Let’s begin with a quick review of the physiology of heat production/heat loss. The human body can generate heat through an increase in basal metabolism rate via the sympathetic nervous system and muscular activity. It will also attempt to keep organs warm through vasoconstriction. Heat loss occurs through radiation, conduction, evaporation, and convection (table 2).

There are many predisposing or contributing factors putting patients at risk for cold injuries. Nicotine, atherosclerosis, or tight restrictive clothing or jewelry can cause a decrease in local tissue perfusion. Alcohol, drug intoxication, and many medications can cause vasodilatation allowing for an increase in radiation and loss of vasoconstriction as a protective mechanism. Diseases that may interfere with the body’s ability to react or identify a cold stress increase the risk, i.e. cardiovascular disease, diabetes, neurologic diseases. Additionally, a lack of preparation for cold stresses, not wearing protective clothing, poor nutrition, and fatigue put people at risk.

CHILBLAINS

Chilblains, or frostnip, is a localized skin reaction that occurs when skin is exposed repeatedly to cold. There is no actual tissue freezing and the subcutaneous tissues are spared.

The skin can be blanched, or begin to have reddish purple macular lesions. This injury is easily reversible with no permanent sequaelae. Management includes rewarming of the affected areas at room temperature. Massage can be harmful and should be avoided.

FROSTBITE

Definition

Frostbite is also a localized cold injury, but actual freezing of tissues occurs. Frostbite can be considered superficial or deep. It tends to affect areas of endarterial flow- most commonly toes and fingers. Any unprotected body surface can be affected. Although frostbite occurs most commonly in below freezing temperatures, it can occur if other conditions exist, such as wind, prolonged exposure, or impaired vascular integrity.

Description

Superficial frostbite initially appears white and waxy. The patient often complains of coldness or numbness. With thawing the areas become hyperemic and vesiculated. Blisters may begin to develop. Deep frostbite is also white, waxy, but tend to feel harder. With thawing the area remains hard. Both levels of frostbite have resulting edema and the formation of eschar.

Pathophysiology

When the skin is first exposed to the cold there is a reflex arteriolar spasm with decreased capillary blood flow. Ice crystals form initially in the extracellular space creating a hypertonic state and thereby pulling water out of the cells. This creates toxic levels of electrolytes in the cells leading to cell death. These ice crystals often expand and cause mechanical destruction of tissue as well. The cold also increases blood viscosity, promotes vasospasm and precipitates microthrombus formation. It may be that prostaglandin’s mediate this cascade of injurious events (1).

Management

Ideally rapid rewarming is the treatment of choice. This is most often accomplished using immersion in warm water (40 — 42⁰C). The tissues must be very carefully protected from mechanical injury throughout the process. The water used for rewarming needs to be kept at a consistent temperature and the extremity protected for burn injury. Tetanus prophylaxis needs to be remembered. A fasciotomy may be needed if extensive edema occurs. ). Antiprostaglandins may be helpful in stopping the cascade of injury.

Transport issues

Assess the patient with a core temperature to rule out coexisting hypothermia. Protect the injured part with tenting. Do NOT rewarm the injured areas if there is a chance of refreezing as this greatly increases the tissue damage. Throughout the transport the patient may need analgesia. If rewarming has occurred prior to the transport, the extremity should be elevated, cotton or gauze placed between the toes and fingers (if they are the affected part). Transport to a facility with experience in these types of injuries, a regional burn center is often ideal.

Sequaelae

Superficial frostbite eventually leaves the injured area with shiny red skin, which remains, sensitive to heat and cold. Deep frostbite leaves nonviable skin with mummifying and sloughing. Patients frequently lose digits and require plastic or reconstructive surgery. Infection and chronic pain are also noted in many patients.

HYPOTHERMIA

Definition

Hypothermia is divided into 3 categories based on core temperature (table 3). The reduction of core and cellular temperature has a parallel decrease in all vital activity as the enzymatic rate of metabolism decreases. Some authors also categorize hypothermia as acute or chronic. Acute hypothermia occurs in a period of less than six hours. Chronic hypothermia occurs when pt is exposed to cold for more than 24 hours, this occurs more frequently on land. Urban hypothermia is a form of chronic hypothermia that is associated with factors such as age, debilitation, drug and alcohol use, and predisposing disease allowing for warmer than expected temperatures (ambient temperatures as high as 90^oF) to cause a patient to experience hypothermia.

Reports of survival after up to 66 minutes, and a recorded temperature of 16^oC (60.8^oF) fascinate us with this cold injury as well as reminding us that patients must be warm before death can be confirmed.

Description

Mild hypothermia (35 - 33^oC) causes a patient to shiver and sees an increase in respiratory rate, heart rate, and cardiac output to increase the bodies heat production. The blood glucose drops as it is used for energy. These patients are often clumsy, apathetic, and irritable. Reflexes are hyperactive.

Moderate hypothermia (<33 — 28.4^oC) patients present with lethargy, confusion, ataxia, and may hallucinate. A cough reflex is often absent, making aspiration a risk. Hyperglycemia may occur, as the insulin is no longer capable of transporting glucose into cells. This occurs only if prolonged shivering did not occur. Respiratory rate begins to become shallow, decreased cardiac output with a decrease in heart rate also begins to appear.

In severe hypothermia (<28.4^oC) the body can no longer generate any heat by itself. The patient will present comatose and the metabolic rate continues to decrease. Apnea will most likely occur between 21 —24^oC. Pupils are dilated and nonreactive. Deep tendon reflexes are often absent. Oxygen binds tenaciously to hemoglobin resulting in hypoxia to the cells. This will lead to lactic acid production. Ventricular fibrillation can begin to present at approximately 29^oC and below and often occurs with rough handling, intubation, or cardiac compressions.

Cardiac dysrhythmias begin to occur below 29^oC, atrial fibrillation with a slow ventricular rate is common (this will usually convert to sinus rhythm with warming). Changes in conduction tend to occur at 27^oC with a widening of the QRS and prolonged PR and QT intervals. The Osborne (J wave) is seen clearly at 25^oC.

Pathophysiology/Complications

Hypothermia occurs when the bodies heat-producing mechanisms cannot keep up with heat loss. Cold exposure has an immediate vasoconstriction of peripheral vessels and an increase in sympathetic nervous system. Once the patient shivering stops cooling is rapid. The complications from hypothermia are mainly related to the metabolic derangements.

The bronchial system suffers two insults, a decrease in rate and volume and bronchorrhea. Bronchorrhea is a marked increase in tracheal and bronchial secretions.

The circulatory system is affected with dysrhythmias as previously discussed, but there are significant derangements of the blood. The blood has a hemoconcentration from the shift of fluids. The vasoconstriction to shift fluids to the core organs combined with the increase in blood viscosity gives a perceived overhydration. The body responds to this by removing the extra volume through diuresis. Prolonged hypothermia can cause plasma to leak from the capillaries further increasing the blood viscosity. Coagulopathies occur due to the colds inhibition of enzymatic coagulation cascade. This all puts the patient at risk for thrombosis. Platelet function also is impaired by the cold injury and white blood cell count may be altered due to leukocyte sequestration.

Medication administration is altered due to the protein binding that is increased with cold. Many of the receptors have a decreased sensitivity to medication as well. Acid base balance is also affected and correction for temperature needs to be made prior to any treatment (Table 4).

Management

The first step in management is to keep a high index of suspicion. The rest of the management is providing supportive care, preventing and identifying complications, and looking for secondary problems while preventing further heat loss and augmenting heat production. In all patients provide oxygenation, cardiac monitoring, blood glucose monitoring and intravenous fluids.

Mild hypothermia is best treated with passive external warming with blankets. The addition of insulation and preventing further heat loss to allow the body’s own mechanisms to generate heat. This provides a gradual rewarming. The average increase in temperature is approximately 0.5 — 2.0.^oC per hour. There are times that a more active approach will be needed — in patients who are incapable of shivering, are intoxicated or malnourished. If the patient is in wet clothing, be sure to remove these.

Moderate hypothermia may be treated with passive rewarming if the patient’s mentation allows cooperation. However, active external rewarming is more likely. Active external rewarming can be used in otherwise healthy patients. If vasoconstriction is significant it will limit the ability for this to work. Active external rewarming is the application of heat to the skin often using immersion in a water tank. There is the possibility with the external rewarming that an afterdrop could occur. This occurs as the blood courses through extremities that are still cold and then returns to the core. Conduction warming uses water filled heat exchange blankets. In a setting where these techniques are not available using warmed packs to the groin, axilla, and neck. In some centers a form of forced warm air convection is being trialed. None of these active external rewarming techniques should be used if the patient is not capable of protecting their airway.

Severe hypothermia requires a more aggressive form of rewarming — active core rewarming. These techniques transfer heat to the body’s core, achieving warming from the core out as warmed blood circulates. The easiest techniques for this are warmed oxygen administration via and ET tube or mask (40 — 45^oC), warming of IV fluids, gastric or bladder lavage. More invasive techniques include peritoneal, mediastinal, or thoracic tube lavage, cardiac bypass, and hemodialysis.

The administration of warmed humidified oxygen works by warming alveolar blood that returns to the heart, warming the myocardium. The heat also warms the lungs themselves as well as eliminating a major source of heat loss. With humidified oxygen there is the additional benefit of replacing some of the needed fluids or at least not having further loss through the bronchial system.

In all the lavage settings rates as high as 4 to 12L/hr may be needed. The fluid should be warmed to approximately 45^oC with a dwell time of 1 — 2 minutes before removing the fluid. In the bladder it is recommended that the fluid be administered in 100 —200 cc boluses to avoid over distention. In gastric lavage beware of dilutional issues with the fluid; be sure to use an isotonic solution.

Transport issues

In the transport situation for mild hypothermia, prevent further heat loss with passive external warming — blankets and warm environment. Protect the patient from any wind source, cover the patient’s head, and provide warm oral fluids (after assuring a gag reflex is present).

Gentle handling of all hypothermia patients with stimulation minimized as much as possible. When removing clothing, gently cut off instead of pulling it off, and remove any jewelry the patient may be wearing. Remind the team to reduce the amount of movement in the vehicle as much as possible.

Administration of oxygen is a priority in all hypothermia patients, warmed if at all possible. This may be accomplished with a warming unit on the humidifier or wrapping the tubing around a hand warmer (be careful not to allow the tubing to become too warm).

Rehydration of the patient can be accomplished with oral fluids in mild hypothermia and IV fluids with moderate or severe hypothermia. Be sure the fluid is not cold, (it can be if stored in a vehicle that has been outdoors). The fluid of choice is NS (with D5 if hypoglycemia is an issue). The fluid is administered at approximately 40^oC at a rate of 200 — 250ml/hr (pediatrics 4-5 ml/kg/hr) monitoring for fluid overload. The IV fluids can be warmed with a warming device or as mentioned with the oxygen. Wrapping the IV bags in a warming device or insulating in a blanket or jacket in the vehicle with the heater on can warm fluids in route.

As with any patient during a transport close monitoring of VS is imperative. Remember that with severe hypothermia a respiratory rate of 4 — 6 may be adequate to oxygenate the vital organs. The pulse may only be found using a doppler. With mild hypothermia cardiac monitoring and blood pressure monitoring can be very difficult due to muscle tremors.

Airway management should include intubation only if airway reflexes are absent. The risk of cardiac dysrhythmias form intubation is increased with temperature decreases. Preoxygenation may help prevent the vfib.

Cardiac dysrhythmias present a controversy if the patient is in vfib or asystole. In some sources CPR is held in patients with core temperatures less than 28^oC. There is no evidence that defibrillation is effective at these temperatures either. However most authors agreed that an attempt at defibrillation in vfib should occur, if unsuccessful then wait for rewarming. Medications are used with the knowledge that the body is less receptive or unresponsive to medications at core temps under 28^oC.

Patients with hypothermia present special problems during transport. The understanding of the pathophysiology and treatment protocol, as well as planning before hand for these emergencies may make the difference.

Special situations

Children, especially infants are at an increased risk of hypothermia. Newborns born out of the hospital may have hypothermia even in an environment that seems warm to the providers. They have less insulation and their head is larger in size proportionally than adults, leading to greater heat loss. Children often have limited energy reserves, and poor motor development limiting their ability to shiver.

Elderly people start with lower basal metabolic rates and body temperatures. As we age are ability to adapt to temperature changes, with vasoconstriction and shivering greatly diminished. The other great danger is the difficulty recognizing hypothermia in the elder who may have confusion or dementia prior to the insult of hypothermia.

Alcohol and other toxic states interfere with thermoregulation. Vasodilation contributes to the heat loss, as does the persons altered perception. Hypoglycemia is a cofactor as the energy reserves are diminished for shivering. Alcohol intoxication is frequently the cofactor in urban hypothermia, even in environmental temperatures of 70^oF.

Trauma patients may be susceptible to hypothermia. If the environmental temperatures are cold and prolonged extrication occurs, removal of clothing for assessment, administration of cold IV fluids and oxygen may add to the potential for hypothermia. In head injury patients (or CVA) the ability to thermoregulate may be disrupted.

Conclusion

As with any injury, having an index of suspicion is the most critical starting point. Cold injuries can be local or systemic. The treatment of each is dependent on the severity and environmental conditions during transport.

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Semonin-Holleran, R. (1997). Environmental Emergencies. In NFNA (1997) Flight Nursing Core Curriculum (pp. 641-644). Park Ridge, Il: NFNA.

Sanders, M. (1994). Environmental Emergencies. In Mosby’s Paramedic Textbook. (pp. 810-815). St. Louis: Mosby.

Holleran, R. (Ed). (1996) Cold-Related Emergencies In Flight Nursing: Principles and Practice (2^nd ed., pp. 526-541). St. Louis: Mosby.

Roberts: Clinical Procedures in Emergency Medicine. 3^rd Ed. 1998 W.B. Saunders Philadelphia. MD Consult L.L.C. http://www.mdconsult.com

CE is no longer available for continuing education credits for hypothermia and heat related illnesses.