Frostbite and hypothermia case file

Frostbite and hypothermia case file

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 42

A 44-year-old undomiciled man is found on a park bench in the middle of winter. He is cold and wet from the falling snow. A concerned citizen called EMS to transport the patient to the Emergency Department. The patient is minimally arousable and his clothes are soaked from the waist down. A pack of cigarettes and a small bottle of whiskey are found in his jacket pocket. On examination, he is thin, disheveled, malodorous, and his extremities are pale and cold. His blood pressure is 110/70 mm Hg, heart rate is 90 beats per minute and irregular, respiratory rate is 18 breaths per minute, and his rectal temperature is 30°C (86°F). There is no evidence of trauma and the patient is not shivering.

⯈ What is your next step?

⯈ What is the most likely diagnosis?

⯈ What is your next step in treatment?

ANSWER TO CASE: 42

Frostbite and Hypothermia

Summary: A 44-year-old undomiciled man with poor nutrition and a history of ethanol abuse and cigarette smoking was exposed to freezing temperatures and now has a decreased level of consciousness. The patient has an irregular heart rhythm, likely atrial fibrillation. He is not shivering and his rectal temperature is 30°C (86°F).

• Next step: Transfer to the ED and prevent further systemic heat loss. Remove any wet or constrictive clothing. Wrap the patient in warm, dry blankets. The affected areas should be immobilized, insulated, and kept away from dry heat sources
• Most likely diagnosis: Cold exposure injury leading to frostbite and hypothermia
• Next step in treatment: Rapid core rewarming

ANALYSIS

Objectives

1. Recognize the spectrum of cold exposure injuries.
2. Understand the pathophysiology of frostbite and hypothermia and how it affects various organ systems.
3. Know the treatments for frostbite and hypothermia.

Considerations

Accidental hypothermia is a multifaceted entity encompassing a range of clinical features. Frostbite occurs when the skin and body tissues are exposed to cold temperature for a prolonged period of time. To minimize soft tissue injury in this patient, the rewarming process should not be delayed. Evaluation of core body temperature is necessary to determine if hypothermia exists and to what degree. Once his wet and constrictive clothing are removed, passive rewarming techniques can be used to increase the core body temperature. Individuals who are at greatest risk for hypothermia include the elderly, diabetics, smokers, alcoholics, people with peripheral vascular disease, peripheral neuropathy, Raynaud disease, and those who are exposed to windy weather, which increases the rate of heat loss from skin.

Approach To:

Frostbite and Hypothermia

DEFINITIONS

HYPOTHERMIA: Condition in which the core body temperature drops below that required for normal metabolism, which is less than 35°C (95°F).

FROSTNIP: Deposition of superficial ice crystals on the skin. It can be a warning sign for impending frostbite. Typically it is a retrospective diagnosis because it is defined by the absence of tissue damage upon rewarming.

FROSTBITE: Occurs when the skin tissue freezes. Superficial frostbite involves the skin; whereas deep frostbite involves deeper structures such as muscle, tendon, and bone.

TRENCH FOOT: Results from prolonged exposure of the extremities to a cold, wet environment, without freezing. Prolonged exposure to this environment leads to decreased peripheral circulation. This was a common condition in trench warfare during World War I.

CHILBLAINS (PERNIO): A nonfreezing cold-related injury that occurs in cool, humid environments. It is characterized by red, scaly lesions, often on the face, hands, or feet.

CLINICAL APPROACH

Physiology

The human cold response is aimed at maintaining the core body temperature and the viability of the extremities. The skin’s thermoreceptors are densest on the upper torso. These peripheral thermoreceptors signal a central thermostat, located in the preoptic region of the anterior hypothalamus to activate autonomic as well as behavioral heat loss and gain mechanisms. Peripheral cooling of the blood leads to a cascade of events including catecholamine release, thyroid stimulation, shivering thermogenesis, and peripheral vasoconstriction. Heat loss is reduced by peripheral vasoconstriction mediated by sympathetic stimulation and catecholamine release. By using stored glycogen, shivering thermogenesis can provide several hours of heat, however once glycogen stores are depleted shivering stops. The extremities are protected by the hunting reaction, which consists of irregular, 5- to 10-minute cycles of alternating periods of vasodilation and vasoconstriction that protect the extremities against sustained periods of vasoconstriction. If the body is exposed to cold of prolonged duration or magnitude and the core body temperature is threatened, this mechanism is abandoned—the so-called life-versus-limb mechanism. Once the body has physiologically lost the ability to compensate for the cold, injury is inevitable. The physiologic consequences of cold injury are thus considered by a systems approach.

Heat loss occurs through four basic mechanisms: conduction, convection, radiation, and evaporation. Conduction occurs through heat transfer from the warmer body to a cooler object; in a wet environment, this occurs at a much greater rate. Convection is the transfer of heat from movement, where wind acts as a confounding

factor that draws heat away from the body. Radiation is heat transfer by electromagnetic waves from the noninsulated areas on the body. Evaporation of water leads to heat loss through exhalation of warm air.

There are many predisposing factors for the development of hypothermia (see Table 42–1). These can be generalized into four overlapping categories: disrupted circulation, increased heat loss, decreased heat production, and impaired thermoregulation.

Two high-risk populations include individuals who consume ethanol and the elderly. Ethanol use predisposes to hypothermia in many ways. First, it impairs judgment and thermal perception, therefore, increasing the risk to cold exposure. Ethanol predisposes to hypoglycemia, impedes shivering (ie, lack of fuel interferes with shivering), and causes peripheral vasodilation (ie, increases heat loss). In addition, ethanol’s affect on the hypothalamus results in a lower thermoregulatory set point, resulting in a reduction of the core temperature. The elderly exhibit age-related impairments in many of the systems of thermoregulation. The elderly often have an impaired shivering response, decreased mobility, and malnutrition. They are less able to discriminate cold environments and often lack the ability to vasoconstrict adequately. Their risks are also increased secondary to their medications, particular cardiac medications, which may impede thermoregulation. The risk of falls is increased in the elderly. It is also critical to rule out sepsis as the cause of hypothermia in the elderly; particularly hypothermic individuals who are found indoors. For systemic effects of hypothermia, see Table 42–2.

Abbreviations: BP = blood pressure; CT = computed tomography; EEG = electroencephalogram.

Cardiovascular

Cardiovascular complications are common throughout the spectrum of cold injury. Initially during mild cold stress, tachycardia is noted, as temperatures decline, the response of the cardiovascular system shifts from tachycardia to progressive bradycardia that is refractory to atropine. A multitude of cardiac dysrhythmias are seen in hypothermia with atrial fibrillation being the most common. The Osborn or J wave is a well-known manifestation of hypothermia seen on ECGs (see Figure 42–1). It is characterized by elevation at the junction of the QRS complex and the ST-segment and is typically seen at temperatures below 32°C (89.6°F). As temperatures drop below 28°C (82.4°F), ventricular fibrillation occurs. As the core body temperature drops so does oxygen consumption. It is thought that in some people this decline in oxygen consumption may explain why profoundly hypothermic patients have been successfully resuscitated.

Figure 42–1. The J (Osborn) wave (arrows) appears on electrocardiograms of approximately 80%

of hypothermic patients. In general, the amplitude and duration of the Osborn wave are inversely

related to core temperature. (Reproduced, with permission, from Hall JB, Schmidt GA, Wood LDH,

eds. Principles of Clinical Care. 3rd ed. New York, NY: McGraw-Hill; 2005:1681.)

Respiratory

Initially in response to cold, respirations increase and similarly to the cardiovascular system with continued cold exposure the hyperactivation of the system begins to slow down. Respiratory depression occurs with resultant respiratory acidosis from carbon dioxide retention. Protective airway mechanisms are impaired due to decreased ciliary motility, bronchorrhea, and thickening of respiratory secretions.

Renal

Mild dehydration and hypotension cause a decrease in renal blood flow and glomerular filtration rate. However, central hypervolemia from peripheral vasoconstriction, inhibition of ADH, impaired renal tubular function, and the loss of concentrating abilities result in large-volume cold diuresis.

Gastrointestinal

Poor perfusion to the liver results in the inability to clear toxins, the retention of lactate, and the formation of a metabolic acidosis.

Neurological

As temperature declines, an individual’s level of conscious also declines. Pupillary light response and deep tendon reflexes also decline while muscular tone tends to increase.

Hematologic

Hypothermia leads to many hematologic changes. The most common include a progressive hemoconcentration of the blood resulting in an increase in hematocrit. In addition, low temperature inhibits enzymatic reactions of the clotting cascade, leading to a progressive coagulopathy.

Figure 42–2. ECG shows J waves in a hypothermic patient. (Reproduced, with permission, from Knoop KJ,

Stack LB, Storrow AB. Atlas of Emergency Medicine. 2nd ed. New York, NY: McGraw-Hill; 2002:516.)

FROSTBITE

Maintenance of core temperature takes precedence over rewarming of the extremities. When the body is exposed to a magnitude or duration of cold that is significant enough to disrupt the core body temperature, continuous and intense vasoconstriction occurs, promoting frostbite to the exposed tissue. Frostbite occurs when tissue temperatures are less than 0°C (32°F). There are two mechanisms for tissue damage: architectural cellular damage from ice-crystal formation and microvascular thrombosis and stasis. The initial phase of frostbite, the “prefreeze phase,” is characterized by tissue temperatures dropping below 10°C (50°F), and cutaneous sensation being lost. There is microvascular vasoconstriction and endothelial leakage of plasma into the interstitium. Crystal formation does not occur until tissue temperatures drop below 0°C (32°F). Areas of skin that experience a slow rate of cooling will develop ice crystals in the extracellular matrix, whereas cells that undergo rapid cooling develop intracellular ice crystals, the latter of which is less favorable to cell survival. During the freeze–thaw phase, extracellular ice crystals form. In an attempt to maintain osmotic equilibrium, water leaves the cells causing cellular dehydration and intracellular hyperosmolality. This leads to cellular collapse and demise. The third phase is the progressive microvascular collapse phase. Red cells sludge and form microthrombi during the first few hours after the tissues are thawed. The exact mechanism is unclear. Hypoxic vasospasm, hyperviscosity, and direct endothelial damage all adversely affect flow. Ultimately, there is plasma leakage and arteriovenous shunting resulting in thrombosis, increased tissue pressure, ischemia and necrosis also known as the late ischemic phase. In superficial frostbite, clear vesicles may appear, whereas hemorrhagic blisters appear in deep frostbite injuries.

MANAGEMENT

The ultimate goal of prehospital treatment is preservation of life. Frostbite and hypothermia often coexist and prevention of further systemic heat loss is the priority. Field rewarming should not be performed if there is any potential for interrupted or incomplete thawing, unless the possibility of evacuation does not exist, because tissue refreezing is disastrous. However, it is appropriate to remove wet, constricting clothing and replace with dry clothing. There is a direct relationship between the length of time the tissue is frozen and the extent of cellular damage.

As with all patients who present to the ED with serious conditions, evaluation and stabilization occurs simultaneously and the ABCs should always be promptly addressed. The patient should be placed on a cardiac monitor and have an intravenous catheter placed. Once this occurs, a thorough history should be obtained including ambient temperature, wind velocity, duration of exposure, type of clothing worn, medication history, and preexisting medical problems that could affect heat loss. A core temperature needs to be determined. This is best achieved by obtaining a rectal temperature. Most standard hospital thermometers only read as low as 34°C (93.2°F). Therefore, in patients suspected to be hypothermic, it is critical to measure core temperature using a specialized thermometer that is capable of reading low temperatures.

Diagnostic studies that may be useful include a bedside capillary blood glucose. Correcting hypoglycemia early in presentation may prevent the need for more invasive rewarming techniques. As temperature declines, pulse oximetry may not be reliable, so an arterial blood gas can determine oxygen saturation. An ECG should be obtained to evaluate cardiac dysrhythmias including atrial fibrillation. Laboratory studies may reveal an elevated hematocrit secondary to hemoconcentration, and low platelet counts due to splenic sequestration. Hyperkalemia is indicative of cellular acidosis and is a marker for a poor prognosis. Elevation in the blood urea nitrogen (BUN) and creatinine (Cr) is commonly encountered in hypothermic patients. Low thyroid and cortisol levels may reveal a person predisposed to hypothermia. A high index of suspicion must be maintained for an occult traumatic injury as trauma and hypothermia commonly occur together. Consider a head CT scan and other radiographic studies on patients who have an altered mental status or who do not improve with rewarming.

After stabilizing the core temperature and addressing associated conditions, rapid thawing should be initiated. The core temperature will continue to fall even after the patient is extricated from the cold environment due to temperature equilibration between the core and peripheral blood. Most patients are dehydrated. Warm intravenous fluids (crystalloid) should be administered. For frostbite, rapid rewarming of frozen or partially thawed tissue is accomplished by immersion in gently circulating water that is carefully maintained at a temperature of 37°C to 41°C (99°F-106°F). Rewarming is continued until the tissue is pliable and distal erythema is noted, usually about 10 to 30 minutes. Active, gentle motion is encouraged but direct tissue massage should be avoided. Parenteral analgesics should be administered because tissue rewarming causes throbbing, burning pain, and tenderness. Sensation is often diminished after thawing and then disappears with bleb formation. Sensation does not normalize until healing is complete.

After thawing, the injured extremities should be elevated to minimize swelling. Sterile dressings should be applied and involved areas handled gently. Digital exercises are encouraged to help avoid venous stasis. Treatment also includes NSAIDs, topical aloe vera, debridement of clear blisters (hemorrhagic blisters should be left alone), and tetanus vaccine if indicated. Antibiotics are also often given. In cases of gangrene, amputation is often delayed for up to 3 weeks, because the extent of tissue injury is difficult to initially assess.

Based on the severity of hypothermia, various rewarming schemes are followed. These include passive rewarming, active external rewarming for moderate hypothermia, and active core rewarming in severe hypothermia.

Passive external rewarming allows patients to warm by endogenous heat production. This requires the ability to shiver. Individuals who are malnourished, hypoglycemic, or have a core temperature below 30°C are not candidates for passive external rewarming. Therefore, this is a good option in healthy patients with a mild degree of hypothermia. The patient should be removed from the cold or wet environment, and be wrapped in blankets, sleeping bags, or other insulating materials.

The decision to actively rewarm a patient implies a greater degree of hypothermia and possibly a coexisting medical condition. Active external rewarming involves the application of heat directly to the skin by way of forced air surface warming, warm water immersion, radiant heat sources, and warm water bottles. In the hospital setting, forced air rewarming is most practical.

Active core rewarming refers to techniques that warm the patient from the inside out and are used to rewarm severely hypothermic patients. There are several methods used in active core rewarming including positive pressure ventilation using warm air, peritoneal and pleural irrigation with warmed saline, and extracorporeal blood rewarming. These methods are reserved for severely hypothermic patients and those presenting with cardiac arrest.

Hypothermic patients may experience complications secondary to rewarming. Afterdrop refers to the continual decline in core body temperature after the patient is removed from the cold environment. The current theory holds that rewarming causes disequilibrium across a gradient such that the body is cooled from the periphery to the inside and the core body temperature will continue to drop until core temperature is equal to peripheral temperature. This was thought to predispose to ventricular fibrillation. However, there is little evidence to support this. Nonetheless, ventricular fibrillation is typically resistant to defibrillation until core temperatures are above 28°C (82.4°F).

For patients who are pulseless and show no signs of life, death pronouncement only occurs when the individual’s core body temperature is greater than 35°C. Since the physiologic response to hypothermia is extremely varied, the well known adage, “no one is dead until they are warm and dead” is often valid.

COMPREHENSION QUESTIONS

42.1 A 72-year-old woman with dementia is reported missing by nursing home staff late one December night. The patient was found 2 hours after the police were called lying on a park bench, soaking wet, in a thin night gown with no shoes on. EMS has arrived on the scene. Which of the following is the most appropriate next step in management?

A. Check capillary blood glucose and try to feed the patient.

B. Immediately place the patient on a stretcher, start an IV, and give fluids.

C. Check for airway, breathing, circulation, and then maintain core body temperature by removing wet clothes and wrapping in warm, dry blankets.

D. Cover the patient with any available materials so that passive rewarming can start.

42.2 An avid outdoorsman was hiking in the mountains when his boot broke through the ice on the edge of a stream submerging one foot. The patient has a long history of diabetes with known peripheral neuropathy. He was able to hike out to the ranger’s station but had lost complete sensation of his wet foot afterwards. The patient has frostbite on his cheeks, hands, and this wet foot shows evidence of trench foot. All wet clothing is removed, he is wrapped in blankets and on arrival to the emergency department, his vitals signs are stable except for a core body temperature of 34°C. Which of the following is the most appropriate next step in management?

A. Initiate extracorporeal blood warming until a core temp of 37°C is reached.

B. Begin rapid rewarming with water 40°C to 42°C (103°F-104°F).

C. Rub the skin dry where there is evidence of trench foot to decrease the chance of blisters developing.

D. Treat the patient’s diabetes and peripheral neuropathy then reassess sensation in each extremity.

42.3 A 14-year-old adolescent boy wandered into the woods chasing after his dog and lost his bearings. When he was finally found, he was brought to the ED with severe frostbite of the fi ngers of both hands. Initially, they appeared very blue, but are beginning to look black. He has not regained sensation 24-hours after the exposure. Which of the following describes the most appropriate time to wait before deciding on amputation of the affected fi ngers?

A. 24 hours after the episode

B. 48 to 72 hours after the episode

C. 3 to 7 days after the episode

D. 7 to 10 days after the episode

E. 2 to 3 months after demarcation

42.4 An undomiciled man of unknown age presents to the ED unresponsive. Bystanders believe he was outside all night in a snow storm. His core temperature is 30°C. What is the most common cardiac dysrhythmia seen in hypothermia?

A. Sinus tachycardia

B. Sinus bradycardia

C. Ventricular fibrillation

D. Atrial fibrillation

E. Prolonged QT syndrome

42.5 A 35-year-old undomiciled woman, with a history of schizophrenia, presents to the ED complaining of tingling in her fingers. The nursing staff removes her wet clothes and places her in a warm hospital gown. Her vital signs include a blood pressure of 130/75 mm Hg, heart rate of 80 beats per minute, and temperature of 36.05°C (96.9°F). On examination, you note discolored, frostbitten hands. Which of the following features is a poor prognostic indicator in frostbite?

A. Hemorrhagic blisters

B. Demarcation line of viable tissue

C. Clear fluid-filled blisters

D. Edematous subcutaneous tissue

ANSWERS

42.1 C. The first step in emergency care is always to address and stabilize the airway, breathing, and circulation (ABCs). Passive rewarming methods are appropriate including removing wet clothing. It is critical that rapid rewarming be avoided if the patient may be delayed to receiving definitive care. Incomplete thawing and refreezing is detrimental to tissue. Checking a blood glucose is important in a patient with altered mental status but should be done after ABCs are addressed.

42.2 B. Rapid rewarming in the field is rarely practical, however, in the Emergency department it should be started as soon as possible. It is critical to avoid the deleterious effects of incomplete thawing and prevent refreezing. Although comorbid conditions such as diabetes influence the management of a hypothermic patient, the patient’s lack of sensation is due to cold injury and this should be rapidly treated, not just treating the diabetes.

42.3 E. Generally, 3 weeks is the minimum time required to assess the viability of tissue after frostbite to see whether amputation is required. Tissue thought to be necrotic sometimes turns out to be viable. The line of demarcation between viable and nonviable tissue becomes clear in 1 to 2 months after the initial cold injury, but surgery may be delayed until 2 to 3 months.

42.4 D. Atrial fibrillation is the most common dysrhythmia in hypothermia and is characteristically seen at a core temperature of 30°C. Prolongation of any interval, bradycardia, asystole, atrial fibrillation/fl utter, and ventricular tachycardia may also be seen. In this patient a 12-lead ECG was obtained showing an Osborne (J) wave, which is indicative of a junctional rhythm and is consistent with hypothermia. J waves may be seen at any temperature below 32.2°C (89.9°F), most frequently in leads II and V6. Below a core temperature of 25°C (77°F), they are most commonly found in the precordial leads (especially V3 and V4) and their size increases. J waves are usually upright in aVL, aVF, and the precordial leads.

42.5 A. Hemorrhagic blisters are a poor prognostic indicator due to their association with deep tissue injury. These blisters should not be debrided or drained because it leads to tissue desiccation and worsening of the injury. Clear blisters, on the other hand, should be drained because the fluid contains thromboxane, which is thought to be destructive to healthy tissue. A demarcation line of healthy tissue is a late sign in hypothermia. Edematous soft tissue is not a prognostic indicator in frostbite.

CLINICAL PEARLS

⯈ Because hypothermia and frostbite often occur simultaneously, prevention of further systemic heat loss is the highest priority.

⯈ Field rewarming is rarely warranted because of the potential for incomplete or interrupted rewarming. Injured parts should be protected, core temperature stabilized and patient transferred to the ED for rapid rewarming. A rewarming bath should be maintained at a temperature of 37°C to 41°C (98.6°F-105.8°F).

⯈ Standard hospital thermometers only read as low as 34°C (93°F), so a specialized low-temperature thermometer is required to obtain an accurate core body temperature.

⯈ A severely hypothermic patient can present with rigidity, asystolic, and with fixed pupils; however, he or she should not be pronounced deceased until the core body temperature has been warmed to at least 35°C (95°F).

⯈ Hypoglycemia, sepsis, and hypothyroidism are conditions that may mimic or coexist with hypothermia.

⯈ Ethanol abusers and the elderly are at high risk for cold-exposure injuries.

References

Ahya SN, Flood K, eds. The Washington Manual of Medical Therapeutics, 33rd ed. St Louis, MO: Lippincott Williams & Wilkins; 2010. 

Aslam AS, Aslam AK, Vasavada BC, Khan IA. Hypothermia: evaluation, electrocardiographic manifestations, and management. Am J Med. 2006;199:297-301. 

Bessen HA, Ngo B, Hypothermia. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011. 

Danzl DF. Frostbite. In: Rosen P, Barkin R, eds. Emergency Medicine, Concepts and Clinical Practice. 7th ed. Philadelphia, PA: Mosby; 2009. 

Danzl DF. Accidental hypothermia. In: Rosen P, Barkin R, eds. Emergency Medicine, Concepts and Clinical Practice. 7th ed. Philadelphia, PA: Mosby; 2009. 

Hermann L, Weingart S. Hypothermia and other cold-related emergencies. Emerg Med Pract. 2003;5(12):1-22. 

Ikaheimo TM, Junila J, Hirvonen J, Hassi J. Frostbite and other localized cold-related injuries. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011. 

McCauley RL, Killyon GW, Smith DJ, Robson MC, Heggers JP. Frostbite. In: Auerbach PS, ed. Wilderness Medicine. 5th ed. Philadelphia, PA: Mosby Elsevier; 2007:195-210. 

Olin JW. Other peripheral arterial diseases. In: Goldman L, Bennett JC, eds. Cecil Textbook of Medicine. 24th ed. Philadelphia, PA: WB Saunders; 2011. 

Van der Ploeg GJ, Goslings JC, Walpoth BH, Bierens JJ. Accidental hypothermia: rewarming treatments, complications and outcomes from one university medical centre. Resuscitiation, 2010:1550-1555.

HomeEmergency Medicine Case FileFrostbite and hypothermia case file