines, 2010) (3).
Passive external rewarming (PER) by covering the victim with a blanket or wrap is ideal in an alert patient whose core temperature is greater than 32°C (90°F).
Below 90°F, rewarming should proceed with active core rewarming (ACR) concurrent with active external rewarming (AER). ACR can be accomplished with IV D5NS warmed to 40-42°C (104-108°F) or the inhalation of humidified oxygen warmed to 104-108°F. More invasive techniques include peritoneal lavage with dialysate warmed to 104-108°F, thoracic lavage with normal saline at 104-108°F, or warming of the gastrointestinal tract with gastric/colonic lavage (LOE C).
AER (fires, hot water bottles, and heating pads) should be employed when ACR has already begun to avoid the life-threatening risk of core temperature afterdrop. This devastating process occurs when sudden exposure of vasoconstricted cool extremities to AER causes peripheral vasodilatation, a drop in central blood pressure, and a sudden influx of cool blood from the periphery to the core that can trigger dysrhythmias and shock (4). Table 42.1 provides an overview of hypothermia severity and ideal treatment modalities (4).

Prevention

Good conditioning, proper nutrition, experienced leadership in backcountry environments, normal hydration, avoidance of ethanol or tobacco and habituation to the cold environment (both physiologic and behavioral), and the use of proper clothing help prevent hypothermia (6).
Clothing choice centers on the 3 Ls: layered, loose, and lightweight. A waterproof outer layer is key. If exercise is occurring in a temperature of < 0°F, three-layered hand and footwear are optimal for the prevention of frostbite.

FROSTBITE

Epidemiology

Frostbite is most common in active individuals from 30-49 years of age. High-risk outdoor activities in inclement environments account for a large percentage of injuries.
Risk factors for frostbite are shown in Table 42.2. Ethanol and psychiatric problems underlie up to 70% of most cases of frostbite. The need for amputation correlates more with the duration of cold exposure rather than the lowness of the temperature. This explains why the impaired judgment resulting from ethanol use and psychiatric illness account for such a large percentage of injuries.
Anatomic sites of injury include the following, in order of most common occurrence: feet and hands (90% of all frostbite), ears, nose, cheeks, and the penis (a particular concern for runners).

Table 42.2 Risk Factors for Frostbite

Predisposing Factors
Behavioral	Organic
Ethanol use	Prior cold injury
Psychiatric illness	Wound infection
Motor vehicle problems	Atherosclerosis
Homelessness	Diabetes mellitus
Smoking	Fatigue
Improper clothing
High-risk outdoor activities (back-country skiing/mountaineering)