elapids will remain attached and "chew'' on their victim to

inject the venom. Although this makes it more difficult fur

these snakes to deliver a clinically significant amount of

venom, it also makes it more difficult to clinically assess a

patient with a potential bite, as there may not be bite or fang

marks in a patient who has had a potentially life-threatening

envenomation.

..... Spiders

Like snakes, there are 2 major groups of spiders that cause

medically significant envenomations in North America: the

black widow (genus Latrodectus) and the brown recluse

(genus Loxosceles). It is difficult to estimate the true incidence of spider bites, because the history of a bite is often ­

times unreliable, with many patients and physicians

reasoning that a rash, abscess, or cellulitis originated from a

spider bite when no spider was seen. Additionally, with the

CHAPTER 65

Figure 65-2. North American cora l snake.

Reproduced with permission from Knoop K}/

Stock LB/ Storrow AB/ et of. The Atlas of

Emergency Medicine. 3rd ed. New York:

McGraw-Hill Medical/ 2009. Figure 1 6.30.

Photo contributor: Steven Holt MD.

possible exception of the female black widow spider, the

general public has difficulty distinguishing medically rele ­

vant spiders from those that are generally benign. That

being said, bites from brown recluse and black widow

spiders can be deadly in extreme circumstances and can

unquestionably cause substantial morbidity and pain.

There are 5 species of black widow spiders found in

the United States. These spiders are medium-sized, typically black colored, and have species-specific ventral

markings. The female Latrodectus mactans has the characteristic red hourglass ventral marking and has a larger

body and fangs than her male counterpart, making the

female more likely to cause envenomation (Figure 65-3 ).

The clinical effects of a black widow spider envenomation

in humans are thought to be caused by the neurotoxin

a-latrotoxin.

There are 2 major species of recluse spiders found in

the United States: the Loxosceles reclusa (brown recluse)

and Loxosceles deserta (desert recluse). The brown recluse

is found primarily in the southern and midwestern United

States, and the desert recluse's range is in the southwestern

portion of the country. North American recluse spiders

are brown to gray-colored with dark dorsal markings

that have a violin pattern, giving it its other names, fiddle ­

back or violin spider (Figure 65-4) . The toxin in recluse

spider bites is complex, but is thought to contain

proinflammatory and necrosis-inducing substances

similar to phospholipase D and hyaluronidase.

CLINICAL PRESENTATION

� Snakes

The severity of a crotaline envenomation depends on

multiple factors, including the amount of venom delivered, the potency of the venom, and the location of the

venom (anatomically and by depth), as well as clinical

Figure 65-3. Black widow spider,

 

Asymptomatic

- CXR, consider labs

(electrolytes, blood count)

- Evaluate primary vs secondary

drowning

- Evaluate for traumatic injury

mit to monitored bed Discharge home

Figure 64-2. Drown ing incidents diag nostic algorithm. CXR, chest x-ray; ICU, intensive care unit.

DISPOSITION

Patient condition will largely determine disposition. Poor

prognostic factors include:

• Submersion for > 10 minutes

• > 10 minutes before initiation of basic life support

measures in an apneic/pulseless patient

• >25 minutes of pulselessness

• Initial temperature <33°C (92°F)

• Initial Glasgow score <5

• Need for cardiopulmonary resuscitation in the ED

• Submersion in water colder than l 0°C (50°F)

• Initial arterial blood gas pH <7.1

� Admission

Admission is indicated for any symptomatic patient. Those

who are intubated, have persistently altered mental status,

are hypothermic, or require high-flow oxygen should be

admitted to an intensive care unit. Cardiac monitoring is

indicated for any patient with oxygen requirements or

changes on chest radiograph.

� Discharge

Patients who present asymptomatic and remain asymp ­

tomatic for at least 6 hours may be safely discharged home.

Discharged patients should be instructed to return for

development of difficulty breathing, fever, or mental status

changes.

DROWNING INCIDENTS

SUGGESTED READING

Causey, AL, Nichter, MA. Drowning. In: Tintinalli JE, Stapczynski

JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th ed.

New York, NY: McGraw-Hill, 201 1, pp. 137 1-1374.

Causey AL, Tilelli JA, Swanson ME. Predicting discharge in

uncomplicated near-drowning. Am J Emerg Med. 2000;1 8:9.

Layon AJ, Modell JH. Drowning: Update 2009. Anesthesiology.

2009;1 10:1390.

Papa L, Hoelle R, Idris A. Systematic review of definitions for

drowning incidents. Resuscitation. 2005;65:255.

Salomez F, Vincent JL. Drowning: A review of epidemiology,

pathophysiology, treatment and prevention. Resuscitation.

2004;63:26 1.

van Beeck EF, Branche CM, Szpilman D, Modell JH, Bierens JJ.

A new definition of drowning: Towards documentation and

prevention of a global public health problem. Bull World

Health Organ. 2005;83:853.

Envenomation

Patrick M. La n k, MD

Key Points

• In addition to any focused or antidotal therapy available, aggressive symptom-based supportive care is

important for all envenomations.

• Knowledge of local venomous species may be helpful,

although be aware that patients may have contact with

non local or exotic venomous animals.

INTRODUCTION

In 2010, there were more than 60,000 calls made to United

States Poison Centers related to bites and envenomations.

Although there are many venomous animal species in

North America, a majority of these calls involved insects

(including bees, wasps, hornets, and ants), arachnids

(including spiders and scorpions), and snakes. From information provided in the 20 10 Annual Report of the

American Association of Poison Control Centers' National

Poison Data System, there were a total of 5 fatalities related

to all bites or envenomations and approximately 2,500

instances of antivenin being given.

The clinical presentations of the various forms of

venom exposure vary greatly and are dependent on multiple factors including the species of the animal, the

amount of venom delivered, and potential baseline medi ­

cal problems in the envenomed patient. Patients presenting with an animal envenomation may therefore display a

variety of symptoms ranging from local reaction to a bite

or sting to generalized yet nonspecific effects (eg, vomiting, headache, hypertension) or toxin-specific findings

(eg, paralysis or coagulopathy) . This chapter focuses on

the presentation, evaluation, and treatment of 2 of the

most clinically relevant North American envenomations:

snakes and spiders.

• North American venomous bites are rarely unprovoked.

• Contact your local poison control center (1-800-222-1 222)

for assistance with diagnosing and managing all envenomations.

� Snakes

Venomous snakes found in North America are most easily

divided into their 2 families: Elapidae and Viperidae (subfamily Crotalinae). The majority of venomous snakebites

occurring yearly in North America are caused by snakes in

the Crotalinae subfamily, which includes rattlesnakes

(genus Crotalus), copperheads, and cottonmouths (genus

Agkistrodon). Less than 5o/o of venomous snakebites are

from the Elapidae family, which includes the coral snake.

Fewer still may be from bites by exotic, nonnative snakes

usually being kept as pets.

Venomous snakes found natively in North America are

generally nonpredatory to humans. Bites, therefore, take place

on provocation of the snake-either intentional or accidental.

These bites are typically located on extremities, but particu ­

larly troublesome cases have been reported in which venomous bites have involved the face, neck, or tongue. The vast

majority of venomous snakebites occur in young men, with

an appreciable association with alcohol intoxication. Children

are also at a higher risk for being bitten by a venomous snake.

There are a few characteristics that can help identify a

North American snake as being part of the Crotalinae subfamily. These snakes have vertical slit-like pupils, long

fangs, and a triangular head. This subfamily is also referred

to as "pit vipers" because they have heat-sensing pits

274

ENVENOMATION

Poisonous (pit vipers) Harmless

Nostri l

Figure 65-1. Differences between venomous pit vipers and nonvenomous

North American snakes.

located on their heads j ust behind the nostrils and in front

of the eyes (Figure 65- 1). Crotaline venom contains a combination of chemicals that cause primarily local tissue

damage and hematologic effects.

Elapidae native to North America are the coral snakes.

These snakes, found mostly in the Southeast United States

(particularly Florida and Texas), have a characteristic color

pattern that distinguishes them from the similar-appearing but

nonvenomous scarlet king or milk snake. People often remember this pattern difference by reciting the rhyme, "Red on yellow kills a fellow. Red on black, friend of Jack'' (Figure 65-2).

Elapid venom has a curare-like neurotoxic effect and is said to

be one of the most potent North American venoms. However,

multiple characteristics of the snake make clinically significant

bites from these snakes rare. They tend to reside in remote

unpopulated areas and even if confronted will attempt to flee

before biting. Unlike the crotalids, the elapids' fangs are short

and unlikely to penetrate thick clothing or shoes. After biting,

 

Hallam MJ, Cubison T, Dheansa B, I mray C. Managing frostbite.

BM]. 201 0;341:1 151.

Ulrich AS, Rathlev NK. Hypothermia and localized c old injuries.

Emerg Med Clin North Am. 2004;22:28 1.

Heat-Related Illness

Natalie Radford, MD

Key Points

• Always consider secondary causes of hyperthermia.

Heat exhaustion and heat stroke should be diagnoses

of exclusion.

• Do not fluid overload elderly patients while rehydrating

them in the emergency department (ED). Remember

that their fluid and electrolyte deficits developed over

INTRODUCTION

Heat exhaustion and heat stroke are on a continuum of disease severity. Heat exhaustion occurs when the body can no

longer dissipate heat adequately, resulting in hyperthermia.

Heat stroke is the result of complete thermoregulatory dysfunction. Classic heat injury occurs in the elderly or ill with

prolonged exposure to high environmental temperatures.

Physical exertion is not required. Elevated temperatures and

high humidity overwhelm the body's normal c ooling mechanisms. Ex:ertional heat injury occurs in physically fit individ -

uals who exert themselves during conditions with high heat

and humidity. Heat gain from the environment combined

with internal heat production overwhelms the body's normal

cooling mechanisms, creating hyperthermia.

There are about 400 deaths from heat-related illness in

the United States every year. Extremes in weather condi ­

tions can greatly affect these numbers. The Midwest heat

wave in July 1 995 caused 465 deaths in the city of Chicago

alone. The mortality rate in patients with heat stroke can

range between 10% and 70% and is affected by a patient's

physical ability to adapt to changes in the ambient tern ­

perature and medical comorbidities.

The body normally maintains its core temperature

between 36°C (96.8°F) and 38°C (100.4°F). In hyperthermia,

as opposed to fever, there is an elevated body temperature

without a resetting of the hypothalamic t emperature center.

days, and they do not need to be fully repleted while

in the ED.

• Begin cooling the severely hyperthermic patient as

soon as other life-threatening conditions and airway,

breathing, and circulation have been addressed. Delays

in treatment can increase morbidity and mortality.

The body reacts to a heat stress to decrease body temperature

via 3 main mechanisms: increased sweat production,

decreased internal heat production, and removal from the hot

environment. Any factors that impede these responses can

lead to heat exhaustion or heat stroke.

Evaporation of sweat is the main mechanism through

which the body dissipates heat. Evaporative mechanisms

are impaired by both environmental and physical factors.

High humidity, as seen with an elevated heat index,

impedes the body's ability to evaporate sweat and cool.

Elderly, infants, and those with chronic illness have

decreased ability to adapt to hot conditions. Certain medications including antipsychotics, anticholinergics, betablockers, and diuretics also interfere with sweat e vaporation

and cooling. Alcoholics, those with decreased mobility, and

some patients with chronic medical conditions including

obesity, poor cardiac function, and scleroderma have

impaired abilities to evaporate heat as well.

Radiation, conduction, and convection of heat also

allow the body to lose heat, but only when the ambient

temperature is lower than body temperature. Utilizing these

mechanisms can aid in cooling a hyperthermic patient.

CLINICAL PRESENTATION

In patients presenting with heat exhaustion, core body temperature is usually normal, but can be elevated to 40°C

267

 

 Do not use water warmed above 42°C to avoid

superimposed thermal injury. Never initiate rewarming in

the prehospital setting if there is any potential for refreezing,

as this can worsen tissue injury.

A rewarming period of between 15 and 60 minutes

is adequate for most patients. Use the appearance of the

affected tissues to guide the duration of therapy. Appropriately

rewarmed tissue should appear erythematous and pliable.

Encourage active movement of the affected extremity to

stimulate increased circulation. Rewarming can be exceptionally painful, and parental opioids are frequently required.

Numerous adjunctive therapies have been proposed, although

the evidence supporting their use is lacking ( Table 62- 1).

It may take many weeks for the full extent of the

patient's injuries to declare. That said, certain early findings

do suggest better or worse outcomes. Findings associated

with a better prognosis include the rapid re-establishment

of normal skin temperature and sensation and the

CHAPTER 62

Table 62-1. Adj unctive therapies for frostbite.

Debride clear bl isters.

Leave hemorrhagic blisters intact.

Apply aloe vera cream (Dermaide) every 6 hours to affected

tissue.

Dress affected areas in soft, dry bandages.

Elevate and splint affected extremity.

Administer tetanus prophylaxis.

Administer NSAID (ibuprofen 400 mg every 8 hours).

Administer penicillin orally or intravenously every 6 hours for

48-72 hours.

Admit to hospital for daily hydrotherapy at 40°C.

Strictly prohibit smoking.

development of large clear blisters. Persistent tissue

cyanosis, firm insensate skin, and the delayed formation of

small hemorrhagic blisters all portent a poor prognosis.

DISPOSITION

� Admission

Admit all patients with acute frostbite for a minimum of

24-48 hours, as the full extent of tissue injury may not be

evident on initial presentation. Transfer to a specialized

burn center may be required in severe cases where

significant tissue necrosis will necessitate surgical

debridement. Consider admission for all high-risk patients

(young children, elderly, and homeless) with NFCI and

most patients with significant immersion foot to limit

further progression of disease.

� Discharge

Most patients with frostnip, chilblains, and mild cases of

immersion foot can be safely discharged home provided

they have access to adequate cold-weather clothing and a

warm, dry environment. All discharged patients require

clear instructions on proper wound care and further injury

prevention. Ensure adequate outpatient analgesia and

arrange for close surgical follow-up as necessary.

SUGGESTED READING

Ikaheimo TM, Junila J, Hirvonen J, Hassi J. Frostbite and other

localized cold injuries. In: Tintinalli JE, Stapczynski JS, Cline

DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th ed.

New York, NY: McGraw-Hill, 201 1.

Irnray C, Grieve A, Shillon S, Caudwell Xtreme Everest Research

Group. Cold damage to the extremities: Frostbite and nonfreezing cold injuries. Postgrad Med ]. 2009;85:48 1--488.

 

CHAPTER 63

( 104°F). Patients complain of nonspecific symptoms and

signs including weakness, dizziness, fatigue, nausea, vomiting,

headache, myalgias, tachycardia, tachypnea, hypotension, and

diaphoresis. By definition, mental status remains normal.

Heat stroke patients present with altered mental status (AMS)

ranging from mild confusion to coma. Body temperature is

elevated above 40°C ( 104°F), and they may or may not be

sweating. Patients can exhibit a wide range of neurologic

symptoms and signs, including ataxia, seizures, and hemiple -

gia. Multiorgan system failure consisting of hepatic, renal, and

cardiac impairment may also be present in severe cases .

..... History

Important factors to address in the history include a full

description of the circumstances surrounding the heat

exposure. Has the patient been in a non-air-conditioned

apartment in the summer for several days, or has the

patient been working outside while there is an elevated

heat index? Past medical history should include questioning

for medical conditions that increase the risk of heat illness

and medications that impede the body's ability to cool.

..... Physical Examination

Physical examination should involve complete exposure of

the patient to remove heat-trapping clothing and to assess

for any physical injuries.

DIAGNOSTIC STUDIES

..... Laboratory

A complete metabolic panel (CMP) should be drawn to

evaluate serum electrolytes. Hypo- or hypernatremia may be

present as well as hyperkalemia. Prerenal azotemia may also

be seen on the CMP, indicating impaired renal function. A

creatine phosphokinase should be checked to rule out rhabdomyolysis. As end-organ damage occurs, patients with heat

stroke may develop elevated liver enzymes (peaking at 24-72

hr), disseminated intravascular coagulopathy (DIC; thrombocytopenia, low fibrinogen levels, elevated fibrin split

products, elevated D-dimer), and coagulopathy (elevated

prothrombin time/partial thromboplastin time).

..... Imaging

A noncontrast computed tomography (CT) scan of the

brain should be performed on patients presenting with

AMS. In heat stroke, the CT is normal. Electrocardiogram

should be performed on all patients with heat exhaustion

and heat stroke to evaluate for signs of ischemia or electrolyte abnormalities.

MEDICAL DECISION MAKING

When a patient presents with a potential heat-related ill ­

ness, first priorities include airway, breathing, and circulation (ABCs) and vital signs with temperature (Figure 63-1).

Eliminating other causes for the patient's symptoms is also

important. Differential diagnosis should include meningitis, sepsis, thyroid storm, drug intoxication (PCP, amphetamines, cocaine), cerebral hemorrhage, and status

epilepticus. Neuroleptic malignant syndrome and sero ­

tonin syndrome should both be considered in any patient

taking psychiatric medications. Malignant hyperthermia,

although usually occurring in the context of inhalational

anesthetic or succinylcholine use, should be considered if

symptoms develop in a patient with a previous or family

history of this condition. Vigorous exercise may precipitate

this condition in susceptible individuals.

TREATMENT

Once other diagnoses are excluded, heat exhaustion is the

presumed diagnosis if the patient has normal mental status. Rehydration with either oral or intravenous (N) fluids

is appropriate. Consider oral volume replacement with an

electrolyte-containing solution if the symptoms are mild.

If there is any concern for potential complications from

comorbid conditions, N therapy and laboratory studies

should be instituted. In both cases, treat the patient with

ambient cooling, removal of heavy clothing, and rest .

After eliminating other potential differential diagnoses,

the diagnosis of heat stroke can be made when the patient

with suspected heat illness has an elevated temperature

(>40°C or 1 04°F) and AMS. Begin treatment immediately

with N volume and electrolyte replacement. Start with

250-500 mL of normal saline and replace other electrolytes

based on laboratory values. Be careful not to fluid-overload

older patients or those with cardiac problems .

Evaporative cooling should begin as soon as all life threats

have been assessed and ABCs are secure. Completely expose

the patient and mist with tepid water while a fan is blowing on

him or her. Specially made cool mist fans are highly effective,

but not available in most facilities. Alternatively, a spray bottle

and a box fan are sufficient to lower the patient's temperature.

The patient's core body temperature must be monitored fre ­

quently. A Foley catheter device that provides continuous

temperature evaluation or rectal temperatures recorded every

10 minutes is ideal. Patients may shiver during c ooling, which

is counterproductive by producing heat. Treat shivering with

low-dose benzodiazepines (lorazepaml mg N). When the

patient's temperature reaches 40°C or 104°F, all active cooling

measures should be discontinued. Continuing at lower t emperature can cause overshoot hypothermia. Search for complications from heat stroke such as cardiac ischemia, hepatic

and renal failure, 

 

cardial instability and/or cardiac arrest require active core

rewarming. Available modalities include warmed isotonic

saline (40°C) lavage of the stomach (only if intubated),

HYPOTHERMIA

n�����:�--------:--'��

......._.,.___,f-_.;

f

Figure 61-1. ECG demonstrating Osborn J waves (arrow) in a hypothermic patient.

Shivering

mechanisms intact,

no significant

comorbidities

Impaired

thermogenesis or

significant comorbid

ill ness

rewarming

Admission to

telemetry bed

.6. Figure 61-2. Hypothermia diag nostic algorithm.

CHAPTER 61

bladder, and colon. Peritoneal and pleural irrigation can also

be performed after the insertion of percutaneous catheters.

Emergent thoracotomy with internal cardiac massage and

mediastinal irrigation with warmed saline is a very invasive

technique, but has been used successfully in severely

hypothermic patients with prolonged cardiac arrest. When

available, extracorporeal rewarming with cardiopulmonary

bypass remains the most rapid way (>9°C/hr) to rewarm a

patient with severe symptomatic hypothermia.

Patients with ventricular fibrillation and core temperatures <30°C are often resistant to defibrillation. If the initial

attempt at defibrillation is unsuccessful, begin cardiopulmonary resuscitation and actively rewarm the patient to at least

30°C before reattempting. Standard Advance Cardiac Life

Support medications (eg, atropine, lidocaine, arniodarone)

are typically ineffective for the management of hypothermiainduced dysrhythrnias. Remember that a patient should not

be pronounced dead until first rewarmed to 32°C.

DISPOSITION

� Admission

Most patients with moderate and severe hypothermia

require hospital admission for active rewarming and continued investigation into the etiology of hypothermia if

not clearly environmental. Admit all patients with evidence

of cardiac instability and those undergoing active core

rewarming to an intensive care unit setting.

� Discharge

Patients without serious comorbidities who present with

mild to moderate hypothermia and successfully undergo

passive rewarming can be safely discharged, provided there

is a warm environment for them to go. To prevent recurrent cold exposure, obtain social work consultation to

arrange placement for undomiciled patients and admit to

the hospital if unsuccessful.

SUGGESTED READING

Bessen HA. Hypothermia. In: Tintinalli JE, Stapczynski JS,

Ma OJ, Cline DM, Cydulka RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th ed.

New York, NY: McGraw-Hill, 201 1, pp. 1231-1234.

Jurkovich GJ. Environment cold-induced injury. Surg Clin North

Am. 2007;87:247-267.

U1rich AS, Rathlev NK. Hypothermia and localized c old injuries.

Emerg Med Clin North Am. 2004;22:28 1-298.

Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E.

Lavonas EJ, Jeejeebhoy FM, Gabrielli. Part 12: Cardiac Arrest in

Special Situations: 20 10 American Heart Association Guidelines

for Cardiopulmonary Resuscitation and Emergency

Cardiovascular Care. Circulation. 2010;122:S829-S861.

Wira CR, Becker JU, Martin G, Donnino MW. Anti-arrhythmic

and vasopressor medications for the treatment of ventricular

fibrillation in severe hypothermia: A systematic review of the

literature. Resuscitation. 2008;78:2 1-29.

Cold-Induced

Tissue Inj u ries

Christine R. Stehman, MD

Key Points

• Address hypothermia, dehydration, and any alternative life threats before focusing on cold-ind uced tissue

injuries.

• When in doubt, treat all cold-induced tissue injuries as

frostbite.

INTRODUCTION

Previously the domain of military physicians, the prevalence

of cold-induced tissue injuries in the civilian population has

increased substantially over the past 20 years as a result of

the growth of homelessness and an expanding interest in

cold weather outdoor activities such as skiing and mountain

climbing. Cold-induced tissue injuries are typically divided

into 2 categories: nonfreezing cold injuries (NFCI) and

frostbite. Examples of NFCis include frostnip, chilblains/

pernio, and immersion/trench foot. Of the 2 types of injury,

frostbite is the more devastating and requires more aggressive treatment. That said, chilblains and immersion foot can

also progress to significant disability and require prompt

recognition and intervention.

Although individuals at the extremes of age are at a

higher risk for cold-induced tissue injuries, frostbite is

fairly uncommon in these cohorts. In fact, adults aged

30-49 are the most likely group to suffer frostbite. The

hands and feet account for more than 90% of all reported

frostbite injuries, whereas almost all NFCis involve the feet.

Other areas of the body at risk for cold-induced tissue

injury include the face (eg, nose, ears), buttocks and

perineum, and penis.

There are 3 major categories of risk factors for coldinduced tissue injury. Behavioral risk factors include

• Rewarm frostbitten extremities rapidly in a warm water

bath (4D-42°C) and nonfreezing injuries slowly in a dry

environment.

• Do not discharge patients with cold-induced tissue injuries

without first ensuring they have a warm, dry place to go.

homelessness, inadequate clothing or shelter, alcohol or

drug use/intoxication, and psychiatric illness. Physiologic

risk factors include comorbid diseases that impair distal

circulation ( eg, diabetes, vasculitis), the use of vasoconstric ­