Hypothermia

Hypothermia


 INTRODUCTION

Background: For the sake of brevity, this discussion will include only accidental hypothermia, not intentional hypothermia such as is used in certain surgeries.

Accidental hypothermia is defined as an unintentional decline in core temperature below 35°C (95°F). Primary hypothermia occurs when the patient is hypothermic from accidental exposure to cold. Secondary hypothermia occurs when a disease state causes a failure of thermoregulatory function.

At temperatures below 35°C (95°F), the patient becomes less capable of generating heat, and body temperature continues to fall unless some action is taken. At a core temperature less than 30°C (86°F), the body assumes the temperature of the surrounding environment. While a history of cold exposure makes the diagnosis of hypothermia easy, hypothermia confounding other more obvious medical problems makes treating patients with hypothermia a challenge.

Pathophysiology: Humans are homeothermic endotherms, in that we maintain a uniform body temperature by internal generation of heat. A stable body temperature results from a balance between internal heat production and heat loss to the environment. The CNS processes input from peripheral and central thermal sensors regulating body temperature by keeping a balance between heat production and heat loss. If core temperature begins to fall, voluntary and involuntary muscle activity (movement and shivering, respectively) can increase basal heat production 2-5 times to counter the excessive heat loss to the environment. An adaptive response in the form of behavorial activity to remove oneself from the cold also plays a role in thermoregulation. Disease states that affect cognition or motor function play a role in the genesis of hypothermia when the expected behavior fails to occur.

Primary hypothermia is the result of continued exposure to the cold with failure of heat generation to keep up with heat loss. When heat is lost to the environment, a number of physiologic and behavorial mechanisms maintain or raise core temperature. Because heat is a byproduct of muscle activity, the majority of heat generation occurs through that mechanism. As long as the level of muscle activity required to keep up with heat loss is sustained, core temperature will be maintained. Ultimately, as long as the ambient temperature remains low, fatigue will occur and muscle activity will decline or cease. Poor physical conditioning, dehydration, and lack of caloric intake necessary to feed the muscle activity exacerbate the problem (this often occurs in recreational situations by accident, misfortune, or stupidity). Injury or strokes may prevent muscle activity, and loss or impossibility of behavorial responses to get out of the cold may play a role.

Secondary hypothermia results when a disease state interferes with thermoregulation through interference of any of the multiple pathways that maintain heat balance. Onset of hypothermia can be triggered by events similar to the generation of primary hypothermia. For example, when a patient has a stroke (disruption of thermoregulation due to CNS injury) and falls to a concrete floor, hypothermia may ensue because of cerebral damage and because the body is exposed to a temperature that may be 20°F below normal body temperature. Concrete has greater heat conductivity than a bed, and the patient will be unable to move or cover himself with a blanket. The situations that could cause secondary hypothermia are many and varied. Therefore, a high index of suspicion is necessary to accurately diagnose and treat secondary hypothermia because treatment of the hypothermia also entails identification and correction of the underlying abnormality.

A physiologic heat balance is a result of many variables, including the ability to generate heat, size, age, insulation in the form of clothing, and the temperature of the environment to which the patient is exposed. Heat always flows from a warmer object to a colder object. Under most circumstances, the body generally is warmer than the surrounding environment and heat, therefore, is lost to the environment unless thermoregulation is maintained.

Heat is lost or gained through several physical mechanisms, including radiation, conduction, convections, and evaporation. Radiation may account for 55% of loss, evaporation 30%, and conduction 15%, with convection being a relatively minor component. Being wet or immersed in water causes more rapid heat loss because water is 25 times more conductive than air. Concrete or stone is approximately 100 times more conductive, and direct exposure to this material results in even greater heat loss than with exposure to water. The ground is somewhere between stone and water, depending on its exact composition.

In summary, the environment usually is cooler than the body; therefore, some degree of heat production is necessary under most circumstances. As a result, the body generally loses heat to the environment if thermoregulation is not maintained. In addition, the heat conductivity of the objects to which the body is exposed influences the rapidity of heat lost, and failure to maintain behavorial adaptations to cold compound this heat loss. Because many disease states interfere with thermoregulation, the complex interactions necessary for balanced thermoregulation can and do fail.

Frequency:

Race:

Sex:

Age:

CLINICAL

History: In some cases, hypothermia is suggested by an obvious history, such as a skier who is caught in an avalanche. In other cases, the history may not suggest the diagnosis of hypothermia, for example in an elderly person who comes into the emergency department in cardiac arrest. The signs and symptoms of hypothermia vary according to core temperature and represent a continuum rather than definitive categories. Especially in urban settings, the presentation may be subtle and easily overlooked.

Because hypothermia may accompany a more obvious condition, keeping hypothermia in the differential diagnosis as a comorbidity in any patient, especially elderly patients, who present with unexplained symptoms is critical. Also important is remembering that the symptoms of the primary condition may overshadow the symptoms of hypothermia.

Physical: Physical findings vary with the degree of hypothermia and with the nature of associated injuries or illness. The underlying illness, such as a stroke, may obscure the physical signs of hypothermia. Using a thermometer capable of registering as low as 25°C (77°F) for measuring core temperature is important. Note that the symptoms represent a continuum, and a fair amount of variability exists from patient to patient. Determination of body temperature from the clinical examination, with the exception of a core temperature reading, is not possible

Causes: Humans have developed considerable behavioral adaptations to cold weather. Any disease that interferes with this adaptive behavior places a patient at risk. Because hypothermia itself alters mental status, patients with mild hypothermia may experience a downward viscous cycle of continued heat loss and maladaptive behavorial patterns. Hypothermia is more frequent among persons who are elderly, homeless, mentally ill, trauma victims, outdoor workers, and children.

DIFFERENTIALS

Alcoholism
Anorexia Nervosa
Delirium
Frostbite
Hypopituitarism (Panhypopituitarism)
Hypothyroidism
Myocardial Infarction
Pneumonia, Bacterial
Sepsis, Bacterial
Septic Shock
Shock, Hemorrhagic


Other Problems to be Considered:

Any disease can precipitate hypothermia if the heat-generation/heat-loss balance moves towards heat loss. The list of possible causes is immense. Some of the more common causes include the following:

WORKUP

Lab Studies:

Imaging Studies:

Other Tests:

Procedures:

TREATMENT

Medical Care: Treatment begins in the prehospital environment, with removal of wet clothing, passive rewarming of the victim, and removal from the cold environment. Associated injuries are stabilized, and the patient should be transported as soon as possible. Rough handling of the patient may precipitate ventricular arrhythmias and should be avoided. An axiom in treatment is that a patient with hypothermia may appear dead; therefore, a patient is not considered dead until they are warm and dead.

Consultations:

MEDICATION

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Antiarrhythmic agents -- Indicated for ventricular fibrillation experienced in hypothermia.
Drug Name
 Bretylium tosylate (Bretylium) -- Until it became unavailable, was the DOC for hypothermia-induced ventricular fibrillation. Class III antiarrhythmic agent that lengthens ventricular action potential duration and effective refractory period, increasing the strength needed to induce ventricular fibrillation. Causes an initial catecholamine release and therefore has some positive inotropic properties. Has a half-life of approximately 4 h.
Adult Dose Initial dose: 5 mg/kg over 10 min; may be repeated in 30 min
Pediatric Dose Not established
Contraindications Documented hypersensitivity; systemic lupus erythematosus, digitalis-induced arrhythmias, complete heart block or second-degree or third-degree heart block if a pacemaker is not in place; avoid in torsade de pointes
Interactions Pressor catecholamines and digitalis may increase toxicity; coadministration with ofloxacin may increase risk of cardiotoxicity
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions May cause hypotension, especially in patients with fixed cardiac output (eg, aortic stenosis); caution in renal insufficiency, severe pulmonary hypertension, and aortic stenosis; half-life increases in elderly; with renal clearance of 10-50 mL/min, administer 25-50% of the dose; rapid IV injections may result in transient hypertension, nausea, and vomiting; limit injection to 5 mL (undiluted) at each injection site
Drug Name
 Amiodarone (Cordarone) -- Use of this drug in hypothermia is not supported by research.
May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Prior to administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.
Adult Dose Loading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk; decrease to 600-800 mg/d in 1-2 doses for 1 mo
Maintenance dose: 400 mg/d PO; alternatively, 150 mg (10 mL) IV over first 10 min, followed by 360 mg (200 mL) over next 6 h, and then 540 mg over next 18 h
Pediatric Dose 10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia is attained
Contraindications Documented hypersensitivity, complete AV block, and intraventricular conduction defects; patients taking ritonavir or sparfloxacin
Interactions Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and further decrease myocardial contractility; cimetidine may increase levels
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in thyroid or liver disease

FOLLOW-UP

Further Inpatient Care:

Patient Education:

MISCELLANEOUS

Medical/Legal Pitfalls:

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Constructed by Dr N.A. Nematallah Consultant in perioperative medicine and intensive therapy, Al Razi Orthopedic Hospital , State of Kuwait, email : razianesth@freeservers.com