Accidental Hypothermia

Pathophysiology

Cardiovascular

After an initial tachycardia, a progressive bradycardia develops. The pulse usually decreases by 50% at 28° C

The bradydysrhythmia is refractory to atropine

Osborn (J) wave is seen at the junction of the QRS complex and ST segment

J waves are potentially diagnostic but not prognostic.

temperature less than 32° C

Dysrhythmias

All atrial and ventricular dysrhythmias are common in cases of moderate to severe hypothermia

Because the conduction system is more sensitive to the cold than the myocardium

As hypothermia worsens, the PR interval, then the QRS interval, and finally (and most characteristically) the QT interval become prolonged

Central Nervous System

Hypothermia progressively depresses the CNS

Significant alteration of the brain's electrical activity begins below 33.5° C, and the electroencephalogram goes silent at 19° C to 20° C.

Cerebral auto regulation is maintained with an increase in vascular resistance until 25° C

Renal System

cold diuresis Hypothermia depresses renal

blood flow, reducing it by 50% at 27° C to 30° C

Respiratory System

Hypothermia initially stimulates respiration.

This is followed by a progressive decrease in the respiratory minute volume

Carbon dioxide production decreases 50% with an 8° C fall in temperature

Predisposing Factors

Endocrinologic failure Hypopituitarism  Hypoadrenalism  Hypothyroidism  Diabetes

Insufficient fuel   Hypoglycemia  Malnutrition  Marasmus  Kwashiorkor  Extreme exertion

Neuromuscular inefficiency   Age extremes  Impaired shivering  Inactivity  Lack of adaptation

Environmental   Immersion  Nonimmersion

Induced vasodilation   Pharmacologic  Toxicologic

Erythrodermas   Burns  Psoriasis  Ichthyosis  Exfoliative dermatitis

  

  

  

  

FROSTBITEANDOTHERLOCALIZEDCOLD-RELATED

INJURIES

Chilblains Chilblains,or pernio, is characterized

by usually mild but uncomfortable inflammatory lesions of the skin of bared body areas caused by chronic intermittent exposure to cold weather

Localized edema, erythema, cyanosis, plaques, nodules, and in rare cases, ulcerations, vesicles, and bullae.

Trench foot Immersion foot Early symptoms progress from tingling to

numbness of the affected tissues. On initial examination, the foot is pale,

mottled, anesthetic, pulseless, and immobile, which initially does not change after rewarming.

A hyperemic phase begins within hours after rewarming

As perfusion returns to the foot over 2 to 3 days, edema and bullae form, and the hyperemia may worsen.

Treatment

Management of chilblains is supportive.

The affected skin should be rewarmed, gently bandaged, and elevated.

Oral nifedipine 20 mg three times daily

Topical corticosteroids (0,025% fluocinolone cream) and even a brief burst of oral corticosteroids, such as prednisone, have been shown to be useful.

Effective prophylaxis

keeping warm, ensuring good boot fit, changing out of wet socks several times a day never sleeping in wet socks and boots, and once early symptoms are identified, maximizing efforts to warm, dry, and elevate the feet.

Feet should be kept clean, warm, dry bandaged, elevated, and closely monitored for early signs of infection

Frostbite

Frostbite can occur on any skin surface but generally is limited to the nose, ears, face, hands, and feet, penis

First-degree injury

Characterized by partial skin freezing, erythema, mild edema, lack of blisters, and occasional skin desquamation

The patient may complain of transient stinging and burning, followed by throbbing. Prognosis is excellent.

Second-degree injury

Characterized by full-thickness skin freezing , formation of substantial edema over 3 to 4 h, erythema, and formation of clear blisters . The blisters form within 6 to 24 h

Numbness, followed later by aching and throbbing. Prognosis is good.

Third-degree injury

Characterized by damage that extends into

he subdermal plexus. Hemorrhagic blisters form and are associated with skin necrosis and a blue-gray discoloration of the skin.

The patient may complain that the involved extremity feels like a "block of wood," followed later by burning, throbbing, and shooting pains.

Prognosis is often poor.

Fourth-degree injury

Characterized by extension into subcutaneous tissues, muscle, bone, and tendon.

There is little edema. The skin is mottled, with nonblanching cyanosis, and eventually forms deep, dry, black, mummified eschar.

Vesicles often present late The patient may complain of a deep pain. Prognosis is extremely poor

Treatment

FIELD MANAGEMENT

The hypothermia and dehydration associated with frostbite should be addressed.

Wet and constrictive clothing should be removed.

The involved extremities should be elevated and wrapped carefully in dry sterile gauze, with affected fingers and toes separated.

Further cold injury should be avoided.

Rapid rewarming is the single most effective therapy for frostbite.

Rewarming in the field is often impractical and sometimes is dangerous.

If the victim has frozen feet and the only avenue to evacuation is prolonged ambulation, rewarming can complicate matters significantly.

It can be excessively painful

If rewarming is attempted in the field, only clean water warmed to 40° to 42°C (104° to 107.6°F), as measured by thermometer, should be used.

The use of hot, untested tap water should be avoided

Attempts to directly warm with dry air, such as campfires and heaters, should be avoided

Rubbing snow on frostbitten tissue to stimulate circulation is ineffective, destructive, and absolutely contraindicated.

EMERGENCY DEPARTMENT MANAGEMENT

Rehydration and general warming Rapid rewarming is the core of frostbite

therapy and should be initiated as soon as possible.

The injured extremity should be placed in gently circulating water at a temperature of 40° to 42°C for approximately 10 to 30 min, until the distal extremity is pliable and erythematous.

Frostbitten faces can be thawed using moistened compresses soaked in warm water

Anticipate severe pain during rewarming, and treat with parenteral opiates.

Clear blisters should be debrided or at least aspirated.

Hemorrhagic blisters should not be debrided

Therapy with penicillin G 500,000 U IV every 6 h for 48 to 72 h is recommended in prophylaxis

Topical bacitracin Silver sulfadiazine has no benefit Tetanus immunization Ibuprofen 12mg/kg per d PO

Rewarming Techniques

Passive rewarming: Removal from cold environment Insulation Active external rewarming: Warm water immersion Heating blankets set at 40°C Radiant heat Forced air

Active core rewarming at 40°C: Inhalation rewarming Heated IV fluids GI tract lavage Bladder lavage Peritoneal lavage Pleural lavage Extracorporeal rewarming Mediastinal lavage via thoracotomy

HEAT EMERGENCIES

The body tends to maintain its core temperature between 36°C and 38°C (96.8°F and 100° F).

Native thermal regulation mechanisms begin to fail at core temperatures below 35°C and above 40°C

It is possible to maintain core temperatures of 40°C to 42°C for short periods without adverse effect.

The highest documented core temperature in a survivor of heat stroke is 46.5°

Physiologic response to heat stress

Four primary methods: Dilatation of blood vessels

(particularly in the skin), Increased sweat production Decreased heat production Behavioral heat control.

Blood flow to the skin can increase from a basal level of 0.2 L/min to a maximum of about 8 L/min.

The heart rate increases Elevated cholinergic stimulation to

the skin results in increased sweat production.

Medications often interfere with heat removal mechanisms.

Anticholinergic agents, diuretics, pheno-

thiazine, Beta-blockers, calcium channel blockers, and sympathomimetics

CLINICAL FEATURES

Heat Edema

Heat edema is a self-limited process manifested by the mild swelling of the feet, ankles, and hands that appears within the first few days of exposure to a hot environment.

No special treatment is necessary. Elevation of the legs Diuretics are not effective and can

predispose to volume depletion, electrolyte abnormality

Heat Cramps

Heat cramps are painful, involuntary, spasmodic contractions of skeletal muscles, usually those of the calves, although they may involve the thighs and shoulders.

Heat cramps may occasionally occur during exercise or, more commonly, during a rest period after several hours of vigorous physical activity.

In fact, the pain associated with heat cramps usually does not respond to opiates alone.

Treatment consists of fluid and salt replacement (PO or IV) and rest in a cool environment.

For mild cases, or if an overwhelming number of patients require treatment, a 0.1 to 0.2% saline solution can be given PO.

Two 650 mg salt tablets dissolved in quart of water provide a 0.1 % saline solution.

More severe cases of heat cramps will respond to intravenous rehydration with NS.

Heat Tetany

Heat tetany is produced by hyperventilation associated with exposure to short periods of intense heat stress.

This syndrome presents as typical hyperventilation resulting in respiratory alkalosis, paresthesia of the extremities, circumoral paresthesia, and carpopedal spasm.

Treatment consists of removal from the heat and decreasing the respiratory rate.

Heat Syncope

Heat syncope is a variant of postural hypotension resulting from the cumulative effect of relative volume depletion, peripheral vasodilatation, and decreased vasomotor tone.

Evaluation of patients with heat syncope requires exclusion of metabolic, cardiovascular, and neurological disorders that may produce syncope

Treatment consists of removal from the heat source, oral or intravenous rehydration, and rest.

Heat Exhaustion

Heat exhaustion is an acute heat-related illness that reflects significant volume depletion and mayor may not have an elevated temperature.

Symptoms : weakness, malaise, lightheadedness, fatigue, dizziness, nausea, vomiting, frontal headache, and myalgias.

Clinical manifestations include orthostatic hypotension, sinus tachycardia, tachypnea, diaphoresis and syncope.

The core temperature is variable and can range from normal to 40°C (\ 04°F).

Heat exhaustion is treated with volume and electrolyte replacement and rest.

Mild cases may be treated with oral electrolyte solutions.

Rapid infusion of moderate amounts of intravenous fluids (1 to 2 L of saline solution) may be necessary in some patients who demonstrate significant tissue hypo perfusion.

Heatstroke

The classic definition of heatstroke includes the presence of a core temperature higher than 40°C, CNS dysfunction, and anhidrosis.

Anyone with hyperpyrexia and CNS dysfunction should be considered to have a heatstroke, which is a medical emergency

The CNS is particularly vulnerable in heatstroke, with symptoms such as irritability, confusion, bizarre behavior, combativeness, hallucinations, seizures, or coma.

The cerebellum is highly sensitive to heat, and ataxia can be an early neurological finding.

Virtually any neurologic abnormality may be present in heatstroke, including plantar responses, decorticate and decerebrate posturing, hemiplegia, status epilepticus, and coma.

Seizures are quite common in heatstroke

TREATMENT OF HEATSTROKE

Initial Resuscitation Standard initial resuscitative measures (adequacy of airway, breathing, and circulation; initiation of high-flow oxygen; use of continuous cardiac monitoring and pulse oximetry; and intravenous access) are appropriate.

An initial infusion of NS or LR solution at a rate of 250 mL/h is recommended for most patients.

Glucose level should be promptly assessed with a test strip due to the high incidence of hypoglycemia in exertional heatstroke.

A lumbar puncture and computed tomography of the head may also be indicated as part of the evaluation of altered mental status

Cooling Techniques

Rapid reduction of the core temperature to below 40°C (104°F) is the primary goal of treatment and is accomplished by physical cooling techniques.