Hypothermia

Hypothermia is the pathological state in which the core body temperature falls below 35^oC. Hypothermia can be further subdivided into mild (35-32^oC), moderate (32-28^oC), severe (28-20^oC) and profound (<20^oC) [1-3].

Hypothermia is classified as either primary or secondary. Primary hypothermia occurs when an otherwise healthy individual is exposed to environmental circumstances, such as adverse weather or cold water immersion that causes his/her core temperature to drop. Secondary hypothermia occurs when the drop in core temperature is secondary to a primary disease process such as alcohol intoxication, trauma or a myocardial infarct. Elderly population is prone to suffer from hypothermia due to poor mobility, altered temperature perception in addition to the environmental factors.

Epidemiology

Incidence

The incidence of hypothermia in Great Britain is estimated at 6-8 patients per 1000 patients [4]. Accurately estimating the incidence of hypothermia is extremely difficult as hospital attendances only represent the tip of the iceberg in that they reflect the more severe cases. Most cases of hypothermia occur in an urban setting and are related to environmental exposure attributed to alcoholism, illicit drug use, or mental illness, often exacerbated by concurrent homelessness. In 2020 there were 40 deaths in Scotland that involved hypothermia. Of these 40 deaths, hypothermia was the underlying cause in 4 deaths and a contributing factor in 36.[5]

Age

Primary hypothermia usually affects young males and infants. Secondary hypothermia usually affects patients who are elderly, homeless, mentally ill, victims of trauma, or have multiple co-morbidities [3]. Older adults may present with hypothermia instead of pyrexia in response to an infection.

Pathophysiology

The body maintains the core temperature between 36.5 and 37.5 by balancing heat production and heat loss. Heat is generated by cellular metabolism at a rate of 40-60 kcal of heat /square metre of body surface area. Heat production can be increased by contraction of striated skeletal muscle. Shivering can generate 2-5 times the basal heat production rate. Under normal circumstances, the majority (55-65 %) of heat loss is from radiation. Conduction and convection account for about 15% of heat loss and respiration and evaporation the remainder. The hypothalamus controls thermoregulation via increased heat conservation (peripheral vasoconstriction and behaviour responses) and heat production (shivering and increasing levels of thyroxine and adrenaline). The mechanisms for heat preservation may be overwhelmed in the face of cold stress and core temperature can drop secondary to fatigue or glycogen depletion.

Signs and Symptoms

Hypothermia affects almost every organ system.

Learning bite

All systems respond with an initial increase in activity (compensation), followed by a decrease and then eventual loss of activity (decompensation).

1. Cardiovascular system

Tachycardia and vasoconstriction, the initial response to cold stress, result in an increase in blood pressure and cardiac output.

With worsening hypothermia, bradycardia occurs, oxygen demand decreases and cardiac output falls.

Eventually, severe bradycardia, ventricular fibrillation or asystole ensues.

2. Coagulation system

Patients with moderate-to-severe hypothermia may develop a coagulopathy.

Lower temperatures adversely affect enzymes responsible for the coagulation cascade. This will not be reflected in laboratory studies such as PT or APTT, which may be normal.

Hypothermic patients will also be thrombocytopenic and may develop physiological hypercoagulability similar to DIC.

3. Central nervous system

The response to mild hypothermia starts with impaired judgment and memory.

As the severity of hypothermia worsens, slurred speech, ataxia and drowsiness develop. Patients may exhibit foot stomping and paradoxical undressing.

Finally, in severe hypothermia, coma and death result.

4. Renal system

Initially, peripheral vasoconstriction leads to relative central hypervolemia, leading to a diuresis.

More severe hypothermia results in renal failure and renal shutdown.

5. Respiratory system

The initial response to hypothermia is an increase in respiratory rate and a resultant respiratory alkalosis.

As the body cools, the respiratory rate falls and the patient develops carbon dioxide retention, respiratory acidosis and ultimately respiratory arrest.

Learning Bite

All systems respond by an initial increase in activity (compensation), followed by a decrease and then eventual loss of activity (decompensation)

Afterdrop

This is the fall in the patients core temperature after the initiation of rewarming. Although the exact mechanism for the afterdrop is somewhat controversial, the most likely explanation is the rewarming of peripheral sites and the abated vasoconstriction results in the return of cool blood to the central circulation from the peripheral circulation. Afterdrop may cause a temporary worsening of the physiological parameters and increase the likelihood of dysrhythmia or cardiac arrest. This mandates the use of core temperature monitoring in any patient with a core temperature of less than 32^oC.

Assessment in the ED

The diagnosis of hypothermia may be obvious, particularly when there is a history of severe environmental exposure, for example after a prolonged search and rescue effort in a wilderness setting. However the history may be more subtle in the elderly, housebound patient or the wet patient who has been exposed to less severe cold temperatures. These patients suffer a higher mortality rate due to the longer time to diagnosis and their predisposing age and frailty. Mild or moderate hypothermia can present with misleading symptoms, such as confusion, dizziness, chills, fatigue, hunger or dyspnoea. The patient may exhibit poor judgment, slurred speech, irritability, lassitude or altered mental status. The patient may even demonstrate paradoxical undressing in response to prolonged cold stress or a rocking motion. The slurred speech and ataxia may mimic a stroke, alcohol intoxication or high altitude cerebral oedema.

Learning Bite

Obtaining a full set of vital signs (Temperature, Pulse, Blood Pressure and Respiratory Rate) is vital in the patient with altered mental status to avoid missing subtle cases of hypothermia.

Physical Examination

All that is needed to make a diagnosis of hypothermia is a low temperature recorded on an accurate thermometer. The diagnosis can be easily missed by not obtaining a full set of vital signs on the patient or by being misled by an inaccurate tympanic or oral thermometer. If hypothermia is suspected, a core temperature should be performed to confirm the diagnosis. The diagnosis of hypothermia may also be suspected by Osborn or J waves on ECG. The upward deflection of the terminal S wave (at the junction of the QRS and the ST segment) occurs at or near 32 C. It is first seen in leads II and V6.

• Hypoglycemia (hypothalamic dysfunction secondary to glucopenia)
• Hypothyroidism
• Hypopituitarism
• Hypoadrenalism
• Hypothalamic Dysfunction (Tumor, Stroke, Infarction)
• Sedatives and Alcohol
• Sepsis
• Massive Blood Transfusion, Trauma
• Burns and Exfoliative Dermatitis

Learning Bites

Always think beyond sepsis and environmental causes of hypothermia. Think Endocrine causes!

The classic Osborn J waves can be misdiagnosed as ST elevation myocardial infarction, and can also be caused by intracranial pathology or sepsis. 1

General Approach

The severely hypothermic patient must be handled and moved extremely carefully as the hypothermic myocardium is predisposed to ventricular fibrillation (VF) on patient handling. The management of hypothermia requires initial evaluation and support of the airway, breathing, and circulation; prevention of further heat loss; initiation of re-warming appropriate to the degree of hypothermia; and treatment of complications.

The appropriate intervention depends on the severity of the hypothermia, the available resource and the clinical state of the patient. As the severity of the hypothermia increases, so to the treatment of that hypothermia should become more aggressive. Other medical factors, such as alcohol intoxication, central nervous system disease, trauma and infection should be considered and treated concurrently. Consider Parenteral Thiamine for critically ill, malnourished, alcoholics and in those with unexplained lactic acidosis. Wet or cold clothes must be removed. The patient must be placed on a cardiac monitor, have intravenous access established and active re-warming measures initiated. The general treatment of any coagulopathies is by re-warming and not the administration of clotting factors. Re-warming strategies can be divided into active versus passive and invasive versus non-invasive.

Learning Bite

Supportive measures, with a focus on the Airway, Breathing, Circulation, Disability (including Dont Ever Forget Glucose) and the removal of wet, cold clothes is the cornerstone of management

Additional Diagnostic Measures

Laboratory investigations should be driven by the clinical situation. In most cases, it would be reasonable to obtain urea & electrolytes (U&E), a full blood count (FBC), a clotting screen, an arterial blood gas, a creatinine kinase level, a blood alcohol and a urine toxicology screen. These investigations should be repeated during the rewarming phase. Some of the physiological changes seen with hypothermia would include a shift of the oxyhaemoglobin dissociation curve to the left, an increased haematocrit due to the decrease in circulating plasma volume and a low to normal white blood cell count, even in the setting of infection [8]. Arterial blood gases should not be corrected for temperature. The blood gas analyser warms the blood to 37 C and the uncorrected values for pH and PaCO2 correspond almost perfectly to normal temperature values. An uncorrected pH of 7.4 and a PaCO2 of 5.3 kPa confirm acid base balance at all temperatures. The normal respiratory response to hypothermia is hyperventilation, resulting in a respiratory alkalosis. As the hypothermia worsens, respiratory depression predominates and this results in a respiratory acidosis. In a series of 135 hypothermic patients, 30% were acidotic and 25% were alkalotic. This reflects the unpredictability of the acid-base milieu in the hypothermic patient. Imaging studies should be geared toward the clinical situation.

Learning Bite

Dont correct for hypothermia when analysing the acid-base status normal values can be assumed to meet the needs of the hypothermic tissue

Temperature Monitoring

Core temperature monitoring is important in order to assess the efficacy of the rewarming measures. This should be accomplished by the use of a continuous or serial rectal or oesophageal thermometer. The rectal thermometer may lag behind the core temperature increases due to impaction into frozen faeces. The oesophageal temperature reading may be falsely elevated when concurrent heated, humidified oxygen is being administered. It also requires the patient to be intubated.

Fluid Resuscitation

In general, the hypothermic patient is dehydrated and fluid depleted. They should therefore be given a fluid challenge of warmed 0.9% saline or preferably Dextrose-Saline as they may also be hypoglycaemic. Hartmanns solution may also be used but since the hypothermic liver cannot metabolise lactate, it is best avoided. The patient should be monitored carefully for signs of fluid overload.

Passive Rewarming

This principle allows the patients own thermogenic mechanisms to rewarm them. They should be removed from the cold environment and have wet or cold clothes removed. They can then be covered by a blanket or sleeping bag and have their head covered to reduce heat loss. This technique can be used for the patient suffering from mild hypothermia that can still generate heat by shivering.

Active External Rewarming

This involves heat added to the patient from an external source. It is the treatment of choice in mild-moderate hypothermia patients whose own thermoregulatory mechanisms are impaired. Active external rewarming may be accomplished by a variety of methods including heat packs, heat lamps, blankets, warm water immersion, warmed blankets, and forced air systems. Patients must be monitored carefully for a presumptive aftedrop caused be the return of cool peripheral blood to the central circulation. Forced air systems are one of the most widely used means of active external rewarming in current use. Forced air systems are easy to apply, allow for patient monitoring, and seem to limit afterdrop. Rates of warming with these systems approach 1.0-2.5 C/hr [2-3]. The Bair Hugger is a well-known example.

Active Core Rewarming

Patients will moderate to severe hypothermia will require active core rewarming. This comprises a variety of techniques, from simple to more complex. The simplest example of active core rewarming is the use of warmed intravenous fluids and warmed, humidified oxygen.

Fluids can be warmed to 44 C and run through a large, short intravenous cannula. Warmed humidified air/oxygen should also be heated to 42-44 C. This may require special equipment or modification to the existing heating circuit. More invasive methods of active rewarming include cavity (gastric, bladder, peritoneal and pleural) lavage using warm fluids. These methods achieve the most rapid rewarming rates, but due to there invasiveness and complexity, should be reserved for the most severe and refractory of cases including hypothermic cardiac arrest, the failure of more conservative techniques, frozen extremities and evidence of rhabdomyolyis in conjunction with other electrolyte abnormalities [8].

Extracorporeal Blood Rewarming

This is used to aggressively rewarm blood in the severely hypothermic patient who has been refractory to all other methods of rewarming. There are several methods including haemodialysis, arteriovenous, veno-venous and cardio-pulmonary bypass. The biggest advantage of this method is the speed at which the patient can be rewarmed by directly warming their blood. Additional advantages include the continual delivery of oxygenated blood to the tissues despite the absence of mechanical cardiac activity (cardiopulmonary bypass). Extracorporeal rewarming should be considered for patients without perfusion who have no documented contraindications to resuscitation, patients with severe hypothermia, and those with completely frozen extremities [7]. There are no specific criteria for placing a patient on extracorporeal rewarming, but several centres reserve it for patients with a pH >6.5, a serum potassium <10mmol/L, and a core temperature > 12 C [8].

Hypothermic Cardiac Arrest

Both establishing and treating cardiac arrest in the severely hypothermic patient can be very difficult. The treatment of VF in the hypothermic patient is controversial. The European Resuscitation Council 2010 guidelines recommend up to three defibrillation attempts, to with- hold adrenaline until the core temperature exceeds 30 C, and to double the dose frequency until the temperature is above 35 C.2. The patient should be defibrillated, if VF persists, two further shocks should be given. If a total of three shocks have been given and the patient remains in VF, further defibrillation attempts should be withheld until the core temperature is above 30 C.

Distinguishing between VF and asystole can be extremely challenging, particularly in the prehospital setting. Certain stable arrhythmias, such as atrial arrythmias, will respond to rewarming measures only and antiarrythmics should be avoided. The use of antiarrythmic medications in the hypothermic patient is highly controversial and in the small studies done so far, only bretylium has been shown to be of any benefit. Further studies are needed for validation. Once the diagnosis of cardiac arrest is established, it is unclear as to the rate and force needed for cardio-pulmonary resuscitation (CPR) in the severely hypothermic patient. The hypothermic chest wall and myocardium are stiffer and less compliant. CPR does seem to produce improved survival in the cardiac arrest patient, so the old adage should apply that no one is dead until they are warm and dead, unless the patient is cold because they are dead. CPR should continue until the patient is rewarmed to 30 – 32 C, at which point renewed attempts at defibrillation and resuscitation with Advanced Life Support medications are undertaken [6]. Cardiac Arrest secondary to Hypothermia in children may warrant prolonged resuscitation and expert consultation prior to termination of resuscitation as children may have an increased ability to tolerate and recover from hypoxic brain injury. The lowest recorded neurologically intact survival following hypothermic cardiac arrest (in this case associated with immersion) is 13.7 C [6].

Disposition

Patients with mild hypothermia who respond to passive rewarming are usually able to be discharged from the Emergency Department (ED). Patients with severe hypothermia need to be admitted to a HDU/ITU setting. Patients with moderate hypothermia are the most difficult. Their disposition will depend on the patients age, comorbid factors, social situation and response to ED treatment.

Conclusion

Hypothermia is frequently an easy diagnosis to make but it is a condition which must be considered in the setting of altered mental status, medical illness, multiple trauma patients, and poisoning cases. The treatment strategy will depend on the severity of the hypothermia. Mild hypothermia patients can be treated with passive rewarming, whereas moderate to severe hypothermia patients need for active and invasive methods to achieve rewarming. Active core rewarming should be reserved for those patients with severe and profound hypothermia who have not responded to less aggressive measures. The sequelae of hypothermia, including cardiac arrythmias should be treated with rewarming and antiarrthmic drugs are rarely needed.

Definition

Frostbite is the most common freezing condition of human tissue. It occurs whenever the tissue temperature decreases to less than 0 C [6,9,10]. Ice crystal formation damages the cellular architecture and stasis progresses to microvascular thrombi. It can be classified as either superficial or deep. Superficial frostbite affects the skin and subcutaneous tissues; deep frostbite also affects bones, joints and tendons.

Risk factors

Factors predisposing patients to frostbite can be classified into environmental and medical factors. Environmental factors include individuals stranded in cold weather, homelessness, alcohol consumption, altered mental status, exposure to water or dampness and the use of inadequate or constrictive clothing. Medical factors include malnutrition, infection, peripheral vascular disease and diabetes [11].

Mechanism and pathophysiology

Prior to the onset of frostbite, the life versus limb mechanism which is inherent to human physiology will activate to help prevent systemic hypothermia. Arteriovenous anastomoses in the skin shunt blood away from acral areas to limit radiative heat loss. As tissue temperature decreases to less than 10 C, anaesthesia develops. Endothelial cells leak plasma and microvascular vasoconstriction occurs. Crystallisation is not seen as long as the deeper tissues conduct and radiate heat. As tissue temperature continues to fall, ice initially forms extracellularly, causing water to exit from the cell and inducing cellular dehydration, hyperosmolarity, collapse and death.

History

The patient will typically complain of a coldness or firmness affecting the frostbitten area. They may also note a stinging, burning or numbness and a clumsiness of the distal extremity [12].

Physical examination

The hands and feet are most commonly affected, although the face and shins may also be involved.
Superficial Erythema, oedema, waxy appearance, hard white plaques, and sensory deficit are commonly seen.
Deep Full-thickness damage affecting muscles, tendons, and bone, with resultant tissue loss.
Other features include excessive sweating, hyperaemia and tissue gangrene.

Diagnosis

The diagnosis of frostbite is a clinical one, although imaging may help to assess severity. Routine x-ray at presentation and again at 4-10 weeks post injury may demonstrate specific abnormalities, such as osteomyelitis [13]. The imaging of choice in frostbite assessment is scintigraphy. Tc-99m (Technetium 99) pertechnetate scintigraphy is sensitive and specific for tissue injury. Some studies have shown good correlation between scintigraphy findings at 48 hours after injury and ultimate extent of deep-tissue injury [14]. In addition, scintigraphy is useful in assessing the response of damaged tissue to therapy [15].

Management

Pre-hospital Care:

Get the patient to a warm environment as soon as possible. Whenever possible pad or splint the affected area to minimize injury en route. Wet clothing should be removed and replaced by warm, dry clothing. The frostbitten area should be wrapped in a blanket for transportation to a hospital. Do not rewarm frostbitten tissue if there is a possibility of refreezing before reaching definitive care. This may result in worse tissue damage. The patient should be assessed for hypothermia. Ibuprofen 400mg orally prior to re-warming may improve tissue salvage. Do not rub frostbitten areas in an attempt to rewarm them; this can cause further tissue damage.

Learning Bite

Avoid commencing rewarming of the frostbitten extremity unless it is clear that the process will not be interrupted

Emergency Department Tissue should be rapidly re-warmed by immersion in gently circulating water that is carefully maintained at a temperature of 40-42 C by thermometer measurement [16]. Marginal tissue can be thermally injured when the water temperature exceeds 42 C. Incomplete thawing and increased tissue loss are hazards when lower water temperatures are used. Re-warming should be continued until the part feels pliable and distal erythema is noted. This usually requires 15 to 30 minutes of submersion. Active gentle motion of the part by the patient during re-warming should be encouraged, but direct tissue massage should be avoided. Reperfusion is intensely painful and parenteral analgesia is often required.

A common error is premature termination of re-warming, which results in a partial thaw. Sensation is often diminished after thawing until it disappears with bleb formation. Sensation will not return to normal until healing is complete. Clear blisters should be debrided and aloe vera applied the the affected area every 6 hours. Haemorrhagic blisters should be left infect but aloe vera should again be used topically [13]. The injured extremities should be kept elevated to minimize oedema formation. Sterile dressings should be applied and involved areas handled gently. Persistent cyanosis in the extremities after a complete thaw may reflect increased fascial compartment pressure. Because of the cold-induced anaesthesia, this and other occult soft tissue injuries are often not appreciated by the patient or physician. Tissue pressures should be monitored carefully, although decompressing escharotomies are usually not necessary during the initial treatment rendered in the ED. Tetanus prophylaxis should be considered and antibiotics are not routinely needed unless there are signs of infection, in which case Staphylococcal, Streptococcal and Pseudomonal species should be covered [17].

Further treatment should include referral to a physiotherapist at an early stage. It may be a 4-6 week period before the extent of the injury is known and surgical debridement should not be considered before then.

Disposition

The patient should be admitted if there are any features suggestive of deep frostbite. Superficial frostbite can generally be discharged from the ED with follow up at 24-48 hours and instructions to return if they experience worsening or new symptoms.

Favorable prognostic factors include retained sensation, normal skin color and clear rather than cloudy fluid in the blisters, if present. Poor prognostic features include nonblanching cyanosis, firm skin and dark, fluid-filled blisters. However, no prognostic features are entirely predictive, and weeks may pass before the demarcation appears between viable and nonviable tissues. Long term sequelae of fronstbite may include intermittent pain and numbness, ulceration, hyperhydrosis or anhydrosis. The patient may also experience vasomotor problems, osteoporosis, muscle atrophy and phantom limb pain post amputation [13].

Prevention

The best management of frostbite is, of course, prevention. Preventative measures that may be effective include minimising direct skin exposure, avoiding tight boots or multiple sock layers in large boots, keeping the head, neck and face covered, wearing mittens instead of gloves, staying hydrated, having an adequate caloric intake and avoiding direct skin-metal or skin-fluid contact [18].

Key Learning Points

All systems respond by an initial increase in activity (compensation), followed by a decrease and then eventual loss of activity (decompensation)

Grade D recommendation. Evidence level 5

Obtaining a full set of vital signs (Temperature, Pulse, Blood Pressure and Respiratory Rate) is vital in the patient with altered mental status to avoid missing subtle cases of hypothermia

Grade D recommendation. Evidence level 5

Supportive measures, with a focus on the Airway, Breathing, Circulation, Disability (including Dont Ever Forget Glucose) and the removal of wet, cold clothes is the cornerstone of management

Grade D recommendation. Evidence level 5

Dont correct for hypothermia when analysing the acid-base status normal values can be assumed to meet the needs of the hypothermic tissue.

Grade D recommendation. Evidence level 5

Avoid commencing rewarming of the frostbitten extremity unless it is clear that the process will not be interrupted.

Grade D recommendation. Evidence level 5

1. Currier J. Hypothermia. In: Harwood-Nuss A, Wolfson AB, Linden CH et al, eds. The Clinical Practice of Emergency Medicine. 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2001: 1664-1667.
2. Hanania NA, Zimmerman JL. Accidental hypothermia. Crit Care Clin. 1999 Apr;15(2):235-49. doi: 10.1016/s0749-0704(05)70052-x.
3. Biem J, Koehncke N, Classen D, et al. Out of the cold: management of hypothermia and frostbite. CMAJ 2003;168:305-311.
4. Papenhausen M, Burke L, Antony A, Phillips JD. Severe hypothermia with cardiac arrest: complete neurologic recovery in a 4-year-old child. J Pediatr Surg. 2001 Oct;36(10):1590-2.
5. Hypothermia Deaths in 2020. Main points. National Records of Scotland.
6. ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005 Dec 13;112(24 Suppl):IV1-203.
7. Danzl DF: Accidental hypothermia, in Auerbach PS (ed): Wilderness Medicine. 6th ed. Philadelphia, PA: Mosby, 2012:116142.
8. Aurbach P ed. Accidental hypothermia. In: Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 4th ed., St. Louis, MO: Mosby-Year Book, Inc.; 2001: 135-178.
9. Kroeger K, Janssen S, Niebel W. Frostbite in a mountaineer. Vasa. 2004 Aug;33(3):173-6.
10. Kpper T, Steffgen J, Jansing P. Cold exposure during helicopter rescue operations in the Western Alps. Ann Occup Hyg 2003;47:7-16.
11. Petrone P, Kuncir EJ, Asensio JA. Surgical management and strategies in the treatment of hypothermia and cold injury. Emerg Med Clin North Am. 2003 Nov;21(4):1165-78.
12. Ervasti O, Juopperi K, Kettunen P, Remes J, et al. The occurrence of frostbite and its risk factors in young men. Int J Circumpolar Health. 2004 Mar;63(1):71-80.
13. Reamy BV. Frostbite: review and current concepts. J Am Board Fam Pract. 1998 Jan-Feb;11(1):34-40.
14. Murphy JV, Banwell PE, Roberts AH, McGrouther DA. Frostbite: pathogenesis and treatment. J Trauma. 2000 Jan;48(1):171-8.
15. Cauchy E, Marsigny B, Allamel G, et al. The value of technetium 99 scintigraphy in the prognosis of amputation in severe frostbite injuries of the extremities: A retrospective study of 92 severe frostbite injuries. J Hand Surg Am. 2000 Sep;25(5):969-78.
16. Bhatnagar A, Sarker BB, Sawroop K, et al. Diagnosis, characterisation and evaluation of treatment response of frostbite using pertechnetate scintigraphy: a prospective study. Eur J Nucl Med Mol Imaging. 2002 Feb;29(2):170-5.
17. Su CW, Lohman R, Gottlieb LJ. Frostbite of the upper extremity. Hand Clin. 2000 May;16(2):235-47.
18. Chan TY, Smedley FH. Tetanus complicating frostbite. Injury. 1990 Jul;21(4):245.
19. Soar J, Perkins GD, Abbas G, et al: European Resuscitation Council Guidelines for Resus- citation 2010: Section 8. Cardiac arrest in special circumstances: electrolyte abnormali- ties, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution. Resuscitation 81: 1400, 2010. [PMID: 20956045]

Further resource:

• www.bt.cdc.gov disasters