Chapter 9

Hypothermia and Hyperthermia

John B. Kortbeek

Chapter Overview

Patients suffering from hypothermia or hyperthermia of varying degrees are frequently admitted to the ICU. Treatment of these patients presents many challenges, including metabolic, cardiorespiratory, fluid, and electrolyte derangements which often can only be effectively managed in the ICU setting. The classification of hypothermia and hyperthermia will be presented. Definitions, mechanisms, etiology, pathogenesis, clinical presentation, and principles of management of these entities will assist physicians caring for these critically ill patients in understanding and effectively managing these disorders.

Maintenance of Temperature

Temperature homeostasis, maintenance of normothermia is essential for human life. Body temperature is centrally regulated and affected by changes in muscle activity, metabolism, and the cardiovascular system. The hypothalamus is the center of thermoregulation. The optic nuclei in the anterior hypothalamus receive temperature feedback from peripheral nerves in the skin and mucous membranes as well as from perithalamic thermosensors.

Normal temperature is defined as 36.5°C +/− 0.5°C. There is a normal diurnal variation of up to 1°C with peak mid day and nadir around 4 am. Temperature also varies depending on measurement site with core temperatures (rectal > oral > skin).

Temperature is affected by body mass, body habitus, gender, and ovulation. Physical activity, medications, and illness may affect body temperature and regulation. Temperature typically rises with meals and exercise. Environmental exposure to heat and cold produce physiologic responses to maintain normothermia.

Hypothermia may be classified as mild, moderate, or severe. Mild hypothermia (temperature 32–25°C) presents with tachycardia, tachypnea, shivering, and confusion. The most common arrhythmia is atrial fibrillation. J waves may be present on the electrocardiogram (EKG).1

Moderate hypothermia (temperature 28–23°C) presents with altered level of consciousness. The Glasgow coma scale is typically less than 12 and the patient may be comatose. In patients with diminished GCS and coma, co-existent traumatic brain injury must be excluded. The respiratory pattern varies. Tachycardia frequently progresses to atrial fibrillation or flutter and PVCs may be present. More profound temperature drops may result in bradyarrythmias. The patient is at risk of progressing to ventricular arrhythmias including ventricular tachycardia and ventricular fibrillation.

Severe hypothermia (temperature <28°C) presents with coma and apnea. These patients frequently progress to ventricular fibrillation and asystole. Correct assessment of core temperature requires use of thermometers capable of recording temperatures less than 28°C. Many standard emergency department thermometers have a low set point of 28°C.

Patients presenting following exposure to cold may also present with characteristic associated soft tissue injuries. These include frostbite, chilblain, and trench foot.

Frostbite, like burns, is classified by depth of injury. Superficial epidermal injury (frostnip) presents with whitish discoloration or simple erythema after rewarming. The wound is typically numb but becomes quite painful on rewarming. Second-degree injury involves the epidermis and dermis and presents with white–yellow discoloration and is accompanied by blister formation. Some tissue sloughing may occur during recovery. Third-degree injury involves subcutaneous tissues and may progress to muscle, tendon, nerve, and bone. Necrosis accompanies the loss of perfusion and the development of ice crystals in the tissues. Tissue loss is universal and debridement or amputation may be required.

Chilblains (or pernio) refer to the development of erythematous patches accompanied by pain and pruritus in response to rapid rewarming after exposure to cold. The extremities, particularly digits are involved. The condition is common with some individuals genetically predisposed. It may also develop following previous cold injury.

Trench foot or immersion injury earned is so named as it occurred frequently in soldiers during World War I, subjected to prolonged exposure and immersion of the feet in cold water and mud. Freezing temperatures are not required. The prolonged exposure to a cold wet environment results in vasoconstriction, tissue hypoxia, and subsequent injury. Pain swelling and erythema progressing to blistering and even necrosis may occur.

Pathophysiology

Hypothermia has significant effects on a number of essential homeostatic mechanisms. Importantly it affects central nervous system metabolism, cardiac conductivity, the vascular system, oxygen transport, platelet aggregation, the coagulation cascade, and the immune response to pathogens.2

The brain receives approximately 15% of arterial blood flow and is responsible for approximately 20% of metabolic energy consumption. Hypothermia reduces the metabolic rate dramatically, up to 50% at temperatures of 28°C. Hypothermia has neuroprotective effects in reducing production of lactate through anaerobic metabolism as well as reducing the release of excitatory amino acids such as glutamate. Production of free radicals is reduced, cell membranes are stabilized and cerebral oxygen requirements are lowered. These changes result in resistance to ischemic or hypoxic injury. EEG changes in hypothermia consist of reduced alpha activity with a relative increase in beta and theta activity. Somatosensory evoked potentials are also affected with increased latency. These changes explain the sequential altered level of consciousness observed in hypothermia with progression from confusion to coma.³

Mild hypothermia results in shivering and vasoconstriction. Oxygen requirements are increased and there may be compensatory tachycardia and increased cardiac output. As hypothermia progresses impaired cardiac contractility and conduction occurs along with progressive increases in afterload from vasoconstriction which may decrease stroke volume especially in the patient with border line cardiac reserve. This leads to impaired perfusion and lactic acidosis. With severe hypothermia cardiac arrest eventually results.

Mild hypothermia initially results in an intracellular potassium shift. In addition, the hemoglobin oxygen saturation curve shifts to the left resulting in decreased delivery of oxygen to the tissues. As the shock state unfolds and cardiac arrest occurs, hypoxia and necrosis lead to severe acidosis and hyperkalemia.

The coagulation cascade is directly affected by hypothermia resulting in the increased risk of bleeding and associated mortality in trauma. Fibrinolysis is enhanced, platelet aggregation and adhesion is diminished. The enzymatic coagulation cascade is inhibited.

Leukocyte and immunologic effects have been documented with impaired wound healing and increased risk of sepsis, pneumonia, and surgical site infection. Surgical wounds are directly affected through vasoconstriction and relative tissue hypoxia. Systemic effects are many and include reduced leukocyte chemotaxis, aggregation and phagocytosis, altered cytokine production, delayed TNF clearance and impaired monocyte major histocompatibility surface antigen expression.

The EKG may exhibit a prolonged PR, QRS, and QT intervals, Osborne waves, sinus tachycardia, and atrial fibrillation. Brady-arrhythmias and ventricular arrhythmias are associated with low moderate to severe hypothermia (Fig. 1, J Wave).

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