Hypothermia

Introduction

Physical exam and ancillary studies

Key Points

Body Response

Differential diagnosis

Disposition

Predisposition

Treatment

References

Diagnosis

Rewarming

Introduction

Hypothermia is defined as a core (rectal, esophageal, or tympanic membrane) temperature less than 35° C (95 °F). Exposure to cold is usually present but not necessary to produce this condition. An intoxicated swimmer may be in 60 degree Fahrenheit water and may become hypothermic, despite an air temperature of 90°F. Individuals at the extremes of age and those with altered sensorium for any reason are particularly susceptible. It must be considered in any cold exposure with decreased level of consciousness.

The body regulates core temperature through mechanisms of loss and heat gain.

Heat loss:

  • Conduction - transfer of heat from body to environment (the body loses heat 30 times faster in water than air).

  • Convection - wind chill.

  • Radiation - heat transfer by electromagnetic waves (increased by peripheral vasodilatation, decreased by insulated clothing).

  • Evaporation - sweat, exhaled breath

Heat Gain (or conservation):

  • Peripheral vasoconstriction – increased metabolic rate, shivering, behavior (putting on warm clothes and getting out of the cold).

Body Response

  • 32-35° C: Increased metabolic activity, surface and subcutaneous vessels constrict, decreasing blood flow to the skin, and shivering.

  • <32° C: metabolic activity slows, oxygen (O2) consumption and carbon dioxide (CO2) production drop with loss of the shivering response and loss of vasomotor tone.

  • CNS Response: increasing hypothermia results in depression in the level of consciousness (LOC), mild incoordination leading to confusion, lethargy, and coma. Pupils are often dilated and non-reactive.

  • CV Response: From 32-35° C cardiac output, heart rate and BP increase to attempt to rewarm; but, all begin to drop at < 32° C.

  • ECG – Osborne J waves (broad upright deflection at the end of the QRS complex may be present (see Immersion Injuries chapter for example). As hypothermia worsens, T-wave inversion, prolonged PR, QRS, and QT intervals occur as well as dysrhythmias such as bradycardia, slow atrial fibrillation, ventricular fibrillation and asystole. Thrombosis and embolisms increase due to decreased intravascular volume and increased blood viscosity.

  • Pulmonary Response: Respiratory rate initially increases then begins to decrease as temperature decreases below 32° C. Tidal volume decreases, cough and gag reflexes fail, and the risk of aspiration increases. The oxyhemoglobin dissociation curve shifts to the left resulting in decreased O2 delivery to the tissues. Arterial blood pH appears falsely low and pO2/pCO2 falsely high. These changes improve spontaneously with rewarming.

  • GI Response: Decreased hepatic function alters the metabolism of drugs cleared by the liver (i.e. lidocaine).

  • Renal Response: The body loses its ability to concentrate urine resulting in cold diuresis and volume depletion. Decreased renal blood flow and tissue breakdown products may lead to acute tubular necrosis and renal failure.

Predisposition for hypothermia

Extremes of age, decreased muscle mass, autonomic dysfunction, use of vasoactive drugs such as alcohol predispose hypothermia. Trauma, burns, and other system stressors worsen the body’s response to the cold.

Diagnosis

Diagnosis requires measuring a core temperature with a low reading thermometer. Most thermometers read only to 94ºF. A refrigerator thermometer may be shielded and used if necessary. An axillary temp >35.5º C may be useful as a screening tool in a mass casualty situation.

Physical exam and ancillary studies

The physical exam should begin with establishing the airway, breathing, and circulation (ABC’s) and then vital signs to include pulse, blood pressure, respiratory rate, and a core temperature with a hypothermic thermometer (IVAC only reads to 94°F). A mental status may demonstrate signs that are decreased or depressed from normal limits. A screening exam should be completed, including a search for signs of trauma. Baseline studies (if available) should include a CBC (usually hemoconcentrated), electrolytes, BUN, creatinine, glucose (frequently abnormal but not in a predictable manner), ABG, PT/PTT, and if possible, a urine or serum drug tox screen should be considered. An EKG should be done; Osborn (J) waves are a notch at the junction of the QRS complex and ST junction (suggestive but not diagnostic of hypothermia). A chest x-ray is helpful since pneumonia and pulmonary edema are possible complications.

Differential diagnosis

This includes all potential causes of altered mental status and should not be limited to the following conditions:

  • Alcohol and other intoxicants

  • Endocrine problems

  • Hyper/hypoglycemia

  • Hypoxemia and narcotics

  • Uremia

  • Trauma

  • Infection, both central nervous system (CNS) and systemic

  • Psychiatric problems

  • Subarachnoid hemorrhage and space occupying lesions

Treatment

Treatment includes airway maintenance with respiratory and circulatory support. Avoid rough handling of patient as this may precipitate ventricular fibrillation. Keep the patient supine to avoid orthostatic hypotension. Provide IV (D5 normal saline), supplemental O2, and both cardiac and temperature monitoring. Maintain the ABCs and consider axial spine immobilization in suspected trauma cases. Administer warm IV fluids (43ºC) and O2 (42º-46ºC) if the patient’s core temp is < 34° C. Only life-threatening dysrhythmias (ventricular fibrillation (VF) and asystole) should be treated, the remainder will correct with rewarming. The drug of choice for VF is bretylium. Initial defibrillation with up to three attempts is recommended and not re-attempted until core temp reaches 30ºC. Magnesium sulfate has aided spontaneous resolution of VF. Atropine and lidocaine are ineffective in hypothermia. Suspected aspirations should be treated as outlined in the chapter on Immersion Injuries.

Rewarming

Passive external rewarming – place in warm environment, remove wet clothing, and cover with blankets.

Active external rewarming – application of heat to body surface such as hot water bottles (warmed IV bags) in groin and axillas, warmed blankets, and the use of radiant heaters.

Potential problems with external rewarming

  • Core temp afterdrop – cold blood returning from the periphery further cools the body core.
  • Rewarming acidosis – cold blood returning from the periphery brings lactic acid with it.
  • Rewarming shock – relative hypovolemia occurs secondary to peripheral vasodilatation.
  • Note: To minimize complications use active, external rewarming in combination with active core rewarming.

Active core rewarming – Method of choice when the temperature is < 30° C or the patient demonstrates cardiac instability.

Non-invasive – warmed humidified O2 acts to minimize respiratory heat loss. Warmed intravenous fluid resuscitation (D5 normal saline is preferred).

Invasive – Gastric, colonic, bladder, and peritoneal lavage with warmed normal saline solutions.

Key Points

  • The method of rewarming depends on the core temp and stability of the patient.
  • If the patient has a life threatening dysrhythmia you must rapidly and actively rewarm using both invasive and non-invasive techniques.
  • Do an initial and secondary exam of all hypothermic patients identifying any trauma or underlying medical conditions.
  • In some cases, the patient with severe hypothermia may appear clinically dead. However, in the appropriate setting, resuscitative efforts should continue until the core temperature is at least 86° to 92° F (30 to 33° C). The patient is not expired until warm and expired.

Disposition

Patients with significant hypothermia/exposure should be resuscitated and stabilized to the medical officer's best ability. Transfer to a higher level of care should be considered on an individual basis, based on the severity of the incident and the facilities available, with the patient's best interests in mind. Patients with a documented cold injury should be referred to a higher level of care for consultation before being returned to full duty.

References

  1. Environmental Emergencies, Charles E. Stewart, Williams and Wilkins 1990.
  2. Clinical Practice of Emergency Medicine 2nd edition, Ann L. Harwood-Nuss, Lippincott-Raven 1996.
  3. Emergency Medicine: A Comprehensive Study Guide 4th edition, Judith E. Tintinalli, McGraw-Hill Inc. 1996.
  4. Emergency Medicine Concepts and Clinical Practice 4th edition, Rosen / Barkin , Mosby 1998.

Revised by LCDR Richard DelaCruz, MC, USN, and LCDR Steven L Banks, MC, USN, Department of Emergency Medicine, Naval Medical Center San Diego, San Diego, CA. (1999).

Preface  ·  Administrative Section  ·  Clinical Section

The General Medical Officer Manual , NAVMEDPUB 5134, January 1, 2000
Bureau of Medicine and Surgery, Department of the Navy, 2300 E Street NW, Washington, D.C., 20372-5300

This web version of The General Medical Officer Manual, NAVMEDPUB 5134 is provided by The Brookside Associates Medical Education Division.  It contains original contents from the official US Navy version, but has been reformatted for web access and includes advertising and links that were not present in the original version. This web version has not been approved by the Department of the Navy or the Department of Defense. The presence of any advertising on these pages does not constitute an endorsement of that product or service by either the Department of Defense or the Brookside Associates. The Brookside Associates is a private organization, not affiliated with the United States Department of Defense. All material in this version is unclassified. This formatting © 2006 Medical Education Division, Brookside Associates, Ltd. All rights reserved.

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