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Chapter 71 BITES AND STINGS498

5. What are the distinguishing features of scabies?

The bites are typically in the web spaces between the ﬁngers and toes (also the penis, face, and

scalp in children). They create burrows of pruritic, white, threadlike patterns with small gray spots

at the closed end, where the parasite rests. Treatment is with a thorough application of permethrin

from the neck down and may require a second course of treatment in 2 weeks.

6. How dangerous are scorpion stings?

Scorpions are generally not aggressive. They do not hunt for prey, but rather hide and wait.

Scorpions have paired venom glands located in the last of the ﬁve abdominal segments (the tail).

They hold their prey with their pincers, arch their tail over their body, and sting (not bite) the

victim. The principal toxins are polypeptides and low-molecular-weight proteins, histamine, and

indole compounds (including serotonin). The venom causes an increase in the sodium

permeability of presynaptic neurons, which leads to continuous depolarization. Most scorpions

indigenous to the United States are of low toxicity except for the bark scorpion (Centruroides).

In North America, Centruroides exilicauda (found in Baja California) and Centruroides sculpturatus

(in Sonora, Mexico, and in the Southwestern U.S.—Arizona, Utah, New Mexico, Nevada, and

California) are capable of producing systemic toxicity. They can hitch a ride in unsuspecting

travelers’ luggage. In 2007, the AAPCC reported 16,937 patients with scorpion stings. There was

moderate morbidity in 3.9% of patients, major morbidity in 0.18%, and no deaths.

7. What are the signs of scorpion envenomation?

The sting is acutely painful. Systemic manifestations are rare and mainly occur in small

children and the elderly where a larger venom-to-body weight ratio exists. The principal signs

of systemic toxicity are salivation, tachycardia, roving eye movements, involuntary muscle

jerking, opisthotonos, and tongue fasciculations.

8. What is the treatment for a scorpion sting?

Supportive care with local wound care, analgesia, and benzodiazepines for the neuromuscular

symptoms is the mainstay of treatment. There was a Centruroides scorpion antivenom available

only in Arizona, but it is no longer produced. A new scorpion-speciﬁc fragment antigen binding

(Fab) F(ab)2 antivenom (Anascorp™) is available in Mexico and is undergoing evaluation in the

United States. In critically ill children with neurotoxic effects the antivenom has been shown to

resolve the clinical syndrome within 4 hours, to reduce the need for concomitant sedation with

benzodiazepines, and to reduce the levels of circulating unbound venom.

FORMICOIDEA (ANTS)

9. I have a patient who received multiple stings from ﬁre ants. What do I do?

Don’t panic. Treatment is the same as for a bee sting. Fire ants swarm during an attack, and

each sting contributes to the total antigen load. The individual stings result in intensely pruritic

papules that may evolve to sterile pustules within 24 hours. Local necrosis and scarring may

occur.

HYMENOPTERA (BEES AND WASPS)

10. What types of reactions occur from Hymenoptera stings?

There are four types of reactions:

The toxic reaction is a nonantigenic response to the venom characterized by local irritation

at the sting site and, potentially, vomiting, diarrhea, light-headedness, and syncope. There

may also be headache, fever, drowsiness, involuntary muscle spasms, edema without

urticaria, and occasionally convulsions. Local toxic reactions are treated with supportive

care, including cool packs and analgesics.

Chapter 71 BITES AND STINGS 499

Anaphylactic reactions are most commonly seen in Vespidae stings (i.e., wasps, hornets,

yellow jackets). These reactions can range from mild to fatal and occur from 15 minutes to

6 hours after the sting. These reactions are treated like any other allergic reaction.

Delayed reactions present as a serum sickness-like syndrome 10 to 14 days after the

sting. The delayed reactions are treated with antihistamines and corticosteroids.

Unusual reactions reported after Hymenoptera stings include encephalitis, neuritis,

vasculitis, and nephritis.

11. How does a bee sting differ from a wasp sting?

Bees have barbed stingers that usually remain in the victim, pulling the venom sac off of the

bee. Whereas the bee dies after a single sting, a wasp is capable of stinging multiple times. It

is better to remove the stinger from a bee by scraping it out with a credit card rather than by

pinching and plucking it with ﬁngers or tweezers and risking the inadvertent injection of more

venom. Removal of the stinger should be done as soon as possible because the venom sac

continues to pulse venom after it has detached from the bee.

12. What about killer bees?

African honeybees (Apris mellifera scutellata) were introduced into Brazil in 1956 as a

potential honey producer in the tropical environment. There is little difference between the

Africanized bees and European bees in terms of appearance, the nature of their venom, and

the amount of venom that they carry. The difference lies in their aggressive behavior. Victims

typically receive multiple stings during a swarming attack and, therefore, a greater venom

burden. For this reason, the Africanized honeybees have been called killer bees.

13. After a patient has survived an anaphylactic reaction to a bee sting, what

should be done to prepare the patient in case he or she is stung again

in the future?

First, avoid bees and wasps.

Second, carry medical identiﬁcation describing the bee sting allergy, such as a MedicAlert

bracelet.

Third, carry and learn to use an epinephrine self-injector (the Ana-Kit or the EpiPen).

KEY POINTS: BITES AND STINGS RESPONSIBLE FOR THE

GREATEST NUMBER OF DEATHS AND MODERATE-TO-SEVERE

MORBIDITY IN THE UNITED STATES

1. Snakes (35%)

2. Insects (34.5%)

3. Spiders (22.6%)

4. Mammals (4.3%)

5. Aquatic animals (3.6%)

HELODERMA (LIZARDS)

14. Are there any venomous lizards in the world?

Yes, two species: the Mexican beaded lizard (Heloderma horridum) and the Gila monster

(Heloderma suspectum). Both animals live in the desert areas of the southwestern United

States and in Mexico. The venom of these lizards is somewhat similar to Crotaline venom,

although the clinical course is typically milder. The more serious problem with these reptiles

Chapter 71 BITES AND STINGS500

is their powerful jaws (and their tendency to hold onto their victims). They deliver their venom

by chewing and dripping the venom into the lacerations created by their teeth. Their teeth also

commonly break off in the wounds and become foreign bodies and a nidus for infection if not

removed. The teeth, by the way, are difﬁcult to visualize on radiographs. Envenomation is

present in about 70% of the bites.

CULICIDAE (MOSQUITOES)

15. What is the major clinical signiﬁcance of mosquito bites?

There are more than 3,000 species of mosquito, and they are found on every continent, except

Antarctica. They are responsible for more bites than any other blood-sucking organism. They

are attracted by carbon dioxide, lactic acid, body heat, and sweat. Children younger than age

1 year rarely show a skin reaction to the bite; however, by age 5 years almost all children react.

Both immediate and delayed hypersensitivity reactions can occur. The major signiﬁcance,

however, is in the role of the mosquito as a disease vector: They can transmit more than a half

dozen forms of encephalitis, malaria, yellow fever, dengue fever, ﬁlariasis, West Nile Virus, Ross

River virus, Chikungunya fever, and Rift Valley fever. They transmit disease to over 700 million

people annually with at least 2 million resultant deaths in Africa, South and Central America,

Mexico, and Asia. (See Chapter 52 for more information about mosquito-borne diseases).

MAMMALS (BATS, DOGS, CATS, FOXES, HORSES, HUMANS, RACCOONS, SKUNKS, AND WOODCHUCKS)

16. How many dog and cat bites are there annually in the United States? What is

the risk of infection? What is the mortality from these bites?

The majority of pet bites that require medical attention are from dogs. It is estimated that

more than 4.7 million dog bites occur annually, causing up to 800,000 victims to seek medical

attention. The annual incidence of cat bites is about 1 million. The risk of infection from a bite

is determined by multiple factors, including the location of the bite (hands are worse), the type

of wound (crush injury from dogs and punctures from cats are worse), the biting species, and

host factors (immunocompromising comorbidities). Dog bites to the hand, for example, may

have a risk of infection as high as 30%. Cat bites carry a 15% to 80% rate of infection (the

broad spread is likely due to the determination of what constitutes the denominator). Dog

attacks are fatal for about 10 to 20 people annually. The victims are often infants and children

and usually die from exsanguinating neck injuries.

17. Should I give prophylactic antibiotics to the victim of a dog or cat bite?

This is controversial. Meticulous wound care is the most effective means of reducing infection

potential. In a meta-analysis, Cummings showed a number needed to treat of 14 to prevent one

wound infection after a dog bite. However, if one of the studies that Cummings included had shown

an abnormally high infection rate, the conclusion would have been that low-risk wounds

(immunocompetent patients with nonpuncture wounds that do not involve the hand or foot, which

are treated within 12 hours and show no signs of infection) do not beneﬁt from antibiotics. High-

risk wounds, however, may do better with antibiotics in addition to meticulous wound care. When

choosing antibiotic(s), consider the polymicrobial nature of these infections (Staphylococcus,

Streptococcus, Pasteurella multocida, anaerobes, etc.) and the cost of the antibiotic.

18. What is Capnocytophaga canimorsus?

Capnocytophaga canimorsus (DF2) is a fastidious gram-negative rod that can cause sepsis

after a dog bite. Eighty percent of the patients who become seriously ill from this infection are

immunocompromised (i.e., splenectomy, hematologic malignancy, cirrhosis, HIV/AIDS, or

long-term steroids). Fortunately, it is a rare infection because it carries a 25% to 36%

mortality.

Chapter 71 BITES AND STINGS 501

19. What is the origin of the phrase “the hair of the dog that bit you”?

It is a very, very old expression, probably arising from the Roman belief that similia similibus

curantur (like cures like). To treat the victim of a dog bite, one would obtain samples of its

hair and either burn the hair and apply it to the wound or use the hair in creating a poultice for

the wound. It was thought that this would speed wound healing and recovery from rabies. By

extension, another drink or two after a drinking binge would be the cure for a hangover.

20. What types of bites are at risk for the transmission of rabies?

Rabies is a disease caused by an RNA rhabdovirus transmitted by inoculation with infectious

saliva. It is prevalent in parts of Latin America, Asia, Africa, South America, Europe, the Middle

East, India, and Southeast Asia. Rabies-free areas include Hawaii, England, Australia, Japan,

and parts of the Caribbean. The virus primarily affects the central nervous system and is

almost always fatal. In the United States, animal bites from skunks, raccoons, bats, foxes, and

woodchucks should be considered a risk. Exposures from livestock, rodents, and lagomorphs

should be considered individually but rarely require postexposure prophylaxis because the

host dies before the rabies virus can replicate sufﬁciently. Consult your state health

department for local recommendations.

21. What does postexposure prophylaxis for rabies consist of?

Postexposure prophylaxis means trying to prevent the disease before it manifests after a high-

risk exposure. It begins with a thorough cleansing of the wound. Then administer 20 IU/kg of

human rabies immunoglobulin (50% injected in and around the wound, if possible, and 50%

given intramuscularly in the gluteal muscle). Inject 1 mL of human diploid cell vaccine into the

deltoid muscle (or the anterolateral thigh in young children) on days 0, 3, 7, and 14. Tip: Do

not administer the rabies vaccine and the immunoglobulin in the same site.

22. What is a ﬁght bite?

A ﬁght bite or clenched ﬁst injury is a human bite that occurs when a ﬁst strikes the teeth of

an opponent. This usually involves the knuckles of the dominant hand. The laceration can

involve the extensor tendon and its bursa, the superﬁcial and deep fascia, and the joint

capsule. These structures are contaminated with oral ﬂora at the time of injury and are

notorious for becoming infected. There are at least 42 species of bacteria in human saliva. The

most frequently cultured organism from ﬁght bites is Streptococcus, followed by S. aureus

(usually penicillin resistant); 31% of these wound infections are due to gram-negative

organisms, and 43% are due to mixed gram-negative and gram-positive organisms. Up to

29% of these infections may be due to a facultatively anaerobic gram-negative rod, Eikenella

corrodens. This harmful organism is typically resistant to the semisynthetic penicillins,

clindamycin, and the ﬁrst-generation cephalosporins. However, it is usually sensitive to

penicillin and ampicillin. These wounds should be meticulously cared for, with special

attention given to thorough exploration and irrigation. Consider the polymicrobial nature of

these infections when choosing antibiotics.

MARINE FAUNA (JELLYFISH, SHARK, AND VENOMOUS FISH)

23. How do I treat jellyﬁsh or other coelenterate stings?

Jellyﬁsh envenomate by injecting small harpoon-shaped spines from their nematocysts

into their prey. The discharge is triggered by either physical or chemical stimulation.

Frequently, undischarged nematocysts within the jellyﬁsh tentacles remain in contact with

the victim’s skin. The concern, of course, is that the undischarged nematocysts may be

stimulated to release additional venom into the victim. Acetic acid (vinegar) inhibits

nematocyst discharge in Chironex ﬂeckeri stings but has no effect on cysts that have

already discharged. Further, inhibition of nematocyst discharge is probably species

speciﬁc. Effective inhibitors in one species may trigger nematocyst discharge in another.

Chapter 71 BITES AND STINGS502

Acetic acid has been demonstrated to inhibit nematocyst discharge in all of the species of

medically important Australian jellyﬁsh.

If vinegar is not available, acidic drinks (soft drinks and fruit juices) may be tried. Although

popular in folklore, urine has not been proven to inhibit nematocyst discharge and may even

stimulate nematocyst discharge.

Immersion of the affected extremity in hot water may be of some beneﬁt (after acetic acid

decontamination). The nematocysts that remain in the skin can be removed by applying shaving

cream, talc, baking soda, or ﬂour and then shaving the area. The same treatment can be used for

the stings from sea anemones or ﬁre coral. There is an Australian box jellyﬁsh (Chironex

ﬂeckeri) antivenin available. The recommended dosage for the antivenom is 1 to 3 ampules.

24. Name some venomous ﬁsh, and state what their venoms have in common.

How can that feature of their venom be used in treatment?

Stingray, lionﬁsh, scorpionﬁsh, stoneﬁsh, catﬁsh (i.e., freshwater catﬁsh, sea catﬁsh, coral

catﬁsh), oldwife ﬁsh, zebraﬁsh, butterﬂy cod, spiny dogﬁsh, rabbit ﬁsh, rafﬁsh, stargazer ﬁsh,

surgeon ﬁsh, toadﬁsh, weever ﬁsh, bullrout, sculpin, and stinging sharks all have heat-labile

toxins (heat destroys the toxin). Barbs and spines may remain embedded in the wound and

should be promptly removed. The venoms can be rendered nontoxic by placing the affected

extremity of the victim (usually the foot) into hot water (45°C) for 90 minutes.

25. Question: How do I acquire antivenom for exotic snake or marine

envenomations?

Call your local or regional poison center in the United States (1-800-222-1222) for assistance.

They will have the most success in obtaining antivenom from the local zoo or aquarium or

from another poison center. Note that although zoos and aquaria may possess antivenom for

exotic envenomations, the supply is primarily intended for their workers in case of an

emergency. They may choose to release speciﬁc antivenom under a compassionate use

clause, but they are not obligated to do so.

26. How many people are killed by sharks worldwide annually?

Between 2001 and 2006 an average of 4.3 people died worldwide annually from unprovoked

shark attacks. In contrast, approximately 100 million sharks are killed by people annually.

CROTALINAE ELAPIDAE

(RATTLESNAKES, COPPERHEADS, WATER MOCCASINS, AND CORAL SNAKES)

27. What is a dry snakebite?

A dry snakebite is a bite in which no venom was introduced. About 20% to 25% of all U.S.

rattlesnake bites do not result in envenomation. Coral snakes, lacking fangs, envenomate

by chewing the skin; thus, as many as 50% of their bites are dry. Quick observations

helpful in determining whether rattlesnake envenomation has taken place include the

presence of fang marks that ooze nonclotting blood with surrounding ecchymosis and

severe burning pain. These signs combined with microhematuria are characteristic of

severe envenomation and a poor prognosis. In coral snake envenomation, there is usually

little local tissue damage, and systemic signs may be delayed for as long as 12 hours.

The earliest signs and symptoms include nausea, vomiting, headache, abdominal pain,

diaphoresis, and pallor. Coagulopathy is not a feature of coral snake envenomation, but

respiratory paralysis is the feared outcome.

28. True or false: Snakebites are uncommon but are highly lethal?

True and false. In the United States, snakebites are uncommon, and mortality is rare. The

2007 AAPCC report documented 6,550 snakebites (venomous and nonvenomous), and only

two deaths (one from a rattlesnake and one from an unknown crotaline snake). Rattlesnakes

accounted for more than half of the major medical outcomes, and copperheads one sixth.

Chapter 71 BITES AND STINGS 503

29. List some of the epidemiologic characteristics of snakebites in the

United States.

Seventy-ﬁve percent occur from April to September.

Forty-ﬁve percent occur between the hours of 2 P.M. and 6 P.M.

Male-to-female victim ratio is 7:1.

Fifty-ﬁve percent of victims are age 17 to 27 years.

Eight-ﬁve percent of bites are on the ﬁngers or hand; 15% involve the foot or ankle.

Ethanol intoxication was present in 30% to 60% (especially if “pet” snakes are involved).

Fifteen percent had previous snakebites.

30. List the three main clinical effects and the clinical signs of crotaline (pit viper)

envenomation.

Crotaline snakebite manifests with three main clinical effects:

Local (i.e., pain, edema, or ecchymosis)

Systemic (i.e., hypotension, fasciculations, or multiorgan dysfunction syndrome)

Coagulopathy (i.e., low platelets, elevated international normalized ratio [INR], low

ﬁbrinogen)

Signs of Crotaline snakebite include the following:

Rapid onset of slow spreading edema (80%)

Pain out of proportion to the puncture (72%)

Weakness (65%)

Light-headedness (52%)

Nausea (48%)

Erythema at the bite site (53%)

Bleeding diathesis (52%)

Lymphangitis, hypotension, shock, diaphoresis, and chills (58%)

Paresthesias, taste changes, and fasciculations (33%)

31. What is CroFab? When should it be administered?

CroFab (Crotalidae Polyvalent Immune Fab) is an antivenom produced from the pooled serum

of sheep immunized with one of four crotaline snake venoms, then digested with papain to

produce antibody fragments (Fab and Fc). The more immunogenic Fc portion is eliminated

during puriﬁcation, leaving the four monospeciﬁc Fab preparations that are combined to form

the ﬁnal antivenom. It is provided as lyophilized powder and must be reconstituted (this takes

30 minutes). The goal is to attain initial control (deﬁned as halting progression of all

components of envenomation including local effects, systemic effects, and coagulopathy) by

administering an initial loading dose of 4 to 6 vials. After control has been established,

additional 2-vial maintenance doses are infused at 6, 12, and 18 hours. Since Food and Drug

Administration (FDA) approval in 2000 of CroFab, Wyeth has recently ceased manufacture of

Polyvalent Crotalidae Antivenin (a whole immunoglobulin [IgG] preparation), although some

institutions may have supplies that have not yet been used.

Due to the relatively small Fab molecular size and consequent renal clearing, the effective

CroFab duration of action may be insufﬁcient for one-dose treatment of crotaline

envenomation. Scheduled maintenance dosing is recommended after achieving initial control.

The Mexican pharmaceutical company Bioclon has developed an equine-derived polyvalent

crotaline immune F(ab)2 antivenom for use in Mexico that is effective in neutralizing 15 venoms

from North American snakes.

32. Can a crotaline bite cause a compartment syndrome?

Compartment syndrome may result, but it is unlikely because venom is usually deposited in the

subcutaneous tissue, not in fascial compartments. Children, however, with the smaller body mass

and potential for relatively deeper envenomations are more prone to develop compartment

syndrome. It cannot be diagnosed reliably without directly measuring intracompartmental

pressures because the signs and symptoms of compartment syndrome (i.e., paresthesias,

Chapter 71 BITES AND STINGS504

decreased pulses, and pain on motion) are similar to signs and symptoms of envenomation.

Antivenin may improve compartment pressure. If the pressure is elevated initially, monitor the

compartment pressure while administering antivenin. Perform fasciotomy only when pressures

remain persistently elevated above 30 to 40 mm Hg. One exception may be the envenomated

ﬁnger (i.e., tense, blue or pale with absent or poor capillary reﬁll), which should be discussed with

a toxicologist and surgeon. It can be treated with a digit dermotomy on clinical grounds.

33. What is the importance of the coloring of coral snakes, and what are the

active components of its venom?

This small, thin, brightly colored snake is venomous; however, the king snake, which is

nonvenomous, has similar coloration but a different pattern. Remember:

“Red on yellow, kill a fellow” (coral snake)

“Red on black, venom lack” (harmless snake)

This rhyme helps only with identifying North American Coral snakes. Coral snake venom

contains a neurotoxin that irreversibly binds to presynaptic nerve terminals and blocks

acetylcholine receptors. It may take weeks to regenerate the receptors. The clinical effects are

slurred speech, ptosis, dilated pupils, dysphagia, and myalgias. Death results from

progressive paralysis and respiratory failure. There is virtually no local tissue destruction.

34. How is coral snake envenomation treated?

Supportive care with good wound care, in addition to early treatment with 3 to 5 vials of

elapid equine antivenom (Wyeth), is indicated for eastern coral or Texas coral snake

envenomation. Western coral snake envenomation does not require antivenom. Wyeth no

longer produces the antivenom, but some stock may still exist. Coralmyn®, a coral snake

antivenom produced by the Mexican pharmaceutical company Bioclon, must undergo review

by the FDA before being adopted for use in the United States. Coralmyn is effective in the

neutralization of both clinically important coral snake venoms in the United States.

35. What prehospital treatments have been advocated for rattlesnake bites that

are now considered to be ineffective or harmful?

Incising the wound and attempting to extract the poison by oral suction (cut and suck), venom

extraction devices, electric shock to denature the toxin proteins, carbolic acid, strychnine, enemas,

urine, cauterization, prophylactic antibiotics, ice packs (cryotherapy), and arterial tourniquets are

ineffective and, in some cases, harmful. Venom extraction devices do not remove a signiﬁcant

amount of venom (0.04%–2% in one study). Nonsteroidal anti-inﬂammatory drugs may

compound a crotaline venom-induced thrombocytopenic bleeding diathesis and should be avoided.

36. What prehospital nonantivenin treatments do make sense?

It is prudent to remain calm, avoid activity, remove jewelry or constricting items, use a

lymphatic band, immobilize the extremity, follow good basic life support principles, and

transport rapidly to the ED. A lymphatic constriction band (broad and ﬂat band as opposed to

a ropelike tourniquet) can be applied to exert a pressure great enough to occlude superﬁcial

veins and lymphatic channels (typically .20 mm Hg) but loose enough to admit one or two

ﬁngers. It has been shown in experimental models to delay the systemic absorption of venom

and may have use in cases with prolonged transport time. In an animal model, the time to

death after injection of venom can be prolonged, and the median lethal dose of venom can be

increased, simply by immobilizing all four limbs (including the unbitten extremities). This

technique has not been studied clinically.

37. What about exotic snakes (at least exotic by North American standards)?

In 2007 the AAPCC reported 153 exotic snake exposures (i.e., poisonous, nonpoisonous, and

“unknown if poisonous”). There were 0 deaths, 4 life-threatening outcomes, and 32 moderate

outcomes. An Antivenom Index exists that includes a catalog of all of the antivenoms stocked

by North American zoos and aquariums. Possession of exotic venomous snakes may be

restricted by law, and these cases should be reported to the authorities.

Chapter 71 BITES AND STINGS 505

WEBSITES

American Association of Poison Control Centers: http://www.aapcc.org/

Scorpion envenomation: http://emedicine.medscape.com/article/168230-overview

Snake bite antivenom—resources and producers: http://globalcrisis.info/latestantivenom.htm

Widow spider envenomation: http://emedicine.medscape.com/article/772196-overview

BIBLIOGRAPHY

1. Auerbach PS, editor: Wilderness medicine, ed 4, St. Louis, 2001, Mosby.

2. Boyer LV, Theodorou AA, Berg RA, et al: Antivenom for critically ill children with neurotoxicity from scorpion

stings. N Engl J Med 360(20):2090–2098, 2009.

3. Bronstein AC, Spyker DA, Cantilena LR Jr, et al: 2007. Annual Report of the American Association of Poison

Control Centers’ National Poison Data System (NPDS): 25th Annual Report. American Association of Poison

Control Centers. Clin Toxicol 46(10):927–1057, 2008.

4. Bush SP: Snakebite suction devices don’t remove venom: they just suck. Ann Emerg Med 43:187–188, 2004.

5. Cummings P: Antibiotics to prevent infection in patients with dog bite wounds: a meta-analysis of randomized

trials. Ann Emerg Med 23:535–540, 1994.

6. Freeman TM: Clinical practice. Hypersensitivity to hymenoptera stings. N Engl J Med 351:1978–1984, 2004.

7. Sánchez EE, Lopez-Johnston JC, Rodríguez-Acosta A, et al: Neutralization of two North American coral snake

venoms with United States and Mexican antivenoms. Toxicon 51(2):297–303, 2008.

8. Saucier JR: Arachnid envenomation. Emerg Med Clin North Am 22:405–422, ix, 2004.

9. Steen CJ, Janniger CK, Schutzer SE, et al: Insect sting reactions to bees, wasps, and ants. Int J Dermatol

44(2):91–94, 2005.

10. Swanson DL, Vetter RS: Bites of brown recluse spiders and suspected necrotic arachnidism. N Engl J Med

352:700–707, 2005.

ACKNOWLEDGMENT

Thanks to Lee W. Shockley, MD, for his contributions in the previous version of this chapter.

506

SMOKE INHALATION

CHAPTER 72

Richard E. Wolfe, MD

1. What is the most common way to die in a ﬁre?

Smoke inhalation accounts for as high as 80% of ﬁre-related deaths. It increases mortality

by up to 20% over that predicted by age and extent of cutaneous burn alone.

2. Is smoke inhalation so lethal because it causes thermal injury to the lungs?

Not usually. Air has such a low heat-carrying capacity that it rarely produces lower airway

damage. The upper respiratory tract generally cools hot air before it reaches the vocal cords.

Steam, however, has 4,000 times the heat-carrying capacity of air and causes severe upper

airway burns with fatal glottic edema, as well as bronchial mucosal destruction and alveolar

hemorrhage.

3. Why is smoke inhalation so dangerous?

Carbon dioxide and carbon monoxide (CO), the major components of smoke, are

responsible for a drop in the concentration of ambient oxygen from 22% to 5% to 10%.

CO and, more rarely, hydrogen cyanide block the uptake and use of oxygen, leading to

severe tissue cellular hypoxemia. Depending on the fuel, temperature, and rate of heating,

smoke contains a wide variety of toxins. Soot may act as a vehicle in transporting these

toxic gases to the lower respiratory tract, where they dissolve to form acids and alkali.

Removal of the soot is impaired by action of certain of these toxins on respiratory cilia,

leading to severe, delayed pneumonia.

4. Name the four clinical stages of smoke inhalation.

Stage 1: Acute respiratory distress occurs 1 to 12 hours post-injury and is due to

bronchospasm, laryngeal edema, and bronchorrhea.

Stage 2: Noncardiogenic pulmonary edema (adult respiratory distress syndrome) occurs

6 to 72 hours post-injury secondary to increased capillary permeability.

Stage 3: Strangulation occurs 60 to 120 hours post-injury from cervical eschar formation

in patients with circumferential neck burns.

Stage 4: Onset of pneumonia 72 hours after injury, usually from Staphylococcus aureus,

Pseudomonas aeruginosa, or gram-negative organisms.

5. How should smoke inhalation victims be managed in the ﬁeld?

All victims should be placed on a 100% nonrebreather mask, even if they are

asymptomatic. Oxygen administration dramatically accelerates the washout of CO,

shortening the half-life from 4 hours at room air to about 90 minutes. Endotracheal

intubation is indicated for patients in respiratory distress. When intubated, the patient

should be suctioned aggressively to remove inhaled soot. Patients with a loss of

consciousness or altered mental status should be transported to a facility capable of

providing hyperbaric oxygen (HBO) therapy.

6. What should I ask the emergency medical technicians (EMTs) about the ﬁre?

Ask if the patient was trapped in a closed space because signiﬁcant inhalation injury would

not occur in an open area. Try to determine what material was burning. The fuel is of primary

importance in determining the composition of smoke and the risk to the patient.

Chapter 72 SMOKE INHALATION 507

7. Name some toxins produced by smoke and the materials from which they

derive.

Hydrogen cyanide: combustion of wool, silk, nylons, and polyurethanes found commonly

in furniture and paper.

Aldehydes, acrolein: wood, cotton, paper, and plastic materials.

Hydrogen chloride, phosgene: pyrolysis of chlorinated polymers; polyvinyl chloride (wire

insulation materials); chlorinated acrylics; and wall, ﬂoor, and furniture coverings.

Oxides of nitrogen: nitrocellulose ﬁlm.

Sulfur dioxide, hydrogen sulﬁde: rubber.

8. What are the earliest clinical manifestations of acute inhalation injury

following smoke exposure?

Inﬂamed nares, cough, sputum production, and hoarseness are the ﬁrst signs of injury.

This is because the nasopharynx and larynx are exposed to the highest concentration of

inhaled toxins leading to the most severe chemical burns. Furthermore, the proximal

airway is usually the only part of the airway subjected to thermal burns. However, even

when injured, nasopharyngeal and laryngeal edema may be delayed. Furthermore, rapid

progression to complete airway obstruction may occur in patients with mild symptoms.

For this reason, close observation followed by early airway management is often necessary

to ensure patient safety.

9. Why is HBO therapy thought to be beneﬁcial in smoke inhalation?

HBO therapy provides increased oxygen to poorly functioning mitochondrial enzymes

inhibited by CO and cyanide.

HBO therapy at 3 atmospheres (atm) decreases the half-life of CO to 23 minutes.

HBO therapy has been shown to reduce smoke-induced pulmonary edema.

At a cellular level, HBO therapy decreases the formation of intercellular adhesion molecule-I

on the endothelial membrane, which prevents neutrophils from inﬁltrating the central

nervous system and causing a damaging inﬂammatory reaction and permanent neurologic

sequelae.

10. How do I make the diagnosis of smoke inhalation injury?

Bronchoscopy is needed to conﬁrm the presence of inhalation injury. Soot deposition in the

airway, extensive edema, mucosal erythema, hemorrhage, and ulceration conﬁrm that smoke

inhalation has occurred. The initial bronchoscopy may be relatively normal because hyperemia

and edema formation may take some time to evolve. A normal proximal airway does not rule

out more distal injury.

11. How should asymptomatic patients be managed?

Observe the patient in the ED for a few hours ﬁrst. If still asymptomatic, provide

comprehensive discharge instructions on when to return. Although the physical examination

cannot reliably rule out complications such as delayed noncardiogenic pulmonary edema or

pneumonia, ancillary studies and ED or in-hospital observation are not cost effective. The

patient should be instructed to return to the ED if shortness of breath, chest pain, or fever

occurs.

12. If the patient’s pulse oximetry is normal, would arterial blood gas analysis

yield additional information?

In the presence of carboxyhemoglobin (CO), pulse oximetry may yield a falsely elevated

(normal) reading. Arterial blood gases are of limited use and may be helpful only if the oxygen

saturation is measured directly and not derived from the PaO

measurement. Although an

increased alveolar-arterial gradient may correlate with smoke inhalation injury, it does not

predict the severity of injury. Arterial blood gases are most useful in determining

hypoventilation (increased PCO

) and the presence of a metabolic or respiratory acidosis.