allergic emergencies and anaphylaxis how to avoid getting stung.pdf

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2/20Emergency Medicine Practice 2 April 2000

reactions are usually responses to inhaled antigens,

particularly house dust mites. However, allergies are

also responsible for at least 400-800 deaths in the

United States each year.4,5Recent studies suggest that

there may be 30 cases of anaphylaxis per year per

100,000 individuals.6 In northern climates, anaphylaxis

is most common in the summer months, reflecting the

impact of insect stings.

Pathophysiology: A Simple Primer

Allergic reactions are developed hypersensitivities to

antigens.Antigens are proteins recognized by the

human host as foreign. Alternatively, haptensare

incomplete antigens incapable of causing allergic

reactions, but which become antigenic when bound to

certain proteins. Allergies develop by recurrent

exposure to antigens over time. There is a strong

familial tendency toward atopic disorders linked

to a histocompatibility locus on chromosome 11. 7,8

However, the precise mechanisms that prompt the

immune system to identify antigens as foreign are

not well understood.

The Immune ResponseClassical allergy, also termed immediate hypersensitivity,

is an immune-mediated reaction. The classification

system proposed by Gell and Coombs distills this

complex response into four categories. (SeeTable 1.)

With hypersensitivity, antigen-processing cells (i.e.,

macrophages and other cell types) recognize some

allergens as foreign. They release cytokines and other

mediators to transform B-lymphocytes into plasma

cells, which in turn produce antigen-specific immuno-

globulin.9Antibodies of the IgE class and IgG 4subclass

are most important in the pathogenesis of allergy.10,11T

helper and suppressor cells modulate the production of

these antibodies. (See Figure 1.)

IgE antibodies bind to the cell membranes of

receptor cells, mainly mast cells and basophils. There,they lie in wait for antigens. When subsequent antigen

contact occurs, these receptors are activated via adenyl

cyclase inhibition, calcium channel stimulation, and

other mechanisms. In response, the cells release

preformed mediators as well as producing secondary

agents.12These include such substances as histamine,

leukotriene C4, prostaglandin D2, and tryptase.

Stimulation of the production and release of

inflammatory mediators may bypass the IgE-mediated

pathways. For example, anaphylactoid reactionsrelease

Table 1. Classification Of Immunologic Reactions(Gell And Coombs).

Type Mediator Reaction

I IgE (Rarely IgG4) Immediate

II IgG, IgM (Cell-Ag) Cytotoxic

III Ag-Ab complexes Immune complex

IV T cells Cell-mediated

Note: This classification is an oversimplication.

Adapted from: Middleton E Jr., et al. Allergy: Principles and Practice.St. Louis: Mosby; 1998.

Figure 1. Sensitization Phase Of Allergy (Antigen-Induced Immune Stimulation).

(Genetic predisposition)

T suppressor cells

Cytokinesproduced

Antigen-specific IgE Plasma cells

B cells activatedT helper cells activated

Antigen Processing Cell(macrophage and others)

Allergen


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Urticaria is both the mildest and most common

type of systemic allergic reaction. Also termed hives,

urticaria presents as well-circumscribed, pruritic

wheals involving the superficial dermis. Urticaria

occurs in up to 20% of people during their lifetimes,

and is termed acute if it lasts less than six weeks.15

Angioedema involves the deeper layers of the

skin, including subcutaneous tissue, and presents as

well-demarcated localized edema. The skin, gas-

trointestinal tract, and upper airway are most com-monly involved. Respiratory tract angioedema is

potentially fatal. Hereditary angioedema (HAE) is an

autosomal dominant condition caused by lack of a

functional C1 esterase inhibitor.16The facial, airway, or

extremity edema is often associated with abdominal

pain, nausea, vomiting, and diarrhea.

Anaphylaxis is a clinical syndrome characterized

by a severe reaction of multiple organ systems to an

antigen-induced, IgE-driven mediator release in

previously sensitized individuals. Hypotension,

bronchoconstriction, and severe upper airway obstruc-

tion are presenting components of anaphylaxis.

Individuals with anaphylaxis may have one, two, or all

of these conditions. (SeeTable 3.)

Causes Of Hypersensitivity Reactions

Table 4 presents a list of some causes of hypersensitiv-

Mast Celland

Basophil

Classic Allergic Reaction Late-Phase Reaction

Flushing Eosinophil infiltration

Hypotension Neutrophil infiltration

Increased mucus production Fibrin deposition

Pruritis Mononuclear infiltration

Smooth muscle contraction Tissue destruction

Vascular leakage

Minutes Hours

Figure 3. Time Course Of Allergic Reaction. Table 2. HypersensitivityReactions.

Hypersensitivity reactions canbe of varied severity, depend-

ing upon:

Degrees of hypersensitivity Specific IgE concentration

Allergen affinity

Number of mast cellsand basophils

Quantity, route, and rate ofantigen exposure

Pattern and quantity ofmediator release

Target organ sensitivityand responsiveness

Table 4. Causes Of Hypersensitivity Reactions.*

IgE Mediated

Drugs (e.g., antimicrobials, nonsteroidals)

Food (e.g., peanuts, tree nuts, fish, shellfish, eggs, certain

fresh fruits)

Environmental (e.g., house dust mites, pollens, molds, otherinhaled proteins)

Soaps, lotions, detergents

Envenomations (e.g., Hymenoptera)

Snake antivenin

Latex

Miscellaneous: cold, light, vibration, pressure, exercise

Non-immunologic Causes

Drugs (e.g., narcotics, neomycin, d-tubocurare, salicylates,nonsteroidals)

Radiocontrast agents

*This list is not intended to be all-inclusive.

Table 3. Frequency Of Occurrence Of SignsAnd Symptoms Of Anaphylaxis.

Signs/Symptoms Percent

Urticaria and angioedema 88%

Dyspnea, wheeze 47%

Dizziness, syncope, hypotension 33%

Nausea, vomiting, diarrhea, cramping abdominal pain 30%

Flush 46%

Upper airway edema 56%

Headache 15%

Rhinitis 16%

Substernal pain 6%

Itch without rash 4.5%

Seizure 1.5%



5/205 Emergency Medicine PracticeApril 2000

ity reactions. A wide variety of allergens is responsible

for anaphylaxis; some are widespread, such as peanuts

or shellfish, while others are sporadic, including

reactions to vaccines or even semen. The most common

precipitants in children include foods (57%), drugs

(11%), Hymenoptera venom (12%), exercise (9%),

idiopathic (6%), vaccines (2%), additives (1%), specific

immunotherapy (1%), and latex (1%).17

EnvenomationsThere are slightly fewer than 100 cases of sting-related

deaths in the United States each year. Hymenoptera

(e.g., wasps, bees, and fire ants) venom precipitates

serious systemic reactions in 1-3% of patients.18 Once a

patient has a severe systemic reaction from a Hy-

menoptera sting, up to 35-60% will experience anaphy-

laxis to a subsequent sting.19,20Other arthropods

besides Hymenoptera can cause anaphylaxis, including

the kissing bug and a variety of ticks.

Drugs And MedicationsWhile numerous medications can cause allergic

reactions, the most important drug allergy involves

penicillin. Penicillin is responsible for three-quarters of

all deaths from drug-related anaphylaxis. Fatal

anaphylaxis occurs approximately once per 7,500,000

exposures, leading to approximately 100 deaths each

year in the United States.21Parenteral (IM or IV)

penicillin is much more likely to produce anaphylaxis

than orally administered drugs. In fact, only six

fatalities have ever been reported with oral penicillin.22

While penicillin allergy may be more frequent in

people with atopy, a family history of penicillin allergy

does not predict individual sensitivity.

Not all adverse reactions patients experience in

regards to the beta-lactam drugs are allergic in nature.

In particular, most children who develop erythematous

rashes associated with amoxicillin are able to tolerate

beta-lactams and even amoxicillin without problems in

10 Allergy Pearls

1. Hypoxia k ills. Hoarseness or stridor should prompt

immediate concern about a severe hypersensitivity

reaction. Use epinephrine and supplemental oxygen

in this setting and determine the need for intubation.

2. Treat shock. Give small, repeated aliquots of IV

epinephrine to patients in shock. Subcutaneousepinephrine is inadequate.

3. Recognize limits. Antihistamines and steroids may

not be effective in managing acute angioedema.

4. Whos in tr ouble? Voice change, hoarseness, stridor,

and dyspnea suggest the need for airway control in

patients with angioedema. Palatal edema is an

ominous sign in all allergic reactions.

5. Its a famil y affair. Hereditary angioedema presents

with recurrent extremity, gastrointestinal, and upper-airway edema without urticaria. A family history of

similar problems is an important hint. Treat hereditary

angioedema with fresh frozen plasma.

6. Around the blo ck. Patients with allergic reactions

who are on beta-blockers may not respond to

standard therapy. Remember glucagon for serious

hypersensitivity, as well as inhalational ipratroprium if

bronchospasm predominates.

7. Prevention. Prevention of further allergic reactions is

key. Referral for immunotherapy is important for

systemic hypersensitivity reactions to Hymenoptera

stings, including bees, wasps, and fire ants.

Recognition of the precipitating agent or event

requires a careful historythen educate the patient

on future avoidance.

8. Self-stimulation. Epinephrine self-injectable

syringes save lives if patients have serious allergic

reactions outside the hospital. Give a prescription for

several, so the patient can store them in different

placeshome, car, work, and so on. Teach the patient

how and when to use it.

9. Allergy is an acquir ed disorder. Patients who

state or think they cannot be allergic to something

because they have taken it before without problems

often are making a critical mistake. Patientsmay develop angioedema after discontinuing an

ACE inhibitor.

10. Be suspicious . Remember to include anaphylaxis

in the differential diagnosis of shock. Hypotension

with isolated difficulty breathing, chest pain,

back pain, and subtle angioedema often are not

recognized as early anaphylaxis. Delays in

diagnosis can be fatal.



the future.23In one study of 86 consecutive children

with antibiotic use for upper respiratory infection who

developed a rash, 80% were younger than 3 years of

age. Most (85%) had nonspecific erythematous rash,

but 15% had an urticarial rash. When these patients

were re-challenged with the suspected antibiotics

while healthy, none developed rash.24

A particularly interesting reaction to procaine

penicillin is Hoignes syndrome. This dramatic but

non-allergic phenomenon is an idiosyncratic responseto procaine (Bicillin C-R, Wycillin) characterized

by psychosis, anxiety, hallucinations, hypertension,

and tachycardia.25Patients who suffer this effect

do not need to avoid beta-lactams in the future

(only procaine).

Penicillin Allergy And Cephalosporin Use

Penicillin allergy is an absolute contraindication to

cephalosporin use only if severe angioedema or

anaphylaxis occurs with penicillin. Estimates of cross-

sensitivity of cephalosporins and penicillins vary

widely, ranging from 2% to 16%.26However, even in

patients with a stated penicillin allergy, true anaphy-

laxis to cephalosporins is extremely rare (< 0.02%).27

In fact, cross-reactions appear limited to patients given

first-generation cephalosporins; studies of second-

and third-generation cephalosporins show no increase

in allergic reactions in patients who have a history

of penicillin allergy.27In addition, penicillin skin

tests do not predict the likelihood of allergic reactions

to cephalosporins in patients with histories of penicil-

lin allergy.

Aspirin And Nonsteroidal Anti-inflammatory Drugs

Certain agents precipitate hypersensitivity reactions byaltering arachidonic acid metabolism (e.g., salicylates

and nonsteroidals). These drugs inhibit the degrada-

tion of arachidonic acid by cyclooxygenase, allowing

production of more inflammatory allergic mediators

through an alternate lipoxygenase pathway. The new

cyclooxygenase II inhibitors appear to avoid this

biochemical problem.

Aspirin and older NSAIDs remain an important

cause of serious allergic reactions. These drugs may

precipitate bronchospasm in as many as 20% of

asthmatic patients.28A history of nasal polyps may

increase the likelihood of an allergic reaction.

Illicit DrugsA substantial number of hypersensitivity reactions are

non-immunologic and precipitated through direct

mediator release from effector cells.29 For example,

injecting opiates into an upper-extremity vein may

cause swelling and erythema in that arm. Smoking

crack cocaine can produce a pulmonary syndrome of

crack lung,characterized by fever, eosinophilia, and

pulmonary infiltrates.30

LatexTwo-thirds of latex reactions are mild and local (e.g.,

hand erythema and itching), but some patients develop

fatal anaphylaxis.31Latex sensitization has been

reported in about 2.6% of nurses, 9% of surgeons, and

29% of spina bifida patients. In one study of dental

students, 10% developed some form of latex sensitivity

by the end of their four years of training.32 Children

with spina bifida can have such frequent and striking

hypersensitivity reactions to latex that a joint councilsuggests that they have all medical, surgical, and

dental procedures performed in a latex-controlled

environment regardless of a history of latex allergy.33

Radiocontrast MediaAs with latex and medication allergies, anaphylaxis

due to radiocontrast media is an important iatrogenic

affliction. While the vast majority of these reactions

are not immunologic in nature, a few patients may

have an IgE-mediated component to radiocontrast

allergy.34 One to two percent of patients exposed to

these agents suffer an anaphylactoid reaction, with

fatal results in 1 per 50,000-100,000.35This adds up to

an estimated 2667 reactions with 500 deaths annually

in the United States.36

Risk factors for radiocontrast reactions include

previous allergic reactions to these agents (35%

recurrence rate), history of atopy, shellfish allergy,

increased age, dehydration, renal or hepatic dysfunc-

tion, and cardiac disease. Other considerations

involve dye factors such as dose, osmolality, or ionic

content.37A history of asthma or use of beta-blockers

may be among the strongest predictors of a contrast-

associated reaction.38

Methods of risk reduction for radiocontrastreactions include using another imaging technique that

does not involve these agents, using nonionic low-

osmolality agents, and pre-treating 12-24 hours prior to

dye load.39Administering diphenhydramine 1 mg/kg

every six hours and prednisone 1 mg/kg over that

period reduces the reaction rate to radiocontrast media

to under 5% for patients with previous reactions.40One

study demonstrated a very low reaction rate if low-

osmolality, non-ionic agents were used.41However, the

costs associated with these more expensive imaging

dyes are substantial.41

Food AllergiesFood allergies are the predominant cause of anaphy-

laxis seen in the ED.42While food allergy occurs in

about 1.4% of young children and 0.3% of adults, most

reactions are minor.43

Anaphylactic reactions to foods usually occur

immediately after the food is ingested.44Of interest, as

many as one-third of patients with food allergy

demonstrate a biphasic reaction. Many can experience

prolonged symptoms, lasting as long as several



weeks.45Some food allergies occur only when particu-

lar food is followed by exercise.46In addition to

causing urticaria or respiratory symptoms, food

allergens frequently precipitate a gastrointestinal

insurrection. Patients typically complain of nausea,

vomiting, abdominal cramping, and/or diarrhea.

Some food hypersensitivity reactions are due to

agents added during food production (e.g., penicillins

and sulfites). A limited number of foods are respon-

sible for the vast majority of food-induced allergicreactions. In children, the culprits include milk, eggs,

peanuts, fish, and tree nuts; in adults, prime offenders

consist of peanuts, tree nuts, fish, and shellfish.47As

the American palate expands toward the gourmet,

emergency physicians are seeing reactions to new

foods, such as kiwi-chamomile tea. Peanut allergies are

both common and severe, leading some airlines to stop

serving this staple as the in-flight snack. Of all aller-

gies, however, some consider beer anaphylaxis to be

the most tragic.48

There are several interesting non-allergic food

reactions known collectively as the restaurant syn-

dromes.The Chinese restaurant syndrome is a

reaction to MSG that consists of chest pain, facial

burning, flushing, paresthesias, sweating, dizziness,

headaches, palpitations, nausea, and vomiting. Symp-

toms usually begin during or shortly after the meal but

can be delayed for up to 14 hours.49

Scombroid poisoning occurs after eating spoiled

fish, usually tuna, mackerel, or mahi-mahi (dolphin).

Symptoms include flushing (usually a sunburn-type

rash), urticaria, headache, nausea, vomiting, and

abdominal cramping.50This reaction due to

histamine-like toxins can be treated with diphenhy-

dramine or cimetidine.

Exercise

Other poorly understood mechanisms cause directmediator release from allergy effector cells. Exercise-

induced allergy is usually limited to urticaria and nasal

congestion, but some reactions are fatal.39More than

50% of patients with exercise-induced reactions have

atopy, and more than half of those with exercise-

induced anaphylaxis develop the syndrome only if

they ate just prior to marked exertion.51Prevention

includes modifying the exercise activity, avoiding

high-risk foods within four hours of exercise, and

prophylaxis with antihistamines and leukotriene-

receptor antagonists.

Diagnosis Of Hypersensitivity Reactions

The diagnosis of an allergic reaction often depends

upon the patient drawing a connection between an

exposure and subsequent hives or wheezing. However,

making the correct diagnosis is complicated when

Table 5. Diagnosis Of Hypersensitivity Reactions.

History

Precipitating event:Medications, including OTCs (especially NSAIDs)

Foods (peanuts, nuts, fresh fruits, fish, shellfish,eggs, milk)

Environmental exposures

Physical agents/events

Previous episodes:

Frequency

Duration

Effects of treatment

Physical Exam

Vital signs

Skin

Urticaria

Angioedema

Upper respiratory tract

Rhinitis

Oral and laryngeal edema

Lower respiratory tract

Bronchospasm

Increased secretions

Cardiovascular

Hypotension

Tachycardia (rarely bradycardia)

Dysrhythmias

Cardiac arrest

Gastrointestinal tract

Abdominal colic

Vomiting (nausea)

Diarrhea

Central nervous system

Confusion

Agitation

Coma

Eyes

Conjunctivitis

Chemosis



chest discomfort, back pain, or vascular collapse occurs

in isolation, especially if the patient is confused or

moribund. Serious allergic reactions may occasionally

be confused with vasovagal episodes after an injection,

sting, or other exposures.

Although identifying the etiology often depends

on an appropriate history, a physical exam demonstrat-

ing urticaria, angioedema, bronchospasm, or vascular

collapse provides a compelling diagnostic picture.

(SeeTable 5.) Occasionally, therapeutic intervention

must be based on the physical findings alone; clinical

improvement with therapy may be the best and only

diagnostic confirmation.

HistoryThe single most important question to ask of a

patient with an allergic reaction is How is your

breathing?The inability to answer this question

speaks volumes. Syncope and dyspnea are the most

acutely worrisome complaints during an allergic

reaction. Other symptoms with dangerous overtones

include hoarseness, a lumpin the throat, chest pain,or trouble swallowing.

The next priority is to determine the time course of

the reaction. Most people likely to die of anaphylaxis

have dramatic progression of symptoms. Severe

reactions are characterized by shortness of breath,

syncope, or lightheadedness within 30 minutes of

exposure. The more rapid the progression of symp-

toms, the greater the need for emergency intervention.

Many patients with allergic reactions complain of

generalized pruritus in addition to real or imagined

swelling of various body parts. Gastrointestinal

symptoms are frequent, and may include crampy

abdominal pain, nausea, vomiting, and diarrhea. Yet,while skin and respiratory complaints are common,

some patients with severe allergic reactions may have

no pruritus or dyspnea. Anaphylaxis can produce

isolated cardiovascular collapse.52

Identifying The Agent

Clearly, the physician would like to identify the

inciting agent. Recognizing the precipitant (seeTable 4)

of a hypersensitivity reaction can prevent or ameliorate

subsequent episodes by avoidance or possibly immu-

notherapy. Patients who believe they have had an

allergic reaction are eager to provide a variety of

theories as to the possible allergen. Unfortunately,because the tempo of allergic reactions is so var iable,

the assumed connection between an exposure and a

reaction may be misleading. Certainly, a list of medica-

tions and new environmental exposures (soaps,

perfumes, foods, and so on) is helpful. A careful

inventory must include over-the-counter (OTC)

medications, which many patients fail to recall unless

prompted. It is important to realize that anyone may

become sensi tized to almost anything, even after

decades of tolerance. The fact that they never had a

reaction to shellfish in the past does not eliminate

shellfish from the list of current suspects.

Past Medical And Family History

Past medical history is important, particularly the

history of prior allergic reactions. If the patient re-

counts a distant history of sulfa allergy, this may

incriminate a current drug such as Silvadene cream.

Family history of drug allergies is less significant. The

fact that the patient has a family history of penicillin

allergy may increase the possibility of multiple drug

allergies, but not necessarily penicillin.53

Physical Exam inat ion

The physical exam in hypersensitivity reactions should

initially focus on the immediate life threatslaryn-

gospasm and hypotension.

Airway

Evaluate the patient for stridor, drooling, and signs of

respiratory distress. The patient in extremis may be

bolt upright, strap muscles bulging, and ribs retracting.An inability to speak, muffled voice, or hoarseness

may reflect the need for urgent intubation. Ask the

patient to open his or her mouth, if he or she is able.

Palatal edema is an important sign that may presage

laryngeal edema. Upper airway edema is present on

autopsy in about 60% of fatal cases.54Visualization of

the cords with a fiberoptic scope or ENT mirror may be

helpful in some cases if suspicion for laryngeal edema

is high despite a normal palate. Upper respiratory

findings in allergic reactions include rhinitis and

laryngeal edema.

Some patients with psychological problems

present with factitious stridor, known asMunchausensstridor. These patients intentionally adduct their vocal

cords and can appear to be in profound respiratory

distress. Indirect laryngoscopy can reveal the non-

anatomic nature of the stridor. Or more simply, ask the

patient to cough during the acute episode, which may

cause the stridor to disappear for a brief period.55

Breathing

The patient with laryngospasm may demonstrate a

paradoxical torso movement, with sternal collapse

accompanied by abdominal distention on inspiration.

Tachypnea may represent bronchospasm or can be due

to increased metabolic demand. Bronchospasm withincreased airway secretions reflects lower airway

involvement. Wheezing is frequent in severe reactions,

and should be distinguished from stridor, which is a

more ominous sign. Stridor tends to be loudest over

the larynx or sternal notch, while wheezing is more

prominent in the lateral fields.

Circulation

Severe hypersensitivity reactions may present with

circulatory collapse, hypoperfusion, and tachycardia.



However, the moribund patient may be bradycardic,

and dysrhythmias are seen in some cases. Quickly

determine the presence of shock by evaluating pulses,

skin perfusion, and mental status.

Skin And M ucous Membra nes

The most typical manifestations in allergy are found by

carefully evaluating the skin and upper respiratory

tract. Isolated urticaria or angioedema may be early

signs of a serious allergic reaction, especially if it

involves the lips, tongue, or palate. Detection of

urticaria may require palpation in dark-skinned

patients. Some patients with urticaria demonstrate an

unusual skin reaction called dermatographism.

Drawing on their back with a finger will cause the skin

to develop wheals in the stimulated area. Acute

conjunctival hyperemia and swelling of the sclera

(chemosis) also suggests an allergic reaction. (SeeTable

5.) Angioedema may be difficult to recognize in its

early stages, and the patient or family may be most

helpful with confirming early changes.

Laboratory EvaluationThe laboratory evaluation of allergic reactions in the

ED has limited utility. Define the level of oxygenation,

realizing that hypoperfusion may limit the ability of

pulse oximetry to accurately report oxygen saturation.

Consequently, arterial blood gas (ABG) analysis may

be more useful than pulse oximetry in anaphylactic

shock. Metabolic acidosis is common in severe anaphy-

laxis.56Other laboratory tests available to the emer-

gency physician are not useful in the initial evaluation

of hypersensitivity reactions but may be used to

eliminate alternate diagnoses.

While the emergency physician is concerned with

stabilizing the patient, a future consulting physician

will likely be concerned with the etiology of the

patients reaction. Allergists believe that tests which

confirm an event as allergic can have future utility.

Serum histamine peaks early and transiently, and for

this reason is unlikely to be helpful. Serum tryptase

levels, however, peak 1 to 1.5 hours after the onset of

anaphylaxis and remain elevated far longer than

Table 6. Differential Diagnosis Of Anaphylaxis And Anaphylactoid Reactions.

Physical factors

Exercise

Cold, heat, sunlight

Airway disease

Reactive airway disease

Epiglottitis

Foreign body

Pulmonary embolism

Cardiovascular disease

Dysrhythmias

Myocardial ischemia

Capillary leak syndrome

Flush syndromes

Carcinoid

Postmenopausal

Chlorpropamidealcohol

Medullary carcinoma thyroid

Restaurant syndromes

Monosodium glutamate (MSG)

Scombroid poisoning

Sulfites

Shock

Hemorrhagic

Cardiogenic

Endotoxic

Excess endogenous production of histamine

Systemic mastocytosis

Urticaria pigmentosa

Leukemias

Psychiatric disease

Panic attacks

Munchausens stridor

Neurologic

Vasovagal syncope

Seizure

Stroke

Drug reaction

Red man syndrome (vancomycin)

Reaction to anti-seizure medication

Miscellaneous

Hereditary angioedemaProgesteroneanaphylaxis

Urticarial vasculitis

Pheochromocytoma

Hyperimmunoglobulin E, urticaria syndrome




plasma histamine. Elevated tryptase levels persist

for five hours after the onset of symptoms.57However,

the utility of this test for emergency management

remains unknown.58

Differential Diagnosis

A number of disorders mimic allergic reactions. (See

Table 6.) Necrotizing vasculitis, erythema multiforme,

and serum sickness may cause urticaria. Cutaneousmastocytosis is a rare disorder that causes reddish-

brown macules and papules that develop urticar ia and

itching if traumatized. Systemic mastocytosis is

another rare disorder that causes episodic flushing

with or without urticaria.

Angioedema is most commonly allergy-mediated,

but it also may occur in its acquired and hereditary

forms. Hereditary angioedema is due to a deficiency of

C1esterase inhibitors. Hereditary angioedema is

suggested by a family history (i.e., autosomal domi-

nant inheritance), absence of urticaria and itching,

prominence of recurrent self-limited attacks of circum-

cised subepithelial edema of the skin, and involvement

of the gastrointestinal tract (e.g., abdominal colic) and

upper respiratory tract (e.g., airway angioedema).59

It is usually a clinical diagnosis, because the definitive

test, a functional assay of C1esterase inhibitor, is

not rapidly available. Recognizing hereditary an-

gioedema is very important because it is not respon-

sive to epinephrine, antihistamines, or corticosteroids.

Fresh frozen plasma infusion will abolish acute

episodes, and danazol reduces attack frequency.

Acquired angioedema may occur with some

lymphoproliferative disorders.

Angiotensin-converting enzyme (ACE) inhibitors

may produce angioedema, predominantly of the upper

airway. This idiosyncratic reaction may begin soon

after starting the medication or suddenly arise after

years of symptomless use. This disorder responds

poorly to standard allergic therapy and is mainly due

to unmetabolized kinins.60 Aggressive airway manage-

ment is particularly important because serious upper

airway angioedema may threaten the ability to breathe.

Occasionally, urticaria and angioedema must be

differentiated from contact sensitivity, which is a

localized, vesicular eruption progressing to chronic

skin thickening with continued allergen exposure.

Atopic dermatitis occasionally mimics hypersensitivity

reactions.61 The lack of abrupt-onset or migratory

patterns common with typical urticaria may signify a

non-allergic disorder.

Treatment Of Allergic Reactions

The major causes of death from hypersensitivity

reactions are respiratory failure and circulatory

collapse. Consequently, identify and treat shock and

respiratory insufficiency. Patients with severe reactions

need emergent resuscitation and require a team

approach. Monitoring should include ECG leads, pulse

oximetry, and serial automated blood pressure mea-

surements. Invasive hemodynamic and urine output

monitoring are important in severe hypersensitivity

reactions, particularly in the elderly and those with

significant concomitant medical problems.

AirwayThe most immediate threat to life in an allergic

reaction is upper airway obstruction. If the patient

is not profoundly hypotensive, allow him or her to

Cost-Effective Strategies In DealingWith Acute Allergic Reactions And Angioedema

1. Do not order radiographs or laboratory tests in most

patients with acute allergic reactions.

Laboratory tests (e.g., CBC and electrolytes) are

not usually indicated in patients with acute

allergic reactions.

Risk M anag ement Caveat : Laboratory tests may be useful

in diagnosing maladies that mimic allergic reactions.

For example, shortness of breath may be due to cardiac

ischemia or acute anemia, in which case an ECG or stat

hemoglobin may be helpful.

2. Do not order chest x-rays in patients with acute

allergic reactions and mild respiratory distress.

In many cases, respiratory distress in mild allergic

reactions is due to bronchospasm. This can be treated

effectively with nebulized beta-adrenergic agonists.

Risk M anag ement Caveat : A chest radiograph may be

used to exclude pneumonia and pneumothorax in

patients with atypical presentations for allergy.

3. Use less expensive, generic medications.

Many patients can be treated effectively with generic

diphenhydramine and cimetidine, rather than more

expensive H1and H

2antihistamines. In fact, most of the

studies regarding H1and H

2blockers in allergy were

done using diphenhydramine and cimetidine.



sit upright and make best use of his or her respiratory

mechanics. All dyspneic patients require 100%

oxygen by face mask. Heliox may improve

ventilation in severe airway compromise

by reducing airway turbulence.

Some patients may require urgent or emergent

intubation; however, massive swelling of the tongue

or upper airway may pose a nightmarish scenario

for the emergency physician. Orotracheal intubation

is usually preferred to the nasotracheal route because

mucosal edema may limit success and cause bleeding

during the latter approach. If time permits, look at

the back of the patients throat. If you are unable to

see the entirety of the soft palate, the intubation will

be challenging.62

Rapid-sequence intubation (RSI) is the most

commonly employed approach to emergency intuba-

tion. However, it may create special problems in the

patient with pronounced airway edema. If a breathing

patient is given paralytics but is unable to be intubated

secondary to distorted anatomy associated with

anaphylaxis, upper airway obstruction may render thebag valve mask useless. There are several alternatives

to RSI in the patient with airway edema. Awake

intubation is often suggested. If time permits, such

patients may be pretreated with nebulized lidocaine to

anesthetize the airway and with a sedative agent as

indicated. Fiberoptic nasotracheal intubation is another

alternative. The emergency physician may decide to

involve the anesthesiologist in this procedure depend-

ing upon his or her degree of experience with this

technique. If RSI is ultimately chosen for the patient

with airway edema, be prepared to perform an imme-

diate cricothyroidotomy if intubation fails. Being

prepared in this instance involves applying Betadine tothe patients neck and having an opened

cricothyroidotomy tray at the bedside. (Dont let the

patient see the tray, especially if the Betadine on their

neck alarms them.)

Epinephrine is an important adjunct in

patients with upper airway edema, as described

in subsequent sections.

BreathingWhile patients with anaphylaxis certainly demonstrate

wheezing, most profound respiratory distress is due

to upper airway problems rather than bronchospasm.

As with all aspects of anaphylaxis, epinephrine byany route can decrease the bronchospastic component

of this disease. Inhaled epinephrine may be useful

in mitigating both bronchospasm and laryngeal

edema (i.e., 0.5 mL of epinephrine nebulized in 2.5

mL of saline).63

Other inhaled sympathomimetics such as albuterol

and metaproterenol are useful for allergy-induced

bronchospasm. Nebulized ipratropium bromide

(Atrovent) will also ameliorate bronchospasm, particu-

larly in allergy patients on beta-blockers. While often

recommended by older textbooks for allergic broncho-

spasm, there is no empiric evidence for the use of

aminophylline in anaphylaxis.

CirculationAfter airway obstruction, shock is the most likely cause

of death from anaphylaxis. Hypotensive patients

require large-bore IVs and aggressive resuscitation.

Epinephrine is the drug of choice in severe allergic

emergencies. Epinephrine has alpha-agonist activity

that improves vascular tone, and beta activity that

bronchodilates and stimulates the heart. In addition,

epinephrine blocks the release of allergic mediators

through cyclic-AMP stimulation.

There are no absolute contraindications to the use o f

epinephrine in a true anaphylactic emergency. Epinephrine

is safe even for older adults. In one study on asthma,

patients as old as 96 years of age were safely given

three doses of epinephrine. In this study there was no

significant difference in ventricular arrhythmias

between patients younger than 40 vs. those older than

40 years old, and the mean arterial pressure, heart rate,and respiratory rate decreased with treatment in the

older population.64

In mild-to-moderate reactions where peripheral

perfusion is maintained, give epinephrine subcutane-

ously or intramuscularly at 0.01 mg/kg (i.e., 0.1 mL/

kg) up to 0.3 to 0.5 mg (1:1000 solution=1 mg/mL).

Some authorities believe that the IM route is so

safe and effective that the subcutaneous route

should be abandoned.65

The appropriate dose, concentration, and route of

epinephrine delivery in anaphylactic shock have not

been studied. The following recommendations are

based on non-peer-reviewed, published recommenda-tions and the experience of the authors. In more severe

reactions, give 1-5 mL of a 1:10,000 solution (0.1 mg/

mL) intravenously over two to three minutes. Alterna-

tively, one can titrate an epinephrine infusion (1 mg in

250 cc D5W=4 mcg/cc) to symptoms and signs.66 The

low-dose titration method may be most appropriate for

patients at risk for cardiac complications from epi-

nephrine therapy.67Cardiac monitoring is appropriate

for all patients receiving intravenous epinephrine.68

If vascular access cannot be obtained in the

intubated patient, intratracheal dosing using 1-5 mL of

1:10,000 epinephrine can be used. Sublingual injection

of epinephrine is another consideration.

Complications Of Epineph rine

Complications of epinephrine used for allergic reac-

tions are rare. In one case, a patient was given epineph-

rine for a presumed allergic reaction and suffered a

fatal intracranial bleed. The crucial issue here involved

the fact that the patient was not having an allergic

reaction but was in the midst of a hypertensive crisis.

He had a blood pressure of 220/160 mmHg prior to

receiving the drug.69In another case, a 30-year-old man



developed a myocardial infarction after self-adminis-

tering an Epi-Pen for an episode of idiopathic anaphy-

laxis. The patient had numerous risk factors for

coronary artery disease.70All told, there are only a

handful of cases in the English-language literature that

document adverse outcomes when epinephrine is used

to treat allergic reactions.66,68,71

Non-pharmacologic TherapyFluids are an important adjunct in the treatment of

anaphylaxis. Some patients with anaphylactic shock

are unresponsive to epinephrine, possibly due to

secretion of endogenous epinephrine, norepinephrine,

and production of angiotensin II.72,73

Use large volumes of IV crystalloid to resuscitate

severely allergic patients with hypoperfusion. Resusci-

tation may require several liters of isotonic saline or

lactated Ringer s solution to replete the intravascular

space. Avoid hypo-osmolar and dextrose-containing

solutions, which quickly ooze into the extravascular

space from the associated capillary leak syndrome.

The Pneumatic Antishock Garment (PASG)(formerly known as MAST) has been used to treat

shock associated with allergic reactions.74,75However,

this device has not been subject to rigorous study in

patients with anaphylaxis.

Additional InterventionsDecrease Antigen Loa d

If possible, eliminate the antigen or delay its absorp-

tion. (See Clinical Pathway: Treatment Of Allergic

Reactionson page 13.) If the antigenic material was

injected into an extremity, as in the case of an enveno-

mation, some authorities suggest applying a loose

tourniquet to impede lymphatic but not arterial flow.Bees, but not wasps, may leave a stinger in the wound,

attached to a glob of bee parts (the venom sac). If a

stinger is present, remove it by scraping rather than

compression; squeezing the venom sac can inject more

antigen. Local application of ice may delay central

antigen delivery, but it may also cause cold injury to

local tissue.

The utility of decreasing the gastric absorption of

an ingested antigen remains unknown. While the use

of charcoal seems reasonable in this situation, there is

essentially no clinical or laboratory data supporting

its use.

Antihistamines

The use of H1-blocking antihistamines (e.g., diphenhy-

dramine) is standard therapy in patients with allergic

reactions. The dose for mild reactions is usually

diphenhydramine or hydroxyzine 25 to 50 mg given

PO or IM. Oral alternatives with limited sedation are

cetirizine 10 mg or loratadine 10 mg.76,77

Patients with more severe reactions should be

treated with intravenous H1antihistamines. In these

cases, most authorities recommend diphenhydramine

50 to 75 mg IV.

H2blockers (e.g., cimetidine), either alone or in

combination with an H1agent, are also useful in the

treatment of allergic reactions. The best-studied H2antagonist is cimetidine. It is usually given in a 300 mg

dose (PO, IM, or IV). The H2blockers offer a non-

sedating alternative (or addition) to the H1blockers

and seem equally effective.78,79 One study of 93 patients

compared diphenhydramine and cimetidine and found

them both useful in treating acute allergic reactions.78

Runge et al found cimetidine and diphenhydramine

togethermore effective than either alone in treating

acute urticaria in 39 patients.80There are also some

data indicating that cimetidine may be effective when

H1antihistamines are not.81

CorticosteroidsAlthough antihistamines may be sufficient in mild

allergic reactions, they are inadequate if used alone for

severe anaphylaxis. Corticosteroids are useful in most

allergic reactions that require an ED visit. They block

arachidonic acid production through cell membranestabilization; however, this effect may take several

hours. Steroids also attenuate the late-onset component

of hypersensitivity reactions, although the significance

of this component of allergy is unclear. Prednisone is

effective in the outpatient management of acute

urticaria, resolving rash and itching significantly faster

than placebo.82 Although optimal dosing has not been

studied, prednisone 1 mg/kg/d used for three to five

days appears reasonable. This short course does not

require a tapering dose. Consider risks and benefits in

patients with diabetes mellitus or peptic ulcer disease.

Inhaled corticosteroids mitigate allergic effects isolated

to the respiratory tract and may be particularly usefulin allergic rhinitis.83

GlucagonThe patient with a significant hypersensitivity reaction

who is taking beta-blocker drugs poses a special

challenge. These patients often respond poorly to

epinephrine. In case of epinephrine failure, consider

the use of glucagon in these patients. This drug may

also be effective in anyone with anaphylaxis who is

unresponsive to other therapies. Glucagon bypasses

the receptors obstructed by the beta-blockers.84 Its

positive chronotropic and inotropic effects are inde-

pendent of catecholamine receptors, possibly throughstimulation of cAMP synthesis.

The use of glucagon for allergic reactions in

patients taking beta-blockers is based on case reports.85

Since glucagon is short-acting, it may be dosed at 1-2

mg IV every five minutes titrated to symptomatic

improvement. Some patients may require a glucagon

drip at 1-5 mg/h. Common side effects include

hyperglycemia, nausea, and vomiting.

Cont inued on page 14



Clinical Pathway: Treatment Of Allergic Reactions

Allergenexposure PO charcoal

Loose tourniquet if peripheral Stinger removal by scraping

Local SC epinephrine 0.01 mg/kg? Ice?

Urticaria and/or mildangioedema

Bronchospasm

Oral

Sting, bite

Poorresponse

Goodresponse

H1and/or H

2antagonist

PrednisoneRarely epinephrine SC

Inhaled sympathomimetic Inhaled ipratropium (Atrovent)

Ensure adequate oxygenation (Intubate if necessary)

Epinephrine 1:10,000 solution in 1 cc aliquots IV q 2-3 min until

improvedAND/OR 1 mg in 250 cc D

5W, titrate to response

Aggressive IV normal saline or Ringers lactate (2-3 L/h

if hypoperfusion)

Hemodynamic and O2saturation monitoring

H1and/or H

2antagonist

Corticosteroid

Consider glucagonIV, especially if onbeta-blockers

Taper epinephrineand IV fluid

Consider disposition

This cl inical pa thw ay is intended to supplement, rather tha n

subst i tute, professional jud gm ent an d m ay be chang ed

depending upon a pat ient s individu al n eeds. Failure to com ply

wi th this pathw ay does not represent a breach of the standard

of care.

Copyright2000 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants permission to reproduce this

Emergency Medicine Practicetool for institutional use.

Hypersensitivityreaction

Airwayangioedema,

anaphylaxis



Controversies In Practice

Approach To ACE AngioedemaAngioedema is an immunologically mediated, non-IgE

edema that is generally restricted to the soft tissues of

the head and neck. Antihistamines and steroids may

not be effective in managing acute angioedema,86

leaving some patients at risk for upper airway obstruc-

tion. Many emergency physicians wonder, Whenshould these patients be admitted, and how should

their airways be managed?Unfortunately, there are

few data available to answer this question.

Ishoo et al retrospectively studied 93 episodes of

angioedema.87Intubation or tracheostomy was necessary

in nine (9.7%) of the cases. Voice change, hoarseness,

stridor, and dyspnea were significantly associated with

the need for airway control. These authors suggest that

patients with facial rash, facial edema, lip edema, or soft

palate edema may be managed with supportive care and

observation. Alternatively, they suggest that patients with

laryngeal edema or progressing symptoms be admitted

to an ICU setting. In addition to being a retrospective

study based on a relatively small number of patients, the

admission algorithm developed by these authors was not

prospectively validated.

ACE-inhibitor angioedema is not known to be

biphasic; thus, patients who stabilize and improve tend

to do well. It seems reasonable that patients who

present to the ED with lip or tongue swelling and no

respiratory signs or symptoms can be monitored in the

ED to determine whether the condition improves or

worsens over the course of several hours. In one

retrospective chart review over an eight-year period,

no case of ACE-inhibitor mediated angioedema

required intubation or surgical airway.88Obviously,

such patients must be instructed not to take their ACE

inhibitor and to return immediately for any worsening.

On the other hand, all cases of ACE-inhibitor-induced

angioedema are not benign, and the literature is full of

case reports of respiratory compromise.89,90Patients

with respiratory complaints, palatal edema, or progres-

sive course require admission and are candidates for

intubation; patients whose symptoms have plateaued

may be watched . . . with a cricothyroidotomy tray atthe bedside!

Cont inued f rom page 12

Ten Excuses That Dont Work In Court

1. I thought he had cardiogenic shock. He complained of

chest pain.

Anaphylaxis can present initially with chest discomfort,

hypotension, and tachycardia. Urticarial wheals may beabsent. Unfortunately, this patient did not get the

epinephrine he needed until he developed ventricular

fibrillation. Now this physician is consulting with the

hospital lawyer.

2. I thought it was just hives involving the lips

and tongue.

This patient actually had angioedema related to ACE

inhibitor use. The diphenhydramine and steroids he

received for an allergic reaction were ineffective for his

angioedema, and the patient collapsed on the way home

with airway obstruction. Angioedema is non-IgE-mediated and usually involves the head and neck.

Angioedema due to ACE inhibitor use may not respond

to antihistamines or steroids, but may progress rapidly to

upper airway obstruction.

3. I didnt think the patient was at risk for a

contrast reaction.

This patient got IV contrast for a head CT to exclude HIV-

related toxoplasmosis. Unfortunately, he developed

acute renal failure and is now a candidate for

hemodialysis. Risk factors for radiocontrast media

reactions are a prior history of similar reactions, a history

of asthma, increased age, dehydration, renal or hepaticdysfunction, beta-blocker use, and cardiac disease.

4. Since he collapsed during exercise, I thought he had a

heart attack.

Exercise-induced allergic reactions are usually associated

with urticaria and nasal congestion, but sometimes they

are fatal. If the treating physician had spoken with the

patients wife, he would have learned that the patient

develops allergic symptoms during exercise and forgot

his Singulair today.

5. I thought this was just simple urticaria.The patient was treated with diphenhydramine and

released with the diagnosis of allergic reaction.

Unfortunately, the treating physician ignored the

patients fever, myalgias, arthralgias, and use of penicillin

10 days ago. This physician thought about possible

serum sickness later that night and called the patient to

return for re-evaluation. The patient returned the next

morning with a creatinine of 5.0 mg/dL.

Cont inued on page 15



Management Of Recurrent UrticariaSome patients treated in the ED for mild-to-moderate

allergic reactions are discharged and return later with

recurrent symptoms. The first step in managing these

patients is to carefully repeat the history and physical,

looking for keys to the diagnosis that were possibly

missed on the first visit, such as new body products,

clothing, pets, or medications. Occult infections and

malignancy may present with urticaria, and the

physical examination should look for these etiologies.

Blood work is usually not part of the initial visit for

urticaria; however, for recurrent cases a CBC may be

helpful in identifying an occult processes such as a

myeloproliferative diseases including thrombocytosis,

which will cause histamine release.91Some clinicians

obtain a sedimentation rate on patients with recurrent

urticaria in an attempt to identify underlying inflam-

matory processes; unfortunately, the lack of sensitivity

and specificity of this test limits its usefulness.92

Pharmacologic management of recurrent urticaria

should involve either switching the patient to another

category of antihistamine (remember, there are eightcategories of antihistamine, each with its own thera-

6. I didnt think about prescribing an Ana-Kit.

Having a patient die following ED discharge from

anaphylaxis after ano t he r bee sting is a definite

malpractice risk. These kits contain epinephrine anddiphenhydramine. Self-administered medications should

be prescribed at ED discharge following an allergic

reaction due to an envenomation. The one caveat is that

older patients with cardiac disease should not use

epinephrine unless i n ext remis.

7. I didnt think that patient with angioedema

needed intubation.

One retrospective study associated voice change,

hoarseness, stridor, and dyspnea with the need for

airway control. Consider airway control in patients

with these findings (although not all patients withthese signs and symptoms require emergent

intubation). Unfortunately, this emergency physician

did not control the airway despite stridor, and now

the patient has a large cricothyroidotomy hole in

his neck.

8. I didnt use epinephrine because he was so old. I

thought he would do okay with Benadryl and steroids.

He didnt. Epinephrine is the drug of choice for life-

threatening anaphylaxis. When the chips are down,

nothing else will do. It is indicated even in elderly

patients and those with a history of hypertension and

cardiac disease whenever they have a dangerousallergic reaction.

9. I just didnt understand why that patient did not

respond to standard therapy.

Patients on beta-blockers may not respond to standard

anti-allergy therapy, including epinephrine. One

alternative in this setting is glucagon. This physician now

wishes he had thought of using glucagon in this patient

who developed anaphylactic shock.

10. I didnt think it could be hereditary angioedema

because it is so rare.Although hereditary angioedema is an unusual

diagnosis in the ED, the treatment of this disorder is

different enough from standard angioedema or

allergic reactions to merit note. These patients can

be treated with fresh frozen plasma in addition to

airway management. Being aware of the possible

need for FFP in hereditary angioedema may save a

patients life, as well as preclude a large retainer for

your defense lawyer.

Ten Excuses That Dont Work In Court(continued)

peutic profile). Another approach is to add an H2-

blocker or steroids. In one double-blind, randomized,

prospective trial, adding prednisone to an antihista-

mine regimen shortened the clinical duration of

urticaria without apparent adverse effects.82

A crucial component to managing patients with

recurrent urticaria is education about the natural

history of allergic reactions. Tell these patients they

should expect a waxing and waning course. While the

medication may mitigate the severity of symptoms

(i.e., itching and rash), it will not completely extirpate

those symptoms. When patients have realistic expec-

tations about their allergic reaction, they are less

likely to return to the ED.

Disposition: Admission, Discharge,Or Observation?

The disposition of allergy patients requires significant

clinical judgment. Most patients with allergic reac-

tions can be discharged. Hospitalize or observe

patients with severe reactions such as airway an-

gioedema, persistent bronchospasm, hypoperfusion,



or cardiac problems, especially if the condition is not

promptly resolved by therapy. Other high-risk groups

include those on beta-blocker therapy who have

significant reactions and those with severe late-phase

or prolonged reaction. Some patients who have

problematic social situations (such as no phone) or live

far from medical care may also require admission or

prolonged observation. (SeeTable 7.)

The amount of time a patient needs to be observed

after an allergic reaction is also unknown. Most

authorities suggest that patients with significant

allergic reactions should be observed for four to six

hours if discharge is being considered. When they are

discharged, instructions must include immediate

return to the ED for shortness of breath or syncope.

Discharge MedicationsBecause some reactions are biphasic, drugs prescribed

at discharge may blunt a late allergic relapse. Prescribe

H1and/or H2antagonists for at least 24 to 48 hours,

and corticosteroids for several days, to modify any

delayed inflammatory response. Montelukast andother leukotriene-receptor antagonists may inhibit

exercise-induced anaphylaxis.93

If a patient had a severe reaction to a food or insect

sting, prescribe self-administered injectable epineph-

rine (Epi-Pen or Ana-Kit, both available in adult and

pediatric strengths). Make sure the patient knows

when and how to use the device.

Education And ReferralRemember to educate the patient about antigen

avoidance. Aspirin is present in many over-the-counter

combination medications, and cross-sensitivity with

other non-steroidal agents may exist. With predictable

exposure to agents that might initiate the allergy

mechanism (e.g., iodinated radiocontrast agents),

pretreatment with antihistamines and corticosteroids

may be appropriate. Recommend Medic Alert bracelets

for those with severe allergies.

Finally, make an allergist referral on a case-by-case

basis. This is most appropriate for patients with

anaphylaxis due to Hymenoptera stings. Immuno-

therapy has become the standard of care for severe

(i.e., not simple, localized) stinging insect reactions and

may reduce the risk of anaphylaxis with re-sting from

60% to about 5%.94,95 Immunotherapy may not be

necessary for children who have isolated hives after

bee stings. In one study, children who had only

cutaneous reactions were not at risk for future anaphy-

laxis to stings.96

Summary

Allergy is a complex illness that involves inflammatory

mechanisms. Most patients with allergic reactions have

mild symptoms. However, life-threatening airway

angioedema as well as anaphylaxis require prompt

recognition and aggressive therapy. Patients in distress

require appropriate oxygenation and occasionally

intubation. Epinephrine and IV fluids remain the

mainstays of therapy for severe reactions. Give antihis-

tamines and corticosteroids for most reactions.

Above all, treat allergic reactions with respect.

The average emergency physician will encounter

many severe hypersensitivity reactions during his

or her career.

References

Evidence-based medicine requires a critical appraisal

of the literature based upon study methodology and

number of subjects. Not all references are equally

robust. The findings of a large, prospective, random-

ized, and blinded trial should carry more weight than a

case report.

To help the reader judge the strength of each

reference, pertinent information about the study, such

as the type of study and the number of patients in the

study, will be included in bold type following the

reference, where available. In addition, the mostinformative references cited in the paper, as deter-

mined by the authors, will be noted by an asterisk (*)

next to the number of the reference.

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2. Portier P, Richet C. De laction anaphylactique des certain

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3. Lichtenstein LM. Allergy and the immune system. Sci Am

1993 Sep;269(3):116-124. (Review)

4. Yunginger JW, Nelson DR, Squillace DL, et al. Laboratory

Table 7. Disposition Of Hypersensitivity Reactions.

When in doubt, hospitalize:

All severe reactions not promptly resolved by therapy:

Airway angioedema, bronchospasm

Hypoperfusion or cardiac problem

All patients on beta-blocker therapy

Anticipated severe late-phase reaction (for example, if there is history of the same in the past)

Patients with inadequate support system

Discharge plan:

Observe patients significant reactions for at least four to six hours prior to discharge

Prescribe H1and/or H

2antagonists for at least 24-48 hours

Consider steroids (for most allergic reactions)

Beta-agonists

Education about antigen avoidance

Self-injectable epinephrine

Appropriate referral



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*22. Patterson R, Anderson J. Allergic reactions to drugs and

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26. Levine BB. Antigenicity and cross-reactivity of penicillins

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Ann Allergy Asthma Immunol 1995;74(2):167-170. (Review)

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29. Fisher MM, Harle DG, Baldo BA. Anaphylactic reactions to

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Physician CME Questions

31. The most common cause of death in patients with

a severe allergic reaction is:

a. cerebrovascular accident.

b. circulatory collapse.

c. complications of medical therapy.

d. multiple organ failure.

e. respiratory failure.

32. IV epinephrine is not indicated in which of the

following allergic reaction situations?

a. An 8-year-old female with hypotension and

severe tachycardia

b. A 32-year-old male with hoarseness and

stridor

c. A 38-year-old male with airway angioedema

d. A 48-year-old female with urticaria alone

e. A 64-year-old male with hypotension and

abdominal pain

33. All of the following are potential causes of

anaphylactic shock except:

a. C1esterase inhibitor deficiency.

b. exercise.

c. Hymenoptera stings.

d. latex.

e. peanut oil ingestion.

34. A patient on beta-blocker therapy presentshypotensive and bradycardic shortly after

multiple bee stings. Epinephrine does not help.

Which medication should be given next?

a. cimetidine.

b. diphenhydramine.

c. glucagon.

d. high-dose epinephrine.

e. methylprednisolone.

35. A young female presents with vomiting and

diarrhea along with facial and hand swelling, as

well as airway stridor. She has experienced thisbefore but never has had urticaria. Other family

members have a similar problem. The medication

of choice is:

a. cimetidine.

b. epinephrine.

c. fresh frozen plasma.

d. hydroxyzine.

e. methylprednisolone.

36. A patient with known severe penicillin allergy is

accidentally given an oral dose of penicillin. He

is asymptomatic so far. Treatment should include

which of the following?

a. Benadryl

b. Intravenous epinephrine

c. Or al charcoal

d. Prednisone

e. Subcutaneous epinephrine

37. Which of these clinical scenarios is not sugges-

tive of an allergic reaction?

a. Acute back pain with hypotension

b. Acute bronchospasm with hypotension

c. Confusion with fever of 103F

d. Isolated facial angioedemae. Urticaria with vomiting and diarrhea

38. The most frequent cause of allergic

symptoms is:

a. food sensitivity.

b. inhaled antigens.

c. insect s tings.

d. medicat ions.

e. non-immunogenic.


20/20

Physician CME Information

This CME enduring material is sponsored by Carolinas HealthCare System

and has been planned and implemented in accordance with the Essentials

and Standards of the Accreditation Council for Continuing Medical

Education. Credit may be obtained by reading each issue and completing

the post-tests administered in December and June.

Target Audience:This enduring material is designed for emergency

medicine physicians.

Needs Assessment:The need for this educational activity was determined

by a survey of medical staff, including the editorial board of this publica-

tion; review of morbidity and mortality data from the CDC, AHA, NCHS,

and ACEP; and evaluation of prior activities for emergency physicians.

Date of Original Release:This issue ofEm ergency Medicine Practice

was published April 1, 2000. This activity is eligible for CME credit through

April 1, 2001. The latest review of this material was March 28, 2000.

Discussion of I nvestigational Information:As part of the newsletter,

faculty may be presenting investigational information about

pharmaceutical products that is outside Food and Drug Administration

approved labeling. Information presented as part of this activity is

intended solely as continuing medical education and is not intended

to promote off-label use of any pharmaceutical product.Disclosure of

Off-Label Usage:This issue ofEm ergency Medicine Practice discusses no off-

label use of any phamaceutical product.

Faculty Disclosure: In compliance with all ACCME Essentials, Standards,

and Guidelines, all faculty for this CME activity were asked to complete afull disclosure statement. The information received is as follows: Dr.

OBrien. Dr. Howell, Dr. Zull, and Dr. Salomone report no significant

financial interest or other relationship with the manufacturer(s) of any

commercial product(s) discussed in this educational presentation.

Accreditation:Carolinas HealthCare System is accredited by the

Accreditation Council for Continuing Medical Education to sponsor

continuing medical education for physicians.

Credit Designation: Carolinas HealthCare System designates this

educational activity for up to 2 hours of Category 1 credit toward the

AMA Physicians Recognition Award. Each physician should claim only

those hours of credit actually spent in the educational activity.Emergency

Medicine Practice is approved by the American College of Emergency Phy-

sicians for 24 hours of ACEP Category 1 credit (per annual subscription).

Earning Credit:Physicians with current and valid licenses in the United

States, who read all CME articles during each Em ergency Medicine Practice

six-month testing period, complete the CME Evaluation Form distributed

with the December and June issues, and return it according to the

published instructions are eligible for up to 2 hours of Category 1 credit

toward the AMA Physicians Recognition Award (PRA) for each issue. You

must complete both the post-test and CME Evaluation Form to receive

credit. Results will be kept confidential. CME certificates will be mailed to

each participant scoring higher than 70% at the end of the calendar year.

Class I

Always acceptable, safe

Definitely useful

Proven in both efficacy

and effectiveness

Must be used in the

intended manner for

proper clinical indications

Level o f Evidence:

One or more largeprospective studies

are present (with

rare exceptions)

Study results consistently

positive a

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