Accidental hypothermia

Background

Definition: Core Temp < 35°C (95 °F)

1. Mild hypothermia (32-35°C) (90-95)
2. Moderate hypothermia (28-32°C)
3. Severe hypothermia (<28°C)

immersion in any water colder than 16°C to 21°C (60.8°F to 69.8°F) can lead to severe hypothermia

Patients are at risk for dysrhythmias at body temperatures below 30°C (86°F); the risk rises as body temperature decreases.

he typical sequence is a progression from sinus bradycardia to atrial fibrillation with a slow ventricular response, to ventricular fibrillation, and ultimately to asystole.

The hypothermic myocardium is extremely irritable, and ventricular fibrillation may be induced by a variety of manipulations and interventions that stimulate the heart, including rough handling of the patient

Cold-induced bronchorrhea, along with a depression of cough and gag reflexes, makes aspiration pneumonia a common complication

Hypothermia causes a leftward shift of the oxyhemoglobin dissociation curve, potentially impairing oxygen release to tissues. Patients may have minimal oxygen reserves despite diminished oxygen requirements, which warrants the administration of supplemental oxygen.

Hypothermia impairs renal concentrating abilities and induces a cold diuresis, which leads to volume loss.

e immobile hypothermic patient is prone to rhabdomyolysis, and acute renal failure may occur because of myoglobinuria and renal hypoperfusion. Intravascular volume is also lost due to a shift of plasma to the extravascular space.

The combination of hemoconcentration, cold-induced increase in blood viscosity, and poor circulation may lead to intravascular thrombosis and embolic complications. Disseminated intravascular coagulation may occur because of the release of tissue thromboplastins into the blood stream, especially when circulation is restored during rewarming. Because cold inhibits both platelet function and the enzymatic reactions of the coagulation cascade, hypothermic patients are prone to bleeding.

TREATMENT Treatment includes both general supportive measures and specific rewarming techniques. The patient should be removed from the cold environment, wet clothing should be removed, and the patient should be dried. Therapy begins with careful, gentle handling because manipulation can precipitate ventricular fibrillation in the irritable hypothermic myocardium. Pulses may be difficult to detect in the profoundly hypothermic patient, and chest compressions may cause ventricular fibrillation. To avoid inappropriate chest compressions, a patient who is unmonitored or in a "nonarrested rhythm" (a rhythm other than ventricular fibrillation or asystole, such as sinus bradycardia or atrial fibrillation) should be examined carefully for respiratory activity and pulses. Thirty to 45 seconds should be spent attempting to detect respiratory activity and palpate a pulse. If none is detected, CPR should be initiated.

Oxygen and IV fluids should be warmed, and the patient's core temperature, cardiac rhythm, and oxygen saturation should be monitored constantly. Pulse oximetry is usually accurate in hypothermic patients, although unreliable data may be obtained with profound vasoconstriction or a very low cardiac output. If central venous lines are placed, care should be taken to avoid entering and irritating the heart. In general, indications for endotracheal intubation are the same as in the normothermic patient. Concern has been raised regarding induction of dysrhythmias during intubation, but there is a very low complication rate with careful intubation after oxygenation.8,9 Medications used for rapid-sequence intubation may be ineffective at temperatures of <30°C (<86°F).8

Although dysrhythmias in the hypothermic patient may represent an immediate threat to life, most rhythm disturbances (e.g., sinus bradycardia, atrial fibrillation or flutter) require no therapy and revert spontaneously with rewarming. The activity of antiarrhythmic and cardioactive drugs is unpredictable in patients with hypothermia, and the hypothermic heart is relatively resistant to atropine, pacing, and countershock. Ventricular fibrillation may be refractory to therapy until the patient is rewarmed. The American Heart Association's 2005 guidelines suggest a single defibrillation attempt. If this is unsuccessful, CPR should be instituted and rapid rewarming begun. Defibrillation should be reattempted when the core temperature reaches 30°C (86°F).7

Because a number of hypothermic patients are thiamine-depleted alcoholics (and because Wernicke disease may cause hypothermia), consider giving IV thiamine, 100 milligrams. Between 50 and 100 mL of 50% glucose should be administered if a test-strip serum glucose measurement is low or if a rapid glucose test is unavailable

thorough search for infection is indicated.

Hydrocortisone (100 milligrams) should be given to the patient who has a history of adrenal suppression or insufficiency or is in myxedema coma. Routine corticosteroid therapy is not necessary.

In severe hypothermia or hypothermia secondary to an underlying illness, patients may fail to rewarm passively; active rewarming is then indicated. Active rewarming is also indicated for patients with cardiovascular compromise.

IV fluids and blood should also be warmed to 40°C (104°F) before administration, especially in patients receiving massive volume resuscitation. Commercial fluid warmers allow the temperature of infused fluids to be precisely controlled.

Both inhalation rewarming and administration of heated fluids should be used in all patients, because these are simple techniques without complications, as long as the temperature is controlled.

lavage with warmed saline is simple, and patients can be lavaged with large volumes of warm fluid over a short time. However, the obtunded hypothermic patient may develop pulmonary aspiration if lavaged with an unprotected airway. The urinary bladder can also be lavaged with warm saline solution through a urinary drainage catheter.

Pleural lavage using thoracostomy tubes has provided effective rewarming in animal studies and a few human cases.15 Lavaging the left thoracic cavity delivers heated fluid in close proximity to the heart, which potentially allows rapid cardiac warming. Two thoracostomy tubes (for fluid inflow and outflow) generally have been employed. If this technique is chosen, care must be taken to monitor the net fluid infusion, because increased intrathoracic pressure and tension hydrothorax may complicate the procedure. The risk of precipitating dysrhythmias during chest tube insertion is unknown.

Approach to Rewarming Patients with mild hypothermia, who are still in the excitation stage, generally improve spontaneously, as long as endogenous heat production mechanisms are functional. At temperatures of >30°C (>86°F), the incidence of dysrhythmias is low, and rapid rewarming is rarely necessary.

By far the most important consideration in the selection of rewarming techniques is the patient's cardiovascular status; a secondary consideration is the presenting temperature. Some feel that patients with a stable cardiac rhythm (including sinus bradycardia and atrial fibrillation) and stable vital signs do not need rapid rewarming, even if the temperature is very low. They recommend passive rewarming and noninvasive rewarming modalities (e.g., forced-air rewarming, administration of warm moist oxygen, and use of warm IV fluids) in this setting. Others argue that profoundly hypothermic patients, even if currently in "stable" condition, are at risk of developing life-threatening dysrhythmias. They recommend rapid rewarming until the temperature has reached 30°C to 32°C (86.0°F to 89.6°F) to minimize the time period during which dysrhythmias may develop. The relative merits of each approach have not been studied.

Patients with cardiovascular insufficiency or instability, including persistent hypotension and life-threatening dysrhythmias, need to be rewarmed rapidly.

Unless there is strong evidence that the patient is incapable of survival, resuscitative efforts should be continued until core temperature is at least 30°C to 32°C (86.0°F to 89.6°F).

ECG Changes

1. Osborn (J) wave
2. T-wave inversions
3. PR, QRS, QT prolongation
4. Muscle tremor artifact
5. Dysrhythmias
   1. Sinus bradycardia
   2. A fib or flutter
   3. Nodal rhythms
   4. AV block
   5. PVCs
   6. V-fib
   7. Asystole

DDx

1. Accidental (environmental) exposure
2. Metabolic disorders
   1. Hypoglycemia
   2. Hypothyroidism
   3. Hypoadrenalism
   4. Hypopituitarism
3. Hypothalamic and CNS
   1. Head trauma
   2. Tumor
   3. Stroke
   4. Wernicke encephalopathy
4. Drugs
   1. Ethanol
   2. Sedatives-hypnotics
5. Sepsis
6. Dermal disease
   1. Burns
   2. Exfoliative dermatitis
7. Acute incapacitating illness
8. Massive fluid or blood resuscitation

Treatment

Passive RewarmingActive External RewarmingActive Core Rewarming 2005 AHA guidelinesVfib--> Attempt defib ONCE; no meds until >30°C (86°F)Repeat defib once >30°C (°86F)

Source

Tintinalli