Assessment and Management of Patients With Allergic Disorders

Chapter

53Chapter

53Assessment andManagement of PatientsWith Allergic Disorders

LEARNING OBJECTIVESOn completion of this chapter, the learner will be able to:

1. Explain the physiologic events involved with allergic reactions.2. Describe the types of hypersensitivity.3. Describe the management of patients with allergic disorders.4. Describe measures to prevent and manage anaphylaxis.5. Use the nursing process as a framework for care of the patient with

allergic rhinitis.6. Discuss the different allergic disorders according to type.

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Chapter 53 Assessment and Management of Patients With Allergic Disorders 1581

substance that is normally harmless (eg, dust, weeds, pollen, dan-der). Chemical mediators released in allergic reactions may pro-duce symptoms ranging from mild to life-threatening.

The many cells and organs of the immune system secrete var-ious substances important in the immune response. These partsof the immune system must work together to ensure adequate de-fense against invaders (ie, virus, bacteria, other foreign sub-stances) without destroying the body’s own tissues by an overlyaggressive reaction.

FUNCTION AND PRODUCTION OF IMMUNOGLOBULINSAntibodies formed by lymphocytes and plasma cells in responseto an immunogenic stimulus constitute a group of serum proteinscalled immunoglobulins. Grouped into five classes (IgE, IgD,IgG, IgM, and IgA), antibodies can be found in the lymph nodes,tonsils, appendix, and Peyer’s patches of the intestinal tract or cir-culating in the blood and lymph. Each antibody molecule is com-posed of two identical heavy (H) chains and two identical light(L) chains. Each chain contains one variable region and one ormore constant regions. The constant regions determine the class(IgE, IgD, etc.) of each antibody and allow each class of antibodyto interact with specific effector cells and molecules. The variableregions contain antigen-binding sites (Porth, 2002). Antibodiesare capable of binding with a wide variety of antigens, which in-clude macromolecules and small chemicals (Abbas & Lichtman,2001). Antibodies of the IgM, IgG, and IgA classes have definiteand well-established protective functions. These include neutral-ization of toxins and viruses and precipitation, agglutination, andlysis of bacteria and other foreign cellular material. (See Chap. 50for further discussion of these functions.)

Immunoglobulins of the IgE class are involved in allergic dis-orders and some parasitic infections, evidenced by elevation ofIgE levels. IgE-producing cells are located in the respiratory andintestinal mucosa. Two or more IgE molecules bind together toan allergen and trigger mast cells or basophils to release chemi-cal mediators, such as histamine, serotonin, kinins, slow-reactingsubstance of anaphylaxis (SRS-A), and the neutrophil factor,which produces allergic skin reactions, asthma, and hay fever.

The human body is menaced by a host of potential invaders—allergens as well as microbial organisms—that constantly threatenits surface defenses. After penetrating those defenses, these aller-gens and organisms compete with the body for its nutrients and,if allowed to flourish unimpeded, disrupt its enzyme systems anddestroy its vital tissues. To protect against these agents, the bodyis equipped with an elaborate defense system.

The epithelial cells coating the skin and making up the lining ofthe respiratory, gastrointestinal, and genitourinary tracts provide thefirst line of defense. The structure and continuity of these surfacesand the resistance to penetration are initial deterrents to invaders.

One of the most effective defense mechanisms is the body’s ca-pacity to equip itself rapidly with weapons (antibodies) individu-ally designed to meet each new invader, namely specific proteinantigens. Antibodies react with antigens in a variety of ways: (1) by coating the antigens’ surfaces if they are particular sub-stances, (2) by neutralizing the antigens if they are toxic, and (3) byprecipitating the antigens out of solution if they are dissolved.

The antibodies prepare the antigens so that the phagocyticcells of the blood and the tissues can dispose of them. In somecases, however, the body produces inappropriate or exaggeratedresponses to specific antigens, and the result is an allergic or hyper-sensitivity disorder.

Allergic Reaction: Physiologic OverviewAn allergic reaction is a manifestation of tissue injury resultingfrom interaction between an antigen and an antibody. Allergy isan inappropriate and often harmful response of the immune sys-tem to normally harmless substances. In this case, the substanceis termed an allergen. Atopy refers to allergic reactions charac-terized by the action of IgE antibodies and a genetic predisposi-tion to allergic reactions.

When the body is invaded by an antigen, usually a proteinthat the body’s defenses recognize as foreign, a series of events oc-curs in an attempt to render the invader harmless, destroy it, andremove it from the body. When lymphocytes respond to the anti-gen, antibodies (protein substances that protect against antigens)are produced. Common allergic reactions occur when the im-mune system of a susceptible person responds aggressively to a

Glossaryallergen: substance that causes manifesta-

tions of allergyallergy: inappropriate and often harmful im-

mune system response to substances thatare normally harmless

anaphylaxis: clinical response to an immedi-ate immunologic reaction between a spe-cific antigen and antibody

angioneurotic edema: condition character-ized by urticaria and diffuse swelling ofthe deeper layers of the skin

antibody: protein substance developed bythe body in response to and interactingwith a specific antigen

antigen: substance that induces the produc-tion of antibodies

antihistamine: medication that opposes theaction of histamine

atopic dermatitis: type I hypersensitivity in-volving inflammation of the skin evi-

denced by itching, redness, and a varietyof skin lesions

atopy: term often used to describe IgE-mediated diseases; genetically determinedallergic disorders

B lymphocyte: cells that are important inproducing circulating antibodies

bradykinin: polypeptide that stimulatesnerve fibers and causes pain

eosinophil: granular leukocyteepitope: an immunologically active site on

an antigen; a single antigen can have sev-eral different epitopes that elicit responsesfrom different antibodies

erythema: diffuse redness of the skinhapten: incomplete antigenhistamine: substance in the body that causes

increased gastric secretion, dilation of cap-illaries, and constriction of the bronchialsmooth muscle

hypersensitivity: abnormal heightened reac-tion to a stimulus of any kind

immunoglobulins: a family of closely relatedproteins capable of acting as antibodies

leukotrienes: a group of chemical mediatorsthat initiate the inflammatory response

lymphokines: substances released by sensi-tized lymphocytes when they contact spe-cific antigens

mast cell: connective tissue cells that containheparin and histamine in their granules

prostaglandins: unsaturated fatty acids thathave a wide assortment of biologic activity

rhinitis: inflammation of the nasal mucosaserotonin: chemical mediator that acts as a po-

tent vasoconstrictor and bronchoconstrictorT lymphocyte: cells that can cause graft re-

jection, kill foreign cells, or suppress pro-duction of antibodies

urticaria: hives

1582 Unit 11 IMMUNOLOGIC FUNCTION

Antibodies combine with antigens in a special way, likened tokeys fitting into a lock. Antigens (the keys) only fit certain anti-bodies (the locks). Hence, the term “specificity” refers to the spe-cific reaction of an antibody to an antigen. There are manyvariations and complexities in these patterns. The strength withwhich one antigen-binding surface of an antibody binds to oneepitope, an immunologically active site on an antigen, is knownas the affinity of the interaction (Abbas & Lichtman, 2001).

Antibody molecules are bivalent; that is, they have two com-bining sites. Therefore, the antibody easily becomes a cross-linkbetween two antigen groups, causing them to clump together (ag-glutination). By this action, foreign invaders are cleared from thebloodstream. Agglutination is the means for determining bloodgroup in laboratory tests.

Role of B CellsThe B cell, or B lymphocyte, is programmed to produce one spe-cific antibody. On encountering a specific antigen, a B cell stim-ulates production of plasma cells, the site of antibody production.The result is the outpouring of antibodies for the purpose of de-stroying and removing the antigen.

Role of T CellsThe T cell, or T lymphocyte, assists the B cells in producing an-tibodies. T cells secrete substances known as lymphokines thatencourage cell growth, promote cell activation, direct the flow ofcell activity, destroy target cells, and stimulate the macrophages.Macrophages present the antigen to the T cells and initiate theimmune response. They also digest antigens and assist in remov-ing cells and other debris. The antigen-binding site of a T cell hasa structure much like that of an immunoglobulin. It recognizesepitopes through complementary interactions. Unlike a specificantibody, a T cell does not bind free antigens (Parslow, Stites,Terr & Imboden, 2001).

FUNCTION OF ANTIGENSAntigens are divided into two groups: complete protein antigensand low-molecular-weight substances. Complete protein antigens,such as animal dander, pollen, and horse serum, stimulate a com-plete humoral response. (See Chap. 50 for a discussion of humoral

immunity.) Low-molecular-weight substances, such as medica-tions, function as haptens (incomplete antigens), binding to tis-sue or serum proteins to produce a carrier complex that initiatesan antibody response. The term “hapten” is derived from theGreek word haptien (to fasten). The proteins or other immuno-gens that haptens are fastened to are known as carriers (Parslow et al., 2001).

In an allergic reaction, the production of antigen-specific IgEantibodies requires active communication between macrophages,T cells, and B cells. When the allergen is absorbed through therespiratory tract, gastrointestinal tract, or skin, allergen sensitiza-tion occurs. The macrophage processes the antigen and presentsit to the appropriate T cell. B cells that are influenced by the T cell mature into an allergen-specific IgE immunoglobulin-secreting plasma cell that synthesizes and secretes antigen-specificIgE antibody.

FUNCTION OF CHEMICAL MEDIATORSMast cells, which have a major role in IgE-mediated immediatehypersensitivity, are located in the skin and mucous mem-branes. When mast cells are stimulated by antigens, powerfulchemical mediators are released that cause a sequence of physi-ologic events resulting in symptoms of immediate hypersensi-tivity (Fig. 53-1). There are two types of chemical mediators:primary, which are preformed and found in mast cells or ba-sophils, and secondary, which are inactive precursors formed orreleased in response to primary mediators. The most prevalentknown primary and secondary mediators are described next.Table 53-1 summarizes the actions of primary and secondarychemical mediators.

Primary MediatorsIgE-mediated inflammation occurs when an antigen binds to theIgE antibodies that occupy certain receptors on mast cells.Within minutes, this binding causes the mast cell to degranulate,releasing certain preformed mediators. A two-phase responseresults. There is an initial immediate effect on blood vessels,smooth muscle, and glandular secretion. This is followed a fewhours later by cellular infiltration of the involved site. This typeof inflammatory response is commonly known as an immediatehypersensitivity response (Parslow et al., 2001).

FIGURE 53-1 Allergen triggers B cell to make IgE antibody, which attaches to mast cell. When that allergen re-appears, it binds to the IgE and triggers the mast cell to release its chemicals. Courtesy of U.S. Dept. of Health andHuman Services, National Institutes of Health.


HISTAMINEHistamine plays an important role in the immune response. His-tamine is released from mast cell granules where it is stored. Max-imal intensity is reached within about 15 minutes after antigencontact (Parslow et al., 2001). The effects of histamine release in-clude erythema; localized edema in the form of wheals; pruritus;contraction of bronchial smooth muscle, resulting in wheezingand bronchospasm; dilation of small venules and constriction oflarger vessels; and increased secretion of gastric and mucosal cells,resulting in diarrhea. Histamine action results from stimulationof histamine-1 (H1) and histamine-2 (H2) receptors found on dif-ferent types of lymphocytes, particularly T-lymphocyte suppres-sor cells and basophils. H1 receptors are found predominantly onbronchiolar and vascular smooth muscle cells. H2 receptors arefound on gastric parietal cells.

Certain medications are categorized by their action at these re-ceptors. Diphenhydramine (Benadryl) is an example of an anti-histamine, which is a medication displaying an affinity for H1

receptors; cimetidine (Tagamet) and ranitidine (Zantac) are ex-amples of other pharmacologic agents that target H2 receptors toinhibit gastric secretions in peptic ulcer disease.

EOSINOPHIL CHEMOTACTIC FACTOR OF ANAPHYLAXISPreformed in the mast cells, this chemotactic factor, which affectsmovement of eosinophils (granular leukocytes) to the site of al-lergens, is released upon degranulation to inhibit the action ofleukotrienes and histamine.

PLATELET-ACTIVATING FACTORPlatelet-activating factor (PAF) is responsible for initiatingplatelet aggregation at sites of immediate hypersensitivity reac-tions. It also causes bronchoconstriction and increased vascularpermeability. PAF also activates factor XII, or Hageman factor,which induces the formation of bradykinin.

PROSTAGLANDINSProstaglandins, composed of unsaturated fatty acids, producesmooth muscle contraction as well as vasodilation and increasedcapillary permeability. The fever and pain that occur with in-flammation are due in part to the prostaglandins.

Secondary MediatorsLEUKOTRIENESLeukotrienes are chemical mediators that initiate the inflamma-tory response. They are metabolites released by mucosal mast cells.They collectively make up what was once termed “slow-reactingsubstance of anaphylaxis” (SRS-A). Leukotrienes cause smoothmuscle contraction, bronchial constriction, mucus secretion in theairways, and the typical wheal and flare reaction of the skin(Parslow et al., 2001). Compared with histamine, leukotrienes are100 to 1,000 times more potent in causing bronchospasm. Manymanifestations of inflammation can be attributed in part toleukotrienes. Medications categorized as leukotriene antagonistsor modifiers (zileuton [Zyflo], zafirlukast [Accolate], montelukast[Singulair]) block the synthesis or action of leukotrienes and pre-vent the signs and symptoms associated with asthma.

BRADYKININBradykinin is a polypeptide with the ability to cause increasedvascular permeability, vasodilation, hypotension, and contractionof many types of smooth muscle, such as the bronchi (Parslow et al.,2001). Increased permeability of the capillaries results in edema.Bradykinin stimulates nerve cell fibers and produces pain.

SEROTONINSerotonin is released during platelet aggregation, acting as a po-tent vasoconstrictor and causing contraction of bronchial smoothmuscle.

Table 53-1 • Chemical Mediators of Hypersensitivity

MEDIATORS ACTION

Primary Mediators(Preformed and found in mast cells or basophils)Histamine (preformed in mast cells)

Eosinophil chemotactic factor of anaphylaxis (ECF-A)(preformed in mast cells)

Platelet-activating factor (PAF) (requires synthesis by mastcells, neutrophils, and macrophages)

Prostaglandins (chemically derived from arachidonic acid;require synthesis by cells)

Basophil kallikrein (preformed in mast cells)

Secondary Mediators(Inactive precursors formed or released in response to primary

mediators)Bradykinin (derived from precursor kininogen)

Serotonin (preformed in platelets)Heparin (preformed in mast cells)Leukotrienes (derived from arachidonic acid and activated by

mast cell degranulation) C, D, and E or slow-reacting sub-stance of anaphylaxis (SRS-A)

VasodilationSmooth muscle contraction, increased vascular permeability, increased

mucus secretionsAttracts eosinophils

Smooth muscle contractionIncites platelets to aggregate and release serotonin and histamineD and F series → bronchoconstrictionE series → bronchodilationD, E, and F series → vasodilationFrees bradykinin, which causes bronchoconstriction, vasodilation, and

nerve stimulation

Smooth muscle contraction, increased vascular permeability, stimulatespain receptors, increased mucus production

Smooth muscle contraction, increased vascular permeabilityAnticoagulantSmooth muscle contraction, increased vascular permeability


HYPERSENSITIVITYAlthough the immune system defends the host against infectionsand foreign antigens, immune responses can themselves cause tis-sue injury and disease. An immune response to an antigen mayresult in sensitivity to challenge with that antigen; hypersensi-tivity is a reflection of excessive or aberrant immune responses(Abbas & Lichtman, 2001).

A hypersensitivity reaction is an abnormal, heightened reactionto any type of stimuli. It usually does not occur with the first ex-posure to an allergen. Rather, the reaction follows a re-exposureafter sensitization in a predisposed individual. Sensitization initi-ates the humoral response or buildup of antibodies. To promoteunderstanding of the immunopathogenesis of disease, hypersen-sitivity reactions have been classified into four specific types of re-

actions (Fig. 53-2). Most allergies are identified as either type I ortype IV hypersensitivity reactions.

Anaphylactic (Type I) HypersensitivityThe most severe form of a hypersensitivity reaction is anaphy-laxis. This systemic reaction is characterized by edema in manytissues, including the larynx, and is often accompanied by hy-potension (Abbas & Lichtman, 2001). Type I or anaphylactic hy-persensitivity is an immediate reaction beginning within minutesof exposure to an antigen. This reaction is mediated by IgE anti-bodies rather than IgG or IgM antibodies. Type I hypersensitiv-ity requires previous exposure to the specific antigen. In turn, theplasma cells produce IgE antibodies in the lymph nodes, wherehelper T cells aid in promoting this reaction. The IgE antibodies

Type II. A cytotoxic reaction, which involves the binding of either the IgG or IgM antibody to a cell-bound antigen, may lead to eventual cell and tissue damage. The reaction is the result of mistaken identity when the system identifies a normal constituent of the body as foreign and activates the complement cascade. Examples of type II reactions are myasthenia gravis, Goodpasture's syndrome, pernicious anemia, hemolytic disease of the newborn, transfusion reaction, and thrombocytopenia.

Type I. An anaphylactic reaction is characterized by vasodilation, increased capillary permeability, smooth muscle contraction, and eosinophilia. Systemic reactions may involve laryngeal stridor, angioedema, hypotension, and bronchial, GI, or uterine spasm; local reactions are characterized by hives. Examples of type I reactions include extrinsic asthma, allergic rhinitis, systemic anaphylaxis, and reactions to insect stings.

Type 1

Antigen

IgE antibody

Mastcell

Release of vasoactive aminesand other mediators

Antigen

RBC

Complement

IgG orIgM antibody

Phagocytosis

Lysis of RBC

Type II

FIGURE 53-2 Four types of hypersensitivity reactions.


bind to membrane receptors on mast cells found in connectivetissue and basophils. During re-exposure, the antigen binds to ad-jacent IgE antibodies, activating a cellular reaction that triggersdegranulation and the release of chemical mediators (histamine,leukotrienes, and eosinophil chemotactic factor of anaphylaxis[ECF-A]).

Primary chemical mediators are responsible for the symptomsof type I hypersensitivity because of their effects on the skin,lungs, and gastrointestinal tract. When chemical mediators con-tinue to be released, a delayed reaction may occur lasting for up to24 hours. Clinical symptoms are determined by the amount ofthe allergen, the amount of mediator released, the sensitivity ofthe target organ, and the route of allergen entry. Type I hyper-sensitivity reactions may include both local and systemicanaphylaxis.

Cytotoxic (Type II) HypersensitivityType II, or cytotoxic, hypersensitivity occurs when the systemmistakenly identifies a normal constituent of the body as foreign.This reaction may be a result of a cross-reacting antibody, possi-bly leading to cell and tissue damage. Type II hypersensitivityinvolves the binding of either IgG or IgM antibody to the cell-bound antigen. The result of antigen–antibody binding is activa-tion of the complement cascade (see Chap. 50) and destructionof the cell to which the antigen is bound.

A type II hypersensitivity reaction is associated with severaldisorders. For example, in myasthenia gravis, the body mistak-enly generates antibodies against normal nerve ending receptors.In Goodpasture syndrome, antibodies against lung and renal tis-sue are generated, producing lung damage and renal failure.

Type III. An immune complex reaction is marked by acute inflammation resulting from formation and deposition of immune complexes. The joints and kidneys are particularly susceptible to this kind of reaction, which is associated with systemic lupus erythematosus, serum sickness, nephritis and rheumatoid arthritis. Some signs and symptoms include urticaria, joint pain, fever, rash, and adenopathy (swollen glands).

Complement

Antigenantibodycomplex

Infiltrationof PMNleukocytes

PMNleukocyte

Lysosomal enzymes

Damage toadjacent cells

Antigenpresenting cell

Antigen

MHC

Sensitizedt cell

Active immuneresponse resultingin tissue damage

Type III

Type IV

Type IV. A delayed, or cellular, reaction occurs 1 to 3 days after exposure to an antigen. The reaction, which results in tissue damage, involves activity by lymphokines, macrophages, and lysozymes. Erythema and itching are common; a few examples include contact dermatitis, graft-versus-host disease, Hashimoto's thyroiditis, and sarcoidosis.

FIGURE 53-2 (Continued)


A type II hypersensitivity reaction resulting in red blood cell de-struction is associated with drug-induced immune hemolytic ane-mia, Rh-hemolytic disease of the newborn, and incompatibilityreactions in blood transfusions (see Chap. 33).

Immune Complex (Type III) HypersensitivityType III, or immune complex, hypersensitivity involves immunecomplexes formed when antigens bind to antibodies. These com-plexes are then cleared from the circulation by phagocytic action.When these type III complexes are deposited in tissues or vascu-lar endothelium, two factors contribute to injury: the increasedamount of circulating complexes and the presence of vasoactiveamines. As a result, there is an increase in vascular permeabilityand tissue injury. The joints and kidneys are particularly suscep-tible to this type of injury. Type III hypersensitivity is associatedwith systemic lupus erythematosus, rheumatoid arthritis, certaintypes of nephritis, and some types of bacterial endocarditis. Theseare discussed elsewhere in this text.

Delayed-Type (Type IV) HypersensitivityType IV, or delayed-type hypersensitivity, also known as cellularhypersensitivity, occurs 24 to 72 hours after exposure to an aller-gen. It is mediated by sensitized T cells and macrophages. An ex-ample of this reaction is the effect of an intradermal injection oftuberculin antigen or purified protein derivative (PPD). SensitizedT cells react with the antigen at or near the injection site. Lym-phokines are released and attract, activate, and retain macrophagesat the site. These macrophages then release lysozymes, causing tis-sue damage. Edema and fibrin are responsible for the positive tu-berculin reaction.

An example of a type IV hypersensitivity reaction is contactdermatitis resulting from exposure to allergens such as cosmetics,adhesive tape, topical medications, medication additives, andplant toxins. The primary exposure results in sensitization. Re-exposure causes a hypersensitivity reaction composed of low-molecular-weight molecules (haptens) that bind with proteins orcarriers and are then processed by Langerhans cells in the skin.The symptoms that occur include itching, erythema, and raisedlesions.

AssessmentHEALTH HISTORY AND CLINICAL MANIFESTATIONSA comprehensive allergy history and a thorough physical exami-nation provide useful data for the diagnosis and management ofpatients with allergic disorders. An assessment form is useful forobtaining and organizing this information (Chart 53-1).

The degree of difficulty and discomfort experienced by the pa-tient because of allergic symptoms and the degree of improve-ment in those symptoms with and without treatment are assessedand documented. The relationship of symptoms to exposure topossible allergens is noted.

Diagnostic EvaluationDiagnostic evaluation of the patient with allergic disorders com-monly includes blood tests, smears of body secretions, skin tests,and the radioallergosorbent test (RAST). Results of laboratory

blood studies provide supportive data for various diagnostic pos-sibilities; however, they are not the major criteria for the diagno-sis of allergic disease.

COMPLETE BLOOD COUNT WITH DIFFERENTIALThe white blood cell (WBC) count is usually normal except withinfection. Eosinophils, granular leukocytes, normally make up1% to 3% of the total number of WBCs. A level between 5% and15% is nonspecific but does suggest allergic reaction. Higher levelsare considered moderate and severe. In moderate eosinophilia,15% to 40% of blood leukocytes as eosinophils are found inpatients with allergic disorders as well as in patients with malig-nancy, immunodeficiencies, parasitic infections, and congenitalheart disease, and those receiving peritoneal dialysis. In severeeosinophilia, 50% to 90% of blood leukocytes as eosinophils arefound in the idiopathic hypereosinophilic syndrome.

EOSINOPHIL COUNTAn actual count of eosinophils may be obtained from blood sam-ples or smears of secretions. A total eosinophil count can be ob-tained from a blood sample by using special diluting fluids thathemolyze erythrocytes and stain the eosinophils. During symp-tomatic episodes, smears obtained from nasal secretions, con-junctival secretions, and sputum of atopic patients usually revealeosinophils, indicative of an active allergic response.

TOTAL SERUM IMMUNOGLOBULIN E LEVELSHigh total serum IgE levels support the diagnosis of atopic dis-ease. A normal IgE level, however, does not exclude the diagno-sis of an allergic disorder. IgE levels are not as sensitive as thepaper radioimmunosorbent test (PRIST) and the enzyme-linkedimmunosorbent assay (ELISA). Indications for determining IgElevels include the following:

• Evaluation of immunodeficiency• Evaluation of drug reactions• Initial laboratory screening for allergic bronchopulmonary

aspergillosis• Evaluation of allergy among children with bronchiolitis• Differentiation of atopic and nonatopic eczema• Differentiation of atopic and nonatopic asthma and rhinitis

SKIN TESTSSkin testing entails the intradermal injection or superficial appli-cation (epicutaneous) of solutions at several sites. Depending onthe suspected cause of allergic signs and symptoms, several dif-ferent solutions may be applied at several separate sites. These so-lutions contain individual antigens representing an assortment ofallergens, including pollen, most likely to be implicated in the pa-tient’s disease. Positive reactions (wheal and flare) are clinicallysignificant when correlated with the history, physical findings,and results of other laboratory tests.

The results of skin tests complement the data obtained fromthe history. They indicate which of several antigens are mostlikely to provoke symptoms and provide some clue to the inten-sity of the patient’s sensitization. The dosage of the antigen (al-lergen) injected is also important. Most patients are hypersensitive


Chart 53-1 • ASSESSMENT

Allergy Assessment Form

Name _______________________________________________ Age _______________ Sex _______________ Date _______________I. Chief complaint: _________________________________________________________________________________________

II. Present illness: ___________________________________________________________________________________________III. Collateral allergic symptoms: _________________________

Eyes: Pruritus ______ Burning ________ Lacrimation_______Swelling______ Injection _______ Discharge_________

Ears: Pruritus ______ Fullness ________ Popping__________Frequent infections ________

Nose: Sneezing _____ Rhinorrhea _____ Obstruction_______Pruritus ______ Mouth-breathing ___________Purulent discharge__________

Throat: Soreness______ Postnasal discharge_________Palatal pruritus _________ Mucus in the morning _________

Chest: Cough _____________ Pain ________________ Wheezing ________Sputum ____________ Dyspnea_____________Color______________ Rest ________________Amount____________ Exertion_____________

Skin: Dermatitis __________ Eczema _____________ Urticaria_________IV. Family allergiesV. Previous allergic treatment or testing: __________________________________________________________________________

Prior skin testing: _________________________________________________________________________________________Medications: Antihistamines Improved____________ Unimproved __________

Bronchodilators Improved____________ Unimproved __________Nose drops Improved____________ Unimproved __________Hyposensitization Improved____________ Unimproved __________

Duration __________Antigens __________Reactions__________

Antibiotics Improved____________ Unimproved __________Corticosteroids Improved____________ Unimproved __________

VI. Physical agents and habits: __________________________________________________________________________________Bothered by:

Tobacco for _____ years Alcohol _____________ Air cond._____________Cigarettes _____ packs/day Heat _______________ Muggy weather ________Cigars _____ per day Cold _______________ Weather changes _______Pipes _____ per day Perfumes ____________ Chemicals ____________Never smoked ________________ Paints_______________ Hair spray ____________Bothered by smoke_____________ Insecticides __________ Newspapers___________

Cosmetics ___________ Latex ________________VII. When symptoms occur: ____________________________________________________________________________________

Time and circumstances of 1st episode: ________________________________________________________________________Prior health: _____________________________________________________________________________________________Course of illness over decades: progressing __________ regressing __________Time of year: ______________________________________ Exact dates: ____________________________________________

Perennial __________Seasonal __________Seasonally exacerbated __________

Monthly variations (menses, occupation): ______________________________________________________________________Time of week (weekends vs. weekdays): ________________________________________________________________________Time of day or night: ______________________________________________________________________________________After insect stings: ________________________________________________________________________________________

VIII. Where symptoms occur:____________________________________________________________________________________Living where at onset:______________________________________________________________________________________Living where since onset: ___________________________________________________________________________________Effect of vacation or major geographic change:___________________________________________________________________Symptoms better indoors or outdoors: _________________________________________________________________________Effect of school or work:____________________________________________________________________________________Effect of staying elsewhere nearby: ____________________________________________________________________________Effect of hospitalization:____________________________________________________________________________________Effect of specific environments: ______________________________________________________________________________Do symptoms occur around: ________________________________________________________________________________

old leaves _____ hay _____ lakeside _____ barns _________summer homes _____ damp basement _____ dry attic _____lawnmowing _____ animals ______ other ______ (continued)


to more than one pollen. Under testing conditions, they may notreact (although they usually do) to the specific pollens that inducetheir attacks.

In cases of doubt about the validity of the skin tests, a RASTor a provocative challenge test may be performed. If a skin test isindicated, there is a reasonable suspicion that a specific allergenis producing symptoms in an allergic patient. Several precau-tionary steps, however, must be observed before skin testing withallergens:

• Testing is not performed during periods of bronchospasm.• Epicutaneous tests (scratch or prick tests) are performed be-

fore other testing methods in an effort to minimize the riskof systemic reaction.

• Emergency equipment must be readily available to treatanaphylaxis.

Types of Skin TestsThe methods of skin testing include prick skin tests, scratch tests,and intradermal skin testing (Fig. 53-3). After prick or scratchtests, intradermal skin testing is performed with allergens that didnot elicit positive reactions. Because a larger antigen challenge isbeing used, local or systemic reactions could occur if the sameantigens that produced positive skin or scratch reactions are used.The back is the most suitable area of the body for skin testing be-cause it permits the performance of many tests. The multitest ap-plicator is a commercially available device with multiple testheads that allows simultaneous administration of antigens bymultiple punctures at different sites.

Interpretation of Skin Test ResultsFamiliarity with and consistent use of a grading system are es-sential. The grading system used should be identified on a skintest sheet for later interpretation. A positive reaction, evidencedby the appearance of an urticarial wheal (round, reddened skinelevation) (Fig. 53-4), localized erythema (diffuse redness) in thearea of inoculation or contact, or pseudopodia (irregular projec-

tion at the end of a wheal) with associated erythema is consideredindicative of sensitivity to the corresponding antigen.

There may be false-negative results due to improper tech-nique, outdated allergen solutions, and prior use of medicationsthat suppress skin reactivity. Corticosteroids and antihista-mines, including allergy medications, suppress skin test reactiv-ity and are usually withheld 48 to 96 hours before testing,depending on the duration of their activity. False-positive skintests may result from improper preparation or administration ofallergen solutions.

Interpretation of positive or negative skin tests must be basedon the history, physical examination, and other laboratory test

Chart 53-1 • ASSESSMENT (Continued)

Allergy Assessment Form

Do symptoms occur after eating:cheese _____ mushrooms _____ beer _____ melons _____bananas _____ fish _____ nuts _____ citrus fruits _____other foods (list)________________________________________________________________________________________

Home: city _____ rural _____house _____ age _____apartment _____ basement _____ damp _____ dry _____heating system _____pets (how long) _____ dog _____ cat _____ other _____

Bedroom: Type Age Living room: Type AgePillow _____ _____ Rug _____ _____Mattress _____ _____ Matting _____ _____Blankets _____ _____ Furniture _____ _____Quilts _____ _____Furniture _____ _____Anywhere in home symptoms are worse: _______________________________________________________________________

IX. What does patient think makes symptoms worse? _________________________________________________________________X. Under what circumstances is patient free of symptoms? _____________________________________________________________

XI. Summary and additional comments: ___________________________________________________________________________

FIGURE 53-3 Intradermal testing. A 0.5-mL or 1-mL sterile syringe witha 26/27 gauge intradermal needle is used to inject 0.02 to 0.03 mL of intra-dermal allergen. The needle is inserted with the bevel facing upward and thesyringe parallel to the skin. The skin is penetrated superficially, and a smallamount of the allergen solution is injected to create a bleb (raised area) ap-proximately 5 mm in diameter. A separate sterile syringe and needle are usedfor each injection. From Taylor, C., Lillis C., & LeMone, P. (2001). Fun-damentals of nursing: The art and science of nursing care (4th ed.). Philadel-phia; Lippincott Williams & Wilkins.


results. The following guidelines are used for the interpretationof skin test results:

• Skin tests are more reliable for diagnosing atopic sensitivityin patients with allergic rhinoconjunctivitis than in patientswith asthma.

• Positive skin tests correlate highly with food allergy.• The use of skin tests to diagnose immediate hypersensitivity

to medications is limited because metabolites of medica-tions, not the medications themselves, are usually responsi-ble for causing hypersensitivity.

PROVOCATIVE TESTINGProvocative testing involves the direct administration of the sus-pected allergen to the sensitive tissue, such as the conjunctiva,nasal or bronchial mucosa, or gastrointestinal tract (by ingestionof the allergen) with observation of target organ response. Thistype of testing is helpful in identifying clinically significant aller-gens in patients with a large number of positive tests. Major dis-advantages of this type of testing are the limitation of one antigenper session and the risk of producing severe symptoms, particu-larly bronchospasm, in patients with asthma.

RADIOALLERGOSORBENT TESTRAST is a radioimmunoassay that measures allergen-specific IgE.A sample of the patient’s serum is exposed to a variety of sus-pected allergen particle complexes. If antibodies are present, theywill combine with radiolabeled allergens. After the serum is cen-trifuged, radioimmunoassay detects the allergen-specific IgE an-tibody. Test results are then compared with control values. Inaddition to detecting an allergen, RAST indicates the quantity ofallergen necessary to evoke an allergic reaction. Values are re-ported on a scale from 0 to 5. Values of 2+ or greater are consid-ered significant. The major advantages of RAST over other testsinclude decreased risk of systemic reaction, stability of antigens,and lack of dependence on skin reactivity modified by medica-

tions. The major disadvantages include the limited allergen se-lection, reduced sensitivity compared with intradermal skin tests,lack of immediate results, and cost.

Allergic DisordersThere are two types of IgE-mediated allergic reactions: atopicand nonatopic disorders. While the underlying immunologic re-actions of the two types of disorders are the same, predisposingfactors and manifestations are different. The atopic disorders arecharacterized by a hereditary predisposition and production of alocal reaction to IgE antibodies produced in response to com-mon environmental allergens (Kay, 2001a). The nonatopic dis-orders lack the genetic component and organ specificity of theatopic disorders (Porth, 2002). Examples of atopic disorders areallergic rhinitis, allergic asthma, and atopic dermatitis (Kay,2001a).

A type I hypersensitivity response results in atopic (allergic) dis-eases, which affect 10% to 20% of the U.S. population. Geneticfactors play a role in susceptibility to these diseases. Disorders char-acterized as atopic include anaphylaxis, allergic rhinoconjunctivi-tis, atopic dermatitis, urticaria and angioedema, gastrointestinalallergy, and asthma. Latex allergy may be a type I or type IV hyper-sensitivity reaction, although true latex allergy is considered to bea type I hypersensitivity reaction (Brehler & Kütting, 2001). Latexallergy is discussed later in this chapter. Contact dermatitis is con-sidered a type IV hypersensitivity reaction.

ANAPHYLAXISAnaphylaxis is a clinical response to an immediate (type I hyper-sensitivity) immunologic reaction between a specific antigen andan antibody. The reaction results from IgE antibody. An ana-phylactic reaction can be triggered by exposure to an antigenthrough inhalation, injection, ingestion, or skin contact. It is a se-vere, life-threatening allergic reaction. It is estimated that 3.3 to43 million persons in the United States (1.24% to 16.8% of the

Reaction Guide

Negative wheal

1+ wheal

2+ wheal

3+ wheal

4+ wheal

4+

3+2+1+

0.51.01.52.0

3.0

4.0cm

FIGURE 53-4 Interpretation of reactions: Negative =wheal soft with minimal erythema. 1+ = wheal present (5–8 mm) with associated erythema. 2+ = wheal (7–10 mm)with associated erythema. 3+ = wheal (9–15 mm), slightpseudopodia possible with associated erythema. 4+ = wheal(12 mm+) with pseudopodia and diffuse erythema.


population) are at risk for anaphylaxis (Neugut, Ghatak &Miller, 2001).

PathophysiologyAnaphylaxis is caused by the interaction of a foreign antigenwith specific IgE antibodies found on the surface membrane ofmast cells and peripheral blood basophils. The subsequent re-lease of histamine and other bioactive mediators causes acti-vation of platelets, eosinophils, and neutrophils and thecoagulation cascade. Smooth muscle spasm, bronchospasm,mucosal edema and inflammation, and increased capillary per-meability result. These systemic changes characteristically pro-duce clinical manifestations within seconds or minutes ofantigen exposure (Neugut et al., 2001). Closely related to ana-phylaxis is an anaphylactoid (anaphylaxis-like) reaction, whichis described in Chart 53-2.

Substances that most commonly cause anaphylaxis includefoods, medications, insect stings, and latex (Chart 53-3). Foodsthat are common causes of anaphylaxis include peanuts, tree nuts,shellfish, fish, milk, eggs, soy, and wheat. Many medications havebeen implicated in anaphylaxis. Those that are most frequentlyreported include antibiotics (including penicillin), radiocontrastagents, intravenous anesthetics, aspirin and other nonsteroidalanti-inflammatory drugs (NSAIDs), and opioids. Antibiotics andradiocontrast agents cause the most serious anaphylactic reac-tions, producing reactions in about 1 of every 5,000 exposures.Penicillin is the most common cause of anaphylaxis and accountsfor about 75% of fatal anaphylactic reactions in the U.S. eachyear (Neugut et al., 2001).

Clinical ManifestationsAnaphylactic reactions may be categorized as mild, moderate, andsevere systemic reactions. The time from exposure to the antigento onset of symptoms is a good indicator of the severity of the re-action: the faster the onset, the more severe the reaction (Neugutet al., 2001).

Mild systemic reactions consist of peripheral tingling and asensation of warmth, possibly accompanied by fullness in themouth and throat. Nasal congestion, periorbital swelling, pruri-tus, sneezing, and tearing of the eyes can also be expected. Onsetof symptoms begins within the first 2 hours of exposure.

Moderate systemic reactions may include flushing, warmth,anxiety, and itching in addition to any of the above symptoms.

More serious reactions include bronchospasm and edema of theairways or larynx with dyspnea, cough, and wheezing. The onsetof symptoms is the same as for a mild reaction.

Severe systemic reactions have an abrupt onset with the samesigns and symptoms described above. These progress rapidly tobronchospasm, laryngeal edema, severe dyspnea, cyanosis, and hy-potension. Dysphagia (difficulty swallowing), abdominal cramp-ing, vomiting, diarrhea, and seizures can also occur. Cardiac arrestand coma may follow.

PreventionStrict avoidance of potential allergens is an important preventivemeasure for the patient at risk for anaphylaxis (Neugut et al.,2001). Patients at risk for anaphylaxis from insect stings shouldavoid areas populated by insects and should use appropriateclothing, insect repellent, and caution to avoid further stings.

If avoidance of exposure to allergens is impossible, adminis-tration of epinephrine is a critical measure to prevent an anaphy-lactic reaction. People sensitive to insect bites and stings, thosewho have experienced food or medication reactions, and thosewho have experienced idiopathic or exercise-induced anaphylac-tic reactions should always carry an emergency kit that containsepinephrine. The EpiPen from Dey Pharmaceuticals is a com-mercially available first-aid device that delivers premeasured dosesof 0.3 mg (Epipen) and 0.15 mg (Epipen Jr.) of epinephrine (Fig. 53-5). The autoinjection system requires no preparation, andthe self-administration technique is uncomplicated. The patientmust be given an opportunity to demonstrate the correct tech-nique for use; an Epipen training device is available. Verbal andwritten information about the emergency kit, as well as strategiesto avoid exposure to threatening allergens, must also be provided.

Screening for allergies before a medication is prescribed or firstadministered is an important preventive measure. A careful his-tory of any sensitivity to suspected antigens must be obtained be-fore administering any medication, particularly in parenteralform, because this route is associated with the most severe ana-phylaxis. Nurses caring for patients in any setting (hospital,home, outpatient diagnostic testing sites, long-term care facilities)must assess patients’ risk for anaphylactic reactions. The patientis asked about previous exposure to contrast agents used for diag-

Anaphylactoid (Anaphylaxis-Like) Reaction

Closely related to anaphylaxis is an anaphylactoid (anaphylaxis-like)reaction, caused by the release of mast cell and basophil mediatorstriggered by non–IgE-mediated events. An anaphylactoid reactionmay occur with medications, food, exercise, and cytotoxic antibodytransfusions. The reaction may be local or systemic. Local reactionsusually involve urticaria and angioedema at the site of the antigenexposure. Although possibly severe, anaphylactoid reactions arerarely fatal. Systemic reactions occur within about 30 minutes of ex-posure involving cardiovascular, respiratory, gastrointestinal, and in-tegumentary organ systems. For the most part, an anaphylactoidreaction and its treatment are identical to that of anaphylaxis(Neugut et al., 2001).

Chart53-2

Chart53-2

Common Causes of Anaphylaxis

FoodsPeanuts, tree nuts (walnuts, pecans, cashews, almonds, etc.), shell-fish (shrimp, lobster, crab, etc.), fish, milk, eggs, soy, wheat

MedicationsAntibiotics, especially penicillin and sulfa antibiotics, allopurinol,radiocontrast agents, anesthetic agents (lidocaine, procaine), vac-cines, hormones (insulin, vasopressin, ACTH), aspirin, nonsteroidalanti-inflammatory drugs (NSAIDs)

Other Pharmaceutical/Biologic AgentsAnimal serums (tetanus antitoxin, snake venom antitoxin, rabiesantitoxin), antigens used in skin testing

Insect StingsBees, wasps, hornets, yellow jackets, ants, including fire ants

LatexMedical and nonmedical products containing latex

Chart53-3

Chart53-3


nostic tests and any allergic reactions, as well as reactions to anymedications, foods, insect stings, and latex. Persons predisposed toanaphylaxis should wear some form of identification, such as amedical alert bracelet, naming allergies to medications, food, andother substances.

People who are allergic to insect venom may require venom im-munotherapy, which is used as a control measure and not a cure.Immunotherapy following an insect sting is very effective in re-ducing the risk of anaphylaxis from future stings (Neugut et al.,2001). Insulin-allergic diabetic patients and penicillin-sensitivepatients may require desensitization. Desensitization is based oncontrolled anaphylaxis, with a gradual release of mediators. Pa-tients who undergo desensitization are cautioned that there shouldbe no lapses in therapy, because this may lead to the reappearanceof an allergic reaction when the medication is reinstituted.

Medical ManagementManagement depends on the severity of the reaction. Initially,respiratory and cardiovascular functions are evaluated. If the pa-tient is in cardiac arrest, cardiopulmonary resuscitation is insti-tuted. Oxygen is provided in high concentrations duringcardiopulmonary resuscitation or when the patient is cyanotic,dyspneic, or wheezing. Epinephrine, in a 1�1,000 dilution, is ad-ministered subcutaneously in the upper extremity or thigh andmay be followed by a continuous intravenous infusion. Antihis-tamines and corticosteroids may also be given to prevent recur-rences of the reaction and to treat urticaria and angioedema. Tomaintain blood pressure and normal hemodynamic status, IV flu-ids (ie, normal saline solution), volume expanders, and vasopres-sor agents are given. In patients with episodes of bronchospasmor a history of bronchial asthma or chronic obstructive pul-monary disease, aminophylline and corticosteroids may also beadministered to improve airway patency and function. If hy-potension is unresponsive to vasopressors, intravenous glucagonmay be given for its acute inotropic and chronotropic effects. Pa-tients with severe reactions are observed closely for 12 to 14 hours.Because of the potential for recurrence, patients with even mildreactions must be educated concerning this risk.

Nursing ManagementIf a patient is experiencing an allergic response, the nurse’s initialaction is to assess the patient for signs and symptoms of anaphy-laxis. The nurse assesses the airway, breathing pattern, and othervital signs. The patient is observed for signs of increasing edemaand respiratory distress. Prompt notification of the physician andpreparation for initiation of emergency measures (intubation,administration of emergency medications, insertion of intra-venous lines, fluid administration, oxygen administration) areimportant to reduce the severity of the reaction and to restore car-diovascular function. The nurse documents the interventionsused and the patient’s response to treatment, vital signs, and lab-oratory values.

The patient who has recovered from anaphylaxis needs an ex-planation of what occurred and instruction about avoiding futureexposure to antigens and administering emergency medicationsto treat anaphylaxis. The patient must be instructed about anti-gens that should be avoided and about other strategies to preventrecurrence of anaphylaxis. All patients who have experienced ananaphylactic reaction should receive a prescription for preloadedsyringes of epinephrine. The nurse instructs the patient and fam-ily in their use and has the patient and family demonstrate correctadministration (Chart 53-4).

ALLERGIC RHINITISAllergic rhinitis (inflammation of nasal mucosa; hay fever,chronic allergic rhinitis, pollinosis) is the most common form ofrespiratory allergy presumed to be mediated by an immediate(type I hypersensitivity) immunologic reaction. It affects about8% to 10% of the U.S. population (20% to 30% of adolescents).The symptoms are similar to viral rhinitis but are usually morepersistent and demonstrate seasonal variation (Tierney, McPhee& Papadakis, 2001). It often occurs with other conditions, suchas allergic conjunctivitis, sinusitis, and asthma. Allergic rhinitis isassociated with impaired work and school performance and de-creased quality of life (Ratner, Ehrlich, Fineman et al., 2002).When untreated, many complications may result, such as allergicasthma, chronic nasal obstruction, chronic otitis media with hear-ing loss, anosmia (absence of the sense of smell), and, in children,orofacial dental deformities. Early diagnosis and adequate treat-ment are essential to reduce complications and relieve symptoms.

Because allergic rhinitis is induced by airborne pollens ormolds, it is characterized by the following seasonal occurrences:

• Early spring—tree pollen (oak, elm, poplar)• Early summer—rose pollen (rose fever), grass pollen

(Timothy, red-top)• Early fall—weed pollen (ragweed)

Each year, attacks begin and end at about the same time. Air-borne mold spores require warm, damp weather. Although thereis no rigid seasonal pattern, these spores appear in early spring,are rampant during the summer, and taper off and disappear bythe first frost.

PathophysiologySensitization begins by ingestion or inhalation of an antigen. Onre-exposure, the nasal mucosa reacts by the slowing of ciliary ac-tion, edema formation, and leukocyte (primarily eosinophil) in-filtration. Histamine is the major mediator of allergic reactionsin the nasal mucosa. Tissue edema results from vasodilation andincreased capillary permeability.

FIGURE 53-5 The EpiPen and EpiPen Jr. Autoinjectors are commerciallyavailable first-aid devices that administer premeasured doses of epinephrine.An EpiPen training device is available for patients to practice correct self-injection technique. Courtesy of Dey Pharmaceuticals, Napa, CA.


Clinical ManifestationsTypical signs and symptoms of allergic rhinitis include nasal con-gestion; clear, watery nasal discharge; intermittent sneezing; andnasal itching. Itching of the throat and soft palate is common.Drainage of nasal mucus into the pharynx initiates multiple at-tempts to clear the throat and results in a dry cough or hoarseness.Headache, pain over the paranasal sinuses, and epistaxis can ac-company allergic rhinitis. The symptoms of this chronic conditiondepend on environmental exposure and intrinsic host responsive-ness. Allergic rhinitis may affect quality of life by also producing fa-tigue, loss of sleep, and poor concentration (Ratner et al., 2002).

Assessment and Diagnostic FindingsDiagnosis of seasonal allergic rhinitis is based on history, physi-cal examination, and diagnostic test results. Diagnostic tests in-clude nasal smears, peripheral blood counts, total serum IgE,epicutaneous and intradermal testing, RAST, food eliminationand challenge, and nasal provocation tests. Results indicative of allergy as the cause of rhinitis include increased IgE andeosinophil levels and positive reactions on allergen testing. False-positive and false-negative responses to these tests, particularlyskin testing and provocation tests, may occur.

Medical ManagementThe goal of therapy is to provide relief from symptoms. Therapymay include one or all of the following interventions: avoidancetherapy, pharmacotherapy, and immunotherapy (Kay, 2001b).Verbal instructions must be reinforced by written information.Knowledge of general concepts regarding assessment and therapy inallergic diseases is important so that patients can learn to managecertain conditions as well as prevent severe reactions and illnesses.

AVOIDANCE THERAPYIn avoidance therapy, every attempt is made to remove the aller-gens that act as precipitating factors. Simple measures and envi-ronmental controls are often effective in decreasing symptoms.Examples include use of air conditioners, air cleaners, humidifiersand dehumidifiers, and smoke-free environments. In many cases,it is impossible to avoid exposure to all environmental allergens,so pharmacologic therapy or immunotherapy is needed.

PHARMACOLOGIC THERAPY

Antihistamines. Antihistamines, now classified as H1-receptorantagonists (or H1-blockers), are used in managing mild allergicdisorders. (H2-receptor antagonists are used to treat gastric andduodenal ulcers.) H1-blockers bind selectively to H1 receptors,preventing the actions of histamines at these sites. They do notprevent the release of histamine from mast cells or basophils. TheH1-antagonists have no effect on H2-receptors, but they do havethe ability to bind to nonhistaminic receptors. The ability of cer-tain antihistamines to bind to and block muscarinic receptors un-derlies several of the prominent anticholinergic side effects ofthese medications.

Oral antihistamines, which are readily absorbed, are most ef-fective when given at the first occurrence of symptoms becausethey prevent the development of new symptoms by blocking theactions of histamine at the H1-receptors. The effectiveness ofthese medications is limited to certain patients with hay fever, va-somotor rhinitis, urticaria (hives), and mild asthma. They arerarely effective in other conditions or in any severe conditions.

The patient is taught how to inject epinephrine in the event of ananaphylactic reaction. The patient should be encouraged to prac-tice this technique using a training device.1. Carefully uncap the Epipen device, holding it so that the

injecting end is upright.

Chart 53-4 • PATIENT EDUCATIONSelf-Administration of Epinephrine

2. Position the device at the middle portion of the thigh.

3. Push the device into the thigh as far as possible. The Epipendevice will autoinject a premeasured dose of epinephrine intothe subcutaneous tissue.

Ep

iPen

epin

ephrin

e

EpiPen EpiPen

EpiPen EpiPen


Antihistamines are the major class of medications prescribedfor the symptomatic relief of allergic rhinitis. The major side ef-fect is sedation, although histamine H1 antagonists are less sedat-ing than earlier antihistamines (Kay, 2001b). Additional sideeffects include nervousness, tremors, dizziness, dry mouth, palpi-tations, anorexia, nausea, and vomiting. Antihistamines are con-traindicated during the third trimester of pregnancy; for nursingmothers and newborns; in children and elderly people; and in pa-tients whose conditions can be aggravated by muscarinic blockade(ie, asthma, urinary retention, open-angle glaucoma, hyperten-sion, and prostatic hyperplasia).

Newer antihistamines are called second-generation or non-sedating H1-receptor antagonists. Unlike first-generation H1-receptor antagonists, they do not cross the blood–brain barrierand do not bind to cholinergic, serotonin, or alpha-adrenergic re-ceptors. They bind to peripheral rather than central nervous sys-tem H1-receptors, causing less sedation. Examples of thesemedications are loratadine (Claritin), cetirizine (Zyrtec), and fex-ofenadine (Allegra). These are summarized in Table 53-2.

Adrenergic Agents. Adrenergic agents, vasoconstrictors of mu-cosal vessels, are used topically (nasal and ophthalmic) in addi-

tion to the oral route. The topical route (drops and sprays) causesfewer side effects than oral administration; however, the use ofdrops and sprays should be limited to a few days to avoid reboundcongestion. Adrenergic nasal decongestants are used for the reliefof nasal congestion when applied topically to the nasal mucosa.They activate the alpha-adrenergic receptor sites on the smoothmuscle of the nasal mucosal blood vessels, reducing local bloodflow, fluid exudation, and mucosal edema. Topical ophthalmicdrops are used for symptomatic relief of eye irritations due to al-lergies. Potential side effects include hypertension, dysrhythmias,palpitations, central nervous system stimulation, irritability,tremor, and tachyphylaxis (acceleration of hemodynamic status).Examples of adrenergic decongestants and their routes of admin-istration are found in Table 53-3.

Mast Cell Stabilizers. Intranasal cromolyn sodium (Nasalcrom)is a spray that acts by stabilizing the mast cell membrane, thus re-ducing the release of histamine and other mediators of the aller-gic response. In addition, it inhibits macrophages, eosinophils,monocytes, and platelets involved in the immune response (Ratneret al., 2002). Cromolyn interrupts the physiologic response tonasal antigens and is used prophylactically before exposure to

Table 53-2 • Chemical Classes of H1 Antihistamines

CLASSIFICATION AND EXAMPLE MAJOR SIDE EFFECTS NURSING IMPLICATIONS

SedatingEthanolamines

Ex: diphenhydramine (Benadryl)

PiperazinesEx: hydroxyzine (Atarax)

AlkylaminesEx: chlorpheniramine (Chlor-Trimeton)

EthylenediaminesEx: tripelennamine (PBZ)

PhenothiazinesEx: promethazine (Phenergan)

Nonsedatingloratadine (Claritin)

fexofenadine (Allegra)

cetirizine (Zyrtec)

Drowsiness, confusion

Dry mouth, nausea, vomiting

PhotosensitivityUrinary retentionDulls mental alertness; drowsiness

Dry mouth

Less CNS depression than other groups;best class for daytime use

Gastrointestinal upset

Drowsiness

Palpitations

Heavy sedation and drowsiness

Nasal congestionHypotension

Gastrointestinal upset

Occasional drowsiness and fatigue

Drowsiness, dry mouth

Teach patient to avoid alcohol, driving, or engaging inany hazardous activities until CNS response to drugtreatment is stabilized.

Suggest sucking on hard candy or ice chips for relief ofdry mouth.

Encourage use of sunscreen and hat while outdoors.Assess for urinary retention; monitor urinary output.Teach patient to avoid alcohol, driving, or engaging in

any hazardous activities until CNS response to drugtreatment is stabilized.

Suggest sucking on hard candy or ice chips for relief ofdry mouth.


Administer medication with food or milk to decrease GIdistress. Increase fluid intake.


Instruct patient to sit and relax a few minutes beforeactivity.


Encourage use of humidification at home.Instruct patient to rise from a sitting position slowly.

Counsel patient to take the medication on an emptystomach.




allergens to prevent the onset of symptoms and to treat symptomsonce they occur. It is also used therapeutically in chronic allergicrhinitis. This spray is as effective as antihistamines but less effec-tive than intranasal corticosteroids in the treatment of seasonalallergic rhinitis. Patients must be informed that the beneficial ef-fects of the medication may take a week or so to occur. The med-ication is of no benefit in the treatment of nonallergic rhinitis.Adverse effects (ie, sneezing, local stinging, and burning sensa-tions) are usually mild.

Corticosteroids. Intranasal corticosteroids are indicated in moresevere cases of allergic and perennial rhinitis that cannot be con-trolled by more conventional medications such as decongestants,antihistamines, and intranasal cromolyn. These medicationsinclude beclomethasone (Beconase, Vancenase), budesonide(Rhinocort), dexamethasone (Decadron Phosphate Turbinaire),flunisolide (Nasalide), fluticasone (Cutivate, Flonase), and tri-amcinolone (Nasacort).

Because of their anti-inflammatory actions, these medicationsare equally effective in preventing or suppressing the major symp-toms of allergic rhinitis. Corticosteroids are administered bymetered-spray devices. If the nasal passages are blocked, a topicaldecongestant can be used to clear the passages before the adminis-tration of the intranasal corticosteroid. Patients must be aware thatfull benefit may not be achieved for several days to 2 weeks. Ad-verse effects of intranasal corticosteroids are mild and include dry-ing of the nasal mucosa and burning and itching sensations causedby the vehicle used to administer the medication. Systemic effectsare more likely with dexamethasone. Recommended use of thismedication is limited to 30 days. Beclomethasone, budesonide, flu-nisolide, fluticasone, and triamcinolone are deactivated rapidlyafter absorption, so they do not achieve significant blood levels.Corticosteroids suppress host defenses, so they must be used withcaution in patients with tuberculosis or untreated bacterial infec-tions of the lungs. Patients on corticosteroids are at risk for infec-tion and for suppression of typical manifestations of inflammationbecause host defenses are compromised. Inhaled corticosteroids donot affect the immune system to the same degree as systemic cor-ticosteroids (ie, oral corticosteroids). As corticosteroids are inhaledinto the upper respiratory tract, tuberculosis or untreated bacte-rial infections of the lungs may become apparent and progress.Whenever possible, patients with tuberculosis and other bacterialinfections of the lungs should avoid inhaled corticosteroids.

Oral and parenteral corticosteroids are used when conven-tional therapy has failed and symptoms are severe and of short du-ration. They can control symptoms of allergic reactions such ashay fever, medication-induced allergies, and allergic reactions to

insect stings. Because the response to corticosteroids is delayed,they have little or no value in acute therapy for severe reactionssuch as anaphylaxis. Patients who receive corticosteroids must becautioned not to stop taking the medication suddenly or withoutspecific instructions from the physician. The patient is also in-structed about side effects, which include fluid retention, weightgain, hypertension, gastric irritation, glucose intolerance, andadrenal suppression. Further discussion of corticosteroids is pro-vided in Chapter 42.

IMMUNOTHERAPYAllergen desensitization (allergen immunotherapy, hyposensitiza-tion) is primarily used to treat IgE-mediated diseases by injectionsof allergen extracts. This type of therapy provides an adjunct tosymptomatic pharmacologic therapy and can be used when aller-gen avoidance is not possible (Parslow et al., 2001). Specific im-munotherapy has been used in the treatment of allergic disordersfor about 100 years. It consists of administering increasing con-centrations of extracts of specific allergens over a long period (Kay,2001b). Goals of immunotherapy include reducing the level ofcirculating IgE, increasing the level of blocking antibody IgG,and reducing mediator cell sensitivity. Immunotherapy has beenmost effective for ragweed pollen; however, treatment for grass,tree pollen, cat, and house dust mite allergens has also beeneffective.

Correlation of a positive skin test with a positive allergy his-tory is an indication for immunotherapy if the allergen cannot beavoided. The value has been fairly well established in instances ofallergic rhinitis and bronchial asthma that are clearly due to sen-sitivity to one of the common pollens, molds, and householddust. Although helpful in most patients, immunotherapy doesnot cure the condition. Before immunotherapy is initiated, thepatient must understand what to expect and the importance ofcontinuing therapy for several years. When skin tests are per-formed, the results are correlated with clinical manifestations;treatment is based on the patient’s needs rather than on skin tests.

The most common method of treatment is the serial injectionof one or more antigens that are selected in each particular caseon the basis of skin tests. This method provides a simple and ef-ficient technique for identifying IgE antibodies to specific anti-gens. Specific treatment consists of injecting extracts of thepollens or mold spores that cause symptoms in a particular pa-tient. Injections begin with very small amounts and are graduallyincreased, usually at weekly intervals, until a maximum tolerateddose is attained. Maintenance booster injections are given at 2- to 4-week intervals, frequently for a period of several years,before maximum benefit is achieved.

Table 53-3 • Adrenergic Decongestants and Their Routes of Administration

ADRENERGIC DECONGESTANT TRADE NAME ROUTE OF ADMINISTRATION

naphazoline hydrochlorideoxymetazoline hydrochloride

phenylephrine hydrochloridepseudoephedrine hydrochloridetetrahydrozoline hydrochloride

xylometazoline hydrochloride

PrivineAfrin, Dristan long-lasting,

Neo-Synephrine 12 hour, Sinex long-lasting

Neo-SynephrineSudafedCollyrium, Murine Plus, Visine

Neo-Synephrine II, Otrivin

TopicalTopical

TopicalOralTopical ophthalmic and nasal

preparationsTopical

There are three methods of injection therapy: coseasonal, pre-seasonal, and perennial. When treatment is given on a coseasonalbasis, therapy is initiated during the season in which the patientexperiences symptoms. This method has been proved ineffectiveand is used infrequently. Also, there is an increased risk of sys-temic reactions. Preseasonal therapy injections are given 2 to 3 months before symptoms are expected, allowing time for hypo-sensitization to occur. This treatment is discontinued after theseason begins. Perennial therapy is administered all year round,usually on a monthly basis, and is the preferred method becauseit has more effective, longer-lasting results.

Any patient who receives specific immunotherapy is at risk forgeneral, and potentially fatal, anaphylaxis. This occurs most fre-quently at the induction or “up-dosing” phase. Attempts havebeen made to minimize the risk of systemic reactions by pre-treating allergen extracts with agents such as formaldehyde. Thisapproach decreases the binding of the allergen by IgE, but it alsoresults in decreased immunogenicity (Kay, 2001b).

• Deficient knowledge about allergy and the recommendedmodifications in lifestyle and self-care practices

• Ineffective individual coping with chronicity of conditionand need for environmental modifications

COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONSBased on assessment data, potential complications may includethe following:

• Anaphylaxis• Impaired breathing• Nonadherence to the therapeutic regimen

Planning and GoalsThe goals for the patient may include restoration of normalbreathing pattern, increased knowledge about the causes and con-trol of allergic symptoms, improved coping with alterations andmodifications, and absence of complications.

Nursing InterventionsIMPROVING BREATHING PATTERNThe patient is instructed and assisted to modify the environmentto reduce the severity of allergic symptoms or to prevent their oc-currence. The patient is instructed to reduce exposure to peoplewith upper respiratory infections (URIs). If a URI occurs, the pa-tient is encouraged to take deep breaths and cough frequently toensure adequate gas exchange and prevent atelectasis. The patientis instructed to seek medical attention because allergy symptomsalong with a URI may compromise adequate lung function.Compliance with medications and other treatment regimens isencouraged and reinforced.

PROMOTING UNDERSTANDING OF ALLERGY AND ALLERGY CONTROLInstruction includes strategies to minimize exposure to allergens,desensitization procedures, and correct use of medications. Thenurse informs and reminds the patient of the importance of keep-ing appointments for desensitization procedures because usuallydosages are adjusted on a weekly basis, and missed appointmentsmay interfere with the dosage adjustment.

Patients also need to understand that medications for allergycontrol should be used only when the allergy is apparent. Thisis usually on a seasonal basis. Continued use of medicationswhen not required may cause an increased tolerance to the med-ication, with the result that the medication is not effective whenneeded.

COPING WITH A CHRONIC DISORDERAlthough allergic reactions are infrequently life-threatening, theyrequire constant vigilance to avoid allergens and modification ofthe lifestyle or environment to prevent recurrence of symptoms.Allergic symptoms are often present year-round and create dis-comfort and inconvenience for the patient. Although patientsmay not feel ill during allergy seasons, they often do not feel welleither. The need to be alert for possible allergens in the environ-ment may be tiresome, placing a burden on the patient’s abilityto lead a normal life. Stress related to these difficulties may in turnincrease the frequency or severity of symptoms.

To assist the patient in adjusting to these modifications, thenurse must have an appreciation of the difficulties encountered


NURSING ALERT Because the injection of an allergen may in-duce systemic reactions, such injections are given only in a setting(ie, physician’s office, clinic) where epinephrine is immediatelyavailable.

!Because of the risk for anaphylaxis, injections should not be

given by a lay person or by the patient. The patient remains in theoffice or clinic for at least 30 minutes after the injection and is ob-served for possible systemic symptoms. If a large, local swelling de-velops at the injection site, the next dose should not be increased,because this may be a warning sign of a possible systemic reaction.

Therapeutic failure is evident when a patient does not experi-ence a decrease of symptoms within 12 to 24 months, fails to de-velop increased tolerance to known allergens, and cannot decreasethe use of medications to reduce symptoms. Potential causes oftreatment failure include misdiagnosis of allergies, inadequatedoses of allergen, newly developed allergies, and inadequate en-vironmental controls.

NURSING PROCESS: THE PATIENT WITH ALLERGIC RHINITISAssessmentThe examination and history of the patient reveal sneezing, oftenin paroxysms, thin and watery nasal discharge, itching eyes andnose, lacrimation, and occasionally headache. The health historyincludes a personal or family history of allergy. The allergy as-sessment identifies the nature of antigens, seasonal changes insymptoms, and medication history. The nurse also obtains sub-jective data about how the patient feels just before symptoms be-come obvious, such as the occurrence of pruritus, breathingproblems, and tingling sensations. In addition to these symp-toms, hoarseness, wheezing, hives, rash, erythema, and edema arenoted. Any relationship between emotional problems or stressand the triggering of allergy symptoms is assessed.

DiagnosisNURSING DIAGNOSESBased on the assessment data, the patient’s major nursing diag-noses may include the following:

• Ineffective breathing pattern related to allergic reaction


by the patient. The patient is encouraged to verbalize feelings andconcerns in a supportive environment and to identify strategiesto deal with them effectively.

MONITORING AND MANAGING POTENTIAL COMPLICATIONS

Anaphylaxis and Impaired BreathingRespiratory and cardiovascular functioning can be significantlyaltered during allergic reactions by the reaction itself or by themedications used to treat reactions. The respiratory status is eval-uated by monitoring the respiratory rate and pattern and by as-sessing for breathing difficulties or abnormal lung sounds. Thepulse rate and rhythm and blood pressure are monitored to assesscardiovascular status regularly or any time the patient reportssymptoms such as itching or difficulty breathing. In the event ofsigns and symptoms suggestive of anaphylaxis, emergency med-ications and equipment must be available for immediate use.

Nonadherence to Therapeutic RegimenKnowing about the treatment regimen does not ensure adher-ence. Having the patient identify potential barriers and exploreacceptable solutions for effective management of the condition(eg, installing tile floors rather than carpet, not gardening in thespring) can increase adherence to the treatment regimen.

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-CareThe patient is instructed about strategies to minimize exposureto allergens, the actions and adverse effects of medications, andthe correct use of medications. The patient should know thenames, dose, frequency, actions, and side effects of all medicationstaken.

Instruction about strategies to control allergic symptoms isbased on the needs of the patient as determined by the resultsof tests, the severity of symptoms, and the motivation of thepatient and family to deal with the condition. Suggestions forpatients sensitive to dust and mold in the home are given inChart 53-5.

If the patient is to undergo immunotherapy, the nurse re-inforces the physician’s explanation regarding the purpose andprocedure. Instructions are given regarding the series of injec-tions, usually given initially every week and then at 2- to 4-weekintervals. These instructions include remaining in the physician’soffice or the clinic at least 30 minutes after the injection so thatemergency treatment may be given if the patient has a reaction;avoiding rubbing or scratching the injection site; and continuingwith the series for the period of time required. In addition, thepatient and family are instructed about emergency treatment ofsevere allergic symptoms.

Because antihistamines often produce drowsiness, the patientis cautioned about this and other side effects of the particularmedication. Operating machinery, driving a car, and performingactivities requiring intense concentration should be postponed.The patient is also informed about the dangers of drinking alco-hol when taking these medications because they tend to exagger-ate the effects of alcohol.

The patient must be aware of the effects caused by overuse ofthe sympathomimetic agents in nose drops or sprays. A conditionreferred to as rhinitis medicamentosa may result (Fig. 53-6). Aftertopical application of the medication, a rebound period mayoccur in which the nasal mucous membranes become more ede-matous and congested than they were before the medication wasused. Such a reaction encourages the use of more medication, anda cyclical pattern results. The topical agent must be discontinuedimmediately and completely to correct this problem.

Chart 53-5Home Care Checklist • Allergy Management

At the completion of home care instruction, the patient or caregiver will be able to:

• Verbalize how to maintain a dust-free environment by removing drapes, curtains, and venetian blinds and replacing them with pull shades; covering the mattress with a hypoallergenic cover that can be zipped; and removing rugs and replacing them with wood flooring or linoleum. ✓ ✓

• Identify rationale for washing the floor and dusting and vacuuming daily. ✓ ✓

• Identify rationale for replacing stuffed furniture with wood pieces that can easily be dusted. ✓ ✓

• State rationale for wearing a mask whenever cleaning is being done. ✓ ✓

• Identify rationale for avoiding use of tufted bedspreads, stuffed toys, and feather pillows and replacing them with washable cotton material. ✓ ✓

• State rationale for avoiding the use of any clothing that causes itching. ✓ ✓

• Verbalize ways to reduce dust in the house as a whole by using steam or hot water for heating rather than air and using air filters or air conditioning. ✓ ✓

• Verbalize ways to reduce exposure to pollens or molds by identifying seasons of the year when pollen counts are high; wearing a mask at times of increased exposure (windy days and when grass is being cut); and avoiding contact with weeds, dry leaves, and freshly cut grass. ✓ ✓

• State rationale for seeking air-conditioned areas at the height of the allergy season. ✓ ✓

• State rationale for avoiding sprays and perfumes. ✓ ✓

• State rationale for use of hypoallergenic cosmetics. ✓ ✓

• State rationale for taking prescribed medications as ordered. ✓ ✓

• Identify specific foods that may cause allergic symptoms. (Examples of foods that can cause allergic reactions are fish, nuts, eggs, and chocolate.) ✓ ✓

• Develop a list of foods to avoid. ✓ ✓

Patient Caregiver


Continuing CareFollow-up telephone calls to the patient are often reassuring tothe patient and family and provide an opportunity for the nurseto answer any questions. The patient is reminded to keep follow-up appointments and is informed about the importance of con-tinuing with treatment. The importance of participating inhealth promotion activities and health screening is emphasized tothe patient.

EvaluationEXPECTED PATIENT OUTCOMESExpected patient outcomes may include:

1. Exhibits normal breathing patternsa. Demonstrates lungs clear on auscultationb. Exhibits absence of adventitious breath sounds (crack-

les, rhonchi, wheezing)c. Has a normal respiratory rate and patternd. Reports no complaints of respiratory distress (shortness

of breath, difficulty on inspiration or expiration)2. Demonstrates knowledge about allergy and strategies to

control symptomsa. Identifies causative allergens, if knownb. States methods of avoiding allergens and controlling in-

door and outdoor precipitating factorsc. Removes from the environment items that retain dustd. Wears a dampened mask if dust or mold may be a

probleme. Avoids smoke-filled rooms and dust-filled or freshly

sprayed areasf. Uses air conditioning for a major part of the dayg. Takes antihistamines as prescribed; participates in hypo-

sensitization program, if applicableh. Describes name, purpose, side effects, and method of

administration of prescribed medicationsi. Identifies when to seek immediate medical attention for

severe allergic responsesj. Describes activities that are possible, including ways to

participate in activities without activating the allergies3. Experiences relief of discomfort while adapting to the in-

conveniences of an allergya. Relates the emotional aspects of the allergic responseb. Demonstrates use of measures to cope positively with

allergy4. Absence of complications

a. Exhibits vital signs within normal limits

b. Reports no symptoms or episodes of anaphylaxis (ur-ticaria, itching, peripheral tingling, fullness in the mouthand throat, flushing, or difficulty swallowing) or cough-ing, wheezing, or difficulty breathing

c. Demonstrates correct procedure to self-administer emer-gency medications to treat severe allergic reaction

d. Correctly states medication names, dose and frequencyof administration, and medication actions

e. Correctly identifies side effects and untoward signs andsymptoms to report to physician

f. Discusses acceptable lifestyle changes and solutions foridentified potential barriers for compliance with treat-ment and medication regimen

CONTACT DERMATITISContact dermatitis (dermatitis venenata), a type IV delayed hy-persensitivity reaction, is an acute or chronic skin inflammationthat results from direct skin contact with chemicals or allergens.There are four basic types: allergic, irritant, phototoxic, andphotoallergic (Table 53-4). Eighty percent of cases are due toexcessive exposure to or additive effects of irritants (eg, soaps,detergents, organic solvents) (Tierney et al., 2001). Skin sensi-tivity may develop after brief or prolonged periods of exposure,and the clinical picture may appear hours or weeks after the sen-sitized skin has been exposed.

Clinical ManifestationsSymptoms include itching, burning, erythema, skin lesions (vesi-cles), and edema, followed by weeping, crusting, and finally dry-ing and peeling of the skin. In severe responses, hemorrhagicbullae may develop. Repeated reactions may be accompanied bythickening of the skin and pigmentary changes. Secondary inva-sion by bacteria may develop in skin abraded by rubbing orscratching. Usually, there are no systemic symptoms unless theeruption is widespread.

Assessment and Diagnostic FindingsThe location of the skin eruption and the history of exposure aidin determining the condition. In cases of obscure irritants or anunobservant patient, however, diagnosis may be extremely diffi-cult, often involving many trial-and-error procedures before thecause is determined. Patch tests on the skin with suspected of-fending agents may clarify the diagnosis.

ATOPIC DERMATITISAtopic dermatitis is a type I immediate hypersensitivity disor-der. A family history is common. The incidence of atopic der-matitis is highest in infants and children. Atopic dermatitis(eczema) affects 10% to 20% of children in Western populations(Kay, 2001b). Most patients have significant elevations of serumIgE and peripheral eosinophilia. Pruritus and hyperirritability ofthe skin are the most consistent features of atopic dermatitis andare related to large amounts of histamine in the skin. Excessivedryness of the skin with resultant itching is related to changes inlipid content, sebaceous gland activity, and sweating. In responseto stroking of the skin, immediate redness appears on the skinand is followed in 15 to 30 seconds by pallor, which persists for

Relief

Nasalcongestion

Reboundreaction

Topical applicationof sympathomimetic

drugs

FIGURE 53-6 Rhinitis medicamentosa. This cyclic pattern results fromoveruse of sympathomimetic nose drops or sprays.


1 to 3 minutes. Lesions develop secondary to the trauma of scratch-ing and appear in areas of increased sweating and hypervascularity.Atopic dermatitis is chronic, with remissions and exacerbations.This condition has a tendency to recur, with remission fromadolescence to age 20 (Tierney et al., 2001). Treatment must beindividualized.

Medical ManagementGuidelines for treatment include decreasing itching and scratch-ing by wearing cotton fabrics, washing with a mild detergent,humidifying dry heat in winter, maintaining room temperatureat 20°C to 22.2°C (68°F to 72°F), using antihistamines such asdiphenhydramine (Benadryl), and avoiding animals, dust, sprays,and perfumes. Keeping the skin moisturized with daily baths tohydrate the skin and topical skin moisturizers is encouraged.Topical corticosteroids are used to prevent inflammation, andany infection is treated with antibiotics to eliminate Staphylococ-cus aureus when indicated. Use of low doses of cyclosporine(Neoral, Sandimmune), an immunosuppressive agent, may beeffective (Kay, 2001b).

Nursing ManagementPatients who experience atopic dermatitis and their families re-quire assistance and support from the nurse to cope with the dis-order. The symptoms are often disturbing to the patient and

disruptive to the family. The appearance of the skin may affectthe patient’s self-esteem and may affect the patient’s willingnessto interact with others. Instructions and counseling about strate-gies to incorporate preventive measures and treatments into thelifestyle of the family may be helpful.

Patients and family members need to be aware of signs of sec-ondary infection and of the need to seek treatment if infection oc-curs. The nurse also teaches the patient and family about the sideeffects of medications used in treatment.

DERMATITIS MEDICAMENTOSA (DRUG REACTIONS)Dermatitis medicamentosa, a type I hypersensitivity disorder, isthe term applied to skin rashes induced by the internal adminis-tration of certain medications. Although individuals react differ-ently to each medication, certain medications tend to induceeruptions of similar types. Rashes are among the most commonadverse reactions to medications and occur in approximately 2%to 3% of hospitalized patients (Tierney et al., 2001).

In general, drug reactions appear suddenly, have a particularlyvivid color, present with characteristics that are more intense thanthe somewhat similar eruptions of infectious origin, and, with theexception of bromide and the iodide rashes, disappear rapidlyafter the medication is withdrawn. Rashes may be accompaniedby systemic or generalized symptoms. Upon discovery of a med-ication allergy, patients are warned that they have a hypersensi-

Table 53-4 • Types, Testing, and Treatment of Contact Dermatitis

TYPE ETIOLOGY CLINICAL PRESENTATION DIAGNOSTIC TESTING TREATMENT

Allergic

Irritant

Phototoxic

Photoallergic

Results from contact ofskin and allergenic sub-stance. Has a sensitizationperiod of 10–14 days.

Results from contact with asubstance that chemicallyor physically damages theskin on a nonimmuno-logic basis. Occurs afterfirst exposure to irritantor repeated exposures tomilder irritants over anextended time.

Resembles the irritant typebut requires sun and achemical in combinationto damage the epidermis.

Resembles allergic dermati-tis but requires light ex-posure in addition toallergen contact to pro-duce immunologicreactivity.

Vasodilation and perivas-cular infiltrates on thedermis

Intracellular edemaUsually seen on dorsal

aspects of hand

Dryness lasting days tomonths

Vesiculation, fissures,cracks

Hands and lower armsmost common areas

Similar to irritantdermatitis

Similar to allergicdermatitis

Patch testing (contraindi-cated in acute, widespreaddermatitis)

Clinical pictureAppropriate negative patch

tests

Photopatch test

Photopatch test

Avoidance of offending materialBurow’s solution or cool water

compressSystemic corticosteroids

(prednisone) for 7–10 daysTopical corticosteroids for mild

casesOral antihistamines to relieve

pruritusIdentification and removal of

source of irritationApplication of hydrophilic cream

or petrolatum to soothe andprotect

Topical corticosteroids and com-presses for weeping lesions

Antibiotics for infection and oralantihistamines for pruritus

Same as for allergic and irritantdermatitis

Same as for allergic and irritantdermatitis

tivity to a particular medication and are advised not to take itagain. Information identifying the hypersensitivity should be car-ried with them at all times.

Skin eruptions related to medication therapy suggest moreserious hypersensitivities. Frequent assessment and prompt re-porting of the appearance of any eruptions are important so thatearly treatment can be initiated. Some cutaneous drug reactionsmay be associated with a clinical complex that involves other organs.These are known as complex drug reactions (Tierney et al.,2001).

URTICARIA AND ANGIONEUROTIC EDEMAUrticaria (hives) is a type I hypersensitive allergic reaction of theskin characterized by the sudden appearance of pinkish, edema-tous elevations that vary in size and shape and itch and cause localdiscomfort. They may involve any part of the body, including themucous membranes (especially those of the mouth), the larynx(occasionally with serious respiratory complications), and the gas-trointestinal tract.

Each hive remains for a few minutes to several hours beforedisappearing. For hours or days, clusters of these lesions maycome, go, and return episodically. If this sequence continues forlonger than 6 weeks, the condition is called chronic urticaria(Tierney et al., 2001).

Angioneurotic edema involves the deeper layers of the skin,resulting in more diffuse swelling rather than the discrete lesionscharacteristic of hives. On occasion, this reaction covers the en-tire back. The skin over the reaction may appear normal but oftenhas a reddish hue. The skin does not pit on pressure, as ordinaryedema does. The regions most often involved are the lips, eyelids,cheeks, hands, feet, genitalia, and tongue; the mucous mem-branes of the larynx, the bronchi, and the gastrointestinal canalmay also be affected, particularly in the hereditary type (see sec-tion that follows). Swellings may appear suddenly, in a few sec-onds or minutes, or slowly, in 1 or 2 hours. In the latter case, theirappearance is often preceded by itching or burning sensations.Seldom does more than a single swelling appear at one time, al-though one may develop while another is disappearing. Infre-quently, swelling recurs in the same region. Individual lesionsusually last 24 to 36 hours. On rare occasions, swelling may recurwith remarkable regularity at intervals of 3 to 4 weeks.

HEREDITARY ANGIOEDEMAHereditary angioedema, although not an immunologic disorderin the usual sense, is included because of its resemblance to aller-gic angioedema and because of the seriousness of the condition.Symptoms are due to edema of the skin, the respiratory tract, orthe digestive tract. Attacks may be precipitated by trauma or mayseem to occur spontaneously.

Clinical ManifestationsWhen skin is involved, the swelling is usually diffuse, does notitch, and is usually not accompanied by urticaria. Gastrointestinaledema may cause abdominal pain severe enough to suggest theneed for surgery. Typically, attacks last 1 to 4 days and are gener-

ally harmless. Occasionally, attacks affect the subcutaneous andsubmucosal tissues in the region of the upper airway and can beassociated with respiratory obstruction and asphyxiation. This dis-order is inherited as an autosomal dominant trait. Approximately85% of patients with this disorder have one nonproductive gene;the other 15% have a gene mutation (Parslow et al., 2001).

Medical ManagementAttacks usually subside within 3 to 4 days, but during this timethe patient should be observed carefully for signs of laryngeal ob-struction, which may necessitate tracheostomy as a life-savingmeasure. Epinephrine, antihistamines, and corticosteroids areusually used in treatment, but their success is limited.

FOOD ALLERGYIgE-mediated food allergy, a type I hypersensitivity reaction, occursin 0.1% to 7.0% of the population. Almost any food can cause al-lergic symptoms. Any food can contain an allergen that results inanaphylaxis. The most common offenders are seafood (lobster,shrimp, crab, clams, fish), legumes (peanuts, tree nuts, peas, beans,licorice), seeds (sesame, cottonseed, caraway, mustard, flaxseed, andsunflower seeds), nuts, berries, egg white, buckwheat, milk, andchocolate (Parslow et al., 2001). Peanut and tree nut (ie, cashew,walnut) allergies are responsible for most severe food allergy reac-tions (Sicherer, Munoz-Furlong, Burks et al., 1999).

One of the dangers of food allergens is that they may be hid-den in other foods and not apparent to those susceptible to theallergen. For example, peanuts and peanut butter are often usedin salad dressings and Asian, African, and Mexican cooking and may result in severe allergic reactions, including anaphy-laxis. Previous contamination of equipment with allergens (ie,peanuts) during preparation of another food product (ie, choco-late cake) is enough to produce anaphylaxis in those with severeallergy.

Clinical ManifestationsClinical symptoms are classic allergic symptoms (urticaria, atopicdermatitis, wheezing, cough, laryngeal edema, angioedema) andgastrointestinal symptoms (itching; swelling of lips, tongue, andpalate; abdominal pain; nausea; cramps; vomiting; and diarrhea).

Assessment and Diagnostic FindingsA careful diagnostic workup is required in any patient with a sus-pected food hypersensitivity. Included are a detailed allergy history,a physical examination, and pertinent diagnostic tests. When test-ing for allergy, skin testing is used to identify the source of symp-toms and is useful in identifying specific foods as causative agents.

Medical ManagementTherapy for food hypersensitivity includes elimination of thefood responsible for the hypersensitivity (Chart 53-6). Pharma-cologic therapy is necessary in patients who cannot avoid expo-sure to offending foods or patients with multiple food sensitivitiesnot responsive to elimination measures. Medication therapy in-volves the use of H1- and H2-blockers, antihistamines, adrenergicagents, corticosteroids, and cromolyn sodium.



Many food allergies disappear with time, particularly in chil-dren. About one third of proven allergies disappear in 1 to 2 yearsif the patient carefully avoids the offending food.

Nursing ManagementIn addition to participating in management of the allergic reac-tion, the nurse focuses on preventing future exposure of the pa-tient to the food allergen. If a severe allergic or anaphylacticreaction to food allergens has occurred, the nurse must instructthe patient and family about strategies to prevent its recurrence.The patient is instructed about the importance of carefully as-sessing food prepared by others for obvious as well as hiddensources of food allergens and of avoiding locations and facilitieswhere those allergens are likely to be present. The patient andfamily must be knowledgeable about early signs and symptomsof allergic reactions and must be proficient in emergency admin-istration of epinephrine if a reaction occurs. The nurse also ad-vises the patient to wear a medical alert bracelet or to carryidentification and emergency equipment at all times.

SERUM SICKNESSThe illness known as serum sickness is an example of an immunecomplex type III hypersensitivity. It has traditionally resulted fromthe administration of therapeutic antisera of animal sources for thetreatment or prevention of infectious diseases, such as tetanus, pneu-monia, rabies, diphtheria, botulism, and venomous snake and blackwidow spider bites. With the advent of human antitetanus serumand antibiotics, classic serum sickness is much less common now.However, various medications (primarily penicillin) may cause aserum sickness–like reaction similar to that caused by foreign sera.

Clinical ManifestationsSymptoms are due to a reaction and immunologic attack on theserum or medication. Antibodies appear to be of the IgE and IgMclasses. Early manifestations, beginning 6 to 10 days after the ad-ministration of the medication, include an inflammatory reactionat the site of injection of the medication, followed by regional andgeneralized lymphadenopathy. There is usually a skin rash, whichmay be urticarial or purpuric. Joints are frequently tender andswollen. Vasculitis may occur in any organ but is most commonlyobserved in the kidney, resulting in proteinuria and, occasionally,casts in the urine. There may be mild to severe cardiac involvement.Peripheral neuritis may cause temporary paralysis of the upper ex-tremities or may be widespread, causing Guillain-Barré syndrome.

Medical ManagementThe usual course lasts for several days to a few weeks if untreated,but the patient responds promptly and completely if treated withantihistamines and corticosteroids. Aggressive therapy, includingventilator support, may be necessary if peripheral neuritis andGuillain-Barré syndrome occur.

Nursing ManagementSee Chapter 64 for nursing management of Guillain-Barrésyndrome.

LATEX ALLERGYLatex allergy, the allergic reaction to natural rubber proteins, hasbeen implicated in rhinitis, conjunctivitis, contact dermatitis,urticaria, asthma, and anaphylaxis. Latex allergy and hypersensi-tivity were first reported in 1927 (Parslow et al., 2001). Althoughthe prevalence of latex allergy is unknown, since 1989 the num-ber of cases of latex allergy has steadily increased (Parslow et al.,2001). This increase may be due to the widespread use of latexgloves with implementation of universal and now standard pre-cautions in response to the AIDS epidemic, changes in the man-ufacturing of gloves to speed the process to meet the increaseddemand for gloves, and greater awareness about latex allergy andits signs and symptoms.

Natural rubber latex is derived from the sap of the rubber tree(Hevea brasiliensis). The conversion of the liquid rubber latex intoa finished product entails the addition of more than 200 chemi-cals. The proteins in the natural rubber latex (Hevea proteins) orthe various chemicals that are used in the manufacturing processare thought to be the source of the allergic reactions. Not all ob-jects composed of latex have the same ability to stimulate an al-lergic response. For example, the antigenicity of latex gloves candiffer widely depending on their manufacturing method.

Populations at risk include health care workers, patients withatopic allergies or multiple surgeries, people working in factoriesmanufacturing latex products, females, and patients with spina bi-fida. Because more food handlers, hairdressers, auto mechanics, andpolice are now wearing latex gloves, they may also be at risk for latexallergy. It is estimated that 1% to 3% of the general population hasan allergy to latex and that 10% to 17% of health care workers aresensitized. Patients are at risk for anaphylactic reactions due to con-tact with latex during medical treatments, especially surgical pro-cedures. About 19% of anaphylactic reactions associated withanesthesia are caused by allergy to latex (Brehler & Kütting, 2001).

Chart 53-6Home Care Checklist • Managing Food Allergies

At the completion of home care instruction, the patient or caregiver will be able to:

• Verbalize understanding of the need to maintain an allergen-free diet. ✓ ✓

• Demonstrate reading of food labels to identify hidden allergens in food. ✓ ✓

• Identify ways to manage an allergen-free diet when eating away from home. ✓ ✓

• State the need to wear a medical alert medallion or bracelet. ✓ ✓

• List symptoms of food allergy. ✓ ✓

• Demonstrate emergency administration of epinephrine. ✓ ✓

• State the importance of prompt treatment and health care follow-up. ✓ ✓

Patient Caregiver


Food that has been handled by individuals wearing latex glovesmay stimulate an allergic response. Cross-reactions have been re-ported in people who are allergic to certain food products, such askiwis, bananas, pineapples, passion fruits, avocados, and chestnuts.

Routes of exposure to latex products can be cutaneous, per-cutaneous, mucosal, parenteral, and aerosol. The most frequentsource of exposure is cutaneous, which usually involves the wear-ing of natural latex gloves. The powder used to facilitate puttingon latex gloves can become a carrier of latex proteins from thegloves; when the gloves are put on or removed, the particles be-come airborne and can be inhaled or can settle on skin, mucousmembranes, or clothing. Mucosal exposure can occur from theuse of latex condoms, catheters, airways, and nipples. Parenteralexposure can occur from intravenous lines or hemodialysis equip-ment. In addition to latex-derived medical devices, many house-hold items also contain latex. Examples of medical and householditems containing latex and a list of alternative products are foundin Table 53-5. It is estimated that over 40,000 medical devicesand nonmedical products contain latex (Brehler & Kütting,2001).

Clinical ManifestationsSeveral different types of reactions to latex are possible. Irritant con-tact dermatitis, a nonimmunologic response, may be due to me-chanical skin irritation or an alkaline pH associated with latexgloves. Common symptoms of irritant dermatitis include erythemaand pruritus. These symptoms can be eliminated by changing glovebrands or using powder-free gloves. Use of hand lotion before don-ning latex gloves may worsen the symptoms because lotions mayleach latex proteins from the gloves, increasing skin exposure andthe risk of developing true allergic reactions (Burt, 1998).

Delayed hypersensitivity to latex, a type IV allergic reactionmediated by T cells in the immune system, is localized to the areaof exposure and is characterized by symptoms of contact der-matitis, including vesicular skin lesions, papules, pruritus, edema,erythema, and crusting and thickening of the skin. These symp-toms usually appear on the back of the hands. This reaction isthought to be due to chemicals that are used for manufacturinglatex products. It is the most common allergic reaction to latex.Although not usually life-threatening, delayed hypersensitivity

Table 53-5 • Selected Products Containing Natural Rubber Latex and Latex-Free Alternatives

PRODUCTS CONTAINING LATEX EXAMPLES OF LATEX-SAFE ALTERNATIVES*

Hospital EnvironmentAce bandage (brown)Adhesive bandages, Band-Aid dressing, Telfa

Anesthesia equipmentBlood pressure cuff, tubing, and bladder

CathetersCatheter leg bag strapsCrutch axillary pads and hand grips, tipsECG padsElastic compression stockingsGlovesIV cathetersIV rubber injection ports

Levin tubeMedication vialsPenrose drainsPrepackaged enema kitsPulse oximetersResuscitation bagsStethoscope tubingSyringes—single use (Monoject, B & D)Suction tubingTapesThermometer probesTourniquetsTheraband

Home EnvironmentBalloonsDiapers, incontinence padsCondoms, diaphragms

Feminine hygiene padWheelchair cushions

Ace bandage, white all cottonCotton pads and plastic or silk tape, Active Strip (3M),

DuodermNeoprene anesthesia kit (King)Clean Cuff, single-use nylon or vinyl blood pressure cuffs

or wrap with stockinette or apply over clothingAll-silicone or vinyl cathetersVelcro strapsCover with cloth, tapeBaxter, Red Dot 3M ECG padsKendall SCD stockings with stockinetteDermaprene, Neoprene, polymer, or vinyl glovesJelko, Deseret IV cathetersCover Y-sites and ports; do not puncture. Use three-way

stopcocks on plastic tubing.Salem sump tubeRemove rubber stopper.Jackson-Pratt, Zimmer hemovac drainsTheravac, Fleet Ready-to-useNonin oximetersLaerdal, Puritan Bennett, certain AmbuPVC tubing; cover with latex-free stockinetteTerumo syringes, Abbott PCA AbbojectPVC (Davol, Laerdal)Dermicel, MicroporeDiatec probe coversX-Tourn straps (Avcor)New Thera-band Exercisers, plastic tubing

Mylar balloonsHuggies, Always, some AttendsPolyurethane products, Durex/Avanti and Reality

products (female condom)Kimberly-Clark productsROHO cushions, Sof Care bed/chair cushions

*Confirmation is essential to verify that all items are latex-free before using, especially if risk of latex allergy.


reactions often require major changes in the patient’s home andwork environment to avoid further exposure.

Immediate hypersensitivity, a type I allergic reaction, is medi-ated by the IgE mast cell system. Symptoms can include rhinitis,conjunctivitis, asthma, and anaphylaxis. The term “latex allergy”is usually used to describe the type I reaction. Clinical manifesta-tions have a rapid onset and can include urticaria, wheezing, dys-pnea, laryngeal edema, bronchospasm, tachycardia, angioedema,hypotension, and cardiac arrest.

Localized itching, erythema, or local urticaria within minutesafter exposure to latex are often the initial symptoms. Symptomsof subsequent reactions can include generalized urticaria, angio-edema, rhinitis, conjunctivitis, asthma, and anaphylactic shockminutes after dermal or mucosal exposure to latex. An increasingnumber of individuals allergic to latex experience severe reactionscharacterized by generalized urticaria, bronchospasm, and hypo-tension (Brehler & Kütting, 2001).

Diagnostic TestingThe diagnosis of latex allergy is based on the history and diag-nostic test results (Parslow et al., 2001). Sensitization is detectedby skin testing, RAST, or ELISA. Skin tests have been unreliablebecause of variability in the techniques used; however, a new stan-dardized skin testing reagent is expected to be available in the nearfuture. Skin tests should be done only by clinicians who have ex-pertise in their administration and interpretation and who havethe necessary equipment available to treat local or systemic aller-gic reactions to the reagent (Hamilton & Adkinson, 1998). Nasalchallenge and dipstick tests may be useful in the future as screen-ing tests for latex allergy.

Medical ManagementThe best treatment available for latex allergy is the avoidance oflatex products, but this is often difficult because of the widespreaduse of latex-based products. Patients who have experienced ananaphylactic reaction to latex should be instructed to wear med-ical identification. Antihistamines and an emergency kit con-taining epinephrine should be provided to these patients, alongwith instructions about emergency management of latex allergysymptoms. Patients should be counseled to notify all health careworkers as well as local paramedic and ambulance companiesabout their allergy. Warning labels can be attached to car win-dows to alert police and paramedics about the driver’s or passen-ger’s latex allergy in case of a motor vehicle crash. Individuals withlatex allergy should be provided with a list of alternative productsand referred to local support groups; they are also urged to carrytheir own supply of nonlatex gloves.

People with type I latex sensitivity may be unable to continueto work if a latex-free environment is not possible. This mayoccur with surgeons, dentists, operating room personnel, or in-tensive care nurses. Occupational implications for employeeswith type IV latex sensitivity are usually easier to manage bychanging to nonlatex gloves and avoiding direct contact withlatex-based medical equipment. Although latex-specific immuno-therapy has been reported, this method of treatment remains ex-perimental (Brehler & Kütting, 2001).

Nursing ManagementThe nurse can assume a pivotal role in the management of bothpatients and staff with latex allergies. All patients should be askedabout latex allergy, although special attention should be given to

Barrier Effectiveness of Latex and Non-latex Gloves

PurposeIn recent years, a variety of non-latex gloves have been used in healthcare in response to the increasing incidence of allergic reactions tolatex, which has occurred with the increased use of gloves to protecthealth care personnel from exposure to body fluids. However, little re-search data about the barrier quality of these new synthetic gloves areavailable. The purpose of this study was to examine the effects of glovestress, type of material, and manufacturer on the barrier effectivenessof medical examination gloves.

Study Design and SampleThe sample consisted of 5,510 medical examination gloves: 1,464 ni-trile, 1,052 latex, 1,006 copolymer, and 1,988 vinyl gloves. Elevenbrands of gloves from five manufacturers were tested for barrier effec-tiveness. The gloves were divided into two groups: stressed and un-stressed. Unstressed gloves were tested by the FDA 1989 water-leaktest in which the gloves were filled with 1,000 mL of water, hung for2 minutes, and observed for leaks. The gloves were rated as ineffectivebarriers if a water leak was detected. The remaining gloves were sub-jected to a laboratory and clinical stress protocol that mimics thestresses on gloves that occur during clinical use. Visible water leaks orleakage on the FDA water-leak test indicated barrier ineffectiveness.Chi-square analyses were used to test the differences between the fre-

NURSING RESEARCH PROFILE 53-1

quencies of failure across glove material, manufacturer, and the stressedvs. nonstressed conditions.

FindingsNitrile gloves had the lowest rate of failure, followed by latex gloves.Copolymer and vinyl gloves had the highest rates of failure. The fail-ure rates were significantly different (p < 0.001). Subjecting gloves tothe stress protocol increased the failure rate significantly (p < 0.002).Failure rates were also significantly different by glove manufacturer (p < 0.001). The data demonstrated that glove material, manufacturer,and stress are important factors that influence the barrier effectivenessof medical examination gloves.

Nursing ImplicationsThe research findings suggest that nitrile medical examination glovesare an acceptable alternative to latex gloves and that vinyl and copoly-mer gloves provide less protection to the wearer. These findings sug-gest the need for health care providers and facilities to use care inselecting the type and manufacturer of gloves to protect the wearerduring patient care. The researchers indicated that studies using largersamples are warranted and should address other variables that may af-fect the barrier effectiveness of gloves during use, including durationof use, presence of powder, glove size, hand dominance, complexityof tasks performed while wearing gloves, and the use of instruments.

Korniewicz, D., el-Masri, M., Broyles, J. M., Martin, C. D., & O’Connell, K. P. (2002). Performance of latex andnonlatex medical examination gloves during simulated use. American Journal of Infection Control, 30(2), 133–138.


those at particularly high risk (eg, patients with spina bifida,patients who have undergone multiple surgical procedures). Everytime an invasive procedure must be performed, the nurse shouldconsider the possibility of latex allergies. Nurses working in op-erating rooms, intensive care units, short procedure units, andemergency departments need to pay particular attention to latexallergy. See Chapter 19 for a latex allergy screening form.

Although the type I reaction is the most significant of the re-actions to latex, care must be taken in the presence of irritantcontact dermatitis and delayed hypersensitivity reaction to avoidfurther exposure of the individual to latex. Patients with latex al-lergy are advised to notify their health care providers and to weara medical information bracelet. Patients must become knowl-edgeable about what products contain latex and what productsare safe, nonlatex alternatives. They must also become knowl-edgeable about signs and symptoms of latex allergy and emer-gency treatment and self-injection of epinephrine in case ofallergic reaction.

Nurses can be instrumental in establishing and participatingin multidisciplinary committees to address latex allergy and topromote a latex-free environment. Latex allergy protocols and ed-ucation of staff about latex allergy and precautions are importantstrategies to reduce this growing problem and to ensure assess-ment and prompt treatment of affected individuals.

New Approaches to Treatmentof Allergic DiseasesAlthough allergen-specific immunotherapy reduces symptomsfor several years after it is discontinued, this approach to man-agement is limited in terms of usefulness because of its potentialadverse effects, particularly anaphylaxis, and the relatively crudeallergen extracts involved. Newer approaches to the treatment ofallergic diseases to overcome these limitations are being evaluatedand include the use of substances such as naturally occurring iso-forms of allergens from plants and trees. These isoforms are lesslikely to stimulate anaphylactic reactions. Use of recombinant al-lergens is expected to eliminate variation between batches of al-lergen. Other experimental approaches include the use of DNAvaccines and monoclonal antibodies and other strategies to blockIgE or its synthesis (Kay, 2001b).

REFERENCES AND SELECTED READINGS

BooksAbbas, A. K., & Lichtman, A. H. (2001). Basic immunology: Functions

and disorders of the immune system. Philadelphia: W. B. Saunders.Antel, P., Birnbaum, G., & Hartung, H. P. (1998). Clinical neuro-

immunology. Malden, MA: Blackwell Scientific.Buttaro, T. M., Trybulski, J., Bailey, P. P., & Sandberg-Cook, J. (1999).

Primary care: A collaborative practice. St. Louis, MO: Mosby, Inc.Delves, P. J. (1998). Encyclopedia of immunology (2nd ed.). San Diego:

Academic Press.Goroll, A. H., & Mulley Jr., A. G. (2000). Primary care medicine

(4th ed.). Philadelphia: Lippincott Williams & Wilkins.Huether, S. E., & McCance, K. L. (2000). Understanding pathophysiol-

ogy (2d ed.). St. Louis, MO: Mosby, Inc.Middleton, E. Jr (Ed.). (1998). Allergy: Principles and practice. St. Louis:

C. V. Mosby.Parkinson, C. F. (2000). Study guide and workbook for understanding

pathophysiology (2d ed.). St. Louis, MO: Mosby, Inc.Parslow, T. G., Stites, D. P., Terr, A. I., & Imboden, J. B. (2001). Med-

ical immunology. New York: McGraw-Hill.Porth, C. M. (2002). Pathophysiology: Concepts of altered health states

(6th ed.). Philadelphia: Lippincott Williams & Wilkins.Roitt, I. M. & Delves, P. J. (2001). Roitt’s essential immunology. Malden,

MA: Blackwell Science.Tierney Jr., L. M., McPhee, S. J., & Papadakis, M. A. (Eds.). (2001). Cur-

rent medical diagnosis and treatment. Stamford, CT: Appleton & Lange.Virella, G. (Ed.). (2001). Medical immunology. New York: Marcel

Dekker.

JournalsAsterisks indicate nursing research articles.Barbarito, C. (1999). Anaphylaxis. American Journal of Nursing, 99(1), 33.Becker, H. S. (2000). An analysis of the epidemiology of latex allergy:

Implications for primary prevention. MedSurg Nursing, 9(3),135–143.

Brehler, R., & Kütting, B. (2001). Natural rubber latex allergy: A prob-lem of interdisciplinary concern in medicine. Archives of InternalMedicine, 161(8), 1057–1064.

Burt, S. (1998). What you need to know about latex allergy. Nursing,28(10), 33–39.

Gehring, L. L., & Ring, P. (1999). Latex allergy: Creating a safe envi-ronment. MedSurg Nursing, 8(6), 358–362.

Gritter, M. (1998). The latex threat. American Journal of Nursing, 98(9),26–32.

Hamilton, R. G., & Adkinson, N. F., Jr. (1998). Diagnosis of naturalrubber latex allergy: Multicenter latex skin testing efficacy study.Journal of Allergy and Clinical Immunology, 102(3), 482–490.

Critical Thinking Exercises

1. A 45-year-old man arrives at the emergency departmentwhere you are employed. He states that he is severely allergicto bees and was stung by a wasp approximately 10 minutesago. He tells you that he has been in anaphylactic shock inthe past as a result of bee stings. He tells you that he receivedallergy injections for bee allergy approximately 10 years ago.Upon assessing the patient, you note that he has generalizedhives and urticaria on his body, and he is complaining of histhroat swelling. What would be your immediate course ofaction?

2. A patient with severe allergies is to receive instructionsabout self-administration of epinephrine if she experiencesanaphylaxis. Develop a teaching plan for this patient andidentify outcomes to measure the effectiveness of your

??

teaching. How would you modify your teaching if the pa-tient reports a severe fear of injection? If the patient has aprofound hearing loss? If the patient is visually impaired?

3. A 28-year-old man has a surgical procedure for a varico-cele. A Penrose drain is inserted into his scrotum duringthe surgical procedure in the operating room. The patientdevelops erythema and significant edema of the scrotuminconsistent with the procedure that was performed. Thecirculating nurse had noted on the operative checklist thatthe patient was allergic to latex. What would be your im-mediate course of action? How could you ensure that asimilar situation would not occur in the future? Whatcourse of action could you take to ensure a latex-free environment for patients who require such anenvironment?


Kay, A. B. (2001a). Advances in immunology: Allergy and allergic dis-eases (first of two parts). New England Journal of Medicine, 344(1),30–37.

Kay, A. B. (2001b). Advances in immunology: Allergy and allergic dis-eases (second of two parts). New England Journal of Medicine, 344(2),109–113.

*Korniewicz, D., el-Masri, M., Broyles, J. M., Martin, C. D., & O’Connell, K. P. (2002). Performance of latex and nonlatex medicalexamination gloves during simulated use. American Journal of Infec-tion Control, 30(2), 133–138.

*Korniewicz, D. M., Garzon, L., Seltzer, J., et al. (2001). Implementinga nonlatex surgical glove study in the OR. AORN Journal, 73(2),435–445.

Lilley, L. L., & Gaunci, R. (1999). Cross sensitivities: Medication errorswaiting to happen. American Journal of Nursing, 99(2), 12.

Neugut, A. I., Ghatak, A. T., & Miller, R. L. (2001). Anaphylaxis in theUnited States: An investigation into its epidemiology. Archives ofInternal Medicine, 161(1), 15–21.

Ratner, P. H., Ehrlich, P. M., Fineman, S. M., et al. (2002). Use ofintranasal cromolyn sodium for allergic rhinitis. Mayo Clinic Pro-ceedings, 77(4), 350–354.

Sicherer, S. H., Munoz-Furlong, A., Burks, A. W., et al. (1999). Preva-lence of peanut and tree nut allergy in the U.S. determined by a ran-dom digit dial telephone survey. Journal of Allergy and ClinicalImmunology, 103(4), 559–562.

Silkoff, P. E., Robbins, R. A., Gaston, B., et al. (2000). Endogenousnitric oxide in allergic airway disease. Journal of Allergy and ClinicalImmunology, 105(3), 438–448.

Walker, S., & Sheikh, A. (2002). Rhinitis. British Medical Journal,324(7334), 403.

Williams, L. W., & Bock, S. A. (1999). Skin testing and food challengesin allergy and immunology practice. Clinical Reviews in Allergy andImmunology, 17(3), 323–338.

RESOURCES AND WEBSITES

American Academy of Allergy, Asthma and Immunology, 611 East WellsStreet, Milwaukee, WI 53202; (800) 822-ASMA; http://www.aaai.org.

Centers for Disease Control and Prevention, 1600 Clifton Road, At-lanta, GA 30333; (404) 639-3311 or (800) 311-3435; http://www.cdc.gov.

Food Allergy & Anaphylaxis Network, 10400 Eaton Place, Suite 107,Fairfax, VA 22030; (800) 929-4040; http://www.foodallergy.org;e-mail: [email protected].

National Institute of Allergy and Infectious Disease, NIAID Office ofCommunications and Public Liaison, NIH, Bldg. 31, Room 7A50,31 Center Drive, MSC 2520, Bethesda, MD 20893; (301) 496-5717; http://www.niaid.nih.gov/.

National Institutes of Health, 9000 Rockville Pike, Bethesda, MD20892; (301) 496-4000; http://www.nih.gov.

Spina Bifida Association of America, 4590 MacArthur Blvd NW, Suite250, Washington, DC 20007; (800) 621-3141; http://www.sbaa.org.

Assessment and Management of Patients With Allergic Disorders

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