Hypothermia
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):
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 bodys 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
(ABCs) 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 patients 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
- Environmental Emergencies, Charles E. Stewart, Williams and Wilkins 1990.
- Clinical Practice of Emergency Medicine 2nd edition, Ann L. Harwood-Nuss,
Lippincott-Raven 1996.
- Emergency Medicine: A Comprehensive Study Guide 4th edition, Judith E.
Tintinalli, McGraw-Hill Inc. 1996.
- 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).
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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.,
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