Chapter 46. Disorders Due to Physical & Environmental Agents

Individuals vary considerably in their response to environmental cold. Factors that increase the possibility of injury due to cold include poor general physical condition, nonacclimatization, childhood or advanced age, systemic illness, and the use of alcohol and other sedative drugs. High wind velocity (wind-chill factor) and moisture may markedly increase the propensity for cold injury at low temperatures.

Systemic Hypothermia

Essentials of Diagnosis

• Signs and symptoms depend on degree of hypothermia
• Rewarming methods include passive external, active external, and active internal rewarming

General Considerations

Healthy Persons

Accidental hypothermia occurs when an external cold challenge overwhelms an individual's capacity to produce or conserve heat. Hypothermia may occur in otherwise healthy individuals during occupational or recreational exposure to cold or as a result of accidents or other misfortunes. Alcohol and drug abuse is a common predisposing cause.

Persons with Predisposing Factors

Systemic hypothermia may follow exposure to even slightly lowered temperatures when preexisting altered homeostasis exists as a result of debility or disease. Accidental hypothermia is more likely to occur in elderly or inactive people and those with cardiovascular, dermatologic, or cerebrovascular disease; mental retardation; myxedema; hypopituitarism; or alcoholism. The use of sedative–hypnotic or antidepressant drugs may be a contributing factor.

Clinical Findings

Because lowered body temperature is the sole finding in some patients brought to the emergency department, the diagnosis often depends on awareness of the possibility of hypothermia.

Temperature

In the hypothermic patient, oral and axillary temperatures are not accurate. Instead, rectal probes should be used. The temperature varies widely in hypothermia, and accurate monitoring is essential.

Symptoms and Signs

Hypothermia is classified as mild when core body temperature is between 34°C (93.2°F) and 36°C (96.8°F). Patients will exhibit tachycardia, tachypnea, and shivering. Hypothermia is moderate between 30°C (86°F) and 34°C. Loss of the shivering reflex and mild alterations in level of consciousness occur. Bradycardia and atrial fibrillation may start to appear. Hypothermia becomes severe below temperatures of 30°C. Patients may appear dead at this stage with fixed, dilated pupils, loss of other reflexes, and coma.

Ventricular fibrillation and asystole may occur spontaneously at core temperatures below 28°C (82.4°F). Note: For this reason, a hypothermic patient should not be considered dead until all reasonable resuscitative measures have failed. No one is dead until he or she is “warm and dead.”

Laboratory Findings

Several laboratory findings are unique to hypothermia. Hypoglycemia, hypomagnesemia, and hypophosphatemia are common, particularly in alcoholics. Hyperglycemia may be seen as a result of hemorrhagic pancreatitis in patients with prolonged exposure to the cold. Sodium and potassium levels may be elevated or depressed. Arterial blood gas samples drawn at cold temperatures are generally analyzed at 37°C (98.6°F), which causes lowering of pH and elevation of PO2 and PCO2 readings. However, clinical therapy is based on the uncorrected determinations recorded at 37°C.The ECG tracing may show prolongation of any conduction interval. Osborne or J wave, may appear below 32°C (89.6°F) (Figure 46–1).

Complications

Metabolic acidosis, pneumonia, pancreatitis, renal failure, sepsis, and ventricular fibrillation may occur. Death due to systemic hypothermia usually results from cardiac arrest associated with ventricular fibrillation, which may occur during rewarming.

Underlying Conditions

Obtain a brief history from witnesses or relatives of a patient with hypothermia, and perform a general physical and laboratory examination to detect underlying conditions that might predispose to hypothermia.

Examination should include an evaluation of renal function (uremia), thyroid function (myxedema), and adrenal function (Addison disease). If sepsis is a diagnostic possibility, obtain appropriate cultures.

Treatment

Bundle the victim of suspected hypothermia in dry, warm blankets at the scene of discovery, and transport the person to the nearest hospital as soon as possible. Remove any wet garments. Note: Transport should be as gentle as possible because of the risk of cardiac arrhythmias due to increased myocardial irritability.

Cardiopulmonary Resuscitation

Adequacy of ventilation and circulation must be ensured by careful clinical observation, continuous ECG monitoring, and serial determinations of arterial blood gases. If cardiac arrest occurs, start cardiopulmonary resuscitation (CPR) (Chapter 9). If the victim has any detectable pulse or breathing, no matter how slow, do not initiate CPR; unnecessary brisk closed chest compression may induce ventricular fibrillation. Because of the protective effects of hypothermia, bradycardia and hypotension are generally well tolerated.

Establish an airway

Intubation of the unprotected airway and frequent suctioning may be required.

Breathing

Depression of the respiratory center in hypothermia causes hypoxemia or hypercapnia, requiring controlled ventilation and supplemental oxygen. Avoid hyperventilation, because a rapid fall in Pco2 may trigger ventricular fibrillation.

Circulation

Check for a pulse for at least 1 minute. If a pulse is present, do not attempt to correct arrhythmia with drugs or cardioversion. This will be unsuccessful most of the time and may precipitate ventricular fibrillation. Begin the rewarming process (see below). If the patient is pulseless, begin CPR. Attempts at defibrillation are usually unsuccessful at temperatures below 30°C (86°F). If ventricular tachycardia/fibrillation is present, attempt a shock at 360 J. If there is no success, continue CPR. At temperatures less than 30°C, withhold further defibrillation and intravenous medications. Begin aggressive rewarming in conjunction with basic CPR. If temperature is 30°C or greater, then continue with ACLS protocol but space intravenous medications longer than standard (decreased metabolism may induce toxicity of drugs).

Correct fluid, electrolyte, and glucose abnormalities

Give thiamine (100 mg intravenously), naloxone (2.0 mg intravenously), and dextrose (25 g intravenously) to all patients with altered mental status who are thought to be hypothermic. Volume expansion with warmed fluid generally helps the rewarming process. Avoid lactated Ringer's solution because the lactate is not metabolized efficiently by a cold liver.

Treatment of Underlying Conditions

Treat underlying and predisposing conditions as necessary (eg, heart disease, hypoglycemia, malnutrition, adrenocortical insufficiency [hydrocortisone, 200 mg intravenously], hypothyroidism [levothyroxine, 400 micrograms intravenously, plus hydrocortisone, 100 mg intravenously]).

Rewarming

Rewarming is essential but potentially harmful, because peripheral vasodilatation may divert blood flow from internal organs to the skin and shunt cooled blood to the central circulation, causing a brief drop in core temperature. Note: Rapid rewarming may be hazardous, because hypothermic patients are particularly vulnerable to lethal cardiac arrhythmias. Core rewarming should be undertaken only if hypothermia is severe and the patient shows cardiovascular instability (eg, cardiac arrest and ventricular fibrillation).

Mild hypothermia (core temperature ≥34°C [93.2°F])

Passive rewarming to prevent further heat loss is sufficient for most patients with mild hypothermia, because their thermoregulatory mechanism is intact, and many of these patients are able to generate heat by shivering. Most patients should be wrapped in dry, heated blankets and carefully monitored. Ambient air temperature can be warmed with radiant heat sources. Patients with mild hypothermia who are otherwise healthy usually respond well to heated blankets and the administration of heated (45°C [113°F]) intravenous solutions. Patients must be carefully monitored when using any of these rewarming methods.

Moderate to severe hypothermia (core temperature <34°C)

Moderate to severe hypothermia often requires additional rewarming measures, because thermoregulation is altered or absent. Individualized supportive care is mandatory, because active rewarming is hazardous. As mentioned previously, active core rewarming is necessary only for patients with cardiovascular instability.

Active external rewarming methods

Heated blankets, forced-air blankets (Bair Hugger), or warm baths have been used, with a rate of rewarming of about 1–3°C/h. Because it is easier to monitor the patient and to carry out diagnostic and therapeutic procedures when heated blankets rather than warm baths are used for active rewarming, heated baths are not widely recommended. There is some potential risk with active external rewarming, because marked vasodilation may occur. Combining active external rewarming with active core rewarming may prevent the resultant hypotension and the core temperature after-drop, which are sometimes seen during rewarming. If active external rewarming is used, the patient should be carefully monitored and supported hemodynamically. The application of commercial heat packs directly to hypothermic skin may cause serious burns.

Active internal (core) rewarming methods

Internal rewarming is suggested for patients with profound hypothermia of long duration in which there is suspected underlying debilitation, for patients with complications of cardiovascular or respiratory insufficiency, and for patients in cardiac arrest.

Repeated peritoneal dialysis may be performed using warm (45°C [113°F]) potassium-free dialysate solution or normal saline. The usual exchange rate is 6 L/h, which can increase the core temperature 1–3°C/h.

Warm fluids (crystalloid solutions) administered by gastrointestinal, colonic, or bladder lavage may be employed. Placement of a nasogastric tube is less invasive but may run the risk of stimulating ventricular dysrhythmias owing to the irritability of the hypothermic heart.

Administration of heated intravenous fluids contributes only 17 kcal/h, which accounts for an increase in body temperature of less than 1/3°C/L. Microwave rewarming of crystalloid solutions to 40–42°C (104–107.6°F) may be safely accomplished in about 2–3 minutes. This technique causes some hemolysis of erythrocytes, and if blood products are used they should be administered through a high-flow countercurrent fluid infuser or reconstituted with warmed normal saline.

Heated humidified oxygen, either via a tight-fitting mask or by endotracheal tube, will raise the core temperature 1 or 1.5–2°C/h, respectively.

Thoracic cavity lavage may achieve rapid rewarming with the added advantage of warming the heart more quickly. Insert two thoracostomy tubes, and continuously infuse fluid warmed to 41°C (105.8°F) through one tube and drain it through the other.

Extracorporeal blood rewarming methods are the gold standard for rewarming in the setting of severe cardiorespiratory compromise/arrest. This may be accomplished via cardiopulmonary bypass or hemodialysis. These methods of course are limited to the institutions that have the abilities to perform these functions.

Antimicrobials

Patients with severe hypothermia—especially those who are comatose—are at high risk for development of aspiration pneumonia; subsequent pulmonary, urinary tract, or intraperitoneal infections; and sepsis. Many hypothermic alcoholic, debilitated, or elderly patients will have an underlying infection, and the cause should be aggressively sought and treatment initiated.

If sepsis suspected, administer broad-spectrum antibiotics. Prophylactic antimicrobial drugs are unnecessary if infection is unlikely.

Complications of Rewarming

Observe the patient for signs of metabolic acidosis, cardiac arrhythmias, acute respiratory distress syndrome, pancreatitis, ischemic bowel, pneumonia, myoglobinuria with renal failure, or clotting abnormalities.

Disposition

Hospitalize all patients who present with core temperatures below 34°C (93.2°F), especially if the sensorium is altered. Patients with coexisting illness and core temperatures under 35°C (95°F) should be hospitalized. The mortality rates in hypothermia are variable and depend on the cause of hypothermia and the patient's underlying condition.

Cold Injury of the Extremities

Essentials of Diagnosis

• Tissue injury or death is caused by ischemia and thrombosis in capillaries or by formation of ice in the tissues
• Treatment of frostbite or chilblains depends on the severity of the skin injury and includes rewarming by both passive and active measures

In healthy individuals, exposure of the extremities to cold produces immediate localized vasoconstriction followed by reflex generalized vasoconstriction. When skin temperature falls to 25°C (77°F), tissue metabolism is slowed, but the relative demand for oxygen exceeds the supply from diminished circulation; thus, the area becomes cyanotic. At 15°C (59°F), tissue metabolism is markedly decreased and the dissociation of oxyhemoglobin is reduced, which may give the skin a pink, well-oxygenated appearance. Tissue damage occurs at this temperature. Tissue death may be caused either by ischemia and thrombosis in capillaries or by actual freezing. Frostbite is tissue freezing caused by formation of ice crystals in tissue. Frostbite occurs when skin temperature drops to 10–4°C (14–24.8 °F). The body's “hunting reaction,” serves to protect the extremity from cold injury by alternating vasoconstriction with vasodilation in 5–10 minute cycles. This occurs with exposure to progressively colder temperatures. The incidence of frostbite depends on factors such as wind, moisture, mobility, venous stasis, trauma, malnutrition, and occlusive arterial disease.

Chilblains (Pernio)

Clinical Findings

Chilblains, occurs with exposure to nonfreezing temperatures and is more common in children and women as well as people with any form of peripheral vascular disease. Chilblains are red or violaceous, painful skin lesions common on the ears, nose, hands, and feet. Lymphocytic vasculitis is common. Chilblains may be associated with edema or blistering and are subsequently aggravated by excessive warmth. With continued exposure, ulcerative or hemorrhagic lesions may appear and progress to scarring, fibrosis, and atrophy.

Treatment and Disposition

Treatment of chilblains is mainly supportive. Elevate the affected part on pillows or sheepskin, and allow it to warm gradually at room temperature.

Do not rub or massage injured tissues or apply ice or heat. Protect the area from trauma and secondary infection. Refer the patient to a primary-care physician or clinic for follow-up. Nicardipine and steroids may also have a role in treatment.

Frostbite

Clinical Findings

Classification

Frostbite is injury of the tissues due to freezing. The classification of injury is applied after rewarming, because the extent of injury is difficult to predict initially. Demarcation is not complete for up to 3–5 weeks.

First degree

Freezing without blistering; peeling is occasionally present.

Second degree

Freezing with clear blistering.

Third degree

Freezing with death of skin, hemorrhagic blisters, and subcutaneous involvement.

Fourth degree

Freezing with full-thickness involvement (including bone); ultimate loss or deformity of body part.

Symptoms and Signs

Frostbitten tissue appears white or blue–white, is firm or hard (frozen), cool to the touch, and generally insensitive. Skin loses sensation at around 10°C. Because cold injury produces anesthesia, many symptoms are not apparent until rewarming begins or the part is closely inspected. In patients with mild frostbite, the symptoms are numbness, paresthesias, pruritus, and lack of fine motor control. With increasing severity, decreased range of motion, blister formation, and prominent swelling are noted. Thawing unmasks local tenderness and throbbing pain. The tissue becomes discolored, loses its elasticity, and becomes immobile. Profound edema, hemorrhagic blisters, necrosis, and gangrene may occur. Long-term sequel includes cold sensitivity, loss of sensation, and hyperhidrosis.

Treatment

Systemic Hypothermia

Treat moderate to severe associated systemic hypothermia before managing frostbite.

Rewarming

Superficial frostbite

Rewarm extremities affected by superficial frostbite (frostnip) by removing wet clothing and applying constant warmth, which can be accomplished by exerting gentle pressure with a warm hand.

Full-thickness frostbite

Rapid rewarming is the most important aspect of management. It should not be attempted, however, if the potential for refreezing exists. Rewarming should be performed with a water bath or whirlpool containing an antimicrobial agent such as iodine or chlorhexidine. Water temperature of 40–42°C (104–107.6°F) is necessary. However, The State of Alaska Cold-injury Guidelines recommend a lower temperature of 37–39°C (98.6–102.2°F). This temperature causes less pain for the patient and only slightly prolongs rewarming. Rewarming should continue until a red-purple color appears and the skin becomes pliable. Recommended rewarming time is anywhere from 15 inutes up to 1 hour.

Resuscitation

Unless concomitant hypothermia exists, intravenous hydration is not usually necessary. Severe cases of frostbite have led to subsequent rhabdomyolysis with renal failure, which then requires aggressive hydration. Intravenous narcotics are almost always necessary secondary to the severe pain associated with rewarming.

Protection of the Injured Part

In the prehospital setting, padding, splinting, and avoidance of rewarming are all that is necessary. Once in the secure hospital setting and after rewarming has been achieved, avoidance of further trauma is important. Affected body parts should be elevated and padded, uncovered or loosely dressed, and left at room temperature. Debride clear blisters because prostaglandins and thromboxane are present in the exudate. Leave hemorrhagic blisters intact. Administer antitetanus prophylaxis. Apply aloe vera cream every 6 hours. Administer ibuprofen, 400–600 mg every 8–12 hours for 72 hours.

Anti-Infective Measures

Infection prevention is important after rewarming. Maintain a sterile environment. Protect skin blebs from physical contact. Whirlpool therapy at temperatures of 32–38°C (89.6–100.4°F) twice daily for 30 minutes for a period of 3 or more weeks helps to cleanse the skin and debride superficial dead tissue. Penicillin prophylaxis is recommended in most cases.

Adjunctive Therapies

Anticoagulation

Consistent benefit from anticoagulation has not been demonstrated.

Vasodilators

Have been used with some success.

Thrombolysis

Small clinical studies with tissue plasminogen activator have demonstrated success in humans, but the results of larger, multicenter trials are needed.

Surgery

Amputation or debridement should not be considered until it is definitely established that tissues are dead. Although rare, the development of a compartment syndrome necessitates fasciotomy. The line of demarcation between injured and normal tissue may not appear until 6–12 weeks after injury; mummification of the injured extremity may require the same length of time. Technetium-99 pyrophosphate and MRI scanning accurately predicts the level of ultimate amputation. Regional sympathectomy performed 24–48 hours after injury has reportedly ameliorated the early sequel of frostbite, including a reduction in edema and decreased subsequent tissue loss. Appropriate clinical studies have yet to be performed to support the use of this therapy.

Hyperbaric oxygen

Disagreement still exists as to effectiveness of HBO therapy. Recent studies in humans have yielded good results.

Disposition

Hospitalize all patients with second- or third-degree frostbite and patients with extensive areas of first-degree frostbite.

Immersion Syndrome (Immersion Foot; Trench Foot)

Essentials of Diagnosis

• Caused by prolonged immersion in cold water
• Alternating vasospasm and vasodilatation results in initial cold and anesthetic feet followed by blistering and ulceration
• Treatment includes rewarming and wound care

Clinical Findings

Immersion foot (or hand) is caused by prolonged immersion in cool or cold water or mud that causes alternating arterial vasospasm and vasodilatation. The affected parts are first cold and anesthetic. Hyperemia follows after 24–48 hours, and the parts become warm, with intense burning and tingling pain. Blistering, swelling, redness, ecchymoses, and ulceration are noted. The posthyperemic phase occurs after 2–6 weeks and causes the limbs to become cyanotic, with increased sensitivity to cold. Complications include lymphangitis, cellulitis, thrombophlebitis, and wet gangrene.

Prevention

Changing out of wet socks and shoes as soon as possible is paramount to the prevention of immersion syndrome. In the military, individuals at risk for immersion foot apply silicone ointment to the bottoms of their feet twice daily as a preventive measure.

Treatment and Disposition

Treatment is best started during or before the stage of reactive hyperemia.

Immediate treatment consists of protecting the extremities from trauma and secondary infection. Rewarm the injured areas gradually by exposing them to air (not to ice or extreme heat). Do not soak or massage the skin. The patient should remain at bed rest until all ulcers have healed. Keep the affected parts elevated to aid in removal of edema fluid, and protect pressure sites (eg, heels) with pillows or booties lined with cotton batting. Give antimicrobials only if infection occurs.

Hospitalize all patients with immersion syndrome.

1This chapter is a revision of the chapter by Shannon Waters, MD, from the 5th edition.

The five main disorders due to environmental heat stress are (1) heat edema, (2) heat syncope, (3) heat cramps, (4) heat exhaustion, and (5) heat stroke.

The body maintains temperature homeostasis via four main mechanisms: (1) conduction, (2) convection, (3) radiation, and (4) evaporation. When the body is unable to adequately regulate body temperature using these methods, heat illness occurs. The extremely young and old, obese, and those with chronic physical and mental impairments have the highest risk of heat illness. The fully heat acclimatized and athletic, healthy individuals are also at risk, however, given the right environmental conditions, if they are impaired by drugs or alcohol, or if they are denied access to hydration and nutrition.

Heat Edema

Essentials of Diagnosis

• Swelling of feet and ankles due to vasodilatation and venous stasis
• Treatment is elevation of the limbs

Nonacclimatized individuals, particularly the elderly, may develop swelling of the feet and ankles that is generally associated with periods of prolonged sitting or standing. The edema is not complicated by manifestations of congestive heart failure or lymphatic disease. The cause of heat edema is muscular and cutaneous vasodilation combined with venous stasis. Interstitial fluid then accumulates in the lower extremities. Because the problem is self-limited, treatment involves use of support hose and simple elevation of the lower limbs. Diuretics are not indicated.

Heat Syncope

Essentials of Diagnosis

• Caused by peripheral pooling of the intravascular volume
• Patient responds promptly to rest, cooling, and rehydration

Simple fainting may occur suddenly after exertion in the heat. Cutaneous and muscular vasodilation redistributes intravascular volume to the periphery of the body. Volume loss and prolonged standing (pooling in the lower extremities) also contribute to the development of inadequate central venous return and insufficient cerebral perfusion. The patient's skin is cool and moist, the pulse is weak, and transient hypotension occurs. In general, core temperature is normal or mildly elevated. The patient usually responds promptly to rest in a recumbent position, cooling, and oral rehydration. Evaluate elderly people who experience syncopal episodes for hypoglycemia, arrhythmias, and fixed myocardial or cerebrovascular lesions.

Heat Cramps

Essentials of Diagnosis

• Spasms of the voluntary muscles of the abdomen and extremities
• Caused by salt depletion
• Treatment consists of fluid and salt replacement

Clinical Findings

Heat cramps are due primarily to salt depletion and manifested by painful spasms of the voluntary muscles of the abdomen and extremities. The skin may be moist or dry, and cool or warm. Muscle fasciculations may be present. The core temperature is normal or only slightly elevated. Laboratory studies (rarely indicated) may reveal hemoconcentration and low serum sodium levels, although this is variable, and normal serum sodium levels are frequently noted. Hypokalemia occurs occasionally.

Treatment and Disposition

Treatment includes oral fluid and salt replacement with 0.1–0.2% salt solution (¼–½ teaspoon table salt in one cup water) or, in severe cases, intravenous normal saline solution. Give supplementary potassium as dictated by measured serum levels. Replace glucose if needed. An alternative therapy for mild symptoms is a commercial electrolyte solution (eg, Gatorade). Place the patient in a cool place, and massage sore muscles gently.

The patient should rest for 1–3 days, depending on the severity of the attack. Hospitalization is usually not required.

Heat Exhaustion

Essentials of Diagnosis

• Caused by either primary water loss or primary sodium loss due to prolonged heat exposure
• Rapidly leads to heat stroke
• Symptoms of dehydration are present, but central nervous system symptoms are not seen
• Treatment includes rehydration and cooling

General Considerations

Heat exhaustion is a systemic reaction to prolonged heat exposure (hours to days) and is due to sodium depletion, dehydration, accumulation of metabolites, or a combination of these factors. It is a premonitory syndrome that rapidly evolves to heat stroke. Central nervous system symptoms are generally not present, and the core body temperature is usually less than 40°C (104°F).

Clinical Findings

Two types of heat exhaustion have been described: hypernatremic (primary water loss) and hyponatremic (primary sodium loss). Heat exhaustion from primary water loss occurs when an individual in a hot environment is denied access to water. Heat exhaustion from primary salt loss occurs when an individual in a hot environment sweats excessive amounts and replaces fluid losses with pure water. It differs from heat cramps in that systemic symptoms are present. Pure forms of either type are rare, and most cases have a mixed salt and water depletion. The signs and symptoms of heat exhaustion are nonspecific and include headache, nausea, vomiting, malaise, muscle cramps, and dizziness. Dehydration is manifested by tachycardia, hypotension, and diaphoresis. In a hypernatremic patient, the water deficit can be calculated by a formula if the current serum sodium and patient's weight and age are known.

Measurement of serum electrolytes and renal function is advisable in most patients, because serum sodium concentration may be markedly low in patients with heat exhaustion. Myoglobinuria indicates subclinical rhabdomyolysis.

Treatment and Disposition

Initial treatment includes placing the patient in a cool place and giving adequate cool water and salted (<200 mOsm/L) fruit drinks or salt tablets according to the estimated amount of water and salt depletion. If the patient is unable to drink fluids, give normal saline or lactated Ringer's supplementation intravenously in accordance with clinical and laboratory findings. If marked hyponatremia with water intoxication is present, administration of intravenous hypertonic saline may be required (Chapter 43).

Hospitalize patients with moderate to severe symptoms and those who are elderly or have comorbid illnesses.

Heat Stroke

Essentials of Diagnosis

• Extremely high body temperatures causing altered mental status and multiorgan dysfunction
• Rhabdomyolysis and severe hepatic damage occur
• Treatment is rapid reduction in body temperature

General Considerations

Heat stroke is caused characterized by dysfunction of the heat regulating mechanism, with altered mental status (ranging from confusion to coma) and elevated core body temperature in excess of 41°C (105.8°F). Sweating is variable. The extremely high body temperature rapidly causes widespread damage to body tissues, with significant rhabdomyolysis and multiorgan dysfunction. Illness and death result from destruction of cerebral, cardiovascular, hepatic, and renal tissue.

Heat stroke usually follows excessive exposure to heat and/or strenuous physical activity under exceptionally hot environmental conditions, although it may develop in elderly, infirm, or otherwise susceptible individuals in the absence of unusual exposure to heat. Cardiovascular disease, diabetes, cystic fibrosis, alcoholism, obesity, recent febrile illness, and debility are predisposing factors. Anesthetics, paralyzing agents, diuretics, sedatives, antidepressants, and anticholinergic drugs may also be contributing factors.

Clinical Findings

Symptoms and Signs

Premonitory findings include headache, dizziness, nausea, diarrhea, and visual disturbances. Most patients have profound central nervous system dysfunction including seizures, delirium, and coma. The skin is hot, flushed, and usually dry (although sweating may be present). Prior to cardiovascular collapse, the pulse may be strong and rapid due to an increase in cardiac output with no change in stroke volume. Blood pressure is initially elevated or unchanged, and hypotension is a late finding that signals circulatory collapse. Hyperventilation may cause initial respiratory alkalosis, which is generally followed by metabolic acidosis. Stigmata of coagulopathy may be present and include hematuria, hematemesis, bruising, petechiae, and oozing at sites of venipuncture. Core body temperatures as high as 46°C (114.8°F) have been reported in some patients who have achieved full recovery.

Laboratory Findings

Laboratory findings include hemoconcentration, decreased blood coagulation, and evidence of disseminated intravascular coagulation. Hypoprothrombinemia, hypofibrinogenemia, or thrombocytopenia may be present. The white blood cell count is routinely elevated. Hypophosphatemia and hypokalemia sometimes occur. Hyperkalemia is associated with acute renal failure due to rhabdomyolysis. The patient has scantly concentrated urine (“machine oil urine”) containing protein, tubular casts, and myoglobin. A consistent finding in patients with heatstroke is severe hepatic injury. Serum transaminase levels rise to tens of thousands, although complete recovery usually ensues if treatment is initiated quickly.

Treatment

Act quickly to prevent further damage. The most critical objectives of treatment are rapid cooling and cardiovascular support.

Airway and Ventilation

Maintain an adequate airway and ventilation; monitor arterial blood gas levels. Give supplemental oxygen, 6–10 L/min, by mask or nasal cannula.

Temperature Reduction

Reduce body temperature promptly. As a first-aid measure, place the patient in a shady, cool place and remove his or her clothing. Sprinkle the patient's entire body with water, and cool by fanning. Alcohol sponge baths are contraindicated and can result in alcohol toxicity. If the victim is near a cold stream, it may be helpful to immerse the patient in the water to facilitate cooling.

In the emergency department, place the patient on a cooling blanket, and place ice packs on the axilla, posterior neck, and inguinal areas (do not apply ice directly to the skin). Water should be sprayed on the patient with a fan blowing on him or her to maximize evaporative cooling. If the temperature cannot be rapidly lowered, or if the victim is unresponsive and the initial core temperature exceeds 42°C (107.6°F), begin peritoneal lavage with cold potassium-free dialysate, 2 L every 10–15 minutes. If a patient requires dialysis, then extracorporeal blood cooling is possible during dialysis. This is also possible via cardiopulmonary bypass, which is a rarely used but extremely effective option. When the rectal temperature drops to 39°C (102.2°F), discontinue active measures to lower temperature to avoid hypothermia, but continue temperature monitoring. Hyperthermia may recur due to thermoregulatory instability, and additional cooling may be required.

Benzodiazepines may be given as needed to control shivering. Because the hypothalamic set point is not elevated as it is in fever, aspirin and acetaminophen have not been found to be helpful. They may even worsen coagulopathy and liver damage.

Maintenance of Urine Output

Maintain adequate urinary output (30–50 mL/h). Insert an indwelling urinary catheter to monitor urine output. If myoglobinuria is present, rehydrate the patient with isotonic saline, alkalinize the urine with intravenous administration of bicarbonate, and consider the use of mannitol, 0.25 g/kg intravenously, to promote diuresis. Maintain blood pressure and urine output with intravenous infusion of crystalloid solutions and inotropic agents as necessary (monitoring of central venous pressure or pulmonary capillary wedge pressure may be required). α-Adrenergic drugs are contraindicated because they produce vasoconstriction and decrease heat exchange. Dobutamine may be preferable to dopamine as an inotropic agent, because it does not have the α-adrenergic renal effects associated with dopamine at rapid rates of infusion.

Disposition

Hospitalize all patients whose core temperature has exceeded 41°C (105.8°F) for treatment of possible complications (disseminated intravascular coagulation, renal failure, hepatic failure, rhabdomyolysis, cardiac arrhythmias, myocardial infarction, and coma).

With early diagnosis and proper care, 80–90% of previously healthy patients should survive. Extreme hyperpyrexia (rectal temperature >42°C [107.6°F]), persistent coma after cooling, markedly elevated alanine aminotransferase (serum glutamic pyruvic transaminase) and aspartate aminotransferase (serum glutamic oxalacetic transaminase) levels, and hyperkalemia associated with extensive rhabdomyolysis are unfavorable prognostic signs.

Lightning Injuries

Essentials of Diagnosis

• Lightning injuries can result not only in burns but also in multiorgan dysfunction
• Respiratory arrest is the most common cause of death; ventricular fibrillation and asystole are also seen in severe cases
• Management is the same as that for a person with blunt trauma

General Considerations

The United States National Weather Service estimates approximately 60–100 deaths in the United States and 24,000 deaths worldwide due to lightening strikes annually. A reported 30% mortality and 70% morbidity is noted. Epidemiology centers in the mountainous states and the southeastern United States. Strike events cluster in the summer months and in the mid-afternoon, with 84% of victims being male. Injuries are caused by a direct strike, splash (ie, from trees, buildings, and fences), step voltage (spreading on ground), upward leaders, and blunt trauma from concussive shockwaves.

Clinical Findings

Suspect lightning injury in a person found dazed, unconscious, or injured in the vicinity of a thunderstorm. Certain pathognomonic clinical signs help to establish the diagnosis. Victims may appear initially pulseless with mottled extremities due to autonomic dystrophies and sometimes cardiac standstill. Triage of lightning strike victims differs from other multiple casualty scenarios in that the dead appearing are addressed first.

Burns

Lightning contact with the body is instantaneous; a flashover phenomenon may channel most of the current along the outside of the body (over the skin) rather than through the victim, as occurs in other types of electrical injury.

Linear burns

Linear burns are first- and second-degree burns that begin at the head and neck and course in a branching pattern down the chest and legs. They tend to follow areas with a heavy concentration of sweat.

Punctate burns

Punctate burns are clusters of discrete, circular, partial- or full-thickness burns that form starburst patterns on the skin.

Feathering burns

Feathering burns are not true burns but rather cutaneous imprints from electron showers that track through the skin. They create a fernlike pattern with delicate branching. These patterns are also called ferning, keraunographic markings, and Lichtenberg flowers or figures.

Thermal burns

Thermal burns from clothing or heated metal are typical second- and third-degree burns. Cranial burns (direct or indirect head strike) and leg burns (ground current) are associated with increased death rates.

Altered Mental Status

Victims of lightning strikes are usually amnestic and may be disoriented, combative, or comatose.

Cardiac Arrest

Cardiopulmonary standstill may be induced by the massive DC countershock of the lightning strike and is the leading cause of mortality. Asystole is more common in lightning strikes as opposed to fibrillation in electrical shock injury. Spontaneous resumption of normal cardiac function is the rule if cardiac standstill is not complicated by simultaneous respiratory arrest (brain-stem shock or contusion). Cardiac necrosis may develop with evolving ECG changes and QT prolongation.

Neurologic Injuries

Central nervous system injuries include traumatic brain and spinal cord injury, coagulation parenchymal injuries, seizure, and anoxic brain injury. Autonomic dystrophies occur. In addition, epidural and subdural hematomas (due to associated falls), subarachnoid hemorrhage, loss of consciousness, and peripheral neurovascular instability are common. Anterograde amnesia and confusion are noted in most patients. Paraplegia and quadriplegia have also been described. Chronic effects include paralysis, chronic pain, and neuropsychologic disorders.

Musculoskeletal Injuries

Victims of lightning strikes are frequently thrown to the ground by tetanic muscle contractions, or they may be injured by falls from heights. Fractures of the spine, ribs, and extremities may occur. Intrathoracic and intra-abdominal injuries result from blunt trauma.

Eye and Ear Injuries

Eye injuries associated with lightning strikes include cataracts, corneal abrasions, hyphema, uveitis, vitreous hemorrhage, and iridocyclitis. Note: Dilated pupils should never be the sole criterion for termination of resuscitative efforts, because they may merely reflect transient autonomic sympathetic discharge or parasympathetic inhibition. Temporary sensorineural hearing loss with or without rupture of the tympanic membrane may result from acoustic and shock wave barotrauma.

Treatment

Maintain the Airway, and Begin Cardiopulmonary Resuscitation

CPR should be instituted immediately. Blown pupils are not a reliable indicator of death as cranial nerve palsy is common. Transport and evacuation should not be delayed; prolonged CPR is only anecdotally successful.

Anticipate Traumatic Injury

Managing the lightning strike victim is analogous to the blunt trauma evaluation. Particular attention to hypothermia, skeletal and spinal fracture, and thoracoabdominal injury is necessary. Indicated studies include appropriate radiographs, ECG, and laboratory tests including CK, cardiac enzymes, electrolytes, urinalysis with myoglobin, lactate, and hemogram. CT of the head is indicated in altered and loss of consciousness.

Begin Burn Therapy and Fluid Replacement

Management of burn wounds follows standard procedures (Chapter 45). Administration of intravenous fluids should be adjusted according to blood pressure readings and urine output. Rhabdomyolysis is rare, and alkalization of the urine and administration of mannitol are not necessary unless myoglobinuria is present. Overhydration may result in cerebral edema. Tetanus should be updated appropriately (Chapter 30).

Disposition

Prolonged cardiac monitoring and serial cardiac enzymes are required only if the patient has a history of cardiac arrest, loss of consciousness, cardiac arrhythmia, abnormal ECG, or if admission is considered for other reasons (burns, trauma). Record results of visual acuity and hearing tests to establish baseline measurement. If the victim has experienced cardiopulmonary arrest and resuscitation efforts have been successful (resumption of spontaneous cardiac activity), allow a minimum of 12–24 hours before weaning the patient from the ventilator to see if spontaneous respiratory activity resumes. If electroencephalographic abnormalities are present, they may clear over 24–72 hours.

Electric Shock and Burns

Essentials of Diagnosis

• Direct current is less dangerous than alternating current (AC)
• AC (most house current) can cause ventricular fibrillation and respiratory arrest
• Burns can result from the electrical current and, although they may look mild, can indicate significant internal damage
• Treatment includes CPR, wound care, and possibly fasciotomy

General Considerations

Electric shock is the response to current flow through the body. Voltage is the pressure behind the current flow. Electrical injuries are the cause of around 1000 deaths in the United States each year. Young men and children are the most commonly injured. The severity of electrical injury is influenced by the type of current as well as the amount of voltage involved.

Alternating current (A/C) refers to an alternating/changing voltage. AC causes tetanic muscle contractions that may lead to inability of the victim to separate from the source, prolonging contact. This may ultimately lead to increased electrical injury to the heart causing fatal arrhythmias.

Direct current refers to unidirectional flow caused by change in voltage difference. For example a utility worker may receive a lethal shock if electric current passes from a high voltage power line in contact with a metal object while the worker is also touching the object. The worker is “grounded” at what is considered 0V (earth). The metal object between the power line and the high voltage wire (7200V) completed the circuit and allowed current to flow from the line to the ground, through the worker.

Tissues of the body differ in resistance to electricity. Skin serves as a protective mechanism at low voltage (<500V). At higher voltage, protective resistance of skin is reduced, generally resulting in more significant injury to internal structures. The protective resistance of skin is decreased with moisture and breaks in the skin. Low resistance pathways include muscular and vascular systems leading to cardiac and vascular damage as well as compartment syndromes.

Clinical Findings

Electric Shock

Electric shock may produce momentary or prolonged loss of consciousness. Ventricular fibrillation is the most serious immediate arrhythmia, although ectopic beats, sinus tachycardia or bradycardia, atrial fibrillation, and asystole occur. Seizures, deafness, blindness, aphasia, and neuropathy can also result from electric shock. Multiple orthopedic injuries may be seen, including posterior shoulder dislocations and femoral neck fractures.

After recovery from mild to moderate electric shock, muscular pain, fatigue, headache, and generalized or focal nervous irritability occur. Physical signs vary according to the sites of action of the current.

Electrical Burns

Small direct electrical burns may hide significant internal organ burns. Extensive skin necrosis and sloughing may not become evident for several days. With internal organ injury, third spacing of fluid is marked. Rhabdomyolosis may also occur.

Treatment

Electric Shock

Free the victim from the current at once. This may be done in many ways, but the rescuer must be protected. Turn off the power, sever the wire with a dry wooden-handled ax, make a proper ground to divert the current, or drag the victim carefully away using dry clothing, a leather belt, rubber, or other dry nonconductive materials. Check cardiac and ventilatory function. If the patient is apneic or pulseless, begin artificial ventilation or CPR (Chapter 9).

Electrical Burns

Treat tissue burns conservatively. The direction and extent of tissue injury may not be apparent for 7–10 days. Treat circulatory shock, if present, with intravenous infusion of crystalloid solutions. Serum CK-MB isoenzyme levels may be falsely elevated immediately after high-voltage electrical injuries and should not be considered a reliable indicator of myocardial damage. Monitor cardiac rhythm to detect rhythm disturbances in unconscious victims, those who have presented with cardiac arrhythmias, or those with an abnormal ECG. If myoglobinuria is present, monitor arterial blood pH at regular intervals to detect acidosis, which requires intravenous bicarbonate therapy to alkalinize the urine and maintain blood pH above 7.45. Consider intravenous mannitol, 2.5 g initially, to promote moderate diuresis in patients whom have inadequate urine output inspite of aggressive hydration with intravenous isotonic solutions.

Assess the need for fasciotomy by measurement of intracompartmental tissue pressures. In children who have bitten electrical cords, be alert for delayed (up to 3 weeks) erosion of the labial artery, which can manifest as significant bleeding.

Disposition

Hospitalize patients who have lost consciousness or experienced cardiac or respiratory arrest, as well as those with ischemic chest pain, myoglobinuria, or significant burn wounds. Cardiac/ICU monitoring may be unnecessary for those without extensive injury, ECG changes, or those without cardiac history. Continued monitoring is not necessary for patients, including children, who are asymptomatic with no initial ECG changes and no increased risk factors for arrhythmias if injury is due to low voltage (220–240 V) source.

Radiation Injuries

Essentials of Diagnosis

• Radiation exposure can cause damage to multiple organ systems
• Organ system damage depends on the dose of radiation delivered

General Considerations

The effects of radiation have been observed in the clinical use of X-rays and radioactive agents, after occupational or accidental exposure, and following the use of atomic weapons or radiologic dispersion device or “dirty bomb.” The harm depends on the quantity of radiation delivered to the body, the type of radiation (X-rays, neutrons, gamma rays, or alpha or beta particles), the site of exposure, and the duration of exposure. Clinical signs and symptoms relate directly to amount received. In radiation terminology, a rad is the unit of absorbed dose and a rem is the unit of dose of any radiation to body tissue in terms of its estimated biologic effect. The gray (Gy) is a unit of measurement for the dose of ionizing radiation equal to 1 J/kg of tissue. One gray is equal to 100 rad.

Clinical Findings

Localized Radiation Exposure

Irradiation causes delayed erythema, epilation, destruction of fingernails, or epidermolysis, depending on the dose. Symptoms develop 1–3 weeks postexposure.

Injury to Internal Organs

Hematopoietic tissues

Injury to bone marrow may cause a decrease in production of blood elements. Lymphocytes are most sensitive, polymorphonuclear neutrophils next most sensitive, and erythrocytes least sensitive. Damage to blood-forming organs may vary from transient depression of one or more blood elements to pancytopenia. The degree of lymphocyte depression within the first 24–48 hours can be used to estimate the dose received.

Cardiovascular system

Pericarditis with effusion or constrictive pericarditis may occur many months after exposure to ionizing radiation. Myocarditis is less common than pericarditis. Smaller vessels (capillaries and arterioles) are more readily damaged than larger blood vessels. If injury is mild, recovery of function occurs.

Gonads

In males, small single doses of radiation (2–3 Gy; 200–300 rads) cause transient aspermatogenesis, and larger doses (6–8 Gy; 600–800 rads) may cause sterility. In females, single doses of 2 Gy (200 rads) may produce sterility. Moderate to heavy irradiation of the embryo in utero results in injury to the fetus or causes embryonic death and abortion.

Respiratory tract

High or repeated moderate doses of radiation may cause delayed pneumonitis (weeks or months).

Mouth, pharynx, esophagus, and stomach

Mucositis with edema and painful swallowing of food may occur within hours to days after exposure to radiation. The salivary glands are relatively radioresistant. Gastric secretion may be temporarily (occasionally permanently) inhibited by moderately high doses of radiation.

Intestines

Loss of mucosa with ulceration and inflammation may follow moderately large doses of radiation leading to massive fluid losses via bloody diarrhea and vomiting.

Viscera and endocrine glands

Hepatitis and nephritis may be delayed complications of therapeutic irradiation. Normal thyroid, pituitary, pancreas, adrenals, and bladder are relatively resistant to low to moderate doses of radiation.

Nervous system

High doses of radiation may damage the brain and spinal cord by impairing their blood supply. Peripheral and autonomic nerves are highly resistant to radiation.

Systemic Reaction (Acute Radiation Sickness)

Symptoms vary with type and amount of exposure. Each phase will be shortened for increasing dosages. The prodromal phase consists of incapacitating vomiting and malaise. Time to onset of vomiting is an excellent screening tool to determine amount of radiation received. An asymptomatic latent phase then follows. A third phase then occurs with dose-dependent symptoms and findings. Bone marrow suppression may occur as early as 24 hours. A gastrointestinal syndrome involving massive fluid losses and bloody diarrhea will begin a few days to a week after exposure to higher doses. The neurovascular syndrome will occur with extremely high doses within a few hours to 1–3 days. This syndrome includes seizures, coma, and eventual death.

Mild acute radiation sickness (ARS)

Exposure consists of 1–2 Gy. There is a prodrome of vomiting 2 hours or more postexposure. Patient otherwise feels well. At 30 days or more, there will be a slight decrease in lymphocyte count and platelets. Patient will feel mild malaise and weakness. Lethality is 0%.

Moderate ARS

Exposure consists of 2–4 Gy. There is prodrome of vomiting approximately 1–2 hours postexposure. There may be a mild headache with slight increase in body temperature. At 3–4 weeks, there will be a more significant decline in lymphocyte and platelet counts. Patient will manifest fever, infection, bleeding, and weakness. Lethality is 0–50%.

Severe ARS

Exposure consists of 4–6 Gy. There is prodrome of vomiting less than 1 hour and bloody but mild diarrhea in 3–8 hours. Patient will have moderate headache. At 1–3 weeks, there will be significant decline in lymphocyte and platelet counts. High fever, infection, bleeding, and epilation will begin. Lethality is 20–70%.

Very Severe ARS

Exposure consists of 6–8 Gy. Prodromal vomiting begins at less than 30 minutes. Massive bloody diarrhea, severe headache, and confusion being at approximately 3 hours. In less than 1 week, extreme decline in lymphocyte and platelet counts occur with high fever, infection, massive vomiting, diarrhea, and disorientation. Lethality is 50–100%.

Lethal ARS

Exposure consists of more than 8 Gy. Vomiting is immediate. Massive diarrhea, coma, and seizures ensure within 1–2 hours. In less than 3 days, lymphocyte count becomes 0.0–0.1 g/L with platelets counts less than 20,000. Patient remains comatose with seizure, bleeding, and infections. Lethality is 100%.

Treatment

Decontamination

Decontamination in most instances will occur prior to arrival at a medical facility. If it does not, simple removal of clothing with placement in marked containers will achieve 90% reduction in contamination. Bare skin and hair should be washed thoroughly with soap and water and the effluent secured for disposal. Radioactive particles will not cause acute injury to medical personnel and should not interfere with emergency management. Wounds should be gently irrigated, debrided, and then covered. Foreign bodies should be removed on an emergency basis. After decontamination, a Geiger counter should be passed over patient to determine effectiveness.

Local Treatment

Treatment consists of pain control and prevention of infection. Once the extent of injury is determined, grafting or amputation may be necessary.

Systemic Treatment

Resuscitation and stabilization of medical and surgical issues should always occur first. After this is accomplished, minimization or prevention of internal contamination should occur. Finally external decontamination should be performed. Treatment of patients with ARS is largely supportive. Massive fluid resuscitation, antiemetics, and blood products may be needed. There are specific medical treatments for radiation, though their effectiveness and safety are still under investigation: (1) colony-stimulating factors have been recommended for healthy victims with exposures >3 Gy and for injured patients >2 Gy; (2) bone marrow transplants have been successfully used in large-dose irradiation cases with subsequent marrow failure; (3) potassium iodine is used orally with radioiodine exposure to prevent thyroid uptake; (4) Prussian blue taken orally increases excretion of cesium and thallium; and (5) Ca− and Zn− DTPA given intravenously chelate plutonium, americium, and curium with subsequent excretion in the urine.

Disposition

All patients with signs or symptoms of radiation exposure must be hospitalized. Advice may be obtained from the Radiation Emergency Assistance Center/Training Site (REAC/TS) in Oak Ridge, TN ([865] 576–3131). The 24-hour emergency network telephone number is (865) 481–1000.

General Considerations

According to the World Health Organization, 409,272 people died from drowning in the year 2000, following only traffic accidents in worldwide mortality. Drowning affects children disproportionately, with residential pools and shallow water drowning (in toilets and buckets comprising as much as 17% in certain populations). Young males suffer an increased rate of mortality as well. Comorbidities leading to drowning include intoxication, trauma (especially in shallow water and high-speed injuries), seizures, arrhythmia, coronary artery disease, hypoglycemia, and hypothermia. Aspiration invariably seems to be present, “dry” drownings probably occur with preaspiration cardiac arrest, or post-event fluid shifts of the aspirate across the alveoli into the circulation. Pulmonary edema and electrolyte abnormalities occur in fresh and saltwater drowning. Decompression illness (DCI) necessitates consideration in scenarios of diving accidents.

Clinical Findings

The victim of near-drowning may present with a wide range of clinical manifestations. Spontaneous return of consciousness often occurs, as does response to brief CPR, both being predictors of good outcome. Vomiting is common. Patients with more severe near-drowning may develop ARDS, hypoxic encephalopathy, or cardiac arrest. A few patients may be deceptively asymptomatic during the recovery period, only to deteriorate as a result of acute respiratory failure in the ensuing 6–24 hours. Reported complications include unique pneumonias such as leptospirosis due to brackish water aspiration, leading to bacterial seeding and brain abscesses.

Symptoms and Signs

The patient may be unconscious, semiconscious, or awake and apprehensive. Cyanosis, trismus, apnea, tachypnea, and wheezing may be present. A pink froth from the mouth and nose indicates pulmonary edema. Cardiovascular manifestations may include tachycardia, arrhythmias, hypotension, shock, and cardiac arrest. Decerebrate or decorticate posturing may be noted in the comatose patient.

Laboratory Findings

Metabolic and respiratory acidosis may coexist. Sodium, potassium, calcium, and magnesium electrolyte disturbances are found. Renal failure and rhabdomyolysis may also evolve.

X-Ray Findings

Initial chest X-rays may show aspiration of fluid; late findings may betray fulminate pulmonary edema or ARDS. Routine chest X-rays are indicated to evaluate for pneumonitis before discharging even in apparent mild cases.

Treatment

Before effective CPR can be accomplished, extract the victim from the water in the prone position. Potential for circulatory collapse exists, with sudden removal of surrounding water pressure in the upright position. Prompt initial resuscitation is best predictor of long-term morbidity. The Heimlich maneuver should not be performed unless there is an airway obstruction. Cervical spine immobilization should be maintained in shallow water, surfing, or trauma victims.

Open Airway and Maintain Ventilation

Open the airway, and ventilate the patient with early intubation for airway protection as necessary. Give oxygen in high concentrations; positive end-expiratory pressure ventilation is used to maintain Pao2 with frequent blood gas measurements. Ventilation is preferred with 6 mL/kg tidal volumes and Fio2 of 0.6 to avoid barotrauma and oxygen toxicity. Effort is made to maintain normocapnea and normoglycemia.

Establish Circulation

Check for a carotid or femoral pulse. Institution of CPR should begin immediately if pulseless; hypothermic vasoconstriction may mask a shallow pulse. Chest compressions and defibrillation in hypothermia may precipitate arrhythmia. Central venous access and monitoring aid in fluid resuscitation.

Treat Hypothermia

Monitor core temperature rectally. Rewarming patients with forced air heating is effective in temperatures as low as 26°C. Hypothermia with cardiac arrest is an indication for extracorporeal rewarming and cardiopulmonary bypass. Complete recovery has been reported after prolonged resuscitative efforts, even when victims have had dilated, fixed pupils. This is particularly true of infants and children, in whom the brain is protected by hypothermia. Recovery is unpredictable; therefore, resuscitation efforts should be attempted in most cases. In adults, mild hypothermia in near-drowning-associated coma, with goal temperature of 33°C for 12 hours, has been shown to be of some benefit, though mortality was increased in a series of therapeutic hypothermia in children.

Disposition

Near-drowning victims who are initially asymptomatic must be monitored for respiratory distress that develops typically within 6 hours. If the patient has a normal physical examination and respiratory effort, a presentation of Glasgow Coma Scale score of 15, and a room air oxygen saturation of 95% or better with a normal chest X-ray, they may be safely discharged home after 6–8 hours.

Decompression Illness (Caisson Disease, “Bends”)

Essentials of Diagnosis

• Caused by release of nitrogen bubbles from plasma and tissues during ascent
• Type1—joint pain; Type2—cardiorespiratory or neurologic involvement
• Treatment is immediate recompression in a hyperbaric chamber

General Considerations

The popular sport of scuba diving has exposed a large number of variably trained individuals to the hazards of decompression illness (DCI). DCI occurs in recreational, commercial, and military endeavors involving diving, but also with barometric changes seen in un-pressurized flight. Divers using conventional diving gear (scuba [self-contained underwater breathing apparatus]) breathe oxygen-containing gas mixtures that are at the same pressure as that of the surrounding water. Boyles law dictates that volumes of gas are dependent relative to varying pressures (P1V1 = P2V2). Ambient pressure at 1 atm (sea level) is 760 mm Hg and increases 1 atm for every 33 ft of seawater depth. Boyles law accounts for the barotrauma seen in rapid descent and ascent involving the pulmonary, ENT, gastrointestinal, and other organ systems. Lung squeeze, a descent phenomenon, occurs as total lung volume decreases to less than the residual volume, causing alveolar hemorrhage, pulmonary edema, and hypoxia. On unequalized ascent, pulmonary over-pressurization syndromes arise, leading to pneumothorax, pneumomediastinum, and systemic arterial gas embolism, addressed in the following section. Dalton's gas law integrates the independent partial pressures of various gases in solution adding to total pressure (Ptotal = PN2 + Po2 + Pco2). Henry's law shows that gas equilibriation across permeable membranes relates to the partial pressure and concentration of each gas. Dalton's and Henry's laws explain, how during rapid ascent, external pressure decreases, dissolved gases (predominantly nitrogen) escape from solution as gas bubbles, causing endothelial inflammation and problematic mass effects in musculoskeletal, cerebral, and cardiac systems. These effects are known as “the bends.” Analogous processes occur in rapid ascend to altitudes above 2000 m (6600 ft) in unpressurized aircraft.

Clinical Findings

Type 1 DCI, or the minor symptom complex, includes deep, aching pain in the large joints and extremities otherwise known as “the bends.” The elbow and shoulder are most commonly affected. Cutaneous marmorata is a pathognomic rash involving gas bubbles in small cutaneous vessels.

Type 2 DCI involves any cardiorespiratory or neurologic symptoms, including generalized fatigue. Typical neurologic findings are ataxia, spinal paralysis, vertigo, visual or speech disturbance, and cognitive deficits. Spinal cord emboli can occur in scuba divers, while the upright position in high-altitude flight predisposes to cerebral gas emboli. Chest pain and shortness of breath occur with involvement of pulmonary and cardiac circulation.

Treatment

Early Measures

Give oxygen, 100%, by mask for at least 2 hours. Give mild analgesics and crystalloid intravenous fluids to maintain hydration.

Recompression

Prompt recompression therapy is indicated in any symptomatic DCI. Resultant chronic symptoms may be altered even by delayed treatment. Persistent symptoms are treated with recompression until resolved or plateau is reached. Navy dive tables for types I and II illnesses are available for the recompression treatment course. Physicians should know the location of the nearest hyperbaric chamber. In the United States, 24-hour clinical advice may be obtained rapidly by telephoning the National Diving Alert Network (DAN) at Duke University [919] 684–9111.

Complications

Further measures may be necessary to relieve some of the complications associated with the bends (eg, shock, spinal cord injury, bladder paralysis, hemoconcentration, and disseminated intravascular coagulation).

Disposition

Transport the patient immediately to the nearest recompression center (hyperbaric chamber) for evaluation and treatment. A patient who is transported to a hyperbaric chamber by aircraft should not be exposed to a cabin altitude higher than 300 m (1000 ft). Commercial flight after DCI should be avoided until resolved or for 1 week. Caution: Never attempt recompression in the water.

Arterial Gas Embolism

Essentials of Diagnosis

• Increased pressure in the lungs causing air to escape from alveoli
• Results in air in the interstitial space or in the pulmonary venous circulation
• Can result in pneumothorax or occlusion of the coronary and cerebrovascular systems
• Treatment is immediate recompression in a hyperbaric chamber

General Considerations

In arterial gas embolism, gas bubbles precipitate from solution and cause problematic mass effects in the circulation. Gas bubbles form in the relatively low pressure venous circulation. Entry into the systemic left-sided circulation occurs through arteriovenous connections, commonly a patent foramen ovale. Dramatic presentations will betray arterial gas embolisms. If symptoms occur more than 10 minutes after surfacing, large air embolism is less likely. Many victims of arterial gas embolism die immediately upon surfacing. If air bubbles enter the cerebral circulation, the victim becomes unconscious or has a seizure during ascent or immediately upon surfacing. Presentation is stroke-like, with blindness, confusion, or symptoms based on anatomic distribution.

Central Circulation

Cerebral embolism is analogous to stroke presentations. If the bubbles have entered the coronary arteries, the person presents with symptoms similar to those of acute myocardial infarction, with chest pain, arrhythmias, and collapse. Complete, sudden circulatory collapse occurs with occlusion of the central circulation. Pulmonary artery or cardiac chamber obstruction has been described as “the chokes.”

Pneumothorax

Signs of pneumothorax or mediastinal emphysema develop more slowly and are not as life-threatening; signs include shortness of breath, hyper-resonance of the chest to percussion, and decreased breath sounds on the affected side. Subcutaneous crepitus that may extend into the neck occurs.

Treatment

Early Measures

Give oxygen, 100%, by mask. Position the victim supine on the left side to prevent aspiration. Chest tube insertion is indicated for symptomatic pneumothorax. Maintain urine output at 1–2 mL/kg/h with intravenous fluids.

Recompression

Immediate recompression is the only effective treatment; the patient should be transported to a hyperbaric chamber immediately (see Decompression Sickness section earlier in this chapter).

Disposition

Transport the patient immediately to the nearest recompression center (hyperbaric chamber) for evaluation and treatment.

High-Altitude Sickness (Mountain Sickness)

General Considerations

High-altitude illnesses are a spectrum of diseases that affect unacclimatized people in the relative hypoxia of altitude. The effects can be seen in high rates of ascent of passengers in unpressurized aircraft as low as 1500 m (4921 ft), to the extremely high altitudes of 5500–8850 m (18,000–29,035 ft) reached by expedition trekkers and climbers. Rapid ascent, a history of altitude illness, physical exertion, obesity, and a myriad of comorbid diagnosis predispose individuals to the effects of altitude. Physical fitness is not itself a protective factor. Hypoxic ventilatory response is the key in acclimatization, with eventual adjustment to the respiratory alkalosis with a metabolic compensation.

Acute Mountain Sickness

Essentials of Diagnosis

• Headache with a myriad of related symptoms
• Treatment is descent, oxygen, and antiemetics
• If descent is not possible, dexamethasone or acetazolamide can be used to aid acclimatization

Clinical Findings

Acute mountain sickness (AMS) is defined as headache at altitude and one of the following: anorexia, nausea, vomiting, fatigue, weakness, dizziness, lightheadedness, or insomnia. AMS is self-limited, but may progress to the more severe manifestations of high-altitude cerebral edema (HACE) or high-altitude pulmonary edema (HAPE). Onset ranges from 1 hour to 3 days.

Treatment

Treat mild cases with rest, allowing physiologic acclimatization before further ascent. NSAIDs and antiemetics may be useful. Avoid alcohol and narcotics/sedatives that may decrease the ventilatory response, especially while sleeping. Moderate cases can be treated with acetazolamide to speed acclimatization, and dexamethazone 4–6 mg PO Q6 hours. Descents of 1000–3000 ft may alleviate symptoms, the definitive treatment for progressive symptoms. Simulated descents of 1000–2000 ft can be achieved with portable pressurized chambers (Gamow bag), when available and rapid descent is not possible in remote settings. Acetazolamide 125–250 mg PO b.i.d. has been shown effective in AMS prophylaxis, starting 1 day prior to ascent, continuing to day 4. Treatment doses are the same; the pediatric acetazolamide dose is 2.5 mg/kg. Avoid acetazolamide in those with sulfonamide/sulfite allergy. Dexamethazone 2–4 mg every 6 hours is also effective. Graded ascents of 600 m per day with rests should allow sufficient acclimatization, preventing AMS.

Disposition

If symptoms persist, descent is the definitive therapy.

Acute High-Altitude Pulmonary Edema

Essentials of Diagnosis

• Noncardiogenic pulmonary edema due to rapid ascent above 2400m(8000 ft)
• Cough and dyspnea on exertion lead to pink, frothy sputum and respiratory distress
• Chest X-ray findings show patchy infiltrates but normal heart size
• Treatment is rapid descent, continuous positive pressure ventilation, oxygen, and nifedipine

Clinical Findings

HAPE carries the greatest mortality of the altitude illnesses. Reported as low as 2400 m (8000 ft), a noncardiogenic pulmonary edema arises after hypoxic vasoconstriction and elevated right heart pressures. Risk for HAPE includes AMS, rapid ascent, congenital absence of one pulmonary artery, and brief sojourn at high altitude by persons acclimatized to living at low altitudes.

Symptoms and Signs

HAPE diagnosis can be made when two from each of the following are present: symptoms—dyspnea at rest, cough, weakness, decreased performance, and chest tightness; signs—crackles, wheezing, central cyanosis, tachypnea, and tachycardia. Rapid progression may occur to florid pulmonary edema and death.

Laboratory Findings

Brain natriuretic peptide levels may differentiate cardiogenic pulmonary edema and HAPE. Secondary signs of inflammation may be seen, with elevated hematocrit. Echocardiogram and/or pulmonary artery wedge pressures may be useful in further differentiating disease.

X-Ray Findings

Findings on chest X-ray are variable. In mild disease, patchy infiltrates in a solitary lung field (commonly the right middle lobe) are noted. The infiltrates rarely coalesce and generally do not involve the base of the lungs. The central pulmonary arteries are dilated, but the cardiac shadow is of normal size. In severe illness, infiltrates are more generalized, but no left atrial enlargement or Kerley B lines are noted. Unilateral pulmonary edema is consistent with unilateral atresia of the pulmonary artery.

Treatment

Early recognition of the disease is crucial. Persistent dry cough and dyspnea in a person who has recently arrived at high altitude should be considered high-altitude pulmonary edema until proven otherwise. Treatment centers on rest and descent. Exertion and cold stress should be avoided. Oxygen is administered by facemask at 4–6 L/min until symptoms are improved, then 2–4 L/min if supplies need to be conserved. Oxygen is continued for 72 hours even after descent from altitude in severe cases. Remotely, the portable Gamow bag can be used with oxygen, with ventilation of CO2 intermittently. Continuous positive-airway pressure will improve oxygenation during evacuation of patients when available. Nifedipine may be given sublingually, then 20–30 mg PO in sustained release b.i.d. β-Agonist may also be useful, acetazolamide may hasten acclimatization but will not alter HAPE, and there is no role for dexamethazone.

Prevention

Preventive measures include (1) education of prospective mountaineers about the possibility of serious pulmonary edema, (2) gradual ascent to permit acclimatization, and (3) rest and avoidance of strenuous exercise for 1–2 days after arrival at high altitudes. Medical attention should be sought promptly if respiratory symptoms develop.

Patients with a history of high-altitude pulmonary edema have a 60% chance of the illness recurring with repeat ascents. Prophylaxis with nifedipine, 20–30 mg of the extended release form every 12–24 hours, is helpful.

Mountaineering parties climbing at 2400 m (8000 ft) or higher should carry a supply of oxygen and equipment sufficient for several days if hospital facilities are not available.

People with symptomatic cardiac or pulmonary disease should avoid high altitudes. Detection of a heart murmur and recurrent episodes of high-altitude pulmonary edema should prompt investigation for a previously existing valvular, shunt, or pulmonary hypertension problem.

Disposition

Hospitalization is generally recommended if symptoms persist for more than a few hours after return to lower altitudes. Hospitalization in mild cases at altitude has been done with supportive therapy and oxygen if descent is undesirable. Commercial airline flight and further physical exertion both should be avoided until oxygen is no longer needed.

High-Altitude Cerebral Edema

Essentials of Diagnosis

• Cerebral edema due to rapid ascent to altitudes above 2400 m (8000 ft)
• Signs and symptoms include headache, ataxia, papilledema, and global encephalopathy
• Treatment is immediate descent, oxygen, and dexamethasone

Clinical Findings

HACE is an end-stage manifestation in the continuum of mountain sickness. It may occur with or without HAPE. Manifestations are principally neurological, with hypoxic failure of cerebral vascular autoregulation. Truncal ataxia and behavior changes may be the first indication of progression to HACE. Symptoms include those of AMS, and may include confusion, apathy, agitation, and focal neurologic signs including cranial nerve palsy, obtundation, and coma. MRI findings show cerebral edema, with death resultant from brainstem herniation. Retinal hemorrhages and papilledema may be seen.

Treatment

Early recognition and intervention is crucial. Because the symptoms of early high-altitude cerebral edema are similar to those of AMS, anyone with headache and fatigue at high altitude must be watched closely for signs of deterioration.

Oxygen should be administered to maintain saturations more than 90%. HACE is an indication for immediate descent/evacuation to preferably an altitude of 1500 m (4000 ft), or at least down 1000 m (3281 ft). Portable hyperbaric chambers may be used if descent is impossible. Dexamethazone, 8 mg and then 4 mg every 6 hours, is indicated. Acetazolamide may be useful, dosed up to 750 mg per day divided b.i.d. When using nifedipine and acetazolamide, monitor closely for hypotension, as cerebral perfusion pressures must be maintained in HACE.

Disposition

Hospitalization is generally recommended if symptoms persist for more than a few hours after return to lower altitudes.

Snake Bites

Essentials of Diagnosis

• Venomous bites can result from either pit vipers or elapids
• Pit viper envenomation results in symptoms related to cytolysis, whereas elapid bites can result in neurotoxic symptoms
• Antivenom is available for both pit viper and elapid bites and should be administered for symptomatic envenomations

General Considerations

Morbidity and mortality from snake envenomation is a significant problem worldwide. Recent estimates put the global number of snake envenomations at around 421,000 annually with an estimated 20,000 deaths. This number is probably higher given very poor tracking of health statistics in underdeveloped countries and rural areas. Only about one out of every four venomous snakebites actually produces venom, with the rest being dry bites. Death from snakebite in the United States is very rare given the low lethality of venom from indigenous species as well as ready access to medical care and antivenin. Two families of venomous snakes exist in the United States. These families are Elapidae or the coral snake and the family Viperidae subfamily Crotalidae or the rattlesnake, water moccasin, and copperhead.

Snake venom is a complex mixture of proteolytic enzymes and toxic proteins. In general, crotalid venom is mainly cytolytic, whereas elapid venom is mainly neurotoxic.

Clinical Findings

The predominantly cytolytic venom of crotalids can cause edema, hemorrhage, and necrosis around the bite site as well as distant from the site in severe envenomations. Systemic signs and symptoms consist of hemolysis, thrombocytopenia, coagulopathy, vomiting, and, rarely, respiratory failure with cardiovascular instability or collapse.

The predominately neurotoxic venom of elapids and the Mojave green rattlesnake may produce few or no early local signs of envenomation, but neurologic symptoms (paresthesias, blurred vision, dysphagia, hypersalivation, ptosis, and respiratory depression) may appear after a delay of 12–24 hours.

Treatment

Emergency First-Aid Measures

Many of the most well-known first-aid measures are no longer recommended. Cryotherapy, tourniquets, and incision and suction have not been shown to be helpful and, in many cases, cause more harm. The best management is to transport the patient to the nearest hospital. Immobilize the bitten part as if it were a fracture. Keep the patient on strict bed rest, if possible. If the patient has a severe envenomation with progression of symptoms, emergency medical service providers may place a constriction band over the site of the bite. A constriction band is a broad, flat band exerting 20 mm Hg of pressure that still permits one or two fingers under the band. However, if the patient is stable, application of a constriction band is not recommended, even if transport time is long. If a constriction band or suction device has been placed prior to the arrival of emergency medical services, it should be left in place for transport. Suction devices have been shown to cause injury themselves, however, and can be removed if no liquid is being extracted. It is very helpful to hospital providers if the progression of any swelling and ecchymosis can be outlined and timed.

Hospital Measures

Assess the patient's respiratory and cardiovascular status. Determine if airway management or cardiovascular resuscitation with crystalloid or vasopressors is needed.

Obtain intravenous access. Assess bite site for local progression. Determine species of snake if possible. Check complete blood count, electrolytes, coagulation profile, and urine myoglobin. Type and crossmatch blood.

Crotalidae polyvalent immune Fab, also known as CroFab, is now the antivenin of choice for North American crotalidenvenomations. CroFab should be administered per the manufacturer's recommendations. It should be noted that CroFab is only approved for use in rattlesnake envenomation but has been successfully used and shown to be safe for use in copperhead envenomation as well. The severity of envenomation should be determined based on the progression of local soft tissue damage as well the presence of systemic side effects. Please see (Table 46–1) for dosing guidelines and goals of treatment. Antivenin must be reconstituted and then administered slowly intravenously as a test dose for 10 minutes. If no signs or symptoms of anaphylaxis occur, then the infusion rate may be increased to be complete in 1 hour. Although the incidence of severe allergic reaction to CroFab should be much less than that to the previous horse serum antivenin, there are reports of it occurring. Treatment, if reaction occurs, should be halting of infusion and administration of steroids, epinephrine and diphenhydramine. CroFab should continue to be administered until initial control of the progression of envenomation is achieved. The manufacturer recommends a scheduled maintenance dosing at 6, 12, and 18 hours after initial control is achieved for rattlesnake envenomations to prevent recurrence of venom effects. No evidence exists to suggest this is necessary for other crotalid envenomations. CroFab is being used in the pediatric population and recent small studies have shown both safety and efficacy in this age group. The same amount of antivenin is used in children but it must be reconstituted in smaller volumes to avoid fluid overload.

For coral snake (Eastern or Texas variety) bites, give five vials of Eastern coral snake antivenin.

Tetanus immunization should be updated for all patients and antibiotics administered only if clinical evidence of infection is present.

Myonecrosis after snake envenomation is thought to be due to local venom effect, not from increase compartment pressures. Fasciotomy for increased compartment pressures does not tend to improve outcome in this patient population. It is felt that fasciotomy should be withheld until several vials of antivenom have failed to reverse effects.

Disposition

Place patients requiring antivenom in the ICU for monitoring. Follow-up administration of two vials of CroFab at 6, 12, and 18 hours is recommended for any patient receiving initial treatment with antivenom due to frequent recrudescence of venom effects. Asymptomatic patients with no local progression and normal laboratory values may be discharged after 8 hours with close wound follow-up.

Bee and Wasp Stings

Essentials of Diagnosis

• Most people who experience a Hymenoptera envenomation have only a painful and urticarial lesion at the site of the sting; more severe reactions can occur and result in anaphylaxis and multiorgan dysfunction
• Oral pain control, tetanus prophylaxis, and diphenhydramine are generally the only treatment needed; in severe reactions, airway management, vasopressors, and even dialysis may be needed

General Considerations

Bees, wasps, and ants are members of the order Hymenoptera. In the United States, domesticated honey bees, feral bumblebees, paper wasps, yellow jackets, and fire ants are the most common attackers, although the aggressive, swarming Africanized bees have been present in the United States since the early 1990s. The venom causes hemolysis and destruction of platelets and leukocytes. It is also capable of destroying vascular endothelium and necrosing skeletal muscle.

Clinical Findings

Patients with Hymenoptera envenomation can present with a wide array of signs and symptoms. The most common effect of a sting is a small pruritic and urticarial-type lesion that also causes pain. Ten percent of people have a large local reaction greater than 5 cm in diameter. These reactions may last longer than the smaller lesions. Less than 1% of patients experience a systemic reaction. Some have a milder reaction with only nausea, vomiting, and diarrhea as well as pruritic urticarial lesions distant from the sting site. Rarely a victim will experience anaphylaxis. Persons who experience multiple stings or who are taking β-adrenergic blocking drugs may experience more severe reactions. Immediate and delayed toxic reactions may occur with envenomation by 50 or more stings. These reactions include hemolysis and rhabdomyolysis with subsequent renal failure, thrombocytopenia, disseminated intravascular coagulopathy, and liver dysfunction.

Treatment

Remove stings or fragments by scraping, not with forceps. Apply topical ice packs. Oral pain control, diphenhydramine, and tetanus prophylaxis are usually all that is necessary for small or large local reaction. Mild systemic reactions may require intravenous diphenhydramine as well as intravenous corticosteroids and a short period of monitoring to allow early intervention for progression to anaphylaxis. Anaphylaxis requires intubation, intravenous access, aggressive fluid resuscitation, aerosolized β-agonists for bronchospasm, subcutaneous or intravenous epinephrine, and possibly pressor agents. Toxic reactions will require the above measures with possible blood products, dialysis, and extensive hospital care.

Disposition

Patients with local reactions may be discharged home. Patients with severe systemic reactions require admission. The Phoenix Poison Control Center recommends mandatory 24-hour admission for children, the elderly, and patients with underlying medical problems or if 50 or more stings are sustained. Otherwise, young healthy individuals with massive envenomation require 6 hours of monitoring with initial and discharge laboratory evaluations of renal and liver function, coagulation studies, and red blood cell count; if no abnormalities are found, patients may be discharged home. Studies of sensitized individuals have found that the vast majority never experience escalating symptoms with future stings; many have less severe reactions. Victims with less severe systemic reactions should undergo immunotherapy and carry an emergency epinephrine pen.

Black Widow Spider Bites

Essentials of Diagnosis

• Symptoms of envenomation include severe pain in the bitten extremity and muscle spasms of the abdomen and trunk
• Abdominal muscle spasms can mimic a surgical abdomen
• Severe hypertension and tachycardia can occur
• Treatment includes narcotic analgesics and antivenom in the seriously ill

Clinical Findings

The female black widow spider (Latrodectus mactans) is shiny black, with a red hourglass marking on its abdomen. Only the female is dangerous. This spider is common in California and other parts of the United States. Other Latrodectus sp. may be found in other countries. The venom is a neurotoxin that results in presynaptic neurotransmitter release. The bite itself is minor and often unnoticed at first. Characteristic symptoms of envenomation occur within 10–60 minutes, including severe pain in the bitten extremity and muscle spasms of the abdomen and trunk. Diffuse paresthesias are noted as well as muscle fasciculation, piloerection, and diaphoresis. Headache, nausea and vomiting, hyperactive deep tendon reflexes, and ptosis may be noted. Victims are in agonizing pain; the rigidity of abdominal muscles may mimic a surgical emergency. Severe hypertension and tachycardia may occur. Deaths are rare; at greatest risk are small infants or older patients with preexisting cardiovascular disease. Symptoms peak at 2–3 hours after the bite and may last up to 3–7 days.

Treatment

Most patients respond to narcotic analgesics. Calcium gluconate has not been found to be very effective for pain control in most recent studies. Local applications of ice should be used judiciously, along with immobilization and loose compression dressing. Antivenom should be reserved for use in seriously ill infants and older patients and should be preceded by horse serum sensitivity testing. One vial of antivenom is sufficient for most patients; give one ampule (2.5 mL) in 10–50 mL of normal saline by slow intravenous infusion. There is a high rate of allergic reaction and one case of fatal anaphylaxis with antivenom administration.

Disposition

All patients who have been bitten by a black widow spider should be observed for 12–24 hours, because hypertension and muscle spasm commonly recur. Hospitalization is necessary for all patients under age 14 years, those older than age 65 years, those with a history of hypertension, and those who present with severe symptoms.

Brown Recluse Spider Bites

Essentials of Diagnosis

• The venom of the brown recluse spider is cytotoxic and causes local tissue destruction
• The bite progresses from an initial pustule to a bull's eye like lesion to a larger crater like ulcer (severe cases)
• Most bites require only tetanus prophylaxis and local wound care; more symptomatic patients may require aggressive wound care including excision

Clinical Findings

The brown recluse spider (Loxosceles reclusa; other Loxosceles sp.) has a dark, violin-shaped area on its back. It is found in old wood piles, attics, closets, and clothes piles and prefers dark, undisturbed places. The venom, which contains sphingomyelinase D, is chiefly cytotoxic, causing local tissue destruction by destroying endothelial cells; it also has a hemolytic component, which on rare occasions may cause massive hemolysis. The enzyme may also disrupt nerve impulses, thus causing skin anesthesia at the bite site.

The bite initially seems mild and often goes unnoticed. Pain at the site begins 1–4 hours later, and an erythematous area with a central pustule or hemorrhagic vesicle may be seen. The typical bull's eye lesion is created when the red blister is encircled by a pale, irregularly shaped, ischemic halo, which in turn is surrounded by extravasated blood. The pustule may gradually grow to form a craterlike lesion over 3–4 days, with associated lymphadenopathy and low-grade fever. Healing is slow, and large lesions may occasionally require skin grafting. Rarely, ulcerating skin lesions may appear years after a bite. A generalized systemic reaction termed loxoscelism may occur 24–48 hours after the bite, with fever, malaise, arthralgias, rash, and hemolysis. Rare fatalities have occurred in small children, who have shown massive intravascular hemolysis, accompanied by hemoglobinuria, jaundice, hypotension, renal failure, pulmonary edema, and disseminated intravascular coagulation. There appears to be little correlation between the development of a systemic reaction and the severity of the skin lesion.

The bites of many other insects may be mistaken for brown recluse spider bites and lead to unnecessary treatment. One helpful clue (although not absolutely reliable) is that spiders tend to bite only once, whereas other insects leave multiple bites.

Treatment

Because of the progressive necrosis associated with many brown recluse bites, early surgical excision is not recommended. Excision of a necrotic area should occur only after the area has stabilized. Many recent studies have failed to show any significant benefit to corticosteroid therapy. Dapsone has historically been a popular treatment for recluse bites. Its use, however, has come into question given the lack of convincing animal and human studies showing any effectiveness in reducing pain and dermonecrosis. Hyperbaric oxygen therapy and wound coverage with nitroglycerin patches have failed to produce consistent effective reduction in progression of the necrosis. Loxosceles antivenom is commercially available although not in the United States. Its use in other countries has shown improvement in wound healing and helped in treatment of systemic loxoscelism. A new ELISA assay has been developed for detection of brown recluse venom and shows promise for diagnosing this arachnid's bite in dermonecrotic skin lesions when a spider was never identified. Many brown recluse spider bites are minor and heal without specific treatment other than tetanus prophylaxis (Chapter 30) and local wound care.

Disposition

Most brown recluse spider bites can be treated on an outpatient basis. Patients with large or infected wounds or those who have signs of a systemic reaction should be hospitalized.

Scorpion Stings

Essentials of Diagnosis

• Most bites produce only local reactions including a painful sting site with or without erythema
• The bite of the Centruroides exilicauda scorpion can produce severe systemic symptoms including extreme restlessness, diaphoresis, seizures, and hypertension
• Severe reactions should be treated in the ICU with neuroleptics, antihypertensives, and atropine; antivenin is available for treatment failures

General Considerations

Most scorpions are relatively harmless, producing only local envenomation reactions. However, C. exilicauda/sculpturatus may produce severe systemic toxicity.

This arthropod is small and yellowish, has a small tubercle (telson) at the base of its stinger, and is 2.5–7.5 cm (1–3 in) long. It is found mostly in the southwestern United States (Arizona, New Mexico, Texas, and along the Colorado River) but may rarely be transported in freight to distant states. Related arthropods are found in many other parts of the world.

The venom of C. exilicauda contains a neurotoxin that may produce severe systemic symptoms. Other North American scorpion stings generally produce only local reactions.

Clinical Findings

The initial sting is intensely painful with little or no erythema or swelling. Light percussion of the wound causes intense pain. Although pain and paresthesias generally resolve within 4 hours, local symptoms may persist for several days. Systemic envenomation initially causes a cholinergic-like toxidrome with typical SLUDGE syndrome. Shortly after, massive norepinephrine release is triggered causing hypertension, tachycardia, hyperpyrexia, and pulmonary edema with possible myocardial infarction. Central nervous system effects generally consist of confusion, restlessness, and dystonic reactions.

Treatment

Periodic applications of ice may relieve local pain; avoid intense cooling. Immobilize the affected part. Do not apply a tourniquet.

Most children recover with supportive care alone but should be observed in an ICU. Strong depressants or tranquilizers do not appear to shorten the duration of symptoms and may produce respiratory depression; specifically, opiate analgesics seem to potentiate the toxicity of the venom. Diazepam or phenobarbital may be used to control seizures; sympatholytic antihypertensive agents may be required to control hypertension. Goat serum antivenom is available in Arizona (Arizona Poison and Drug Information Center [800] 222–1222 or [602] 495–6360) but has not been approved by the FDA and therefore is prohibited from transport outside Arizona. It is effective only for stings from C. exilicauda and is not of benefit for stings from scorpions from South America, Asia, or the Middle East. It seems to abate local pain and paresthesias but does not appear to be very helpful with treatment of systemic effects unless administered within about 1 hour of envenomation.

Many ocean-dwelling animals are potentially harmful to humans because of their ability to traumatize, envenom, or otherwise poison their victims with bites or stings. Most human injuries result from envenomation.

Stingrays

Essentials of Diagnosis

• Envenomation occurs when the tail of the stingray releases venom into its victim
• The sting causes intense local pain as well as nausea and vomiting, weakness, tachycardia, and muscle cramps
• Removal of spines and irrigation with hot water are the mainstays of treatment

General Considerations

Stingrays are the fish most commonly responsible for human envenomations; at least 2000 stings occur annually in the United States. Stingrays are usually encountered in the waters off coastal regions, where they lie partially submerged in the sand. When disturbed, they splash upward with a muscular tail, which carries 1–4 venomous stingers. Injury due to stingrays therefore involves both a traumatic wound (which can be quite severe) and envenomation. The most common sites of injury are the lower extremities, followed by the upper extremities, abdomen, and chest. Wound necrosis is not uncommon.

Clinical Findings

The sting is followed by immediate intense local pain and moderate swelling with bleeding. The pain radiates centrally and can be so severe that it causes disorientation. Systemic symptoms occur within 30 minutes of the sting and include nausea and vomiting, weakness, diaphoresis, vertigo, tachycardia, and muscle cramps. If envenomation has been severe, syncope, paralysis, hypotension, cardiac arrhythmias, and death may occur.

Treatment

Irrigate the Wound

Irrigate the wound with whatever dilutent is at hand (preferably sterile saline or water). Remove any obvious pieces of foreign matter. Immediate basic first aid is necessary to help prevent eventual necrosis, ulceration, and infection.

Anesthetize the Wound

Soak the wound in hot water to tolerance (45–50°C [113–122°F]) for 30–60 minutes. Stingray venom is heat labile and may be denatured in hot water. If heat fails to relieve the pain, infiltrate the wound with lidocaine, 1–2% without epinephrine, or perform regional nerve block. Do not apply ice to the wound.

Explore the Wound

Wound exploration and an X-ray should be performed so that all tissue fragments may be removed. Close the wound loosely around drains, or pack it open.

Give Antibiotics

Administer standard tetanus prophylaxis (Chapter 30), and consider starting treatment with trimethoprim/sulfamethoxazole (160 and 800 mg, respectively, twice a day), ciprofloxacin (500 mg twice a day), or tetracycline (500 mg four times a day) for 7 days.

Surgical Debridement

If necrosis develops, early surgical debridement is recommended. Serial debridement may be necessary to stop any progression.

Hyperbaric Oxygen

Hyperbaric oxygen has been used successfully in the setting of myonecrosis when serial debridement is required. If used, it should be instituted immediately after debridement takes place.

Disposition

Any patient with significant envenomation from a stingray sting should be observed for 4–6 hours for appearance of systemic side effects. Patients who are discharged should have close outpatient follow-up for wound care.

Sea Snakes

Essentials of Diagnosis

• The initial bite is painless, but limb and respiratory paralysis as well as myolysis can occur with envenomation
• Treatment is the same as for land snake envenomation and includes sea snake antivenom if paralysis or myolysis is present

General Considerations

Sea snakes are present in all oceans except the Atlantic and are very similar to terrestrial snakes except for the shape of their tail. Although 90% of sea snake bites are dry, the venom is highly toxic to the nervous system and can cause significant myolysis. The sea snake is not aggressive, and some type of provocation is necessary to be bitten.

Clinical Findings

The initial bite is relatively painless, but with significant envenomation comes rapid limb and respiratory muscle paralysis, ptosis, ophthalmoplegia, and myolysis. Renal failure can occur if myolysis is severe. The hemolysis and coagulopathy associated with U.S. snake bites is not seen.

Treatment

The same basic first-aid principles used for terrestrial envenomation still apply. Monitor respiratory status and prepare for intubation. Screen for signs of myolysis with CK, urine myoglobin, and renal function panel. Signs should be present by 6 hours. If paralysis or myolysis is present, administer sea snake antivenom. Between one and three ampules should be given initially, although more may be necessary. Tiger snake antivenom may be used if sea snake antivenom is not available. Polyvalent snake antivenom is the third-line choice.

Jellyfish

Essentials of Diagnosis

• Jellyfish envenomations are associated with extreme pain both locally and distant from the sting site
• Extensive skin changes may be seen shortly after envenomation
• Systemic signs and symptoms include nausea and vomiting, autonomic changes, and paralysis
• Death is usually caused by respiratory paralysis or drowning secondary to limb paralysis

General Considerations

There are three types of jellyfish that cause the vast majority of the morbidity and mortality associated with jellyfish envenomation of humans: box jellyfish, Irukandji jellyfish, and Portuguese man-o-war. Jellyfish envenomates by touching prey or unsuspecting bathers with long tentacles containing hundreds of stinging cells called nematocysts. The jellyfish sting can cause a wide array of symptoms ranging from skin irritation to death.

Clinical Findings

Most jellyfish stings cause only a localized inflammatory skin reaction and require only symptomatic care. A few jellyfish, however, can cause severe systemic envenomation syndromes.

Box Jellyfish

Severe incapacitating localized pain occurs immediately with the development of wide, erythematous bands on the skin. Confusion progressing to unconsciousness as well as respiratory failure and cardiac arrest can occur within 5 minutes. Death is rare and usually occurs in children. Fatalities are due to the cardiotoxic portion of this complex venom. If the patient lives, skin changes occur over the next few hours with the development of blistering and necrosis that may cause permanent scarring.

Irukandji Jellyfish

The initial sting is hardly felt. Approximately 30 minutes later, the Irukandji syndrome begins. Unbearable pain generally begins in the sacral area and rapidly progresses to the rest of the body. The pain is always present but worsens in waves. Other symptoms include profuse diaphoresis, restlessness, headache, nausea and vomiting, severe hypertension, and tachycardia. Later complications include pulmonary edema, transient cardiomyopathy, and left ventricular dysfunction.

Portuguese Man-O-War

Portuguese man-o-war stings are very painful and leave a “string of beads” appearance. Shortly afterward, an Irukandji-like syndrome can occur, which consists of nausea and vomiting, and muscle cramps, particularly in the abdomen and chest. Pain may be so severe in the chest as to cause hypoxia. Death can occur.

Treatment

Box Jellyfish

Due to the rapidity of possible fatality, basic life support on the scene and advanced cardiac life support once in medical hands must be a priority. Vinegar application to the sting sites will inactivate venom. Compression bandages should be applied next. An antivenom exists and should be used immediately to prevent death from severe envenomations, although most victims survive without its use. The antivenom is useful in controlling pain and possibly with preventing scarring. Intramuscular injection above the sting sites should be performed with three ampules. Intravenous pain control is always necessary in all but the most trivial stings.

Irukandji Jellyfish

Initial first aid is not usually necessary. The role of vinegar is uncertain because it is not known whether vinegar inactivates the nematocysts. Intravenous pain medication will be needed. Control of blood pressure with an α-adrenergic blocking agent will also be necessary. Monitoring for early signs of heart failure with echocardiography within the first 24 hours is recommended. Respiratory and cardiovascular support may ultimately be needed. Development of an antivenom is under way.

Portuguese Man-O-War

First aid consists of removing tentacles. Vinegar is not indicated. Rinsing with seawater, not fresh water, is the treatment of choice. Cold packs and intravenous pain medicine will ease pain. Rarely, respiratory support may be needed.

Disposition

Victims of envenomation should be monitored for 6–8 hours for systemic effects. The elderly or the very young should be monitored for 24 hours.

Scorpion Fish

Essentials of Diagnosis

• Extreme pain at sting site
• Wound sites commonly become ischemic or secondarily infected
• Systemic signs and symptoms include neurologic changes, respiratory failure, and autonomic dysfunction

General Considerations

Scorpion fish are divided into three groups on the basis of appearance and structure of the venom organ: zebra fish, scorpion fish, and stonefish. The venom apparatus consists of 12 or 13 dorsal spines, 3 anal spines, and 3 pelvic spines, all of which can be erected upon stimulation. The venom can be highly toxic (stonefish) and contains chemical fractions analogous to those contained in stingray venom.

Clinical Findings

Scorpion fish stings vary in intensity depending on the species. Most cause immediate pain, with central radiation of discomfort. Local ischemia at the wound site progresses over days to marked swelling, erythema, and cellulitis. Prolonged indolent wound infections sometimes result. Systemic symptoms occur within the first few hours and include vomiting, weakness, diarrhea, delirium, seizures, paresthesias, fever, arthritis, hypertension, cardiac arrhythmias, respiratory failure, hypotension, and death. The portion of the toxin that is responsible for death causes severe vasodilatation.

Treatment

Manage systemic symptoms and dysfunctions supportively. An antivenom is available in Australia for management of stings by the Indo-Pacific stonefish. For scorpion fish stings occurring in coastal waters surrounding the United States, institute the regimen as described next.

Provide Pain Relief

Immerse the wound in hot water to tolerance (45–50°C [113–122°F]) for 30–60 minutes. If heat fails to relieve the pain, infiltrate the wound with lidocaine, 1–2% without epinephrine; or perform regional nerve block. Pain from a stonefish sting may be so severe that it causes delirium requiring parenteral narcotic analgesics for relief.

Manage the Wound

Debride and explore the wound, and remove all foreign material. If there is a chance that a spine may have entered a joint, these procedures should be performed in the operating room, and the surgeon should use magnifying loupes to explore the joint. Do not suture wounds tightly; allow adequate drainage.

Give Antibiotics

Administer standard tetanus prophylaxis (Chapter 30), and consider starting treatment with trimethoprim/sulfamethoxazole (160 and 800 mg, respectively, twice a day), ciprofloxacin (500 mg twice a day), or tetracycline (500 mg four times a day) for 7 days.

Disposition

Patients who have sustained significant envenomation from a scorpion fish sting should be observed for 4–6 hours for development of systemic symptoms. All patients should be seen frequently on an outpatient basis for wound care after discharged.

Essentials of Diagnosis

• Consider toxic marine ingestion with gastroenteritis, neurologic symptoms, and respiratory compromise

Toxic marine poisoning is a worldwide phenomenon involving complex interactions between microbial flora, more than 300 species of fish and shellfish, and regional environmental conditions that may precipitate sometimes epidemic illness. Though varied, the toxins involved are largely heat and gastric acid stable. Treatment is generally supportive and symptomatic. Large ingestions and rapidly progressive symptoms may benefit from activated charcoal, aggressive fluid support, and early airway interventions. Bradycardias generally respond well to atropine. Diagnoses are made by history, epidemiologic, and physical findings.

Ciguatera Toxin Poisoning

General Considerations

Ciguatera fish poisoning is caused by tropical and semitropical marine coral reef fish whose tissues accumulate toxins from the dinoflagellate, Gambierdiscus toxicus. The toxins are multiplied in a food-chain phenomenon in which humans are the final consumer. Ciguaterra, worldwide, is the most common nonbacterial food poisoning. The toxin targets voltage-gated sodium channels; pacific ciguatera toxin has been shown to be ten times as potent as Caribbean isolates with differing regional presentations and severity.

The toxin is ingested by small herbivorous fishes, which are eaten by larger carnivorous fishes. Larger and older fishes are more toxic in ciguatera-endemic areas. The most frequently implicated fishes in the United States include barracuda, jack, snapper, and grouper.

Clinical Findings

Symptom onset ranges from 1–48 hours. First arise perioral parasthesias and mild gastroenteritis or abdominal pain. Symptoms then progress at a rate related to dose, and include parasthesias, pruritis, Lhermitte's phenomenon, myalgias, ataxia, hypotension, and bradycardia. Pathognomonic for ciguatera intoxication is cold allodynia, a sensation of heat–cold reversal. Progressive neurologic symptoms may occur, rarely including respiratory depression and coma. There is a sensitization phenomenon, with subsequent episodes being more pronounced. Untreated, the gastroenteritis usually resolves in 24–48 hours, whereas the neurologic symptoms may become chronic.

Treatment and Disposition

Treat persistent myocardial failure with judicious administration of calcium gluconate, 1–2 g intravenously over 24 hours; the rationale is that the toxin occupies calcium receptor sites that affect the permeability to sodium of the pores in neural and myocardial membranes. Admit patients with cardiovascular symptoms for observation. Antiemetics may be used for gastroenteritis. A double-blinded study recently has shown mannitol to offer no benefit over normal saline administration. Gabapentin has been used recently for chronic neuropathies in anecdotal reports.

Scombroid Poisoning

General Considerations

Scombroid poisoning is caused by ingestion of contaminated or unrefrigerated fish with high levels of vasoactive amines. Any dark fleshed species, such as tuna or mackerel, containing high levels of histadine, can produce toxin by endogenous microbial flora. Case reports have included improperly handled canned tuna. Histamine is the dominant toxic product, and urocanic acid, the other one, is a heat and acid stable direct mast cell degranulator. A pseudoallergic reaction develops. Histamine levels higher than 20–50 mg per 100 mL are noted in toxic fish.

Clinical Findings

Symptoms arise within 15–90 minutes of ingestion and last 8–12 hours. Gastrointestinal symptoms are less pronounced. Findings relate to histamine, including flushing, rash, facial swelling, edema, nausea and vomiting, palpitations, respiratory distress, and shock.

Treatment and Disposition

Treatment is directed at reversing the effects of histamine. Histamine 1 and 2 receptor blockade is indicated using diphenhydramine, cimetidine, or ranitidine. Promethazine may be helpful for uncontrolled emesis. If the reaction is severe, give epinephrine, 0.3–0.5 mL of 1:1000 solution subcutaneously. Admit patients with serious illness for observation.

Puffer Fish (Tetrodotoxin) Poisoning

General Considerations

Tetrodotoxin is one of the most potent nonprotein poisons found in nature, effective in the nanomolar range on neuronal sodium channels. The poison is found in puffer fish and is the commonest cause of lethal marine poisoning. Historically, cases have centered in Japan with ingestion of the delicacy “Fugu,” made by licensed sushi chefs. The toxin accumulates in the skin and liver of the fish.

Clinical Findings

The onset of symptoms can be as rapid as 10 minutes or can be delayed for up to 5 hours. Early symptoms are sensory and include perioral and distal extremity parasthesias. Dizzyness, muscle weakness, ataxia, hypersalivation, dysrythmia, paralysis, respiratory failure, and coma may evolve rapidly. Sixty percent of victims die, most within the first 6 hours.

Treatment

Early recognition of airway compromise is essential, with anticipating the need for ventilatory support. Sedative and amnestics are necessary as the patient may be conscious. Significantly symptomatic patients should be admitted to an ICU; minimal symptoms require monitoring for 8–24 hours dependent on organ system affected.

Paralytic Shellfish Poisoning

Paralytic, diarrhetic, and neurotoxic shellfish poisoning involve the accumulation of toxins in shellfish during phytoplanktonic blooms, largely of dinoflagellate species. Distinction must be made between bacterial and viral shellfish-born infections. Presentation varies geographically and upon the toxin ingested. Symptoms are largely neurologic, including parasthesias, drowsiness, amnesia, respiratory depression, and coma with flaccid paralysis. Gastroenteritis may be an isolated symptom in diarrhetic shellfish poisoning. Symptoms usually resolve in 2–3 days with adequate supportive care.

Treatment

With evidence of dysphagia, obtundation, or progressive paralysis, early airway intervention and endotracheal intubation is indicated. Large ingestions are treated with 50–100 g of activated charcoal. Hypotension is addressed with crystalloid administration. Severe intoxications may lead to arrhythmia; bradycardia responds to atropine, and temporary pacing may be needed for heart block.

Disposition

Patients with respiratory difficulties, cardiovascular symptoms, or paralysis should be hospitalized in an ICU. Patients with symptoms of a minor intoxication, which may be limited to paresthesias and mild dysphagia, should be observed in the emergency department or ICU for at least 8 hours to detect deterioration.