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Emergency Medicine Atlas > Part 2. Specialty Areas > Chapter 16. Environmental Conditions >

High-Altitude Retinal Hemorrhage

Associated Clinical Features

Retinal hemorrhages (Fig. 16.1) are common above 5200 m and above these altitudes need not be associated with acute mountain sickness (AMS). Below 5200 m there is an association with altitude illness. High-altitude retinal hemorrhages (HARH) are rarely symptomatic, but if found over the macula, these hemorrhages may cause temporary blindness.

Figure 16.1

High-Altitude Retinal Hemorrhage (Courtesy of Peter Hackett, MD.)

Differential Diagnosis

The diagnosis can be established by ophthalmoscopy. Without visualization of the lesion, the differential diagnosis of unilaterally decreased vision or blindness at high altitude would include high-altitude cerebrovascular accident as well as all conditions found at sea level.

Emergency Department Treatment and Disposition

HARH generally resolve spontaneously after descent to lower altitudes. No treatment is necessary for asymptomatic HARH. Patients with HARH associated with a decrease in vision should be referred to an ophthalmologist for follow-up.

Clinical Pearls

1. Patients with blurred vision and unilateral mydriasis at the high altitude should be asked about use of medications, including transdermal scopolamine patches.

2. As with almost all altitude-related problems, descent is the primary treatment.

High-Altitude Pulmonary Edema

Associated Clinical Features

High-altitude pulmonary edema (HAPE) is a noncardiogenic form of pulmonary edema (Fig. 16.2). It generally begins within the first 2 to 4 days after ascent above 2500 m. The earliest symptoms are fatigue, weakness, dyspnea on exertion, and decreased exercise performance. Symptoms of acute mountain sickness (AMS) such as headache, anorexia, and lassitude may also be present. If untreated, a persistent dry cough develops, followed by tachycardia and tachypnea at rest with cyanosis. HAPE generally begins and is worse at night. Eventually the victim develops dyspnea at rest and orthopnea with audible crackles in the chest. Pink frothy sputum is a grave sign. There may be mental status changes and ataxia due to hypoxemia or associated high-altitude cerebral edema (HACE).

Figure 16.2

High-Altitude Pulmonary Edema Chest x-ray in patient with HAPE. Note normal heart size with bilateral "patchy" pulmonary infiltrates. (Courtesy of Peter Hackett, MD.)

Differential Diagnosis

Cardiogenic pulmonary edema is rare at high altitude. Respiratory infections may also be present; distinction is made difficult by the fact that fever up to 38.5°C is common with HAPE.

Emergency Department Treatment and Disposition

Mild cases (oxygen saturation in the 90s on low-flow oxygen) at moderate altitudes (below 3500 m) may be treated at altitude with bed rest and oxygen. If supplemental oxygen and a reliable person are available, the patient may be discharged with oxygen therapy and bed rest at home or, more often, in lodgings. More severe cases should descend immediately and may require admission to a hospital at a lower altitude. These patients may require intubation and mechanical ventilation. Nifedipine may be of some benefit but is not a substitute for altitude or descent. Hyperbaric therapy, especially with a portable hyperbaric chamber (Fig. 16.3), has an efficacy equal to that of supplemental oxygen and is mainly helpful in prehospital settings where oxygen availability is limited.

Figure 16.3

"Gamow Bag" Portable hyperbaric chamber (Gamow bag). A HAPE patient is being treated at 4300 m at Pheriche, Nepal. Due to orthopnea, the patient was unable to tolerate lying flat, so the bag was propped up immediately after inflation. (Courtesy of Ken Zafren, MD.)

Clinical Pearls

1. Crackles may be unilateral or bilateral but usually start in the right middle lobe and are heard first in the right axilla.

2. HAPE limited to the left lung in association with a small right hemothorax without pulmonary markings is pathognomonic for unilateral absent pulmonary artery syndrome. These patients develop HAPE at relatively low altitudes, sometimes below 2500 m.

Hypothermia

Associated Clinical Features

Accidental hypothermia is an unintentional decline in core temperature below 35°C. Presentation may be obvious or subtle, especially in urban settings. Symptoms vary from vague complaints to altered levels of consciousness, and physical findings include progressive abnormalities of every organ system. Following initial tachycardia, there is progressive bradycardia (50% decrease in heart rate at 28°C), with decline in blood pressure and cardiac output. ECG intervals may be prolonged; first the PR; then the QRS; and then especially the QTc. A J wave (Osborn wave; hypothermic "hump"; Fig. 16.4) may be seen, but is neither pathognomonic nor prognostic. The J wave is present at the junction of the QRS complex and the ST segment.

Figure 16.4

J Waves J waves in a hypothermic patient with core temperature (rectal probe) of 25.5°C. J waves may be seen at any temperature below 32.2°C, most frequently in leads II and V₆. Below a core temperature of 25°C, they are most commonly found in the precordial leads (especially V₃ and V₄) and their size increases. J waves are usually upright in aVL, aVF, and the left precordial leads. (Courtesy of Alan B. Storrow, MD.)

Differential Diagnosis

J waves may also be associated with central nervous system lesions, focal cardiac ischemia, young age, and sepsis. In mildly hypothermic patients, invisible preshivering muscle tone may obscure P waves.

Emergency Department Treatment and Disposition

Core temperature measurement (using low-reading rectal or esophageal thermometers), gentle handling, and appropriate warming methods are the mainstays of ED treatment. Cardiovascular instability often complicates rewarming; Advanced Cardiac Life Support (ACLS) guidelines for hypothermia provide guidance. If not obvious, a cause should be sought (e.g., hypothyroidism, sepsis), as should associated pathology. Except for previously healthy patients with acute mild hypothermia, most patients require admission for observation or to treat associated injuries or comorbidities.

Clinical Pearls

1. The most common problems with the diagnosis of hypothermia in the ED stem from incomplete data on vital signs.

2. Low-reading thermometers, accurate core temperatures, averaging of respirations over several minutes, and Doppler location of pulses are crucial to appropriate management.

Frostbite

Associated Clinical Features

Frostbite is true tissue freezing resulting from heat loss sufficient to cause ice crystal formation in superficial or deep tissue. Frostbite may affect the extremities, nose, or ears (and the scrotum and penis in joggers). Severity of symptoms is usually proportional to the severity of the injury. A sensation of numbness with accompanying sensory loss is the most common initial complaint. Often, by the time the patient arrives in the ED, the frozen tissue has thawed. The initial appearance of the overlying skin may be deceptively benign (Fig. 16.5). Frozen tissue may appear mottled blue, violaceous, yellowish-white, or waxy. Following rapid rewarming, there is early hyperemia even in severe cases.

Figure 16.5

Thawed Frostbite Typical appearance of frostbite soon after rewarming. Deep frostbite was caused by wearing mountaineering boots that were too tight in extreme cold at high altitude. Note deceptively benign appearance of this devastating injury. (Courtesy of James O'Malley, MD.)

Favorable signs include return of normal sensation, color, and warmth. Edema should appear within 3 h of thawing; lack of edema is an unfavorable sign. Vesicles and bullae appear in 6 to 24 h. Early formation of large clear blebs that extend to the tips of affected digits is a good indicator. Small dark blebs that do not extend to the tips indicate damage to subdermal plexi and are a poor prognostic sign.

Differential Diagnosis

Seen early and after rewarming, frostbite may be indistinguishable from nonfreezing cold injury such as immersion foot. Mixed injuries are common.

Emergency Department Treatment and Disposition

If other injuries are ruled out by history and physical examination, rewarm frostbitten areas in a warm water bath (37 to 41°C). If associated with severe hypothermia, active core rewarming should precede frostbite rewarming. If swelling occurs, measure compartment pressures (including hands and feet) to determine the need for fasciotomy. Admit all patients with associated hypothermia or in whom swelling occurs. Superficial frostbite (minimal skin changes and erythema) may be treated by home care with nursing instructions. Deep superficial frostbite (clear, fluid-filled blebs, swelling, pain; Fig. 16.6) may be treated by home care in a reliable patient. Deep frostbite (proximal hemorrhagic blebs, no swelling, no pulses; Figs. 16.7, 16.8, and 16.9) mandates hospital admission.

Figure 16.6

Deep Superficial Frostbite Clear blebs extending distally are indicators for favorable outcome. (Courtesy of James O'Malley, MD.)

Figure 16.7

Frostbite Blebs Proximal blebs, both clear and hemorrhagic. (Courtesy of Scott W. Zackowski, MD.)

Figure 16.8

Late Frostbite Late appearance of frostbite with demarcation starting to occur. Early surgery should be avoided in favor of autoamputation unless infection supervenes. (Courtesy of James O'Malley, MD.)

Figure 16.9

Deep Frostbite Late appearance of deep frostbite with clear demarcation. (Courtesy of James O'Malley, MD.)

Clinical Pearls

1. Early transfer of the patient to a center experienced in the care of frostbite injuries (even if hundreds of miles away) should be considered. On the other hand, transfer of the patient to a major medical center that does not generally manage frostbite is seldom in the patient's best interest.

2. Treatment of clear versus hemorrhagic blisters is controversial; one approach is to debride clear blisters and use topical aloe vera while leaving hemorrhagic blisters intact.

Pernio

Associated Clinical Features

Pernio, also known as chilblain cold sores, is the result of nonfreezing cold exposure. Pernio appears within 24 h of cold exposure, most frequently on the face, ears, hands, feet, and pretibial areas. A large range of lesions may be seen, with localized edema, erythema, cyanosis, plaques, and blue nodules occasionally progressing to more severe lesions including vesicles, bullae, and ulcerations (Fig. 16.10). The lesions persist for up to 2 weeks and may become more chronic. They are typically very pruritic and associated with burning paresthesias. Following rewarming, pernio often takes the form of blue nodules, which are quite tender.

Figure 16.10

Pernio Pernio or chilblains with localized erythema, cyanosis, and nodules. (Courtesy of Ken Zafren, MD.)

Differential Diagnosis

In the setting of recent cold exposure, pernio might be confused with the more severe syndrome of trench foot and its sequelae. If the history of cold exposure is not elicited, the differential diagnosis is potentially very broad.

Emergency Department Treatment and Disposition

Management is supportive. The skin should be warmed, washed, and dried. Affected extremities can be dressed in soft, dry, sterile dressings and elevated. Nifedipine (20 to 60 mg daily) may be helpful in chronic cases.

Clinical Pearls

1. Healing may be followed by hyperpigmentation.

2. Recurrences are possible following milder exposure.

3. Chilblains are said to be more frequent in young women, especially in association with Raynaud's phenomenon.

Immersion Injury (Trench Foot)

Associated Clinical Features

Immersion injury is a peripheral nonfreezing cold injury resulting from exposure to water, usually at temperatures just above freezing. However, it can occur during prolonged exposure to any wet environment cooler than body temperature. Dependency and immobility predispose to immersion injury. The degree of injury seems to depend on time and temperature. The first symptoms appear in hours; tissue loss may require many days of exposure. Prior to rewarming, the distal extremities are numb and swollen. The skin is first red, then changes to pale, mottled, or black (Figs. 16.11 and 16.12). Cramping of the calves may occur.

Figure 16.11

Immersion Injury Immersion injury to hands (unusual location) several hours after rewarming. The patient spent 18 h bailing out a boat in waters just above freezing in Alaska. (Courtesy of James O'Malley, MD.)

Figure 16.12

Immersion Foot Early appearance of immersion foot in a mentally ill alcoholic homeless patient. (Courtesy of Ken Zafren, MD.)

Differential Diagnosis

Immersion injury is also known as trench foot, peripheral vasoneuropathy, shelter foot, sea boot foot, and foxhole foot. It is distinct from tropical immersion foot or warm-water immersion foot as seen in the Vietnam War. Tropical immersion foot was typically seen after 3 to 7 days of exposure to water at 22 to 32°C. Warm-water immersion foot was seen after 1 to 3 days at 15 to 32°C. These syndromes were characterized by burning in the feet, pain on walking, pitting edema, and erythema, with wrinkling and hyperhydration of the skin. They resolved completely after rest and removal from the wet environment.

Emergency Department Treatment and Disposition

Hypovolemia, hypothermia, and associated injuries are the rule and should be treated first. General treatment of immersion foot (or hand) is the same as that for frostbite that has been rewarmed. Swelling may produce compartment syndrome and require fasciotomy. Most patients require admission to the hospital.

Clinical Pearls

1. Pulses may be difficult to feel but may be found by Doppler.

2. Mixed injuries (frostbite and immersion) are common.

Sun Exposure

Associated Clinical Features

Ultraviolet (UV) radiation causes both acute and chronic skin changes. Sunburn is a partial-thickness burn (Fig. 16.13), which may become a full-thickness injury if infected. "Sun poisoning" is a severe systemic reaction to UV radiation. Patients complain of nausea, vomiting, headache, fever, chills, and prostration. Excessive UV radiation may cause injury to the cornea and conjunctiva, termed ultraviolet keratitis (photokeratitis, snow blindness). This painful condition may occur in skiers, welders, or tanning salon patrons who do not wear proper eye protection.

Figure 16.13

Sunburn Sunburn is characterized by erythema, edema, warmth, tenderness, and blisters. (Courtesy of Kevin J. Knoop, MD, MS.)

Photosensitivity reactions (photodermatoses) are of several types. Phototoxic reactions are an abnormal response to UV radiation caused by a substance that is ingested (e.g., prescription or over-the-counter medications) or applied to the skin (even seemingly innocuous perfumes or shampoos); there is a direct relation between the amount of UV exposure and severity. Photoallergic reactions are clinically similar to contact dermatitis and, like phototoxic reactions, may be precipitated by ingested or applied drugs. Unlike phototoxic reactions, photoallergies may be precipitated by a small amount of light. Phytophotodermatitis (Fig. 16.14, see also Fig. 13.57) is precipitated by skin contact with certain plants followed by exposure to UV radiation. It can resemble either phototoxic or photoallergic reactions.

Figure 16.14

Phytophotodermatitis This reaction may require aggressive systemic steroid therapy. The case illustrated is a mild one caused by exposure to limes and UVA. A clue to the diagnosis is the patchy distribution with linear edges. More severe reactions resemble rhus dermatitis. (Courtesy of Lee Kaplan, MD.)

Differential Diagnosis

Phototoxicity should be suspected in any patient with a severe or exaggerated sunburn. Photoallergy is easily misdiagnosed as allergic eczema or contact dermatitis, especially since onset is often delayed up to 2 days after exposure. Phytophotodermatitis may mimic severe sunburn or contact dermatitis, especially rhus (poison ivy, sumac, or oak; see "Toxicodendron Exposure," below) dermatitis. Endogenous photosensitizers (endogenous photodermatoses) include solar urticaria, porphyria cutanea tarda, polymorphous light eruption, and systemic lupus erythematosus. These may be provoked by visible light as well as by UV radiation. History is the key to the diagnosis of UV keratitis; the differential includes corneal abrasions, ocular foreign body, and conjunctivitis.

Emergency Department Treatment and Disposition

Treatment of sunburn and sun poisoning involves standard burn and supportive care. Sunburn is usually a self-limited problem. Cool compresses and nonsteroidal anti-inflammatory drugs may be beneficial. Steroids may be useful for sun poisoning. Ultraviolet keratitis is treated with mydriatic-cycloplegic eyedrops to decrease pain; initial examination is made easier with topical anesthetics. Severe cases may require bilateral eye patches for 12 to 24 h, antibiotic ointment, and narcotic analgesics. These patients require 24- to 48-h follow-up; ophthalmology referral is indicated to rule out retinal damage.

Treatment of photosensitivity reaction has two components: treatment of the sunburn and recognition of the sensitizing agent or endogenous medical condition. Topical steroids and oral analgesics and antipruritics may be helpful. Systemic steroids may be required. Patients with severe reactions should be referred to a dermatologist for possible photo patch testing.

Clinical Pearls

1. Even para-aminobenzoic acid (PABA) in sunscreens may be a photosensitizer and can cause a photoallergic reaction.

2. The unique properties of individual skin types produce marked differences in response to UV radiation.

3. Victims of UV keratitis typically present 2 to 12 h after exposure. Treatment should not include prolonged use of topical anesthetics or topical steroids.

Lightning Injuries

Associated Clinical Features

Lightning produces injury from high voltage, heat production, and explosive shock waves. Direct injuries include cardiopulmonary arrest, other cardiac arrhythmias, and neurologic abnormalities such as seizures, deafness, confusion, amnesia, blindness, and paralysis. The patient may suffer contusions from the shock wave or from opisthotonic muscle contractions. Chest pain and muscle aches are common. One or both tympanic membranes rupture in more than 50% of victims. Cataracts are usually a delayed occurrence. Hematologic abnormalities including disseminated intravascular coagulation (DIC) have been described. Fetal demise may occur.

Burns may result from vaporization of sweat or moist clothing, heating of clothing and metal objects such as belt buckles, and direct effects of the strike. Linear burns and punctate burns (Figs. 16.15 and 16.16) are thermal burns. Feathering burns (Fig. 16.17) are not actually burns but are skin markings caused by electron showers. They are pathognomonic of lightning injury.

Figure 16.15

Punctate Lightning Burns Punctate burns due to lightning are partial- or full-thickness thermal burns that range from a few millimeters to a centimeter in diameter. They are multiple and closely spaced. (Courtesy of Arthur Kahn, MD.)

Figure 16.16

Linear Lightning Burns Linear burns from lightning are due to thermal effects. (Courtesy of William Barsan, MD.)

Figure 16.17

Feathering Feathering burns (Lichtenberg's flowers, filigree burns, arborescent burns, ferning, or keraunographic markings) are pathognomonic of lightning injury. They are not true burns but are imprints on the skin of electron showers. Note the subtle but typical pattern in the clavicular areas. (Courtesy of Marco Coppola, DO., and Margaret J. Karnes, DO.)

Differential Diagnosis

Diagnosis is easy when there is a thunderstorm, when there are witnesses to the strike, or when there are typical physical findings. Lightning on relatively sunny days (without loud thunder) striking a lone victim may produce a confusing picture. The scattering of clothing and belongings may mimic an assault. Side flashes from metal objects and wiring may produce indoor victims during storms. Differential diagnosis of lightning injury includes cerebrovascular accident or intracranial hemorrhage, seizure disorder, spinal cord injury, closed head injury, hypertensive encephalopathy, cardiac arrhythmias, myocardial infarction, and toxic ingestions (especially heavy metals).

Emergency Department Treatment and Disposition

History and physical examination to rule out associated injuries and standard ED care for critical patients—including cardiac enzymes, urinalysis, and ECG—are necessary. All patients, even those apparently well, require admission for observation, since their condition may change over several hours following the lightning strike.

Clinical Pearls

1. The amount of damage to the exterior of the body does not predict the amount of internal injury.

2. Since lightning most commonly produces cardiac standstill by means of massive direct current countershock, prompt, spontaneous return of normal heart rhythm (by virtue of cardiac automaticity) is the rule. However, respiratory arrest is often more prolonged. In a triage situation, the normal rules do not apply, since victims breathing spontaneously are already recovering. The rule in lightning strikes is to resuscitate the "dead." Ventilatory support is often all that is required.

Ticks

Associated Clinical Features

Ticks are blood-sucking parasites of people and animals. Ticks cause illness by acting as vectors for pathogens, or by secreting toxins or venoms.

Tick paralysis develops 5 to 6 days after an adult female tick attaches. Over the next 24 to 48 h, an ascending, symmetric, flaccid paralysis develops. Alternative presentations include ataxia and associated cerebellar findings without muscle weakness or isolated facial paralysis. Resolution of the paralysis after removal of the tick establishes the diagnosis.

Ticks carry more types of infectious pathogens than any other arthropods except mosquitoes. The most important of these include Borrelia (responsible for Lyme disease and relapsing fever), rickettsia (e.g., Rocky Mountain spotted fever), viral pathogens (e.g., Colorado tick fever), and babesiosis. Rashes are prominent in Lyme disease (see Fig. 13.25) and Rocky Mountain spotted fever (see Fig. 13.6), sometimes present in relapsing fever, uncommon in Colorado tick fever, and absent in babesiosis. The first two are covered in Chap. 13.

Clinically important ticks in North America include Ixodes dammini, the deer tick (Lyme disease and babesiosis; Fig. 16.18); Dermacentor andersonii, the wood tick (Rocky Mountain spotted fever and Colorado tick fever; Fig. 16.19); and Amblyomma americanum, the Lone Star tick (a very widespread tick implicated in the transmission of Lyme disease outside of the range of I. dammini; Fig. 16.20). More than 40 species of ticks can cause tick paralysis. In North America the most common cause is D. andersonii, but A. americanum and Ixodes species have also been associated with tick paralysis.

Figure 16.18

Deer Tick Ixodes dammini, the deer tick, is a vector of Lyme disease and babesiosis. (Courtesy of the Centers for Disease Control and Prevention, Atlanta, GA.)

Figure 16.19

Wood Tick Dermacentor andersonii, the wood tick, is a vector of Rocky Mountain spotted fever and Colorado tick fever. (Courtesy of the Centers for Disease Control and Prevention, Atlanta, GA.)

Figure 16.20

Lone Star Tick Amblyomma americanum, the Lone Star tick, has been implicated as a vector in Lyme disease. (Courtesy of Sherman Minton, MD.)

Differential Diagnosis

Tick paralysis should be considered in any patient provisionally diagnosed with Guillian-Barré syndrome, Eaton-Lambert syndrome, myasthenia gravis, poliomyelitis, botulism, diphtheric polyneuropathy, or any disease producing ascending flaccid paralysis or acute ataxia. The main point of differential diagnosis of tick-borne illnesses is to consider these diseases in the differential of ill patients, especially those who have been outdoors in rural areas during seasons when ticks are active.

Emergency Department Treatment and Disposition

If still embedded, the tick should be removed promptly by grasping it as close to the skin surface as possible, using blunt curved forceps or tweezers. The tick should be pulled out with slow, gentle traction, taking care not to crush or squeeze the body, which may result in injection of contaminated tick fluids. Other methods of tick removal—such as application of fingernail polish, isopropyl alcohol, or a hot match head—have not been proven to effect detachment and may induce regurgitation of tick contents into the wound.

Patients with tick paralysis may require supportive care, including mechanical ventilation. Patients with tick-borne illnesses may require admission for supportive care or intensive antibiotic treatment.

Clinical Pearls

1. Prevention of tick bites includes the use of protective clothing containing N, N-diethylmetatoluamide (DEET).

2. A clear history of a tick bite is present in less than one-third of Lyme disease cases.

3. Unusual neurologic presentations, particularly bilateral peripheral seventh-nerve palsies, should prompt consideration of Lyme disease.

Pit Viper Envenomation

Associated Clinical Features

The pit vipers (Crotalidae family) indigenous to the United States comprise multiple rattlesnake species (Figs. 16.21, 16.22, 16.23), cottonmouths (Fig. 16.24), and copperheads (Fig. 16.25). Pit viper venom is complex and produces hematologic, cardiovascular, and neuromuscular effects. Clinically, snake bites can be divided into four categories. The category of no envenomation consists of only fang marks. Minimal envenomation (Fig. 16.26) consists of fang marks and local swelling but no systemic symptoms. Moderate envenomation (Figs. 16.27, 16.28) includes the above with the addition of nausea, vomiting, and mild changes in coagulation parameters. Severe envenomation (Fig. 16.29) includes all the above with marked local swelling and signs of significant coagulopathy (e.g., subcutaneous ecchymosis and/or hematuria).

Figure 16.21

Eastern Diamondback Rattlesnake The eastern diamondback is the largest U.S. rattlesnake and has a characteristic diamond-shaped pattern on its dorsal aspect. (Courtesy of R. Jason Thurman, MD.)

Figure 16.22

Red Diamond Rattlesnake The elliptical pupils and heat-sensing pits in this red diamond rattlesnake are characteritic of pit vipers. (Courtesy of Sean P. Bush, MD.)

Figure 16.23

Speckled Rattlesnake Note the triangular head, which is characteristic of pit vipers. (Courtesy of Sean P. Bush, MD.)

Figure 16.24

Cottonmouth The cottonmouth is a semiaquatic venomous pit viper that may crawl or swim with its head raised at an angle of 45 degrees. When disturbed, it may open its mouth wide to reveal a white lining. (Courtesy of R. Jason Thurman, MD.)

Figure 16.25

Copperhead The copperhead is frequently encountered in wooded mountains, abandoned buildings, and damp, grassy areas. It is able to climb low bushes and trees in search of food. It is typically a bit more docile than other pit vipers. (Courtesy of R. Jason Thurman, MD.)

Figure 16.26

Rattlesnake Envenomation, Day 1 This rattlesnake bite shows local swelling, some edema beyond the initial bite site, and a hemorrhagic bleb at 6 h. It would be considered mild to moderate at this time. (Courtesy of Sean P. Bush, MD.)

Figure 16.27

Progression of Rattlesnake Envenomation 7 Weeks Seven weeks later, the patient shown in Fig. 16.26 has progressed to tissue loss, eschar formation, and mild changes in coagulation parameters. (Courtesy of Sean P. Bush, MD.)

Figure 16.28

Moderate Crotalid Envenomation Patient was bitten by a rattlesnake on the dorsal aspect of the right hand who presented with edema extending to the wrist as well as nausea and vomiting. (Courtesy of Edward J. Otten, MD.)

Figure 16.29

Severe Rattlesnake Envenomation This patient sustained a rattlesnake bite to his hand and presented with marked and progressive swelling, subcutaneous ecchymosis, and a significant coagulopathy. (Courtesy of Sean P. Bush, MD.)

Differential Diagnosis

Bites by nonpoisonous snakes frequently present to the ED. However, unless clear identification of the snake is possible, all bites should be considered venomous. Physical characteristics of pit vipers include a triangular head, heat-sensing pits, elliptical pupils, and a single row of ventral scales (Figs. 16.22, 16.23, 16.30).

Figure 16.30

Nonvenomous Snake In contrast to the elliptical pupils and triangular head characteristic of pit vipers, this nonvenomous rat snake has a rounded head and circular pupils. (Courtesy of Sean P. Bush, MD.)

Emergency Department Treatment and Disposition

Initial field management of pit viper bites should include immobilization and rapid transport. Application of lymphatic constriction bands and use of extractor devices may be helpful, but these steps are controversial. Tourniquets and local incision are most likely ineffective and may do more harm than good. Electric shock or cryotherapy are not recommended. ED management includes resuscitation, establishing a physiologic baseline, and determining the need for antivenin. Pit viper antivenin of horse serum derivation carries all the risks of any horse serum product. Recommendations for antivenin therapy vary for mild or moderate envenomation. The dose of antivenin increases with the severity of envenomation. The package insert details the current recommendations for antivenin administration and allergy testing. CroFab (Savage Labs), a new recombinant antivenin, eliminates the risk of horse serum allergy and should be used when available. Compartment syndrome is a possible complication; however, prophylactic fasciotomy is not recommended. Patients who do not develop evidence of envenomation after 6 h of observation may be safely discharged home with close follow-up.

Clinical Pearls

1. Approximately one-fourth of all pit viper bites are "dry" (without any injection of venom).

2. In cases of severe envenomation, antivenin should not be withheld, even in individuals with a history of horse serum allergy. Bedside vasopressors (e.g., epinephrine) and a separate intravenous line for their administration should be available.

3. Allergy testing should be performed only in patients who need antivenin therapy.

4. Subcutaneous epinephrine (0.3 mg) given prior to administration of horse serum antivenin may reduce the potential allergic response.

Coral Snake Envenomation

Associated Clinical Features

The United States is home to two members of the Elapidae, or coral snake, family (Fig. 16.31). Coral snakes have small mouths, and bites are usually limited to fingers, toes, or folds of skin. The bite typically produces minimal local inflammation and pain. Paresthesias and muscle fasciculations are common. Systemic symptoms can include tremors, drowsiness, euphoria, and marked salivation. Cranial nerve involvement, represented by slurred speech and diplopia, may be followed by bulbar paralysis with dysphagia and dyspnea. Deaths result from respiratory and cardiac arrest. Onset of severe symptoms may be delayed up to 12 h.

Figure 16.31

Coral Snake United States coral snake with typical coloring and red-on-yellow bands. (Courtesy of Steven Holt, MD.)

Differential Diagnosis

The identification of coral snake bites is more difficult than that of pit viper bites because the fang marks are small and hard to visualize. The identification of coral snakes is complicated because many nonpoisonous snakes mimic their markings. The adage "red on yellow, kill a fellow; red on black, venom lack" (Fig. 16.32) applies to all coral snakes found in the United States but does not hold true in other parts of the world.

Figure 16.32

Nonvenomous Milk Snake As opposed to the red-on-yellow rings seen in the venomous U.S. coral snake, these red-on-black rings indicate a nonvenomous snake. Unfortunately this applies only to animals native to the United States. (Courtesy of Sean P. Bush, MD.)

Emergency Department Treatment and Disposition

Severe systemic symptoms following envenomation by Elapidae may be delayed and cannot be accurately predicted by local wound reactions. It is therefore recommended that four to six vials of antivenin be administered for all such suspected envenomations. Treatment of western coral snake bites is purely supportive because no antivenin is currently available.

Clinical Pearls

1. Treatment with antivenin should be initiated early in cases of eastern coral snake bites, since symptoms are often delayed and severe.

2. Coral snake venom is a potent neurotoxin, in contrast to venom from snakes of the Crotalidae family.

Brown Recluse Spider Envenomation

Associated Clinical Features

The brown recluse spider (Loxosceles reclusa) is the prototypical member of the genus Loxosceles, which as a group can produce the typical necrotic arachnidism following envenomation. These small spiders (approximately 1 cm in body length and 3 cm in leg length) have a worldwide distribution and are identified by the striking fiddle-shaped markings on their anterodorsal cephalothorax (Fig. 16.33). Initial envenomation may be painful, although patients often report no recollection of being bitten. Initial stinging gives way to aching and pruritus. The wound then becomes edematous, with an erythematous halo surrounding a violaceous center (Fig. 16.34). The erythematous margin often spreads in a pattern influenced by gravity, leaving the necrotic center near the top of the lesion (Fig. 16.35). Bullae may erupt, and—over a period of 2 to 5 weeks—the eschar sloughs, leaving a deep, poorly healing ulcer (Fig. 16.36). In unusual cases, systemic symptoms (loxoscelism) may present with hemolytic anemia as a predominant feature. Children are at higher risk of systemic disease. Other symptoms include fever, chills, nausea, vomiting, rash, arthralgia, and weakness. A leukocytosis may be seen.

Figure 16.33

Brown Recluse Spider Brown recluse spider with characteristic fiddle marking on the anterodorsal aspect of the cephalothorax. (Courtesy of Alan B. Storrow, MD.)

Figure 16.34

Early Brown Recluse Spider Bite (8 h) Early brown recluse spider bite (approximately 8 h) with a violaceous center surrounded by faint spreading erythema. (Courtesy of Curtis Hunter, MD.)

Figure 16.35

Later Recluse Spider Bite (24 h) Brown recluse spider bite at approximately 24 h. Note asymmetric spread of erythema and early central ulcer formation. (Courtesy of Edward Eitzen, MD, MPH.)

Figure 16.36

Recluse Necrosis (Weeks) Within about 2 to 5 weeks, significant bites of the brown recluse spider may reveal a deep, poorly healing ulcer with necrosis. (Courtesy of Kevin J. Knoop, MD.)

Differential Diagnosis

The diagnosis of brown recluse spider envenomation is based on typical history, clinical features, and possible exposure to the offending species. The local wound can be confused with cellulitis, decubitus ulcer, burns, and pyoderma gangrenosum. Systemic involvement may present as an isolated hemolytic anemia, thrombocytopenia, jaundice, or hemoglobinuria.

Emergency Department Treatment and Disposition

Most cutaneous lesions secondary to brown recluse spider bites can be managed with cold compresses, elevation, loose immobilization, and attention to tetanus immunization. Severe lesions may require reconstructive plastic surgery several weeks after wound stabilization. The use of dapsone to prevent lesion progression is controversial. Any systemic reaction with evidence of hemolysis, hemoglobinuria, or coagulopathy should prompt admission. Hyperbaric oxygen (HBO) therapy and antivenin have been suggested as possible adjuncts, but no clear consensus of preferred treatment has been established.

Clinical Pearls

1. The asymmetric spread of erythema, due to the local effects of gravity on the toxin, may help to distinguish a brown recluse spider bite from other arthropod envenomations.

2. If dapsone therapy is to be administered, screening for glucose-6-phosphate dehydrogenase (G6PD) deficiency should be considered.

3. Prophylactic antibiotics have been suggested to lessen the chance of secondary infection.

4. Field use of suction devices, if done early, has been suggested to decrease the local reaction and may actually be successful in removing small amounts of venom.

Black Widow Spider Envenomation

Associated Clinical Features

The black widow spider (Latrodectus mactans) is the prototype for the genus Latrodectus, several members of which cause human disease (Fig. 16.37). Members of this genus are common worldwide. The clinical presentation of severe and sustained muscle spasm is produced by a neurotoxic protein which causes the release of acetylcholine and norepinephrine at the presynaptic junction. The initial bite is mild to moderately painful and is often missed (Fig. 16.38). Within approximately 1 h, local erythema and muscle cramping begin, followed by generalized cramping involving large muscle groups such as the thighs, shoulders, abdomen, and back. Associated clinical features can include fasciculations, weakness, fever, salivation, vomiting, diaphoresis, and a characteristic pattern of facial swelling called Latrodectus facies (Fig. 16.39). Rare cases of seizure, uncontrolled hypertension, and respiratory arrest have occurred.

Figure 16.37

Black Widow Spider Latrodectus mactans with characteristic hourglass marking on its abdomen. (Courtesy of Alan B. Storrow, MD.)

Figure 16.38

Black Widow Spider Bite The bite of the black widow spider is clinically subtle. Local reaction is usually trivial, as in this confirmed bite with a small patch of mild erythema. (Courtesy of Gerald O'Malley, DO.)

Figure 16.39

Black Widow Facies A pattern of facial swelling, known as Latrodectus facies, may occur several hours after envenomation. (Courtesy of Gerald O'Malley, DO.)

Differential Diagnosis

The black widow spider is relatively aggressive and will defend her web, which is often found in woodpiles, basements, and garages. Most envenomation occurs between April and October and is located on the hand and forearm. In cases where no history of spider bite can be elicited, a wide differential diagnosis—including causes of acute abdominal pain, muscle spasm, or possible toxic ingestion—must be entertained.

Emergency Department Treatment and Disposition

Treatment of the local wound should include cleansing and tetanus prophylaxis. Severe pain and spasm may require intravenous benzodiazepines and narcotics. Calcium gluconate infusion has long been recommended to reduce symptoms, although evidence for its efficacy is lacking or contradictory. Antivenin exists and carries the same risk as all horse serum products. Antivenin should be strongly considered in cases of respiratory arrest, seizures, uncontrolled hypertension, and pregnancy.

Clinical Pearls

1. Of the five Latrodectus species indigenous to the United States, only three are black and only one has the orange-red hourglass marking (Fig. 16.37).

2. Calcium gluconate infusion is controversial for the treatment of muscle spasm. Benzodiazepines have replaced it as the drugs of choice.

3. Envenomation by L. mactans can mimic an acute abdomen.

Hymenoptera Envenomation

Associated Clinical Features

The order Hymenoptera includes wasps (Fig. 16.40), bees, and ants. Envenomation usually results in local pain, mild erythema, swelling, and pruritus. However, the possibility of more severe reactions makes this subgroup the most important in terms of human envenomation. A systemic or toxic reaction may occur from one or multiple stings. This may manifest as gastrointestinal symptoms, headache, pyrexia, muscle spasms, or seizure. Anaphylaxis may occur within minutes and may cause death. A serum sickness–type reaction may occur 7 to 14 days after envenomation.

Figure 16.40

Paper Wasp Paper wasps are found throughout the world and often establish nests close to or within human dwellings. (Courtesy of Sean P. Bush, MD.)

Solenopsis invicta was imported from South America and is the most prominent fire ant in the United States. It is primarily found in the South and builds mound nests in open grass settings, commonly in urban yards (Fig. 16.41). Disturbing the nests may result in severe swarming attacks. Bites are painful and produce sterile pustules that crust over in a few days (Fig. 16.42).

Figure 16.41

Fire Ant Mound This typical fire ant mound is a raised area of dirt in an urban yard. (Courtesy of Alan B. Storrow, MD.)

Figure 16.42

Fire Ant Bites These fire ant bites on the anterior knee occurred after this patient knelt on a mound. These bites are 3 days old; the initial sterile pustules have begun to crust over. (Courtesy of Alan B. Storrow, MD.)

Differential Diagnosis

Other arthropod envenomations or plant exposures must be considered.

Emergency Department Treatment and Disposition

Anaphylaxis is treated with conventional therapy. Local reactions may be treated with ice packs, steroid cream, and oral antihistamines.

Clinical Pearls

1. Honeybee stings are usually apparent since the stinger apparatus, including barb and venom sac, is often detached and present on the patient's skin (Figs. 16.43 and 16.44).

2. "Brazilian killer" or "Africanized" bees are now present in Texas, Arizona, and California. Their venom is not known to be more toxic; however, their aggressiveness, tendency to swarm in large numbers, and ability to travel long distances make them potentially more dangerous to humans.

Figure 16.43

Honeybee Envenomation Many honeybee stingers (barbs and venom sacs) are seen on this patient's cheek and ear and along the hairline. (Courtesy of Alan B. Storrow, MD.)

Figure 16.44

Honeybee Stingers The barbs and attached venom sacs (stinger apparatus) after removal from the patient. (Courtesy of Alan B. Storrow, MD.)

Caterpillars, Mites, and Centipedes

Associated Clinical Features

The order Lepidoptera contains several families of caterpillars that are venomous to humans. The venom apparatus typically consists of barbed spines arranged in clumps or scattered about the dorsal surface of the insect (Fig. 16.45). They may contain venom or serve as a mechanical irritant. The venoms, about which little is known, are purely defensive in nature. Patients who are stung are often gardening or outdoors when they come in contact with the caterpillar. The typical envenomation presents with acute pain followed by erythema and mild swelling (Fig. 16.46). Caterpillars with a less sophisticated venom apparatus or less toxic venom may cause simple pruritus or urticaria. Systemic symptoms have been reported but are very rare.

Figure 16.45

Caterpillar with Barbed Spines Typical garden caterpillar with barbed spines arranged in clumps. (Courtesy of Alan B. Storrow, MD.)

Figure 16.46

Caterpillar Sting Appearance of a caterpillar sting at 2 h. The patient presented with moderate pain and severe itching. Note how the erythema follows the pattern of the caterpillar. (Courtesy of Alan B. Storrow, MD.)

The puss caterpillar or woolly slug (Megalopyge opercularis) is perhaps the most famous and important venomous U.S. caterpillar (Fig. 16.47). Found throughout the United States, it is very hairy and flat and may reach a length of 4 cm. It lives in shade trees and feeds on their vegetation.

Figure 16.47

Puss Caterpillar The "puss caterpillar" or "woolly slug" is likely the most important venomous caterpillar in the United States. The hairy appearance and small hair tail is characteristic. (Courtesy of Alan B. Storrow, MD.)

Chiggers are the larvae of trombiculid mites and inflict intensely pruritic bites on their victims (Fig. 16.48). They are parasitic only as larvae and infest humans by crawling onto them (usually up the socks) and latching on. The mites secrete a salivary fluid containing digestive enzymes onto the victim's skin. Clothing precautions and repellents are usually effective in reducing unpleasant chigger infestations.

Figure 16.48

Chiggers Chigger bites on a leg appear as puncta surrounded by erythema. (Courtesy of Kevin J. Knoop, MD.)

Centipedes are venomous arthropods that have one pair of legs per body segment, with the number of segments being variable. The first segment contains hollow curved "fangs" (really modified legs and not truly mouth parts) (Fig. 16.49) capable of penetrating human skin. These bear venom glands at the bases. Centipedes largely use their venom to kill their prey. When provoked, however, they may sting humans and produce local burning pain, erythema, and swelling. Severe systemic reactions may occur but are uncommon.

Figure 16.49

Centipede Note the curved "fangs" (actually modified legs) on the first segment of this centipede from Texas. (Courtesy of Alan B. Storrow, MD.)

Differential Diagnosis

Other arthropod envenomations or plant exposures must be considered.

Emergency Department Treatment and Disposition

Treatment of envenomations from caterpillars, mites, and centipedes is purely symptomatic and consists of appropriate pain control, oral antihistamines (such as cyproheptadine or diphenhydramine), topical antipruritic creams, and basic wound care.

Clinical Pearls

1. The caudal appendages of centipedes are not associated with a venom apparatus.

2. Infiltration with local anesthetics may be useful in markedly painful centipede envenomations or for the removal of retained "fang" fragments.

3. Envenomations by the order Lepidoptera are usually from a caterpillar, not from a cocoon or adult stage.

4. Some caterpillars are capable of producing a very painful sting requiring opiate pain control.

5. Attached caterpillar spines may be removed with adhesive tape.

Scorpion Envenomation Diagnosis

Associated Clinical Features

Scorpions are venomous nocturnal arthropods and a worldwide health concern. The most significant morbidity and mortality is attributable to the Buthidae family, which is characterized by a triangular central sternal plate (Figs. 16.50, 16.51). This family includes, among others, the venomous Androctonus genus in northern Africa, Leiurus in the Middle East, Tityus in South America, and Centruroides in North America.

Figure 16.50

Buthidae Sternal Plate The Buthidae family is associated with the most significant envenomations and is characterized by triangular sternal plates (left). Members of the other scorpion families have pentagonal sternal plates (right).

Figure 16.51

Buthidae Sternal Plate The triangular appearance of the sternal plate is well seen in this scorpion, a member of the Buthidae family. (Courtesy of Sean P. Bush, MD.)

Centruroides (Fig. 16.52) is found primarily in the southwestern United States and northern Mexico. It is characterized by a variable subaculear tooth beneath the stinger (Figs. 16.53, 16.54), may be striped, and is yellow to brown in color. These spiders prefer darkness and thus tend to hide in crevices, woodpiles, bedding, clothing, and shoes during the day. Envenomation produces a mild local reaction of pain, swelling, burning, and ecchymosis (Fig. 16.55).

Figure 16.52

Centruroides exilicauda Members of this species are yellow to brown and usually less than 5 cm long. Below the stinger is the telson, within which are two glands containing venom. (Courtesy of Sean P. Bush, MD.)

Figure 16.53

Subaculear Tooth The barb noted at the base of the stinger is variably present in Centruroides (left) and absent in other species (right)

Figure 16.54

Centruroides limbatus Subaculear Tooth A variable subaculear tooth is characteristic of Centruroides. This is an example of a large subaculear tooth on the telson from C. limbatus. C. exilicauda typically has a smaller, sometimes subtle "tooth." (Courtesy of Sean P. Bush, MD.)

Figure 16.55

Scorpion Sting Most scorpion envenomations are mild and produce local pain, swelling, paresthesias, and mild ecchymosis. (Courtesy of Stephen Corbett, MD.)

However, envenomation with the species Centruroides exilicauda, the bark scorpion, can lead to progressive symptoms and death. The venom of C. exilicauda initially produces local paresthesias and pain (grade 1), which may be accentuated by tapping the involved area, also known as the "tap" test. More severe envenomations may produce remote paresthesias (grade II) and either somatic or autonomic nerve dysfunction (grade III). Proteins in the toxin are thought to cause repetitive firing of neurons by binding to sodium channels. These symptoms may include tachycardia, nausea, wandering eye movements, blurred vision, difficulty breathing, trouble swallowing, restlessness, and involuntary shaking. Both somatic and autonomic dysfunction may be present (grade IV). These systemic reactions tend to be more severe in younger patients and may result in death, usually from respiratory arrest, if not treated properly.

Differential Diagnosis

The differential diagnosis of mild scorpion stings includes any insect bite or sting. Major envenomations produce a broad spectrum of neuromuscular symptoms, which may mimic severe black widow spider envenomation, toxic ingestions, or neuromuscular disorders.

Emergency Department Treatment and Disposition

Treatment depends on the severity of envenomation. Grade I or II envenomations are treated with supportive care (ice, oral analgesia) and tetanus immunization. There is no known role for the use of barbiturates, benzodiazepines, steroids, calcium, or epinephrine. The past use of large doses of barbiturates has been suggested to be a major contributor to reported deaths.

Envenomations that progress to grade III or IV must be treated aggressively and may require paralysis and intubation for severe spasms. Goat serum antivenin is available in Arizona (Samaritan Regional Poison Center in Phoenix, 602-253-3334) and can be considered. It does carry a risk of hypersensitivity reactions. Pain and paresthesias from a scorpion sting may persist for up to 2 weeks, but most systemic symptoms improve within 9 to 30 h without antivenin treatment and usually peak at approximately 5 h.

Clinical Pearls

1. Antivenin should be used cautiously, as hypersensitivity reactions are common.

2. If the scorpion is brought in, examine it for a triangular plate and subaculear tooth.

3. Almost all scorpions, including Centruroides exilicauda, fluoresce with intense brightness under cobalt light.

Middle Ear Squeeze

Associated Clinical Features

Middle ear squeeze (barotitis media) results from a relative decrease in middle ear pressure produced as a diver descends. It can occur in as little as 2 to 3 ft of water. The tympanic membrane (TM) bulges inward, causing discomfort. At a depth of approximately 4 ft, the pressure difference is great enough to collapse the eustachian tube and cause obstruction. If attempts to equalize the pressure (e.g., Valsalva or Frenzel maneuver) fail, ascent is necessary. If a diver continues to descend, TM rupture may occur. The influx of water into the middle ear may cause extreme vertigo and lead to a diving disaster.

Barotitis media may present with pain only (grade 0), TM erythema (grade 1), erythema and mild TM hemorrhage (grade 2, Fig. 16.56), gross TM hemorrhage (grade 3), free middle ear blood (grade 4), or free blood with TM perforation (grade 5).

Figure 16.56

Barotitis Media Tympanic membrane erythema and mild hemorrhage consistent with barotitis media. (Courtesy of Richard A. Chole, MD, PhD.)

Differential Diagnosis

The differential diagnosis of diving-related ear pain includes otitis externa, otitis media, and ear canal squeeze.

Emergency Department Treatment and Disposition

Treatment includes ascent, decongestants, and analgesia. Antihistamines may be of use for allergy-related eustachian tube dysfunction. Antibiotics are recommended for preexisting infections or for TM rupture. Most cases resolve spontaneously within hours to days. The patient should not resume diving until the condition has resolved or the TM is completely healed.

Clinical Pearls

1. Barotitis media is the most common medical problem associated with diving.

2. Associated barotrauma should be investigated in cases of barotitis media.

Mask Squeeze

Associated Clinical Features

Mask squeeze results when a diver fails to maintain the balance between the air pressure within his or her mask and the external water pressure during descent. Repeated nasal exhalations into the scuba mask while diving normally accomplish this. When this is not performed properly, extreme negative air pressure can build up inside the mask and may result in the rupture of capillary beds, leading to conjunctival hemorrhage and skin ecchymosis (Fig. 16.57).

Figure 16.57

Mask Squeeze Mask squeeze in a diver who descended to 45 FSW without exhaling into his mask. [Courtesy of Kenneth W. Kizer, MD; reprinted with permission from Auerbach PS (ed): Wilderness Medicine: Management of Wilderness and Environmental Emergencies, 3rd ed. St. Louis: Mosby–Year Book; 1995.]

Differential Diagnosis

Given a recent history of diving, the differential is limited but would include traumatic causes of facial ecchymosis and conjunctival hemorrhage.

Emergency Department Treatment and Disposition

Treatment consists of ascent and essentially supportive care. A history of recent eye surgery should be sought; if discovered, thorough eye examination should be performed and ophthalmologic consultation considered.

Clinical Pearls

1. Diver education and proper diving technique minimize the risk of mask squeeze.

2. Special consideration should be given to patients with recent keratotomy, as corneal incisions heal relatively slowly.

Stingray Envenomation

Associated Clinical Features

Stingray envenomation involves a forceful thrust of the caudal spine or spines of the animal producing a puncture wound (Fig. 16.58) or laceration. Since the animals commonly burrow in sand, they may be accidently stepped on. The stingray has a barbed tail that reflexively impacts the victim, usually in the lower extremity. The force of injection causes the integumentary sheath covering the spine to rupture, potentially releasing venom, mucus, pieces of the sheath, and spine fragments. The wound usually produces immediate intense pain, edema, and bleeding. The initially dusky or cyanotic wound may progress to erythema, with rapid fat and muscle hemorrhage. Systemic symptoms may include nausea, vomiting, diarrhea, diaphoresis, muscle cramps, fasciculations, weakness, headache, vertigo, paralysis, seizures, hypotension, syncope, arrhythmias, and death.

Figure 16.58

Stingray Envenomation Puncture wound from stingray envenomation in a lower extremity. (Courtesy of Daniel L. Savitt, MD.)

Differential Diagnosis

All marine envenomations, specific to the particular environment, must be considered, since visualization of the offending creature is rare. Nonvenomous stings and simple trauma with infection must also be considered.

Emergency Department Treatment and Disposition

Rapid attention to a stingray envenomation is the key to successful treatment. The wound should be irrigated immediately and primary exploration accomplished to remove visible debris. Local suction and proximal constriction bands may be useful but are controversial. Irrigation should be promptly followed by immersion in hot water, to tolerance, for 30 to 90 min. Wounds should be further explored and debrided during soaking. Pain relief should be initiated early, and narcotics may be needed. After soaking, wounds should be formally explored, debrided, and dressed for delayed primary closure or primary closure with drainage. Prophylactic antibiotics are recommended. Patients can usually be discharged home after a 3- to 4-h observation period if no systemic symptoms arise. Tetanus prophylaxis should be given if indicated.

Clinical Pearls

1. Application of cryotherapy to stingray envenomations may prove disastrous.

2. Retained foreign bodies are a common problem in stingray wounds.

3. Bacteria cultured from marine envenomations are extremely diverse. Antibiotics chosen should include coverage of Vibrio species.

Sea Urchin Envenomation

Associated Clinical Features

Sea urchins belong to the phylum Echinodermata and are nonaggressive, slow-moving creatures. Envenomation usually occurs after intentional or accidental handling. Long, brittle, venom-filled spines or the three-jawed globiferous pedicellariae are responsible for the injury. The spines frequently break and pedicellariae can remain attached and active for several hours. They may advance into muscle or joint spaces and cause infection (Fig. 16.59). The usual presentation is burning pain progressing to localized muscle aches. Erythema and edema may be present. Multiple envenomations may produce systemic symptoms including nausea, vomiting, abdominal pain, paresthesia, numbness, paralysis, hypotension, syncope, or respiratory distress. While the envenomation causes a reaction that may be quite painful, it is rarely life-threatening.

Figure 16.59

Sea Urchin Envenomation Four images representing (1) a living sea urchin with characteristic spines; (2) puncture wound of the right middle finger revealing swelling during the chronic phase; (3) radiograph taken shortly after sea urchin injury, revealing the calcified sea urchin spine; and (4) osteolytic process of the right middle phalanx caused by an embedded sea urchin spine. (From Halstead BH: Venomous Marine Animals of the World. Washington, DC: US Government Printing Office, 1965.)

Differential Diagnosis

The differential diagnosis of sea urchin envenomation includes other marine envenomations and local trauma. Delayed presentations can mimic a host of local inflammatory reactions. A careful history of exposure is critical.

Emergency Department Treatment and Disposition

Following envenomation, the affected area should be submersed in nonscalding hot water for 30 to 90 min. Pedicellariae may be removed by applying shaving cream and gently scraping with a razor. Obvious embedded spines should be removed. Hand wounds often require surgical debridement. Retained spines often dissolve spontaneously; however, granulomas may form, producing locally destructive inflammation.

Clinical Pearls

1. Sea urchin envenomation involving a joint may produce severe synovitis.

2. Some species of sea urchin contain dye, which may give the false impression of a retained spine.

3. Sea urchins known to be hazardous to humans are generally found in the Indian Ocean, Pacific Ocean, and Red Sea.

Coelenterate Envenomation

Associated Clinical Features

The phylum Coelenterata contains approximately 10,000 different species, of which several hundred are a danger to humans. This diverse group includes hydrozoans (e.g., Portuguese man-of-war and fire coral, Fig. 16.60), scyphozoans (i.e., "true" jellyfish), and anthozoans (i.e., soft corals, stony corals, and anemones). They account for more marine envenomations than any other phylum. The important species involved in human injuries share sharp stinging cells called nematocysts. Nematocysts are enclosed in venom sacs and are present in tentacles that hang from air-filled structures. After external contact, the nematocysts are discharged from their sacs, often penetrate the skin, and release their venom. Nematocyst venom is an extremely complex substance containing numerous proteins and enzymes. Clinical presentation following envenomation ranges from the mild dermatitis to cardiovascular and pulmonary collapse. Mild envenomations usually result in a self-limited papular inflammatory eruption associated with burning and limited to areas of contact. Moderate to severe envenomations produce a spectrum of neurologic, cardiovascular, respiratory, and gastrointestinal symptoms. Anaphylactoid reactions—including hypotension, dysrhythmias, bronchospasm, and cardiovascular collapse—may play a role.

Figure 16.60

Fire Coral After contact, fire coral most commonly causes immediate local burning pain, followed by erythematous papules or urticarial eruptions. Pruritus may last for several days. (Courtesy of Edward J. Otten, MD.)

Differential Diagnosis

Coelenterate stings often produce a telltale linear pattern corresponding to the shape of tentacles (Figs. 16.61, 16.62). Sea anemones have tentacles loaded with nematocyst variations. Contact may cause painful urticarial lesions, paresthesias, edema, erythema (Fig. 16.63), and, if severe, ulceration, necrosis, and secondary infection. Coelenterate envenomation must also be considered as a potential contributing cause in unexplained cases of collapse resulting from swimming, diving, or near-drowning incidents.

Figure 16.61

Coelenterate Envenomation The sharp angulations and undulations characteristic of jellyfish envenomation. (From Halstead BH: Venomous Marine Animals of the World. Washington, DC: US Government Printing Office, 1965.)

Figure 16.62

Coelenterate Envenomation Jellyfish envenomation on the lower extremities. (Courtesy of the Department of Dermatology, Naval Medical Center, Portsmouth, VA.)

Figure 16.63

Sea Anemone Tattooing Contact with sea anemones results mainly in local skin irritation, initially manifest as pruritus, burning, throbbing, and, sometimes radiation of pain to other areas. The area involved may reveal blistering, local edema, and violaceous petechial hemorrhages. The skin papules are confined to the areas of contact and may persist for 7 to 10 days. (Courtesy of Gerald O'Malley, DO.)

Emergency Department Treatment and Disposition

Concurrently with primary resuscitation, nematocyst decontamination should be accomplished beginning with seawater flushing. The hypotonic nature of fresh water, as well as isopropyl alcohol, may cause additional nematocysts to fire and should be avoided. A 5% solution of acetic acid (vinegar) applied for at least 30 min is the most widely accepted detoxicant. It has been suggested to remove tentacles with the application of shaving cream, followed in 5 min by a careful scraping with a firm, dull object (e.g., tongue blade, credit card). Pruritus may be treated with antihistamines. Pain may be addressed with immersion in hot water or with systemic analgesics. Any victim with systemic symptoms requires at least 6 to 8 h of observation because rebound phenomena are common.

Clinical Pearls

1. The box jellyfish (Chironex fleckeri) is generally considered the most deadly of marine animals and is most predominant in Australian and Southeast Asian waters. It may produce severe systemic symptoms hours after exposure. A sheep-derived antivenin (Commonwealth Serum Laboratory, Australia) is available.

2. The detached tentacles of some species may contain active nematocysts for months, even when fragmented on the beach or floating in water.

3. The Portuguese man-of-war is present in the Floridian Atlantic coast and the Gulf of Mexico. It is known to have a neurotoxin that may cause severe pain and death.

4. There is considerable overlap in degrees of envenomation, from annoying dermatitis to multisystem involvement and death.

Marine Dermatitis

Associated Clinical Features

Marine dermatitis, also known as "sea bather's eruption," is a pruritic condition commonly mislabeled sea lice. Symptoms usually occur a few minutes to 12 h after exposure. The offending organisms are probably numerous and include the larval form of the thimble jellyfish and the planula form of the sea anemone Edwardsiella lineata. The rash consists of erythematous wheals and papules, which may be extremely pruritic (Fig. 16.64). Systemic manifestations include fever, malaise, headache, conjunctivitis, and urethritis. Unlike cercarial dermatitis, marine dermatitis primarily affects areas of the body covered by caps, fins, and bathing suits.

Figure 16.64

Marine Dermatitis Typical appearance of marine dermatitis. (Courtesy of Richard A. Clinchy III, PhD.)

Cercarial dermatitis, or "swimmer's itch," occurs when humans become accidental hosts of nonhuman schistosomes. This causes an immune response that results in itching, erythema, and mild edema. After 60 min, the classic signs are red macules that become pruritic papules 3 to 5 cm in diameter and surrounded by erythema (Fig. 16.65).

Figure 16.65

Cercarial Dermatitis The discrete and highly pruritic papules of cercarial dermatitis commonly occur on exposed body areas. (Courtesy of David O. Parrish, MD. Used with permission from Parrish DO. Seabather's eruption or diver's dermatitis. JAMA 1993;270:2300–2301.)

Differential Diagnosis

A marine dermatitis should be considered when pruritic lesions follow seawater exposure. The incidence increases significantly during the late summer and fall off Long Island and in the late spring and early summer in south Florida. Contact dermatitis and some fungal skin disorders may present in a similar fashion.

Emergency Department Treatment and Disposition

Marine dermatitis is self-limited, rarely persisting beyond 10 days to 2 weeks. The dermatitis may be partially prevented by a vigorous soap-and-water scrub after saltwater bathing. Treatment is symptomatic, and calamine lotion with 1%menthol may bring relief. Topical steroids may provide additional relief. In severe cases, oral antihistamines and corticosteroids may be necessary.

Cercarial dermatitis is treated with isopropyl alcohol or calamine lotion. Severe cases may require systemic corticosteroids, whereas bacterial infection may require topical or oral antibiotics.

Clinical Pearls

1. Marine dermatitis primarily affects areas covered by caps, fins, and bathing suits.

2. Individual lesions may look like insect bites.

Scorpion Fish Sting

Associated Clinical Features

Scorpion fish are colorful venomous marine animals found primarily in tropical waters. Their exotic, beautiful appearance has made them increasingly popular among marine aquarists in the United States, and many envenomations have resulted from mishandling. They are well camouflaged in the wild and stings are usually caused by accidentally stepping on them. Scorpion fish are grouped into the genera Pterois (lion fish) (Fig. 16.66), Scorpaena (scorpion fish proper), and Synanceja (stone fish), with the severity of envenomation progressing respectively. All scorpion fish have multiple spines in association with venom glands; envenomation results from skin puncture followed by venom release into the tissues. Immediately following a scorpion fish sting, the victim experiences intense pain that, untreated, lasts for hours. The site may become warm, erythematous, and edematous and vesicles may arise. Lion fish stings are painful but relatively mild, usually limited to localized pain and tissue responses. Severe systemic effects are more common with stone fish envenomation and may produce a constellation of cardiovascular, pulmonary, neurologic, and gastrointestinal sequelae.

Figure 16.66

Lion Fish The Pterois genus of the Scorpaenidaefamily includes the lion fish. Envenomations occur by erectile spines on the dorsal, pelvic, and anal fins of these fish. Its clinical manifestations are relatively mild and include intense, sharp, throbbing pain, with possible progression of pain radiation, erythema, ecchymosis, systemic symptoms, and necrosis. (Courtesy of Edward J. Otten, MD.)

Differential Diagnosis

History raises a high suspicion for scorpion fish stings in the wild and diagnosis is usually obvious domestically. The differential includes coelenterate, stingray, echinoderm, and sea snake envenomation. As with coelenterates, scorpion fish envenomation should be considered in the event of unexplained near drowning and swimmer collapse.

Emergency Department Treatment and Disposition

Hot water immersion for 30 to 90 min should be initiated as soon as possible. Rebound pain is common and should be treated with repeated hot water immersion. During immersion, the wound should be carefully inspected for pieces of spine and sheath, which may have broken off in the skin. Thorough warm saline irrigation should also be performed along with wound exploration. Severe pain should be treated with local injection of lidocaine without epinephrine and with narcotic analgesia. Antibiotic prophylaxis should be considered in high-risk wounds. Tetanus status should be addressed.

Clinical Pearls

1. Stone fish envenomations are by far the most dangerous of the scorpion fish stings and severe systemic reactions may occur. Stone fish antivenin (Commonwealth Serum Laboratories, Australia) is available.

2. Scorpion fish venom is heat-labile and hot water immersion therapy is effective in treating pain and inactivating venom.

Erysipeloid

Associated Clinical Features

Erysipeloid, also known as "fish handler's disease," is a bacterial skin infection caused by Erysipelothrix rhusiopathiae. This condition is frequently seen in those who handle raw meat, fish, and shellfish. The offending organism enters the body through a break in the skin and causes a local infection within 2 to 7 days. Lesions are characterized by an edematous central purplish-red area, surrounded first by central clearing and then circumscribed by an advancing raised, erythematous ring (Fig. 16.67). The area is usually pruritic and painful and may be associated with fever, malaise, and regional lymphadenopathy.

Figure 16.67

Erysipeloid Envenomation Typical appearance of Erysipelothrix rhusiopathiae skin infection. [Courtesy of Paul S. Auerbach, MD; reprinted with permission from Auerbach PS (ed): Wilderness Medicine: Management of Wilderness and Environmental Emergencies, 3rd ed. St. Louis: Mosby–Year Book; 1995.]

Differential Diagnosis

History aids greatly in the diagnosis, but erysipeloid may be confused with contact or rhus dermatitis, insect bites, and fungal or other cutaneous infections.

Emergency Department Treatment and Disposition

If left untreated, erysipeloid will usually resolve spontaneously in about 3 weeks. Skin infections may be treated with penicillin VK, cephalexin, or erythromycin. If severe infection occurs in association with septicemia, endocarditis, or arthritis, penicillin G 2 to 4 million U IV q4 h for 4 to 6 weeks should be administered. Tetanus status must be addressed.

Clinical Pearls

1. A history of occupational or recreational exposure to fish or shellfish is the key to diagnosis.

2. E. rhusiopathiae is usually resistant to aminoglycoside antibiotics, and these should be avoided.

Toxicodendron Exposure

Associated Clinical Features

Poison ivy, oak, and sumac (Figs. 16.68, 16.69, and 16.70) cause more cases of allergic contact dermatitis than all other allergens combined. At least 70% of the U.S. population is sensitive to the Toxicodendron species.

Figure 16.68

Poison IvyToxicodendron radicans (poison ivy—shrub or climbing vine). Note that the leaves of poison ivy have three leaflets and the stems are commonly reddish orange. Poison ivy occurs throughout the United States. (Courtesy of Lawrence B. Stack, MD.)

Figure 16.69

Poison OakToxicodendron diversiloba (poison oak). Like poison ivy, the terminal part of the branch has a cluster of three shiny leaves. It grows as a tree or woody shrub and occurs west of the Rocky Mountains. (Courtesy of Ken Zafren, MD.)

Figure 16.70

Poison SumacToxicodendron vernix (poison sumac). Note that leaves of poison sumac have 7 to 13 leaflets. It grows as a tree or woody coarse shrub. Only one species of poison sumac is found in the United States. (Courtesy of Lawrence B. Stack, MD.)

The dermatitis begins as pruritus and redness usually within 2 days of exposure in susceptible persons. The degree of dermatitis depends on the patient's degree of sensitivity, amount of allergen exposure, and the reactivity of the skin at the exposed body location. The dermatitis may vary from erythema to erythema with papules to erythema with vesicles and bullae (Figs. 16.71 and 16.72). A linear distribution of the cutaneous lesions is strongly suggestive of toxicodendron dermatitis (Fig. 16.73). This distribution occurs after contaminated fingernails have scratched the skin or plant parts rubbed against it.

Figure 16.71

Poison Sumac Dermatitis A moderately severe local reaction to poison sumac. Note the vesicles, bullae, and exudates characteristic of a contact dermatitis. (Courtesy of Alan B. Storrow, MD.)

Figure 16.72

Poison Oak Dermatitis Erythematous papules and vesicles. This firefighter was exposed to urushiol, the allergen of poison oak, ivy, and sumac, in smoke from burning poison oak. (Courtesy of Ken Zafren, MD.)

Figure 16.73

Poison Ivy Erythematous papules and vesicles in a linear distribution consistent with Toxicodendron dermatitis. (Courtesy of Alan B. Storrow, MD.)

Differential Diagnosis

Medical problems that may appear like a Toxicodendron rash include photodermatitis, cellulitis, thermal burns, and other causes of contact dermatitis.

Emergency Department Treatment and Disposition

An immediate rinse or shower with warm water and soap may minimize the reaction. If symptoms are limited to erythema and papules and a small surface area, calamine lotion or topical steroid sprays may provide adequate symptomatic relief. Pruritus may be decreased with oral antihistamines (e.g., diphenhydramine or cyproheptadine) and oatmeal baths. Vesicles and bullae require Domeboro compresses (for 60 min three times daily) to help dry these lesions and relieve pruritus. Systemic corticosteroids tapered over 3 weeks are used in severe reactions. Secondary infection should be treated with systemic antibiotics against staphylococcal and streptococcal species.

Clinical Pearls

1. Fluid from the vesicles or bullae does not contain any allergen.

2. Removal of the allergen from the skin within 30 min of exposure may prevent dermatitis.

3. Deliberate removal of allergen from under the fingernails may prevent spreading.

4. Treatment with systemic steroids for less than 2 or 3 weeks may result in rebound exacerbations of the dermatitis.

Sporotrichosis

Associated Clinical Features

Sporotrichosis is a fungal skin infection caused by Sporothrix schenckii, an organism primarily found on plants and flowers and in soil; the problem is common among gardeners and florists. It also affects those who handle animals, since the fungus may inhabit animals' claws. Infection arises as contaminated thorns, spines, or claws penetrate the victim's skin. After an average incubation period of 3 weeks, localized infections become apparent. "Fixed" cutaneous infections are localized to the inoculation site and are manifest as 2- to 4-mm papules or nodules. They may ulcerate, become surrounded by raised erythema, and are typically painless (Fig. 16.74). Progression to lymphocutaneous infections occurs in about 70% of cases. Patients present with a nodule at the site of penetration, with later appearance of subcutaneous nodules and skip areas along lymphatic tracks (Fig. 16.75). The lesions may wax and wane over months to years. Patients with cutaneous sporotrichosis typically lack systemic symptoms and, if laboratory profiles are performed, have unremarkable results.

Figure 16.74

Fixed Sporotrichosis The ulcer and surrounding erythema of fixed cutaneous sporotrichosis could be confused with a brown recluse spider bite. (Courtesy of Edward J. Otten, MD.)

Figure 16.75

Lymphocutaneous Sporotrichosis Lymphatic spread is common in cutaneous sporotrichosis. (Courtesy of Kevin J. Knoop, MD.)

Differential Diagnosis

Cellulitis, syphilis, anthrax, brown recluse spider envenomation, and other cutaneous mycoses may be confused with sporotrichosis. Other less common infections such as cat-scratch disease, nocardiosis, and tuberculosis may be considered. A straightforward history of injury is often helpful to pinpoint the diagnosis.

Emergency Department Treatment and Disposition

Sporotrichosis may be successfully treated with oral potassium iodide for one month after clinical manifestations have resolved. Alternative therapy includes oral ketoconazole, while disseminated infections may require intravenous amphotericin B. Outpatient therapy is appropriate for nondisseminated infections. Tetanus status should be addressed.

Clinical Pearls

1. Fungal cultures and tissue biopsy cultures are somewhat useful to confirm the diagnosis.

2. Treatment must be continued for 1 month following clinical resolution to eradicate S. schenckii.

3. Although rare, a pulmonary form of sporotrichosis after inhalation exposure has been reported.

Peyote Ingestion

Associated Clinical Features

Peyote (Liphophora williamsii) is a cactus plant (Fig. 16.76) found primarily in the southwestern United States. The cactus contains a significant amount of mescaline, a potent hallucinogen with structural similarities to norepinephrine. Peyote buttons and seeds are frequently ingested for recreational use but are also used in the religious ceremonies of some Native American groups (peyotism). Toxicity of peyote is generally mild and self-limited. Mescaline induces some sympathomimetic effects due to its similarity to norepinephrine, and marked visual hallucinations and a sense of depersonalization follow. These effects are sometimes accompanied by unpleasant GI symptoms such as severe nausea and vomiting. Full recovery from these symptoms usually occurs within a few hours.

Figure 16.76

Peyote Typical appearance of peyote cactus. Note the individual fleshy "buttons," which may be sliced and dried for storage. (Courtesy of Edward J. Otten, MD.)

Differential Diagnosis

The differential diagnosis of peyote ingestion includes any hallucinogen poisoning. The timing of clinical effects makes mescaline similar to lysergic acid diethylamide (LSD).

Emergency Department Treatment and Disposition

Treatment of peyote ingestion is largely supportive; severe toxic effects are uncommon. Marked agitation may be managed with benzodiazepines.

Clinical Pearls

1. An individual peyote button contains about 45 mg of mescaline; a mescaline dose of 5 mg/kg produces psychic effects.

2. The emotional lability and anxiety produced by mescaline may predispose patients to accidental or self-inflicted trauma.

Dieffenbachia Ingestion

Associated Clinical Features

Dieffenbachia (dumbcane) is a common houseplant (Fig. 16.77) that causes toxic effects when ingested owing to large amounts of insoluble oxalate crystals in its leaves. The oxalate crystals are highly corrosive, and those who ingest the leaves experience painful burning of the lips, tongue, mouth, and esophagus. Marked swelling of the tongue, lips, and oropharynx can occur, and airway patency may become a major issue in managing these patients. Fortunately, calcium oxalate crystals are not absorbed and the profound hypocalcemia associated with soluble oxalates is not seen with Dieffenbachia poisoning.

Figure 16.77

Dieffenbachia Dieffenbachia is a common houseplant because of its colorful appearance and ease of indoor growth. (Courtesy of Kevin J. Knoop, MD.)

Differential Diagnosis

The differential diagnosis of Dieffenbachia ingestion includes exposure to any caustic substances that may cause a similar pattern of burning when ingested.

Emergency Department Treatment and Disposition

Topical anesthetics are helpful in controlling severe pain from burning mucous membranes. Management is largely supportive, as the painful oral burns experienced with Dieffenbachia exposure usually limit ingestion. As with any oropharyngeal burn, airway issues must be addressed. A period of observation is appropriate to make sure that airway compromise does not occur with continued swelling. If leaves are swallowed, GI consultation should be considered to assess the extent of esophageal injury. Decontamination is usually not necessary, as the plant is rarely swallowed in significant amounts.

Clinical Pearls

1. Performance of nasopharyngoscopy may be helpful in assessment of airway patency for more posterior burns.

2. Patients should be instructed not to swallow topical anesthetics, as toxicity may result with extensive use.

Jimsonweed Ingestion

Associated Clinical Features

Jimsonweed (Datura stramonium) is a toxic plant that contains tropane alkaloids consisting of atropine, scopolamine, and cocaine compounds. Ingestion may occur through the drinking of tea made from the leaves or flowers of jimsonweed or from eating the plant's seeds or leaves (Fig. 16.78). Poisoned victims demonstrate an anticholinergic toxidrome resulting from the antimuscarinic receptor effects of atropine and scopolamine. Clinically patients may exhibit altered mental status, xerostomia, xeroderma, xerophthalmia, blurred vision, mydriasis, tachycardia, decreased bowel and bladder motility, and hyperthermia.

Figure 16.78

Jimsonweed Jimsonweed plant with seeds. (Courtesy of Matthew D. Sztajnkrycer, MD, PhD.)

Differential Diagnosis

Jimsonweed poisoning carries a broad differential that comprises any toxin producing an anticholinergic toxidrome, including but not limited to antihistamines, antipsychotics, skeletal muscle relaxants, and tricyclic antidepressants.

Emergency Department Treatment and Disposition

Treatment initially consists of securing the ABCs (airway, breathing, circulation) and stabilization measures. Hypotension resulting from tropane alkaloid ingestion usually responds to fluid boluses, but vasopressor agents may be necessary. Once hemodynamic stability is achieved, the patient's detoxification must be addressed. Gastric lavage followed by activated charcoal is recommended but may be of little use, as toxins are absorbed rapidly. Whole-bowel irrigation is contraindicated with intestinal ileus and must be considered with great caution in jimsonweed ingestion owing decreased bowel motility. Physostigmine may be of benefit to treat severe anticholinergic toxicity, but extreme caution along with toxicology consultation is advisable, as the drug may induce AV block, asystole, seizures, hypotension, and bronchospasm.

Clinical Pearls

1. Examination of the axilla for xeroderma is very helpful to detect peripheral anticholinergic syndrome and distinguish between anticholinergic and sympathomimetic toxidromes.

2. Administering 1% pilocarpine drops does not reverse anticholinergic mydriasis.

Cardiac Glycosides

Associated Clinical Features

Cardiac glycosides (CG) are found in the leaves of the Nerium oleander (Fig. 16.79), Digitalis purpurea (foxglove, Fig. 16.80), and Convallaria majalis (lily of the valley); if ingested, they produce clinical findings similar to digoxin toxicity. Toxicity can also occur if smoke from burning plants is inhaled. Foxglove and oleander tea may be a cause of CG toxicity. Therapeutic effects occur from inhibition of the cardiac cell membrane sodium-potassium adenosine triphosphate pump. These effects result in increased automaticity, improved conduction, and improved inotropy.

Figure 16.79

Nerium Oleander (Yellow Oleander) A common decorative plant in subtropical climates often seen lining roads and highways. Flowers may be white, yellow, red, or purple. Plants may grow to a height of 15 ft. (Courtesy of Lawrence B. Stack, MD.)

Figure 16.80

Digitalis Purpurea (Purple Foxglove) The ornamental plant. (Courtesy of Lawrence B. Stack, MD.)

Toxic effects are an exaggeration of therapeutic effects. Bradydysrhythmias may result from impaired pacemaker function. Tachydysrhythmias may occur from increased automaticity. Nausea, vomiting, confusion, depression, and fatigue may be present. Headaches, paresthesias, weakness, scotomas, and color disturbance (yellow vision) may also be seen.

Differential Diagnosis

Conditions that may mimic CG ingestion include cardiac medication overdose, cardiac ischemia, myocardial infarction, pulmonary embolus, and any condition associated with cardiac disturbances.

Emergency Department Treatment and Disposition

Atropine should be initially given for bradydysrhythmias. Refractory bradydysrhythmias require pacing. Ventricular tachydysrhythmias usually respond to phenytoin or lidocaine. Activated charcoal is the preferred method of decontamination. Cardioversion should be avoided in CG toxicity. Digoxin-specific Fab fragments are the treatment of choice for life-threatening dysrhythmias that fail conventional therapy.

Clinical Pearls

1. Treat CG overdose from plant exposure in the same way as an acute digoxin overdose.

2. Fab fragments have been used successfully to treat CG overdose from plant ingestion.

3. Calcium should be avoided in treating CG-associated hypokalemia, as it may worsen ventricular arrhythmias.

Amanita Phalloides Ingestion

Associated Clinical Features

Mushrooms are the fruits of certain fungi. Amanita phalloides (the "death cap," Fig. 16.81) and Amanita virosa (the "destroying angel") species produce amantoxins and account for most fatalities due to mushroom ingestion. Mushroom poisoning commonly occurs in the early fall, when wild mushrooms are abundant and amateur foragers mistake poisonous mushrooms for edible ones.

Figure 16.81

Amanita phalloides The "death cap" produces amatoxins and accounts for most of the fatalities due to mushroom ingestion. (Courtesy of Edward J. Otten, MD.)

Amantoxin poisoning results in an abrupt onset of nausea, vomiting, diarrhea, and abdominal pain 6 to 24 h after ingestion. Hematemesis, hematochezia, and severe dehydration resulting in hypotension may occur. Metabolic acidosis and electrolyte loss may be found on laboratory evaluation in severe poisoning. Gastrointestinal symptoms may last 12 to 24 h and are followed by a latent period of apparent improvement. This period is followed by a rise in liver enzymes and bilirubin and elevations in the PT and PTT. Liver and renal failure may become apparent.

Differential Diagnosis

The large differential surrounding acute abdominal pain and gastrointestinal bleeding should be entertained. Acute viral hepatitis may present similarly to mushroom ingestion.

Emergency Department Treatment and Disposition

Once the ABCs have been stabilized, gastric decontamination and activated charcoal administration are recommended. Specific interventions that may be helpful but are yet unproved include forced diuresis, charcoal hemoperfusion, high-dose cimetidine, high-dose penicillin, high-dose ascorbic acid, N-acetylcysteine, and hyperbaric oxygen therapy.

Clinical Pearls

1. A history of the ingestion of wild mushrooms by anyone not expert in their identification should prompt suspicion of this problem.

2. A single "death cap" may contain enough toxin to kill an adult.

3. Cooking these mushrooms does not substantially alter their toxicity.

Jequirty (Rosary) Pea Ingestion

Associated Clinical Features

The jequirty pea (Abrus precatorius), also known as the rosary pea, belongs to a family of poisonous plants that contain toxalbumins. The chief toxin of the jequirty pea is abrin, which is structurally very similar to the toxin ricin of the castor bean. Ingestion of jequirty peas rarely results in toxicity, as a majority of the abrin lies within the hard shell of the pea. However, when the peas are chewed or the shell is digested, gastroenteritis usually occurs. Nausea, vomiting, abdominal pain, and diarrhea are common but in severe cases may be accompanied by hemorrhagic gastritis, seizures, arrhythmias, marked dehydration, CNS depression, and even death. Unfortunately, because of the colorful, attractive nature of the jequirty pea (Fig. 16.82), most cases of severe toxicity occur in the pediatric age group.

Figure 16.82

Jequirty Pea Jequirty peas are also known as rosary peas, Indian beans, Buddhist's beads, crab's eyes, and prayer beads. They are about 5 mm in diameter and have a colorful glossy shell, usually red with a black center, although black and white may also be seen. (Courtesy of Kevin J. Knoop, MD.)

Differential Diagnosis

The differential diagnosis of jequirty pea ingestion includes any infectious or toxicologic cause of acute gastroenteritis.

Emergency Department Treatment and Disposition

Treatment of jequirty pea ingestion is largely supportive, as there is no specific antidote for abrin. In all cases, gastric decontamination is indicated and should include activated charcoal, gastric lavage, and whole bowel irrigation. In asymptomatic patients, decontamination, careful observation, and close follow-up is acceptable. With symptoms of toxicity, however, admission is recommended, as the potential for marked clinical worsening is present.

Clinical Pearls

1. Most jequirty pea ingestions are benign, as the vast majority of abrin toxin resides within the undigested shell of the plant.

2. Both toxalbumins, abrin in the jequirty pea and ricin in the castor bean, are structurally similar to botulinum toxin, cholera toxin, diphtheria toxin, and insulin.

3. The jequirty pea is found on a green vine native to India, but it can also be found in other tropical and subtropical areas such as the Caribbean and Florida.

Castor Bean Ingestion

Associated Clinical Features

Ricinus communis (castor bean) shares many similarities with its close neighbor the jequirty pea. Both are toxalbumin-containing plants; the chief toxin of the castor bean is ricin. As in the jequirty pea, most ingestions are not fatal because the toxin in the castor bean is located within the hard coats of the seeds (Figs 16.83 and 16.84). Three seeds are contained in each of the plant's brown capsules. Unless the shell is digested or chewed, ricin is not released and toxicity does not ensue.

Figure 16.83

Castor Bean Plant The castor bean plant is large and leafy; it may reach a height of 10 to 12 ft. (Courtesy of Alex Wilson.)

Figure 16.84

Castor Bean Typical appearance of the castor bean. (Courtesy of Alex Wilson.)

When a toxic ingestion does occur, the clinical picture is very similar to that of jequirty pea ingestions, with nausea, vomiting, abdominal pain, and diarrhea developing in 1 to 3 h. Marked dehydration and hemorrhagic gastritis may occur in severe ingestions, but progression to death is uncommon, as ricin is poorly absorbed from the GI tract. Allergic reactions with anaphylaxis have been reported with handling of the seeds and are also seen among workers in factories where castor oil is produced.

Differential Diagnosis

The differential diagnosis of castor bean ingestion includes any infectious or toxicologic cause of acute gastroenteritis.

Emergency Department Treatment and Disposition

Treatment of castor bean ingestion is largely supportive, as there is no specific antidote for ricin. Gastric decontamination should be performed, including activated charcoal, gastric lavage, and whole bowel irrigation. In asymptomatic patients, decontamination, careful observation, and close follow-up is acceptable. With symptoms of toxicity, admission is recommended for further observation, as there is potential for marked clinical worsening.

Clinical Pearls

1. Like jequirty pea ingestions, castor bean ingestions are usually benign, as a vast majority of the toxin resides within the undigested shell of the plant.

2. The plant is commercially cultivated as a source of castor oil. Such oil has been used for centuries as a purgative and as a lubricant for machines.

Ascaris Ingestion

Associated Clinical Features

Ascaris lumbricoides is a helminth that may cause crampy abdominal pain (Fig. 16.85). Exposure occurs through fecal contamination of food and water. Ascarides are commonly found in tropical climates such as Central America, South America, and Southeast Asia, although they are also endemic in the southeastern United States.

Figure 16.85

Ascaris lumbricoides The helminth Ascaris after passage from the anus. (Courtesy of Bret T. Ackerman, DO.)

Presenting symptoms may include nonspecific abdominal pain and diarrhea. Migration into the biliary system through the ampulla of Vater or into the pulmonary tree may produce biliary colic and respiratory problems, respectively. Examination of the patient is often nonspecific, although an acute abdomen may occur if there is complete biliary or small bowel obstruction from a massive worm burden.

Differential Diagnosis

Other parasites that may cause diseases of the GI tract include Giardia lamblia, Entamoeba histolytica, and Cryptosporidium. Strongyloides stercoralis and the hookworms Necator americanus and Ancylostoma duodenale may produce similar abdominal symptoms.

Emergency Department Treatment and Disposition

The medications of choice for Ascaris include mebendazole, pyrantel pamoate, and albendazole.

Clinical Pearls

1. Microscopic examination of the stool often reveals the ova of Ascaris.

2. Pulmonary involvement of Ascaris is known as Loeffler syndrome.

Acknowledgments

The authors acknowledge the special contributions of Peter Hackett, MD, FACEP, St. Mary's Hospital, Grand Junction, Colorado; Edward Otten, MD, University of Cincinnati, Cincinnati, Ohio; James O'Malley, MD, Providence Alaska Medical Center, Anchorage, Alaska; and the Nova Scotia Museum of Natural History, Halifax, Nova Scotia, Canada. The authors thank Joseph C. Schmidt, MD, and Lawrence B. Stack, MD, for their contributions to the first edition.

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