Definition

• Core body temperature drops below that required for normal metabolism. In primary hypothermia, the healthy individual's compensatory responses to heat loss are overwhelmed by exposure, whereas secondary hypothermia complicates many systemic diseases.
• Stage I-90–95°F (32–35°C)
• Stage II-82–90°F (28–32°C)
• Stage III-75–82°F (24–28°C)
• Stage IV-any temperature <75°F (24°C).

Pathophysiology

• Normal thermoregulation balances heat gained or lost to the environment with heat produced via central thermogenesis. It is controlled by the hypothalamus with input from thermoreceptors. Heat can be gained or lost to the environment via four mechanisms including evaporation, radiation, convection, and conduction. Central thermogenesis generates heat via basal metabolism, muscle activity, and uncoupling of brown fat (neonates).
• Heat production can be augmented via shivering and increased basal metabolic rate. Activation of both the sympathetic nervous and endocrine systems results in increased circulating levels of thyroid-releasing hormone, catecholamines, growth hormone, and glucocorticoids, which all contribute to increased glucose utilization and basal metabolic rate.
• Adaptations to minimize heat loss include cutaneous vasoconstriction, piloerection, and behavioral responses such as curling up, sharing body heat, and seeking shelter.

Systems Affected

• Cardiovascular-in mild hypothermia, sympathetic stimulation induces tachycardia and peripheral vasoconstriction with normal or elevated cardiac output and blood pressure (BP). As the patient becomes colder, depolarization of cardiac pacemaker cells is slowed resulting in bradycardia resistant to treatment with atropine; the resultant fall in cardiac output is balanced by an increase in systemic vascular resistance. At lower temperatures, bradycardia becomes progressively extreme and systemic vascular resistance falls as catecholamine release and adrenergic receptor responsiveness is blunted. Classic ECG findings include the presence of Osborn or J-waves, atrial and ventricular dysrhythmias, and prolongation of the PR, QRS, and QT intervals. Progression from sinus bradycardia through atrial fibrillation to ventricular fibrillation and ultimately asystole.
• Endocrine-sympathetic activation and release of counter-regulatory hormones trigger increased glycogenolysis, gluconeogenesis, and lipolysis as well as inhibit the release and uptake of insulin resulting in hyperglycemia. When hypothermia develops slowly or is long-lasting, glycogen stores become depleted and hypoglycemia develops.
• Gastrointestinal-increased gastric acid production and reduced duodenal bicarbonate secretion may predispose patients to gastrointestinal ulceration. Ileus is common.
• Hemic-plasma shifts to the extravascular space, and the consequent hemoconcentration may lead to hyper- and hypocoagulopathy. Depressed enzymatic activity of clotting factors and platelet hyporeactivity may exacerbate hypocoagulability.
• Hepatobiliary/Pancreatic-hypoxia leads to hepatocellular damage and pancreatitis.
• Musculoskeletal-increased viscosity of joint fluid and muscle stiffness.
• Nervous-as core temperature falls, CNS metabolism and level of consciousness decrease in a linear fashion, and nerve conduction velocity progressively slows. Mild incoordination is followed by lethargy, obtundation and coma.
• Renal-peripheral vasoconstriction increases renal blood flow and glomerular filtration rate resulting in increased urine production. As core body temperature falls, progressive tubular dysfunction and antidiuretic hormone resistance contribute further to cold-diuresis. Later, urine production decreases as a result of falling cardiac output. Acute kidney injury may ensue.
• Respiratory-initial tachypnea is replaced by decreased respiratory rate and tidal volume and increased production of airway secretions. As the temperature falls protective airway reflexes are reduced. At temperatures below 93.2°F (34°C) ventilatory drive is attenuated and increased pulmonary vascular resistance leads to ventilation-perfusion mismatch. Progressive hypoventilation, apnea, and (more rarely) pulmonary edema may develop. Hypothermia also causes the oxyhemoglobin dissociation curve to shift to the left. This effect may be masked by concurrent lactic and respiratory acidosis that may become so profound it results in an overall right-shift.
• Skin-edema develops secondary to increased vascular permeability.

Genetics

Unknown

Incidence/Prevalence

Varies with geographic location

Geographic Distribution

Most common in cold climates

Signalment

Signs

Causes

• Inadequate thermogenesis
  • Normal thermogenesis is overwhelmed
  • Serious illness
• Extreme heat loss
  • Excessive evaporation, conduction, convection, and radiation
  • Inability to vasoconstrict blood vessels or piloerect hair
  • Loss of behavioral adaptations
• Thermoregulatory center failure
  • Hypothalamic injury or disease

Risk Factors

• Extremes of age
• Low body fat and glycogen stores
• Burn injury
• Intracranial injury or disease
• Hypothyroidism
• Diabetic ketoacidosis
• Sepsis
• Trauma
• General anesthesia
• Use of medications including but not limited to beta-blockers, barbiturates, narcotics, phenothiazines

Differential Diagnosis

• Primary CNS disease, hypoglycemia, anemia, hepatic encephalopathy, myxedema, electrolyte disturbances, sepsis, intoxication, neoplasia, and death
• Bradyarrhythmia-cardiac disease, medication side effects, and intoxication

CBC/Biochemistry/Urinalysis

• Results are variable depending on the degree of hypothermia and presence of comorbid conditions
• CBC-hemoconcentration and thrombocytopenia
• Biochemistry-azotemia, hyper- and hypoglycemia, elevated liver enzyme activity, hyperbilirubinemia
• Urinalysis-isosthenuria, glucosuria

Other Laboratory Tests

• Blood gas-variable but metabolic and respiratory acidosis is common.
• Coagulation-hyperfibrinogenemia, DIC. In vivo prolongation of blood clotting times may not be reflected by in vitro assays and should correct with rewarming.
• Thyroid hormone evaluation may confirm underlying hypothyroidism.

Imaging

To investigate recovery complications or comorbid conditions

Diagnostic Procedures

None

Pathologic Findings

• Findings in patients who succumb to primary accidental hypothermia are variable and nonspecific. If body cooling and death occur rapidly, necropsy findings are minimal but may include reddish discoloration of skin, hemorrhagic gastric erosions, and lipid deposits in epithelial cells of renal proximal tubules and other organs.
• Patients who die from secondary hypothermia may have similar findings; however, they will also have evidence of a separate and significant disease process.

Appropriate Health Care

Emergency inpatient intensive care until normothermic and stable

Nursing Care

• Active external rewarming using warm blankets, heating pads, radiant heat, warm baths, or forced warm air, and administration of warm parenteral fluids (stage II) is used in patients with stage I–II hypothermia. Complications include core temperature after-drop whereby the return of cold blood from the periphery to the central circulation causes further core cooling. Rewarming of the trunk should be performed before the extremities to minimize this risk.
• Techniques to warm patients with stage III–IV hypothermia include administration of warm humidified oxygen, warmed intravenous fluids, and bladder or gastric lavage with warm saline. More invasive and technically demanding methods include closed thoracic and peritoneal lavage, hemodialysis, continuous arteriovenous or veno-venous rewarming, and cardiopulmonary bypass.
• Whole-body immersion in hot water is contraindicated, as it will cause massive vasodilatation and hypotension and is likely to provoke dysrhythmias and cardiovascular collapse.
• Fluid therapy-most patients are initially volume depleted but must be closely monitored during resuscitation for volume overload. Crystalloid fluids administered intravenously should be warmed to 104°F (40°C).
• Hypotension is treated with volume resuscitation. The use of inotropic drugs is considered only in cases unresponsive to volume resuscitation.
• Patients with respiratory failure must be mechanically ventilated.

Activity

Minimally affected patients should be encouraged to be active, as muscle activity will generate more endogenous body heat.

Diet

• Withhold oral intake until patient is alert.

Client Education

Prevention of exposure to cold temperatures is imperative in preventing primary hypothermia. Clients with very young and very old patients as well as those with serious medical conditions or taking medications that inhibit thermoregulatory ability should be counseled to keep their pets indoors and to take protective measures if they are to be exposed to cold temperatures.

Surgical Considerations

N/A

Drug(s) Of Choice

Hypoglycemic patients warrant dextrose supplementation.

Contraindications

There is no evidence to support the routine use of steroids or antibiotics.

Patient Monitoring

• Continuous core body temperature.
• Continuous ECG and frequent BP (qlh) during rewarming.
• Frequent assessment (q6–12h) of electrolytes (sodium, potassium, chloride, ionized calcium, magnesium, and phosphorus), acid-base status, packed cell volume, total protein, and blood glucose.
• Daily monitoring of blood urea nitrogen, urine specific gravity, coagulation indices, and liver enzymes in severely affected patients.

Prevention/Avoidance

• Avoid prolonged exposure to cold.
• Monitor and maintain body temperature in anesthetized animals.

Possible Complications

• Peripheral vasodilation during rewarming may further drop body temperature.
• Iatrogenic burns.
• Return of cool peripheral blood to the heart may precipitate cardiac arrhythmias.
• Cardiac arrest.

Expected Course and Prognosis

Variable-affected by severity of hypothermia, underlying cause, and general patient health status.

Associated Conditions

None

Age-Related Factors

Sick or hypoglycemic neonates can become markedly hypothermic in normal environments.

See Also

Shock, Cardiogenic

Abbreviations

• BP = blood pressure
• CNS = central nervous system
• DIC = disseminated intravascular coagulation
• ECG = electrocardiogram

Client Education Handout Available Online