Emergency Medicine Reports June 23, 1997

The Emergencies of Summer: Optimum Management of Injuries Caused By Heat, Water, Bolts, and Venom

Authors: Robert A. Schwab, MD, Mark T. Steele, MD, Robert L. Muelleman, MD, William A. Robinson, MD, Department of Emergency Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center, Kansas City, MO.

Peer Reviewer: Paul Auerbach, MD, MS, FACEP, Chief Operating Officer, Sterling Healthcare Group, Coral Gables, FL.

We have all seen the sweet moments of summer go sour. As every emergency practitioner knows, the bright side of summer frequently has a dark, dangerous lining. The pursuit of outdoor recreation brings with it the potential for serious and life-threatening illnesses, many of which are difficult to manage and require prompt, definitive intervention.

Environmental hazards such as lightning storms and heat spells can turn recreation into tragedy. Water sports always carry the implied risk of near drowning or drowning, and envenomation from snakebites can occur on land or in water. The good news is that most recreational injuries are not life-threatening and can be managed with relative ease. However, when emergency physicians are faced with serious injuries that pose a threat to life or limb, clinical assessment must be swift and interventions must be targeted against the end-organ deterioration and metabolic derangements that pose the greatest risk to patient survival.

Not surprisingly, mastery of therapeutic interventions and clinical judgment of the highest level are required to maximize outcomes in these high-risk groups. Depending upon the nature of the emergency, different issues will need to be addressed. For example, when should antivenin be administered to patients who suffer from snake envenomation, and what precautions are necessary prior to treatment? What is the full spectrum of injuries that can occur in lightning victims, and what are the target organ priorities when resuscitating these victims? What are the most effective strategies for cooling patients with heat illness? Because variable presentations are common, interventions must always be patient-specific.

With these issues and conditions in focus, the purpose of this review is to provide practical clinical strategies for managing summer environmental emergencies that require prompt, life-saving interventions.

—The Editor

Lightning Injuries

Lightning is electrical energy generated by the potential difference between clouds and the ground. When high- and low-pressure air masses meet, charges within the air masses partition themselves in a manner that generates electrical potential. When the potential difference is sufficiently large, a relatively low-energy leader or pilot stroke passes from cloud to ground; it is met by a leader stroke from ground to cloud, and the circuit is completed. Because air resistance is eliminated by the leader stroke, subsequent return strokes are increasingly rapid and powerful. The strobe-like quality of lightning strokes is caused by multiple rapid surges of current along this pathway. Thunder is caused by rapid movement of air, first out of the superheated current pathway, then back into the vacuum as the current dissipates.

Epidemiology. Because there is no central data-collection agency, the exact incidence of lightning-related injury is unknown.1 However, it is estimated that 150-250 lightning-related deaths and more than 1000 injuries caused by lightning occur each year in the United States, predominantly in the southeastern and Rocky Mountain areas.2 Overall, 20-30% of lightning-related incidents result in death. Predictably, most of these injuries occur outdoors during summer months. Golf courses, sporting fields, and large bodies of water are common sites of lightning injury, which involve more than one victim in 30% of cases.2

Physical Hazards Of Electricity. Appreciating the full spectrum of pathophysiological consequences and tissue hazards associated with lightning injuries requires understanding the essential principles that govern the behavior of electricity. In broad terms, electricity refers to the movement of electrons from areas of high potential to areas of low potential. Voltage (V) is the force that moves the electrons, and the amount is usually known since power sources are defined in terms of voltage. Amperage, or current (I), is the volume or number of electrons moving against resistance (R), which is a deterrent to movement. Amperage and resistance are usually not precisely known. The relationship between voltage, amperage, and resistance is described by Ohm’s law:

I = V/R

In any type of electrical exposure, six factors contribute to the extent and type of injuries.3 Table 1 lists and contrasts the characteristics of these factors in lightning, industrial, or household electrical injuries. Tissue injury is caused by heat that is generated as the electrical current attempts to overcome resistance to flow. Joule’s law describes the relationship between energy, amperage, and resistance:

E = I2R

From this equation, it should be clear that amperage is the most direct determinant of the extent of injury. However, the duration of exposure is also important, since prolonged contact increases heat generation, which breaks down skin resistance and enhances conductivity through body tissues. Hence, the amount of energy and duration of exposure required to produce skin penetration depends upon skin resistance, which varies greatly depending upon anatomic location and moisture content. However, once electrical current penetrates the skin, its pathway does not obey predictions based upon the variable resistance of different tissues. (See Table 2.) Rather, experimental work suggests that the body often behaves as a volume conductor with a consistent but unpredictable resistance.4

Alternating current (AC) produces more severe injuries at a given voltage than does direct current (DC), primarily because AC is produced at a frequency that produces tetanic muscle contractions. Because flexors are stronger than extensors, an upper extremity that comes in contact with a source of AC will often become "frozen" to the electrical source, and in the process, produce prolonged exposure and greater injury. In contrast, DC usually produce a single muscle spasm that throws the victim from the source.

Electrical Hazards of Lightning. For practical purposes, lightning can be thought of as a 20 million volt battery that produces a tremendous electrical current. In fact, a current of this magnitude would immolate any unfortunate victim coming in contact with it if not for the type of circuit, duration of exposure, and pathway of the lightning injury.

Although lightning actually involves complex electromagnetic currents, its effects are similar to those produced by DC. Consequently, victims are usually thrown clear of the current and experience a very brief duration of exposure, usually on the order of 1/1,000 of a second.2 This brief exposure does not allow the current to overcome skin resistance, and instead, produces an external pathway or "flashover" in which nearly all of the current travels around the outside of the victim.

Mechanisms of Injury. Lightning-related injuries occur through one of four mechanisms.5 If the victim suffers a direct strike, the full energy of the lightning stroke is directed into and over the body, resulting in significant morbidity and mortality. More commonly, however, the victim suffers injury as a result of side flash or side splash that occurs when the current bolts from its primary target to a secondary target of lower resistance.

Victims who are "struck" while standing under trees are frequently injured by this mechanism. Since the lightning dissipates energy as it overcomes the resistance of the primary target and the intervening air, injuries tend to be less severe, although fatalities often occur as a result of this mechanism. Step voltage causes injury through ground conduction; current spreads centripetally from the site of strike, much like ripples from a pebble dropped in water. Although a great deal of energy is dissipated in overcoming ground resistance, step voltage often causes death of cattle. The fourth mechanism by which lightning causes injury relates to the tremendous explosive forces generated as lightning superheats and expands the air column in its path. Victims can suffer any number of injuries typical of significant blunt trauma.

Pathophysiology. The physical consequences of lightning-induced blunt trauma are not unique; forces strong enough to produce tissue damage can result in fractures and hemorrhaging that lead to severe disability or death. The electrical current produces injury by discharging or short-circuiting electrical tissues, by inducing vascular spasm, and through heat generation. Since the amount of current that enters the body is quite small, one would correctly predict that internal injuries would tend to be less serious than those seen with high-voltage AC, where exposure is prolonged, and internal burns are severe. However, lightning does produce enough internal current to short-circuit the central and autonomic nervous systems, as well as the cardiac conduction system, and, as a result, can produce death or disability from electrical injury alone.

Clinical Manifestations. From a practical, clinical perspective, death from lightning is nearly always the result of respiratory arrest or cardiac dysrhythmias.6 Since approximately one-quarter of all lightning-related injuries result in death, it would appear that these injuries occur about 25% of the time. However, the actual incidence is somewhat higher, since the heart often recovers spontaneously from lightning–induced asystole.7 If respiratory arrest is not prolonged, survival after cardiac arrest is possible. With prolonged respiratory arrest, hypoxia produces ventricular fibrillation and then secondary asystole, which carries a grim prognosis. Although other conduction abnormalities are observed, myocardial infarction is rare.6

In addition to respiratory arrest, which is usually the result of brain stem injury, a number of central nervous system derangements have been associated with lightning injury, including intraventricular hemorrhage, coagulation necrosis, and subdural or epidural hematomata. These disorders can produce a variety of neurologic signs and symptoms.8

Loss of consciousness and amnesia are seen in more than 70% of lightning victims. Injury to the autonomic nervous system produces intense vasospasm, which results in cool, pale, mottled, and flaccid extremities. This keraunoparalysis involves the lower extremities in two-thirds of cases, and generally clears spontaneously within a few hours.2,7

More than 50% of all lightning victims suffer rupture of a tympanic membrane.9 A minority of these also experience conductive or sensorineural hearing loss. Cataracts and other ophthalmologic injuries, such as hyphema, retinal detachment, and vitreous hemorrhage, commonly occur.8

Burns associated with lightning are generally minor and occur in areas where sweat is volatilized to steam or metal objects are worn or carried by the victim.2,8 Feathering burns are thought to be caused by lightning-induced electron showers that produce a fern-like pattern on the skin.10 Although rare, this pattern is pathognomic of lightning injury. Blunt trauma can produce injury to any organ system, although intra-abdominal, pulmonary, and renal injuries are relatively uncommon in victims of lightning strike.2,8 Fractures caused by the electrical discharge or secondary concussion are more common; compartment syndromes are rare. (See Table 3.)

Management Principles. Prehospital providers should adhere to basic principles of prehospital care. Because respiratory arrest precipitated by lightning usually lasts longer than cardiac arrest caused by the same strike, aggressive respiratory support can permit intrinsic cardiac automaticity to restore sinus rhythm and achieve survival. Furthermore, victims who have not experienced cardiopulmonary arrest usually survive and are unlikely to deteriorate acutely.9 Therefore, the essential triage principle in lightning injury is "resuscitate the dead."2,7–9 Prehospital providers should use caution in the field, since lightning can and does strike the same place twice. Victims do not pose significant risk to rescuers.

When victims arrive in the ED, the physician should first assess and manage the ABCs. The cervical spine should be protected at all times, and the resuscitation should follow standard protocols. Initial evaluation should include an electrocardiogram (ECG), cardiac enzymes, urinalysis and urine myoglobin, complete blood count (CBC), and electrolytes. Further laboratory testing should be guided by clinical examination or response to therapy. Intravenous fluids should be administered at a maintenance rate unless shock is present. Remember, too, that internal burns are not a concern, and large external burns are unusual. Radiographs and CT scans should be obtained if clinically indicated. As a rule, cervical-spine films and a chest x-ray will be part of the initial database. A CT scan of the head is mandatory in any patient with loss of consciousness or amnesia and in patients with focal neurologic findings.

Although survival after prolonged cardiopulmonary arrest has been reported,6,7 there is no reason to pursue resuscitation beyond the time period that would normally be allotted for young, otherwise healthy accident victims. Once again, it should be emphasized that the resuscitating team should provide early, effective ventilation that may allow intrinsic cardiac automaticity to restore normal rhythm. In addition, it should be stressed that because ocular injuries are common, the clinician should not rely on dilated pupils alone as a the definitive criterion for brain death.2 Finally, the clinician should obtain a complete set of vital signs, including temperature, and should be prepared to treat hypothermia.

Assessment of the circulation can be confounded by the presence of keraunoparalysis, which can give the false appearance of hypovolemic shock. Usually, only two extremities are involved, so it is important to assess all extremities for the presence of warmth and pulses. If shock is present, look first for a hemorrhagic source, then assess cardiac function before attributing shock to autonomic dysfunction. All patients should have continuous cardiac monitoring, and any arrhythmias should be treated according to established ACLS protocols.

Disposition. All victims of lightning injury should be admitted for observation and cardiac monitoring. Unless cardiopulmonary arrest or ventricular dysrhythmias has occurred in the prehospital or ED setting, or the admission ECG demonstrates a significant injury pattern, admission to a telemetry bed for 24 hours is usually sufficient.6 Occasionally, a victim may appear neurologically intact, have a history characterized by a brief loss of consciousness with amnesia, and have a completely normal diagnostic evaluation. Although admission is still reasonable and recommended, some experts feel these patients may be discharged home with reliable observers. Regardless of the disposition, all victims should be referred for a formal ophthalmologic and otolaryngologic evaluation, including an audiogram, and close follow-up with a primary care provider.8

Prognosis.Victims who suffer cardiopulmonary arrest have a poor prognosis, even if they are resuscitated from the initial arrest.9 Permanent sequelae are seen in most survivors.8 These include psychomotor disturbances as well as ocular and otologic derangements. Victims who suffer a brief loss of consciousness and amnesia without other injuries may recover fully without sequelae.

Prevention. Counseling directed at prevention is advisable. Despite all precautions, however, thunderstorms sometimes occur without warning. If an individual is caught in a storm, shelter should be sought in a building or car; tents should be avoided since they contain enough metal to conduct electricity and can ignite. In the forest, low areas under small trees are safest. If shelter is unavailable, people should be advised to crouch down low, kneel, or curl up on the ground, and, if in a group, individuals should spread out so that a strike is less likely to injure the entire group.

Near Drowning

Definition. Drowning refers to death by asphyxiation within 24 hours following submersion. Secondary drowning refers to death after 24 hours from complications attributable to submersion (e.g., adult respiratory distress syndrome [ARDS], pneumonia, neurogenic pulmonary edema). Because the ultimate outcome of the patient is unknown at the time acute care is administered, this article will use the term near-drowning when discussing patients with at least temporary survival following submersion.

Epidemiology. Drowning is the third most common cause of death associated with unintentional injury for all ages and ranks second for ages 5-44.11 In ten states (Alaska, Arizona, California, Florida, Hawaii, Montana, Nevada, Oregon, Utah, and Washington), drowning surpasses all other causes of injury-related death in children under the age of 15 years.2 In 1988, drowning accounted for more than 6200 deaths,11 and it is estimated that there are 10 saves and five near-drownings for every drowning. In 1985, the total lifetime cost of drowning and near-drowning was estimated to be $6.5 billion in the United States alone.13

Causes of Drowning. Circumstances of drowning vary by geography as well as age. Toddlers and teens are at greatest risk, with recent trends indicating that drowning rates in toddlers have remained fairly constant, whereas the rates in older children have decreased over time.14 In warmer regions of the country, residential swimming pools are the most common sites of drowning, particularly for children 1-4 years old.15 Bathtubs are the usual site for children under one year of age. Bucket-related drownings occur most commonly in infants under 15 months of age.16,17 Up to 75% of all drownings occur in lakes, ponds, rivers, or oceans.

Alcohol and drugs are major risk factors for submersion accidents. In one series, 53% of individuals with a submersion incident over the age of 26 had blood alcohol concentrations greater than 100mg%.18 Drowning and near-drowning also occur in individuals with physical or mental illness. Hypoglycemia, myocardial infarction, cardiac arrhythmias, syncope, and seizures predispose people to drowning, and, in one series, 9% of all suicides were due to drowning.18,19 It should be stressed that drowning and near-drowning may be a manifestation of child abuse. Although all suspicious incidents suggesting this etiology should be reported, studies suggest clinicians fail to link and/or report drowning injuries associated with possible child abuse.20,21

Clinical Consequences. The sequence of tissue and organ damage in drowning is well-characterized. Aspiration of water induces vagal nerve-mediated pulmonary vasoconstriction and pulmonary hypertension. Both fresh and saltwater aspiration lead to surfactant destruction, accumulation of proteinaceous material in the alveoli, and damage to the alveolar-capillary membrane and vascular endothelium. These events result in atelectasis, ventilation-perfusion mismatch, pulmonary edema, and reduced compliance.22 (See Figure 1.) In some cases of near-drowning, these changes do not occur until many hours after the insult.

There are variations on this pathophysiological theme. For example, aspiration of water that is contaminated with chemicals, particulates, or bacteria may produce more severe edema or obstruct the smaller bronchi and bronchioles. Furthermore, bacteria found in fresh water may be resistant to commonly used antibiotics.

Clinically important changes in serum electrolyte are rarely seen in freshwater near-drownings,23 and they have been documented in only 15% of deaths from drownings, probably because most patients who survive near-drowning aspirate less than the 22 mL/kg of body weight required to induce electrolyte changes. However, if a large quantity of fresh water is aspirated, the patient may develop hypervolemia, electrolyte dilution, and red-cell membrane rupture. In contrast, sea-water aspiration can produce hypovolemia and increased serum electrolyte levels. Finally, approximately 10% of drownings are "dry." Death in these patients is usually attributed to laryngospasm, which develops in response to a cold-water stimulus or the mechanical irritation of swallowed water.

Although the lung is the primary target organ in near-drowning, the consequences of hypoxia and acidosis lead to cardiac, central nervous system, and renal abnormalities. Cardiac derangements may be further exacerbated by increased levels of catecholamines secondary to the stress of the incident. Although hypoxic injury accounts for most nervous-system and renal derangements, blunt trauma may play a role in some patients.

Management. In the prehospital phase, the first priority is retrieval of the victim. This must be accomplished without endangering rescuers and may require special equipment. Decisions to withhold or cease resuscitation attempts should not be made in the field unless prolonged duration of submersion can be accurately documented.

If the patient is in cardiopulmonary arrest, resuscitation should be started immediately. Treatment at the scene is the most important factor in determining survival. Do not attempt lung drainage with abdominal thrusts, as such efforts delay ventilation and may induce vomiting. Endotracheal intubation should be performed as soon as possible, and 5-10 cm H20 PEEP should be applied. The team should establish intravenous (IV) access and administer standard drug therapy per ACLS protocol. If the patient is resuscitated, an NG, Foley catheter, and Swan–Ganz catheter should be placed. Fluid replacement should be guided by hemodynamic considerations. It is essential to take the patient’s temperature and treat hypothermia if necessary. Other causes of coma and associated traumatic injuries should be evaluated.

Maintaining oxygenation is the first priority in symptomatic patients. High flow O2 by should be administered by nonrebreather mask. If broncoconstriction is present, an inhaled selective beta-agonist should be administered. Continuous cardiac monitoring is mandatory in anticipation of further deterioration. All symptomatic patients require admission to the hospital.

If the patient is asymptomatic after a submersion episode, obtain a chest x- ray, arterial blood gas, and serum electrolytes. Observe the patient for 4-6 hours. Although admission for observation is accepted practice in all drowning victims, asymptomatic patients with normal diagnostic studies may, in some cases, be discharged after 4-6 hours with close follow-up. Although no controlled studies have been done, one series found that all patients who became symptomatic, did so within four hours.22, 23

Prognostic Indicators. The rate of survival with intact cerebral function varies considerably in retrospective studies. Some unfavorable factors include: submersion for longer than five minutes, CPR delayed for more than 10 minutes, resuscitation for longer than 25 minutes, pH less than 7.1, asystole on arrival to hospital, fixed dilated pupils, and Glasgow Coma Score (GCS) less than 5. None of these factors are absolute, and survival with normal neurologic function has been reported with all of the factors. A recent series of 29 victims under 20 years of age submerged in non–icy waters who presented in cardiac arrest found that 13 (45%) survived to admission, two (7%) survived with mild neurologic impairment, and four (14%) survived with severe neurologic impairment. In this study, submersion duration and resuscitation duration of greater than 25 minutes were associated with death or severe neurologic impairment.22

Prevention. Some prevention-oriented interventions have been shown to be effective.26 These include residential pool barriers, adult supervision of young children, and the presence of life preservers, telephones, and trained rescuers in public swimming areas. Other suggestions include the proper use of pool covers, swimming lessons, limiting alcohol use in swimming and boating areas, and required use of U.S. Coast Guard-approved lifejackets in boats.

Snakebite Injuries and Envenomations

Human snakebite envenomation can produce a wide range of toxic manifestations, from mild, local reactions to severe, life-threatening systemic toxicity. The primary challenge of the emergency physician is to make the diagnosis, determine the severity of envenomation, monitor and support the patient’s vital signs, and treat with antivenin when indicated.

Epidemiology. An estimated 8000 venomous snakebites occur each year in the United States and result in about 10-15 deaths. The American Association of Poison Control Centers (AAPCC) reported about 5200 snakebites (venomous and non–venomous) in 1994, with only two fatalities.27 Most deaths occur 6-48 hours after the bite.28 Only about 5% of deaths occur within the first hour of envenomation and are probably related to the direct intravenous injection of venom.

Most snakebites occur in adolescents and young adults. Males are nine times more likely to be bitten than females. The bite rate is highest in the southern states (North Carolina is No. 1) where snakes are more prevalent. Venomous snakes are found in all states except Maine, Hawaii, and Alaska, and 90% of bites occur between the months of April and October when snakes are most active. The vast majority of bites occur on the extremities.29 In one series, more than half of the bites were provoked, and most of those were associated with alcohol use. Nearly 20 percent of bites in this study were inflicted by pet snakes.30

Venomous Snakes. There are 19 species of venomous snakes indigenous to the United States. The two main families are the Crotalidae (pit vipers) and Elapidae (coral snakes). Crotalidae account for 98% of all venomous bites in the United States and include three genera: Crotalus and Sistrurus (rattlesnakes, 15 species) and two species of Agkistrodon (cottonmouth [water moccasin] and copperhead).

Pit vipers contain a depression or pit in their maxillary bone, which is located halfway between the eye and the nostril on each side of the head. This is a sensory, infrared heat-detecting organ that enables the snake to detect prey up to 14 inches away in absolute darkness. The crotalids can be distinguished from the elapids and non-venomous snakes by the presence of the facial pit, elliptical pupils, triangular head and a single rather than a double row of subcaudal scales. (See Figure 2.)

The crotalids’ venom apparatus consists of the venom gland, venom duct, and one or more fangs on each side of the snake’s head. The glands are connected to two elongated, hollow upper maxillary teeth or fangs that have a slit-like opening near the tip. The fangs are folded against the upper jaw along the roof of the mouth when not in use.

Crotalids generally strike only once and usually from a coiled position. During the strike, the snake’s mouth opens nearly 180 degrees and the fangs rotate down and out so that they are at a right angle to the snake’s jaw. The snake lunges forward, sinking its fangs into its prey and injecting venom. Rattlesnakes discharge anywhere from 25-75% of their venom, which is usually deposited subcutaneously in humans. Strike speeds have been recorded at 8 ft/sec, and the snake’s striking range is usually distance corresponding to one–half the length of its body. Approximately 25-30% of strikes are so–called "dry bites," in which no venom is injected.31 Because reserve fangs may move into position before a functional fang is shed, snakebite victims may have from one to four fang marks.

Coral snakes (Elapidae) include two species; the Arizona coral snake (Micruroides euryxanthus), found mostly in New Mexico and Arizona, and the Eastern coral snake (Micrurus fulvius), located primarily in North Carolina and the Gulf Coast states. Coral snakes are similar to non-venomous snakes in that they have round heads and pupils and a double row of subcaudal scales. Coral snakes have a black snout and red, black, and yellow or white bands that completely encircle their body. Red bands bordered by yellow or white bands indicate a venomous vs. non–venomous snake. Hence, the pneumonic "red on yellow, kill a fellow; red on black, venom lack."

Coral snakes chew rather than strike, and only about 40% of bites result in envenomation.31 There is little or no pain associated with a coral snake bite. The venom is primarily neurotoxic with paresthesias and muscle fasciculations commonly occurring at the bite site. Tremors, drowsiness, euphoria, salivation, slurred speech, diplopia, dysphagia, and dyspnea may occur. Flaccid paralysis and respiratory failure can develop over a period of several hours. The symptoms and signs of elapid envenomation may be delayed up to 12 hours, so hospitalization and early treatment are important. Early treatment with antivenin is indicated because symptoms may be difficult to reverse after venom binds to the nerve sites. Antivenin is currently only available for treatment of bites secondary to the Eastern coral snake. No deaths have been reported secondary to the Arizona coral snake and treatment is supportive.

Exotic snakes account for 1-2% of envenomations in the United States. Species and subspecies of cobras are the most commonly involved. Regional poison control centers are good sources of information for these envenomations, as are local zoos where exotic antivenins can sometimes be obtained.

Clinical Features. The three main functions of venom are immobilization, killing, and digestion of prey. It is a multi-component toxin that consists of water, enzymes, non-enzymatic proteins and peptides, and other, as-yet-unidentified substances. The relative amounts of the components of venom vary among, and even within, species of pit vipers, so clinical manifestations may differ from one patient to the next.3

The vascular endothelium and clotting system are the two principal targets of venom. Loss of vascular volume, hemorrhage, and coagulopathy can cause massive tissue edema, shock, bleeding, and coagulation abnormalities including disseminated intravascular coagulation (DIC), or DIC-like syndromes. Nearly every organ system is susceptible via lymphatic and blood-system spread of venom.

The symptoms and signs of envenomation vary according to the amount and make-up of protein content of the venom deposited, which is dependent upon the snake’s size, age, and species. The clinical effects are also variable and depend upon the patient’s age, size, and health, as well as the location, depth, and number of bites received.

Envenomation is characterized by the presence of one or more fang marks accompanied by the onset of burning pain and edema (within minutes) at the bite site. Edema spreads proximally, typically progressing slowly over 6-12 hours but may involve an entire extremity within an hour. The clinical spectrum of envenomation ranges from mild local pain and edema to a marked local reaction, consisting of ecchymosis or hemorrhagic bleb and bullae formation. Severe cases evolve to systemic coagulopathy, hypotension, shock, and coma. Direct intravenous injection of venom can produce moderate to severe symptoms very rapidly. Nonspecific signs and symptoms of envenomation include weakness, nausea, vomiting, and paresthesias and fasciculations at the bite site.

Crotalid envenomations are classified clinically according to severity as none, minimal, moderate, and severe. (See Table 4.) In one large series of envenomations, about 25% were classified as mild, nearly two-thirds as moderate, and only about 10% as severe.29 Although this classification system is used as the basis for antivenin treatment, it is fairly subjective and imprecise. A more objective 20-point snakebite severity score has recently been developed and retrospectively validated, but awaits prospective study to determine its ease of use, interrator reliability, and its effect on clinical decision-making before it can be recommended for widespread use.32

Prehospital and First Aid Interventions. The victim must be moved from the snake’s striking range to prevent recurrent envenomation. Do not use cryotherapy and arterial tourniquets, as they have been shown to increase tissue necrosis. Immobilize the affected extremity at the level of the heart and limit the patient’s physical activity to decrease systemic absorption of venom. Snakebit victims should be transported to the ED as soon as possible to assess the need for antivenin. If the snake has been killed, it should be transported to the ED for identification. Caution is required, since decapitated snakes can still envenomate up to 60 minutes following decapitation. Remember that precise identification of the species does not change therapy, so prehospital providers should not waste time trying to find and kill the snake.

Some therapeutic measures are controversial. Animal data33 suggest benefit from use of a lymphoconstrictive band, but there currently are no supporting human data. Elective shock therapy, once touted to be beneficial, has been shown to be of no value in animal studies.34,35 Classical surgical incision and suction has been shown to remove up to 50% of venom if employed within three minutes in an animal model.36 The efficacy of this procedure has not been verified in humans,37 however, and its use in untrained hands is fraught with complications, such as increased tissue loss as a result of infection or compromised blood supply and iatrogenic tendon lacerations. A negative pressure suction device has been shown to remove 37% of venom after three minutes in an animal model.38 This device is devoid of the complications associated with surgical incision, and is currently undergoing clinical trials in humans.

ED Management. The main goal is to determine whether envenomation has taken place and, if so, its severity. The ED physician should assess the ABCs and begin resuscitation if necessary. Treat hypotension with isotonic crystalloid solution. Consider changing to a 5% albumin solution if there is no response to 2L of crystalloid because of the increased vascular permeability associated with envenomation.29 Vasopressors should be used only if other measures are not successful.

Establish the time of envenomation and species of snake, if possible, and institute or continue first-aid procedures. The baseline laboratory should include a urinalysis, a CBC and differential, prothrombin and partial thromboplastin times, DIC panel, electrolytes, blood urea nitrogen, creatinine, creatine phosphokinase, and a type and screen. Remove restrictive garments or jewelry from the envenomated extremity and measure the circumference 4-6 inches proximal to the bite site every 15 minutes until swelling has peaked. Then, measurements should be made every hour.

Although the incidence of clinical infection from snakebite is probably low,13 administration of a broad spectrum antibiotic (third-generation cephalosporin) is generally recommended to cover anaerobic and gram-negative bacteria, both of which are found in the mouth cavities of snakes. Coagulopathy should be treated with antivenin and fresh frozen plasma; cryoprecipitate should be administered if active bleeding is present. If any signs of envenomation are present or develop during observation, assess the need for antivenin and hospitalize the patient. (A discussion of antivenin therapy is detailed later in the article.) If no symptoms or signs of envenomation develop, observe the patient 6-8 hours and consider discharge from the ED with follow-up in 24 hours. Symptoms and signs of envenomation are rarely reported after an initial period of observation. Debride bite wounds and provide tetanus immunization if indicated.

Primary surgical excision following snakebite is contraindicated, because this procedure has been shown to increase tissue loss following envenomation. Since venom is generally introduced subcutaneously rather than intramuscularly, compartment syndrome is uncommon. It is difficult to evaluate snakebite victims clinically for the development of compartment syndrome because of the massive soft tissue swelling that can occur. Measurement of compartment pressures should be performed if there is a question of compartment syndrome and fasciotomy is indicated for pressures greater than 30 mmHg. Serial creatine phosphokinase measurements may also be helpful in this setting.

Antivenin Therapy. Antivenin, which binds venom proteins and enhances their elimination, remains the mainstay of treatment29 for moderate to severe envenomations. The package insert for polyvalent Crotalidae antivenin (Wyeth Laboratories) and/or a regional poison control center are good information sources to assist in determining the need for, and procedures for administration of, antivenin. (See Table 5.) Although mild envenomations may not require antivenin (frequently the case with copperhead bites), envenomation severity should be carefully monitored over time, because symptoms can worsen rapidly, in which case antivenin may be indicated.40,41 Generally speaking, antivenin is indicated for moderate-to-severe envenomations. In particular, the ED physician should consider early treatment for Mojave rattlesnake bites, because symptoms with this species are often delayed and may become severe over time.

The intravenous route is the most rapid and effective route of administration. Dosing recommendations are based on envenomation severity. (See Table 6.) Children generally require more antivenin per unit of body weight than adults. Venom probably does cross the placenta barrier, so antivenin along with fetal monitoring is advised in the pregnant patient. Antivenin is most effective when given within 4-6 hours after the bite and may continue to be beneficial for up to 24 hours after envenomation.

If the decision has been made to administer antivenin to a stable patient, the physician should perform a skin test with dilute horse serum testing material. This test can be predictive of hypersensitivity to antivenin, but it should be stressed that a negative test does not rule out the possibility of a hypersensitivity reaction to antivenin. Patients with a history of general allergic disorders, asthma, or an allergy to horse serum are at high risk for hypersensitivty. Moreover, a positive skin test does not preclude the use of antivenin in a patient with severe symptoms. In this circumstance, the patient should be treated with H1 and H2 histamine blockers and corticosteroids, which is followed by slow, dilute administration of antivenin. The clinician should be prepared to treat anaphylaxis in this situation. Skin testing in unstable patients with severe envenomation is not required, but pretreatment with antihistamines and steroids is recommended (See Table 5.)

Complications of antivenin are primarily allergic in nature. Acute anaphylaxis and an anticomplement reaction that clinically resembles anaphylaxis can also occur. Treatment includes administration of crystalloid solution, H1 and H2 histamine antagonists, and IV corticosteroids. Up to 75% of patients treated with antivenin develop serum sickness (Type IV hypersensitivity reaction) in 1-4 weeks following antivenin treatment.36 Signs and symptoms include pruritus, urticaria, fever, arthralgias, swollen joints and edema, lymphadenopathy and peripheral neuritis. Corticosteroids are the mainstay of treatment. Attempts are currently being made to purify antivenin and make it less antigenic. A new product made from sheep–derived purified FAb fragments has recently been tested in the United States and shows promise.29

Prevention. Snakes are generally afraid of humans and usually will not strike unless provoked or cornered. The top speed of a rattlesnake is only about 3 mph so they are generally incapable of chasing down a human. Leather boots and sturdy pants should be worn when entering known habitats such as swamps, caves, wood or stone piles, rocky ledges, and deserted mines and buildings. A walking stick to probe logs and rocks before stepping over them is recommended when hiking. Snakes should not be handled except by experienced personnel with proper equipment.

Heat Illness

Although all forms of heat illness share a common etiology (thermal stress), clinical syndromes range from minor self-limited disorders to fatal emergencies. From 1979 to 1992, between 145 and 1700 persons died each year in the United States as a result of excessive exposure to high temperatures. During this time period, there were three years (1980, 1983, 1988) with heat waves resulting in 1700, 556, and 454 heat-related deaths, respectively.42 Early recognition, aggressive treatment, and appropriate preventative measures can diminish this significant public health problem.

Clinical Aspects of Thermoregulation. Basal metabolism in a fasting adult at absolute rest produces roughly 70 kcal/h. Even a moderate workload can increase this 4-5 times and, during brief periods of intense exercise, heat production may reach 1000 kcal/h. Additionally, high ambient environmental temperatures and direct exposure to sunlight are sources of heat gain. For example, an individual in bright sunlight may gain 150 kcal/h.43

Radiation and evaporation are the two primary mechanisms for dissipating body heat. Radiation, which is facilitated by transfer of heat from the body to a cooler environment, accounts for 65% of cooling, but requires that the air temperature is lower than the body temperature. Roughly 30% of heat loss occurs through evaporation; however, when ambient temperature reaches 35oC or higher, evaporation is responsible for virtually all heat loss. Moreover, when the humidity level exceeds 75%, evaporative heat loss is compromised.

In response to heat exposure, cutaneous blood vessels dilate in order to increase the surface cooling area. To compensate for this redistribution of flow to skin, cardiac output must increase and the splanchnic bed vasculature constricts. In addition, sweat formation will occur, with rates of production reaching 1-2 L/h.

Physiologic adaptation to a hot environment occurs over a period of 10-14 days and is accompanied by decreased energy expenditure and lower rise in body temperature for a given workload.44 For full acclimatization, exercise in the heat is required each day; only partial adaptation occurs by passive exposure to heat. There are several different systems involved in the adaptation process. Activation of the renin-angiotensin system results in increased production of aldosterone-yielding sodium conservation in both urine and sweat. Cardiovascular acclimatization results in increased stroke volume and decreased heart rate for a given cardiac output. Exocrine adaptation produces increased sweat capacity, decreased sweat threshold temperature, and decreased sodium and chloride content of sweat. Work efficiency is increased by an increase in muscle mitochondria per unit of muscle mass, which allows for less heat production for a given intensity of work.

Predisposing Factors to Heat Illness. Since much of the physiologic response to heat involves enhanced cardiovascular function, any intrinsic limitation on this system diminishes the ability to compensate for heat stress and can result in heat illness. In addition, conditions that produce dehydration predispose to heat illness. Obese individuals are at increased risk because they have more insulation and less surface area-to-volume ratio with which to dissipate heat. Any problems that impair sweating mechanisms limit the body’s ability to respond to heat stress. These impairments can be congenital (ectodermal dysplasia, cystic fibrosis, scleroderma) or acquired (burns, miliaria).

Various medications and drugs may also predispose an individual to heat illness.45 Diuretics may produce dehydration. In this regard, phenothiazines, antihistamines, and anticholinergics may reduce sweating. The combination of phenothiazines with butyrophenones can impair thermoregulatory function. Stimulant drugs such as phencyclidine, cocaine, amphetamines, and tricyclic antidepressants can cause increased muscular activity, resulting in increased heat load. Beta blockers limit the compensatory response necessary to increase cardiac output.

Mild-to-Moderate Heat Illness Syndromes. Heat syncope is characterized by sudden fainting in heat while standing or after 15-20 minutes of exercise. The classic example is that of military recruits standing at attention for a prolonged period of time on a hot afternoon. Heat syncope is caused by vasodilation with postural pooling of blood; this leads to decreased venous return and decreased cardiac output with resultant cerebral ischemia. Patients with heart disease and/or those who may be taking diuretics are prone to this problem. Consciousness and blood pressure rapidly return to normal when the patient is supine.

Heat cramps are painful muscle contractions that occur following exercise in the heat. They may be seen in acclimatized individuals who lose large volumes of sweat that is replaced with water. Heat cramps frequently occur at the end of a work day after a cool shower and most often involve heavily–used muscles in the calves, thighs, and abdomen. Treatment consists of rest in a cool environment and passive stretching of the muscles. If heat cramps persist, give a salt solution orally or intravenously (1 L of normal saline). Liberalize salt intake in the diet to prevent recurrence.

The disease process known as heat exhaustion should be viewed as a continuum that starts with minor illness at one end and merges indistinctly into heat stroke on the other end. It may affect anyone regardless of fitness level and acclimatization. Strenuous physical activity in a hot environment or passive exposure to very high temperatures can precipitate the problem.

In its milder forms, heat exhaustion often presents with flu-like symptoms including malaise, headache, anorexia, nausea, vomiting, and muscle cramps. Thermoregulatory mechanisms continue to function so sweating should be present. Central nervous system (CNS) function remains essentially normal during heat exhaustion. Core temperature may be normal or mildly elevated (less that 41oC). Dehydration is usually present resulting in orthostatic hypotension and tachycardia.

Spontaneous cooling is usually sufficient to treat symptoms of heat exhaustion. The patient should stop exercising and be protected from further heat exposure. Have the patient rest supine in a cool place and give oral water or glucose and salt-containing fluids. In more extreme cases of heat exhaustion that are approaching heat stroke, use more aggressive cooling measures and intravenous fluids. With these measures, patients should recover within hours without sequelae.

Heatstroke. In contrast to the previous syndromes, heatstroke represents a true emergency and indicates that the body’s thermoregulatory mechanisms have failed. Two forms are generally recognized. Exertional heatstroke is acute in onset and occurs as a result of strenuous exercise in heat. This syndrome is encountered in healthy, motivated individuals participating in sporting events or undergoing performance tasks. The second form, (i.e., non-exertional or classic heatstroke) is more gradual in onset and typically affects the elderly, the poor, and the chronically ill. This syndrome is more likely to evolve over a period of days in these populations, who are at risk because they are unable to obtain fluids and/or seek refuge in a cooler environment.

The classic clinical criteria for heatstroke are an elevated core temperature, usually defined as 41oC or greater, and CNS dysfunction. Originally, the absence of sweating was described as a criterion for heatstroke; however, it is now clear that sweating may continue, particularly in exertional heatstroke. Significant neurologic findings are the hallmark of heatstroke. Delirium, coma, and seizures are common, although virtually any CNS abnormality may be seen. Cardiovascular abnormalities include high-output (exertional) or low-output (non-exertional) cardiac failure, tachycardia, and hypotension.46 Hyperventilation is common. Complications associated with heatstroke include acute renal failure, rhabdomyolysis, hypoglycemia, hyperkalemia, disseminated intravascular coagulation, lactic acidosis, and hepatocellular injury. All of these abnormalities are seen more commonly in exertional heatstroke.43

Once ABCs are addressed, the prehospital care of heatstroke begins with early recognition and immediate initiation of cooling measures. Remove all clothing, moisten skin, and fan the air around the patient. Although of questionable value, place ice packs in the areas of high blood flow such as the neck, axillae and groin.47,48 Initiate intravenous fluid resuscitation with 5% dextrose in normal saline.

ED care consists of the usual supportive measures and cooling. Remove clothing and institute cooling measures to reduce core temperature to 39oC as quickly as possible. The more rapid the cooling, the lower the mortality, particularly in cases of exertional heatstroke. Regardless of the cooling method employed, discontinue cooling at 39oC to avoid precipitating hypothermia.

Mortality statistics associated with heatstroke have varied widely; however, with current medical therapy it is probably in the 10-20% range.52–55 Morbidity and mortality are related to both the duration of hyperthermia and the core temperature at collapse. Other predictors of poor prognosis include extremes of age, pre-existing illnesses and duration of coma. The majority of patients die or recover completely, with only a small percentage suffering residual neurologic damage.55

Traditional Cooling. Ice water soaks, immersion in ice baths, and use of cooling blankets, as well as application of ice to the groin, neck, and axillae have been used as cooling modalities in heatstroke. These methods are effective, but it should be stressed that the use of iced-soaked towels and fanning is a simple method of cooling that can be used in any ED, requires no special equipment, and provide rapid cooling with little risk.

After removing the patient’s clothes, apply towels or sheets soaked in ice water and ice chips. The sheets or towels keep the ice water in contact with the skin and keep the ice in place. Change the sheets or towels frequently and keep them cold. Direct the breeze from an electric fan over the patient to accelerate the cooling rate. Immersing the victim in a cold water tub is more difficult, and may prove problematic in patients requiring ventilatory support or other critical care therapy and monitoring.

Evaporative Method. Several investigators have abandoned ice water cooling in favor of the more theoretically sound method of evaporative cooling.49–51 Evaporation of water can achieve the removal of 540 kcal/kg of water evaporated, whereas melting ice to water achieves removal of only 80 kcal/kg. This means that evaporation of water from skin will cool the patient up to four times more quickly than an ice water bath. With this method, skin temperature is kept at 30oC-32oC to enhance vasodilation and increase heat flow; shivering is less common than with conventional cooling.

A simple method of evaporative cooling involves fanning the patient while using mist sprayers to wet the skin. High-speed fans ensure the most rapid evaporation. Evaporative cooling works only if the patient has been completely undressed and is not covered with sheets or towels. The patient should be in an air-conditioned area or in an area with low relative humidity so that evaporation will occur. Evaporative cooling also requires intact circulation to take cooled blood from the skin to the body core; use ice water cooling if the patient is in shock.

Other Cooling Methods. Although other cooling methods are available (iced peritoneal, thoracic, bladder or gastric lavage, cardiopulmonary bypass, and chilled oxygen administration) these methos require special equipment, special training, are associated with significant risks, and, in general, have not proved to be more beneficial than external cooling methods.

Prevention. Heat illness spans the spectrum from a minor illness to a life-threatening emergency. As with most environmental disorders, preventative measures are, by far, the best strategy. (See Table 7.) Attention to physical conditioning and acclimatization, use of appropriate clothing, adequate fluid replacement, strategies to help the high-risk populations.

Summary

The majority of life-threatening, summer-related emergencies reflect conditions caused by heat, bolts, water, and venom. In order to maximize outcomes, the ED physician must be aware of the full spectrum of syndromes associated with these insults and make organ- and patient-specific interventions. Indications for therapy will vary according to the severity of the presentation and risk factors of the patient.

References

1. Cherington M. Lightning injuries. Ann Emerg Med 1995;25:516–519.

2. Cooper MA. Lightning injuries. In: Rosen P, Barkin RM, Braen GR, et al, eds. Emergency Medicine: Concepts and Clinical Practice , 3rd ed.. St. Louis: Mosby-Year Book, Inc.; 1992.

3. Kouwenhoven WB. Effects of electricity in the human body. Electrical Engineering 1949;68:199-202.

4. Hunt JL, Mason AD, Masterson TS, et al. The pathophysiology of acute electric injury. J Trauma 1976;16:335-340.

5. Andrews CJ, Darvienza M, Mackerras D. Lightning injury—a review of clinical aspects, pathophysiology, and treatment. Adv Trauma 1989;4:241-247.

6. Kleiner JP, Wilkin JH. Cardiac effects of lightning stroke. JAMA 1978;240:2757-2759.

7. Taussig HB. "Death" from lightning and the possibility of living again. Ann Intern Med, 1968;68:1345-1353.

8. Brown BJ, Gaasch WR. Electrical injuries and lightning. Emerg Med Clin N Am, 1992;10:211-229.

9. Cooper MA. Lightning injuries: Prognostic signs for death. Ann Emerg Med, 1980;9:134-138.

10. Barthlome CW, Jacoby WD, Ramchand SC. Cutaneous manifestations of lightning injury. Arch Dermatol 1975;11:1466-1468.

11. Baker SP, O’Neill B, Ginsburg MJ, et al. The Injury Fact Book, 2nd ed. New York: Oxford University Press, Inc.; 1992:174-185.

12. Waller AE, Baker SP, Szocka. Childhood injury deaths: National analysis and geographic variations. Am J Pub Health 1989;79:310-315.

13. Rice DP, MacKenzie EJ, et al. Cost of Injury in the United States: A Report to Congress, San Francisco, CA: Institute for Health and Age, University of California and Injury Prevention Center, The John Hopkins University; 1989.

14. Brenner RA, Smith GS, Overpeck MD. Divergent trends in childhood drowning rates, 1971-1988. JAMA 1994;271:1606-1608.

15. Wintemute GJ. Drowning in early childhood. Pediatr Ann 1992;21:417-421.

16. Jumbelic M, Chambliss M. Accidental toddler drowning in five-gallon buckets. JAMA, 1990;263:1952-1953.

17. Mann NC, Weller SC, Rauchschwalbe R. Bucket-related drownings in the United States, 1984 -1990. Pediatrics 1992;89:1068-1071.

18. Plueckhahn VD. Drowning: Community aspects. Med J Austr 1979;2:226–230.

19. Avis SP. Suicidal drowning. J Forensic Sci 1993;38:1422-1426.

20. Schmidt P, Madea B. Death in the bathtub involving children. Forensic Sci Int 1995;72:147-155.

21. Feldman KW, Monastersky C, Feldman GK. When is childhood drowning neglect? Child Abuse Negl 1993:17;3:329.

22. Model JH. Drowning. N Engl JMed 1993;328:253-256.

23. Model JH, Graves SA, Ketover A. Clinical course of 91 consecutive near-drowning victims. Chest 1976;70:231-238.

24. Model JH, Davis JH. Electrolyte changes in human drowning victims. Anesthesiology 1969;30:414-420.

25. Quain L, Kinder D. Pediatric submersions: Pre-hospital predictors of outcome. Pediatrics 1992;90:909-913.

26. The National Committee for Injury Prevention and Control. Injury Prevention: Meeting the Challenge. New York: Oxford University Press, Inc.; 1989.

27. Litovitz TL, Felberg L, Soloway RA, et al. 1994 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Ann Emerg Med 1995;13:551-597.

28. Gold BS, Barish RA. (1992). Venomous snakebites—current concepts in diagnosis, treatment and management. (Environmental Emergencies). Emerg Med Clini North Am 1992;10:249-267.

29. Sullivan JB, Wingert WA, Norris RL. North American venomous reptile bites. In: Auerbach PS, ed. Wilderness Medicine–Management of Wilderness and Environmental Emergencies, 3rd ed. St. Louis: Mosby-Year Book; 1995:680-709.

30. Curry CC, Horning D, Brady P, et al. The legitimacy of rattlesnake bites in central Arizona. Ann Emerg Med, 1989;18:658-663.

31. Russell FE, ed. Snake Venom Poisoning. Philadelphia:JB Lippincott; 1980.

32. Dart RC, Hurlbut KM, Garcia R, et al. Validation of a severity score for the assessment of crotalid snakebite. Ann Emerg Med 1996;27:321-326.

33. Burgess JL, Dart RC, Egen NB, et al. Effects of constriction bands on rattlesnake venom absorption: A pharmacokinetic study. Ann Emerg Med 1992;21:1086-1093.

34. Dart RC, Gustafson RA. Failure of electric shock treatment for rattlesnake envenomation. Ann Emerg Med 1991;20:659-661.

35. Howe NR, Meisenheimer JL. Electric shock does not save snakebitten rats. Ann Emerg Med, 1988;17:254-256.

36. McCullough NC, Gennaro JF. Treatment of venomous snakebites. In: Minton SA, ed. Snake Venoms and Envenomations. New York :Marcel Dekker; 1971:137-154.

37. Stewart ME, Greenland S, Hoffman JB. First–aid treatment of poisonous snakebite: are currently recommended procedures justified? Ann Emerg Med 1981;10:331.

38. Bornstein AC, Russell FE, Sullivan JB. Negative pressure suction in field treatment of rattlesnake bite. Vet Hum Toxicol 1985;25:297.

39. Clark RF, Selden BS, Furbee B. The incidence of wound infection following crotalid envenomation. J Emerg Med 1993;11:583-586.

40. Guisto JA. Severe toxicity from crotalid envenomation after early resolution of symptoms. Ann Emerg Med 1995;26:387-389.

41. Hurlbut KM, Dart RC, Spaite D, et al. Reliability of clinical presentation for predicting significant pit viper envenomation. Ann Emerg Med 1988;17:438-439.

42. Heat–related illnesses and deaths-United States, 1994-1995. Morb Mortal Wkly Rep MMWR 1995;44:25, 465-468.

43. Knochel JP. Heat stroke and related disorders. Dis Mon 1989;5:301-377.

44. Williams CG, Bredell GA, Wyndham CH, et al. Circulatory and metabolic reactions to work in the heat. J Appl Physiol, 1993;17:625-638.

45. Kilbourne EM. Heat waves. In: The Public Health Consequences of Disasters. Atlanta: U.S. Department of Health and Human Services, Public Health Service, CDC.; 1989:51-61.

46. O’Donnell TF, Clowes GHA. The circulatory abnormalities of heat stroke. N Engl J Med, 1972;287:15, 734-737.

47. Wyndham CH, Strydom NB, Cooke HM, et al. Methods of cooling subjects with hyperpyrexia. J App Physiol 1959;771-776.

48. Ferris EB, Blankenhorn MA, Robinson HW, et al. Heat stroke: clinical and chemical observations on 44 cases. J Clin Invest, 1938;17:3, 249-262.

49. Weiner JS, Khogali M. A physiological body cooling unit for treatment of heathstroke. Lancet 1980;2:507-509.

50. Graham BS, Lichtenstein MJ, Hinson JM, et al. Non–exertional heatstroke: Physiologic management and cooling in 14 patients. Arch Int Med 1986;146, 87-90.

51. Sweeney WB, Krafte-Jacobs B, Hansen W, et al. A method for shipboard treatment of multiple heat casualties. Mil Med 1992;157:145-147.

52. Hart GR, Anderson RJ, Crumpler CP, et al. Epidemic classical heatstroke: clinical characteristics and course of 28 patients. Medicine 1982;61: 3, 189-197.

53. Yaqub BA, Al–Harthi SS, Al–Orainey IO, et al. Heatstroke at the Mekkah pilgrimage: clinical characteristics and course of 30 patients. Quart J Med 1986;59:523-530.

54. Vicario SJ, Okabajue R, Haltom T. Rapid cooling in classic heatstroke: effect on mortality rates. Am J Emerg Med, 1986;4:5, 394-398.

55. Ramsey CB, Watson WA, Robinson WA. Effect of cooling time on survival in classical heatstroke. J Wild Med 1993:4:1, 27-31.

Physician CME Questions

97. Which of the following is true regarding lightning?

A. Its voltage is lower than most household or industrial electrical sources.

B. Its duration of exposure during a strike is shorter than typical industrial injuries.

C. Its current is lower than most household or industrial electrical sources.

D. It usually takes an internal pathway through the victim.

E. Its circuit is the same as alternating current.

98. Heatstroke can be differentiated from heat exhaustion by which of the following?

A. Presence of CNS dysfunction

B. Ambient temperature

C. Association with exertion

D. Age of the victim

99. Which of the following is not typically seen in victims of lightning?

A. Cataracts

B. Tympanic membrane rupture

C. Cardiorespiratory arrest

D. Compartment syndromes secondary to deep burns

E. Cool, pulseless, paralyzed extremities

100. One of the primary pathophysiological causes of cardiac, CNS, and renal abnormalities in drowning is:

A. hyponatremia.

B. hypoxia.

C. catecholamine release.

D. hypervolemia.

101. All of the following are poor prognostic signs in submerged victims except:

A. hypothermia.

B. pH less than 7.1.

C. submersion longer than 5 minutes.

D. no resuscitation measures for more than 10 minutes.

102. Which of the following features is characteristic of non-venomous snakes?

A. Heat–sensitive facial pit

B. Elliptical pupils

C. Rounded head

D. Single row of subcaudal scales

103. The mainstay of treatment for venomous snakebite is:

A. surgical wound incision.

B. incision and suction.

C. lymphoocclusive constriction band.

D. antivenin therapy.

104. Treatment of heatstroke should include all of the following except:

A. rapid cooling by ice water immersion or evaporation.

B. removal of clothing.

C. intravenous fluids.

D. administration of antipyretics.

E. continuous temperature monitoring.

Corrections: In the table "Guidelines for Treatment of Tick-Borne Diseases" in the May 26 issue, an incorrect dosage was given in the therapy for babesiosis. The sentence should begin "clindamycin 1.2 g bid IV . . ." A sentence in the section asymptomatic tick bites on page 108 should have given the dosage for a 10-day course of doxycycline as 100 mg po bid. Question 84 has been removed from the CME test.We regret any inconvenience caused by these errors.