Practice nursing care for Clients with Immune Function Excess (Allergy)

Practice nursing care for Clients with Immune Function Excess (Allergy)


The inflammatory and immune responses are normally beneficial. They not only protect the body against microorganism invasion and cancer development, but they also stim­ulate tissue growth and repair after injury. However, when in­flammation or immune responses are prolonged, excessive, or occur at an inappropriate time, normal tissues can be damaged instead of protected. These responses are considered "over-actions" to invaders and foreign antigens and are known as hypersensitivity or allergic responses. In addition, inflam­matory and immune responses can fail to recognize self-cells and literally attack normal body tissues. This type of reaction is known as an autoimmune response. Both hypersensitivity and autoimmune responses can damage cells, tissues, or or­gans and have serious consequences.


A hypersensitivity or allergy is a state of increased or excessive response to the presence of an antigen (foreign protein or allergen) to which the client has been previously exposed. These responses cause symptoms that range from uncomfortable (e.g., itchy, watery eyes or sneezing) to life threatening (e.g., allergic asthma, anaphylaxis, bronchoconstriction, or cir­culatory collapse). The terms hypersensitivity and allergy are synonymous and are used interchangeably. Hypersensitivity or allergy reactions are classified into five basic types, which are determined by differences in timing, mechanism, pathophysiology, and clinical manifestations. Each type may occur alone or in combination with one or more other types.

Figure * There are four types of hypersensitivity reaction mediated by immunological mechanisms that cause tissue damage. Types I–III are antibody-mediated and are distinguished by the different types of antigens recognized and the different classes of (more...)


Figure *  IgE-mediated reactions to extrinsic antigens. All IgE-mediated responses involve mast-cell degranulation, but the symptoms experienced by the patient can be very different depending on whether the allergen is injected, inhaled, or eaten, and depending (more...)

Type I (rapid) hypersensitivity, sometimes called atopic allergy, is the most common type of hypersensitivity. This type results from increased production of the immunoglobulin E (IgE) anti­body class. An acute inflammatory reaction occurs when IgE re­sponds to an otherwise harmless antigen (e.g., pollen) and causes the release of histamine and other vasoactive amines from basophils, eosinophils and mast cells. Clinical examples of type I reactions include systemic anaphylaxis, allergic asthma, and atopic (genetic tendency) allergies such as hay fever, allergic rhinitis, and allergies to specific allergens such as latex, bee venom, peanuts, iodine, shellfish, drugs, and thousands of other environmental antigens. Allergens can be encountered in the following ways:

  Inhaled (plant pollens, fungal spores, animal dander,
house dust, grass, ragweed)

  Ingested (foods, food additives, drugs)

  Injected (bee venom, drugs, biologic substances such as
contrast dyes and adrenocorticotropic hormone)

Contacted (pollens, foods, environmental proteins)
Some reactions are confined to the areas exposed to the antigen, such as the mucous membranes of the nose and eyes, causing symptoms of rhinorrhea, sneezing, and itchy, red, and watery eyes. Other reactions may involve all blood vessels and bronchiolar smooth muscle, causing widespread vasodi-lation, decreased cardiac output, and severe bronchoconstric-tion; this condition is known as anaphylaxis.


Allergic Rhinitis


Allergic rhinitis, often called "hay fever," is triggered by hy­persensitivity reactions to airborne allergens, especially plant pollens, molds, dust, animal dander, wool, food, and indus­trial pollutants. Some acute episodes are "seasonal" in that they tend to recur at the same time each year; they coincide with the timing of large environmental exposure and last only a few weeks. Chronic rhinitis, or perennial rhinitis, tends to occur intermittently (with no predictable seasonal pattern) or continuously on exposure to certain allergens. In "nonallergic rhinitis," the same clinical manifestations are present although no allergic cause is identified and the immune system does not appear to be involved.

Figure * Antibody Fc (fragment, crystalline) receptors on basophils and mast cells.


On first exposure to an allergen (an antigen that provokes al­lergic sensitization with IgE), the person responds by making antigen-specific IgE. This antigen-specific IgE binds to the surface of basophils and mast cells. These cells have large numbers of granules containing vasoactive amines (including histamine) that are released when stimulated. Once the antigen-specific IgE has formed, the person is sensitized to that allergen.

In a type I hypersensitivity reaction, the previously sensi­tized person is re-exposed to the provoking allergen. The re­sulting response has a primary phase and a secondary phase. In the primary phase, the allergen binds to two adjacent IgE mol­ecules on the surface of a basophil or mast cell, which breaks or distorts the cell membrane. These membrane changes cause the cell to degranulate and release the vasoactive amines within the granules into the tissue fluids.

The most abundant vasoactive amine is histamine, a short-acting biochemical. Histamine causes increased capillary per­meability, nasal and conjunctival mucous secretion, and itch­ing (pruritus), sometimes accompanied by erythema (redness). These symptoms last for approximately 10 minutes after the histamine is released. When the allergen is continu­ously present, mast cells continuously release histamine and other vasoactive amines, thus prolonging the response.

The secondary phase results from the secretion of other va­soactive amines during the primary phase. These other va­soactive amines draw more white blood cells to the area and stimulate a more general inflammatory reaction through the action of the biochemicals leukotriene and prostaglandins. This reaction occurs in addition to the allergic reaction stim­ulated in the primary phase. The resulting inflammation in­creases the clinical manifestations and is probably responsible for continuing the response.


The tendency to produce IgE in response to antigen exposure is based on genetic inheritance, but no single gene has been found to be responsible. Specific allergies are not inherited. Approximately 50% of clients with allergic rhinitis have one parent with type I hypersensitivities/allergies.






Figure * Degranulation and histamine release. Top, Mast cell with immunoglobulin E (IgE). Bottom, Mast cell degranulation and histamine release when allergen binds to IgE.


A complete blood count and differential may be ordered. An increase in the percentage of eosinophils is consistent with allergic rhinitis. A client with severe seasonal allergic rhinitis may have an eosinophil count as high as 12% (with normal being 1% to 2%). Some clients have an increased total white blood cell count, but the percentage of neutrophils remains normal (55% to 70%). If an acute infection accompanies al­lergic rhinitis, both the total white blood cell count and the number of neutrophils may increase.

Other laboratory tests that indicate the presence of a hy­persensitivity reaction include serum immunoglobulin E (IgE) levels and the Radioallergosorbent Test (RAST). Nor­mal levels of IgE for nonallergic adults is approximately 39 IU/mL (or less than 100 IU/mL). This level can increase many times in the presence of allergies. The usual IgE test does not indicate the specific allergenonly the tendency to have al­lergic responses. The RAST can determine the blood concen­tration of IgE directed against a specific antigen and thus can determine specific allergies. However, the expense of this study limits its use in allergy testing.


Atopic allergies, including allergic rhinitis, affect approxi­mately 10% of the population in North America (Cotran, Kumar, & Collins, 1999). Males and females are affected equally. Racial differences have not been documented.






An accurate and detailed history may provide insight into the possibility of allergic rhinitis. The client is asked to describe the onset and duration of symptoms in relation to possible al­lergen exposure. The nurse asks about work, school, home en­vironments, and possible exposures through hobbies, leisure time, or sports activities. Because a tendency toward type I hypersensitivities can be inherited, the client is asked about the presence of allergies among close relatives.


The client with allergic rhinitis usually has rhinorrhea (a "runny" nose), a "stuffy" nose sensation, and itchy, watery eyes. Mouth breathing may be evident, and the voice can have a nasal sound. Drainage from the nose is usually clear or white. The nasal mucosa appears swollen and pink on inspec­tion. The client may have a headache or feel pressure over the frontal and maxillary sinuses. Transillumination of the si­nuses may be decreased. If nasal secretions drip posteriorly, the client may have a dry, scratchy throat and the appearance


SKIN TESTING. With most type I hypersensitivities, skin testing can reveal which specific allergens are causing the reaction. Skin testing can be performed as scratch test­ing and intradermal testing. Patch testing is generally re­served for contact dermatitis and other manifestations of type IV hypersensitivities.

SCRATCH TESTING. A scratch or prick test results in an immediate hypersensitivity reaction to an allergen. Scratch tests are used in routine allergy testing to determine the pos­sible cause of allergic rhinitis, asthma, urticaria (hives), or any other type I hypersensitivity/allergic reactions. Allergens introduced through a superficial scratch or prick cause a lo­calized reaction (wheal) when the test result is positive. Re­sults are usually determined after 15 to 20 minutes.

CLIENT PREPARATION. For best results, systemic corti-costeroids or antihistamines are discontinued for 5 days be­fore the test; this prevents suppression of the inflammatory re­sponse to an allergen. Nasal sprays to reduce mucous membrane swelling are permitted, except for antihistamine sprays such as azelastine (Astelin). Some allergists recom­mend that aspirin and other nonsteroidal anti-inflammatory agents be withheld before allergy testing.

PROCEDURE. The preferred site for scratch testing is the inside of the arm or the back. Alternate sites may be used if a rash or other skin problem is present in these areas. The skin is gently cleaned with soap and water, and surface oils are re­moved with alcohol.

Small drops of sera containing different known allergens are placed on the skin approximately 20 mm apart. Using a bi­furcated skin testing needle, the skin is scratched or pricked Autoimmunity  through the drop. Skin areas are then examined for the pres­ence and size of a reaction. Areas showing erythema and wheal formation are considered positive for that antigen. The degree of sensitivity is grossly estimated by the size of the response.

Control drops are also applied during the scratch test. Nor­mal saline drops are negative controls, and histamine drops are positive controls. A variation from the expected response to the controls can invalidate the skin test results. If a positive reaction to the saline control occurs, the client may have very sensitive skin or a condition called dermographism. In such cases, the reddened test areas may be skin reactions to the scratch or prick rather than an allergic response to the sera. If the histamine control produces a negative reaction, the client may have used an antihistamine recently.

Serious reactions in response to scratch testing are rare. However, the nurse ensures that emergency equipment is readily available during a scratch test.

FOLLOW-UP CARE. After testing is completed, the nurse washes the solution from the skin. Topical steroids and oral antihistamines may be administered to reduce itching and increase client comfort. If the administered antihistamine can cause sedation, the client will need to have another person drive him or her home.

INTRADERMAL TESTING. Intradermal testing is re­served for substances that are strongly suspected of causing allergy but did not test positive during scratch testing. Intra­dermal testing increases the risk for a greater adverse reaction, including anaphylaxis, but it is a relatively safe procedure. The nurse ensures that emergency equipment is in the room with the client. Small amounts of testing sera (0.1 mL) are injected intradermally on the client's upper arm, and the area is observed for erythema and wheal formation. The de­gree of hypersensitivity is grossly estimated by the size of the response. Client preparation and follow-up care are the same as for scratch testing.

ORAL FOOD CHALLENGE. Some clients experience allergic rhinitis (and other hypersensitivity manifestations) when the allergen does not come into direct contact with the nasal mucosa but is ingested orally. The oral food challenge has been effective for some individuals in identifying specific al­lergens when skin testing has been inconclusive and keeping a food diary has failed to determine the offending food items. This test requires the client to eliminate suspected foods for 7 to 14 days before testing. After this time, the client is directed to eat a defined food for at least one day and to monitor for clin­ical manifestations. When many food allergies are present, the client may need to eat only one food type per day of testing.


Hypersensitivity to specific aller­gens can be tested using an in vitro method. One method, the ALCAT, is available in some areas of the United States and is more widely used in Europe. This method involves drawing blood from a client and exposing it to different panels con­taining food and mold allergens. After incubation, the red blood cells are eliminated, and a Coulter Counter is used to examine the remaining cells (white blood cells and platelets) for size increases and other changes. Positive reactions are those in which the white blood cell size increases by at least 12% and platelets increase aggregation.


Allergy Management: Identification, treatment, and preven­tion of allergic responses to food, medications, insect bites, contrast material, blood, or other substances

  Identify known allergies and usual reaction (e.g., med­
ication, food, insect, environmental).

  Notify caregivers and health care providers of known

  Document all allergies in clinical record, according to

  Place an allergy band on client, as appropriate.

  Monitor client for allergic reactions to new medications,
formulas, foods, and/or test dyes.

  Encourage client to wear a medical alert tab, as

  Provide medication to reduce or minimize an allergic

  Assist with allergy testing, as appropriate.

  Administer allergy injections, as needed.

  Instruct client to avoid allergic substances, as

  Instruct client to avoid further use of substances caus­
ing allergic responses.

  Discuss methods to control environmental allergens
(e.g., dust, mold, and pollen).

  Instruct client and caregiver(s) on how to avoid situa­
tions that put them at risk and how to respond if an ana-
phylactic reaction should occur.

  Instruct client and caregiver on use of epinephrine pen.

Anaphylaxis Management: Promotion of adequate ventila­tion and tissue perfusionfor a client with a severe allergic (antigen-antibody) reaction

  Place client in Fowler's or high Fowler's position.

  Apply tourniquet immediately proximal to the allergen
point of entry (e.g., injection site, IV site, insect bite,
etc.), when possible.

  Administer aqueous epinephrine 1:1000 (0.3-0.5 mL)
subcutaneously at the contact site, if applicable, and
proximal to the tourniquet and repeat every 3 minutes,
as needed.

  Establish and maintain a patent airway.

  Administer oxygen by mask.

  Start an IV infusion of normal saline, lactated Ringer's,
or a plasma volume expander, as appropriate.

  Reassure the client and family members.

  Monitor for signs of shock, airway obstruction, cardiac
arrhythmia, aspiration of gastric contents, and seizures.

  Administer spasmolytics, antihistamines, or cortico-
steroids as indicated if urticaria, angioedema, or bron-
chospasm present.

  Monitor for recurrence of anaphylaxis within 24 hours.

NIC intervention activities selected from McCloskey, J.C., & Bulechek, G.M. (Eds.). (2000). Nursing interventions classification (NIC) (3rd ed.). St. Louis: Mosby. No part of this work is to be altered without prior written permission from the Publisher.


Chart lists NIC interventions for allergy management. Common interventions include avoidance therapy, desensitization therapy, and symptomatic therapy. Many clients use a combination of all three interventions for the effective man­agement of allergic rhinitis and other manifestations of type I hypersensitivity.

AVOIDANCE THERAPY. When specific environmental al­lergens have been identified, the client is encouraged to avoid di­rect or close contact with these agents. For example:


Many airborne allergens can be minimized by the use of air-conditioning/air-cleaning units. Removing cloth drapes, upholstered furniture, and carpeting reduces airborne aller­gens. Covering mattresses and pillows with plastic or ultra-fine mesh hypoallergenic covers also reduces exposure to dust mites and mold.

Pet-induced allergies pose special challenges. Sometimes even simple interventions (e.g., keeping pets out of the bed­room, thoroughly cleaning the room to remove animal hair/dander) may help reduce symptoms. Bathing the pet fre­quently or keeping the pet outdoors can decrease allergen ex­posure. Depending on the severity of the allergy and how well other methods provide relief, pets with feathers or dander may need to be removed from the household.

SYMPTOMATIC THERAPY. When avoidance therapy is impractical, symptomatic therapy can be very effective in re­ducing the intensity of the allergic response and making the client more comfortable.

DRUG THERAPY. Drug therapy involves the use of steroidal and nonsteroidal agents (to reduce inflammation), vasoconstrictors, antihistamines, mast cell stabilizers, and new agents that inhibit the release or action of leukotrienes. Some drugs reduce the response, and others actually prevent the response. Chart 23-2 lists common agents used for symp­tomatic therapy of allergic rhinitis.

Decongestants. Decongestants are available in systemic oral medications or nasal sprays. These agents do not clear the allergen or prevent the release of histamine or leukotrienes. They often have actions similar to those of adrenergic drugs and generally work by causing vasoconstriction in the in­flamed tissue, thereby reducing the edema. Common vaso­constrictors used in decongestant preparations are ephedrine, phenylephrine, phenylpropanolamine, and pseudoephedrine. Secretions are inhibited when the vasoconstrictor is combined with an anticholinergic agent such as scopolamine or at-ropine. Numerous combination decongestants are available by prescription and as over-the-counter cold and allergy med­ications. Common side effects include dry mouth, increased blood pressure, and sleep alterations. Because the effects are systemic, clients with hypertension, glaucoma, and urinary


DRUG THERAPY for Allergic Rhinitis



Usual Dosage

Nursing Interventions





20 mg bid

Take 1 hr before or 2 hr after eating.

Drug absorption is slowed by the

presence of food.





There is an increased incidence

of upper respiratory infections when coadministered

with inhaled corticosteroids.

Drugs reduce local inflammatory

and immune responses.















Reduce dose in clients who

are also taking aspirin.

Aspirin increases plasma concentration of drug.




Zileuton (Zyflo)

600 mg qid

Do not take with terfenadine or


Drug increases plasma concentrations of terfenadine and












1 -2 metered sprays per

nostril, 1 -2 times/day


50 g/metered spray)

Use daily as directed.

Effectiveness depends on regular





Symptoms may persist for 2-3 days after initial


Maximum effectiveness requires continued use for 48-72 hr.









2 metered sprays pernostril qd (approximately 50 (g/metered


Same as for beclomethasone.

Same as for beclomethasone.












Cromolyn sodium


1 spray/nostril 4-6


Use daily as directed.

Effectiveness depends on regular use.





Start therapy 3-4 wk before expected allergy season.

Requires regular use for prophylactic effect.







dozens of others)

1 spray/nostril 4-6 times/day

Caution client not to use more frequently than directed or for longer than 4 days.

Overuse or continued use causes

a rebound nasal congestion

and worsens symptoms.



1 spray/nostril bid

Same as for phenylephrine.

Same as for phenylephrine.

(Afrin, many others)




Additional drugs include Nasacort, Nasonex, and many others.

Antihistamines. Antihistamines compete with histamine at the histamine receptor site and essentially block it from binding to its receptor. This action prevents vasodilation and capillary leak. Many antihistamines also have some anticholinergic ef­fects, which assists in relief by decreasing secretions. First-generation antihistamines, which include diphenhydramine (Allerdryl, Benadryl) and chlorpheniramine (Chlor-Trimeton, Chlor-Tripolon) often induce sedation. Second-generation an­tihistamines, which include loratadine (Claritin), cetirizine (Zyrtec), and fexofenadine (Allegra), are less sedating.

Corticosteroids. Corticosteroids decrease inflammatory and immune responses in many ways, one of which is pre­venting the synthesis of mediators. Local corticosteroids in the form of nasal sprays can be helpful in preventing the symptoms of rhinitis. Systemic corticosteroids can produce severe side effects. Therefore they are avoided for rhinitis and are used only on a short-term basis for other problems associ­ated with type I hypersensitivities.

Mast Cell Stabilizers. Nasal sprays containing mast cell stabilizers, such as cromolyn sodium (Nasalcrom), prevent

mast cell membranes from opening when an allergen binds to IgE. Thus these agents are helpful in preventing the symptoms of allergic rhinitis but are not useful during an acute episode. Leukotriene Antagonists. Two leukotriene antagonists are currently available to treat allergic rhinitis. Zileuton (Zyflo) prevents leukotriene synthesis. Zafirlukast (Accolate) blocks the leukotriene receptor. Both are oral agents and work best in the prevention of allergic rhinitis.


Some clients with allergic rhinitis have found relief through the use of aromatherapy. Possible mechanisms of action in­clude competition and desensitization. Some clients with pollen-induced allergic rhinitis report decreased sensitivity after ingesting unprocessed honey.

DESENSITIZATION THERAPY. Desensitization therapy, commonly called "allergy shots," may be needed when aller­gens have been identified but cannot be avoided consistently. The most common form of desensitization involves subcuta­neous injections of small amounts of the allergen. After the al­lergen has been identified, a very dilute injection solution(1:100,000 or 1:1,000,000) of the allergen is compounded. A 0.05-mL dose of the initial solution is injected subcuta-neously. An increasing dose is usually given weekly (or more frequently) until the client is receiving a 0.5-mL dose. The client is then started on the lowest dose of the next higher con­centration of allergen solution. This process is repeated with increasing concentrations of allergen solutions until the client is receiving the maximum dose of the greatest concentration determined to be needed (usually 1:100), depending on his or her response. In general, injections are given at weekly inter­vals during the first year, every other week for the second year, and every 3 to 4 weeks for the third year. The recom­mended course of treatment is approximately 5 years.

The mechanism of action to reduce allergic responses by desensitization is thought to be competition. In theory, the very small amounts of allergen initially injected are too low to bind to the immunoglobulin E (IgE) already present but are enough to induce the immune system to make immunoglobu­lin G (IgG) against that allergen. Because IgG is not associ­ated with either mast cells or basal cells, allergens that bind to IgG do not trigger degranulation and are removed from the body by precipitation (see Chapter 20). By gradually increas­ing the amount and concentration of the allergen injection, large amounts of IgG are generated specifically against the al­lergen. When the client is exposed to the allergen, IgG will bind to it and clear it from the body before IgE can bind to it and trigger a hypersensitivity reaction. Because so much more IgG can be produced compared with IgE, IgG is successful in the competition to bind the allergen.

Desensitization can also be accomplished orally. Oral desen­sitization (sometimes called oral immunotherapy) is more com­mon in Europe and is not yet widely available in the United States. Instead of injections, the allergen is introduced either by swallowing a gelatin capsule (to prevent the allergen from being destroyed by gastric enzymes and acid) or by allowing sublin-gual absorption. The encapsulated allergen is absorbed in the small intestine, whereas the sublingual allergen is absorbed di­rectly into the circulatory system through the blood vessels un­der the tongue. Two major drawbacks of the oral desensitization method are expense and the difficulty of dose control. Both methods require higher concentrations of the allergen (com­pared to subcutaneous injections), and this increases the cost.

Example of desensitization:




Anaphylaxis, the most dramatic and life-threatening example of a type I hypersensitivity reaction, occurs rapidly and systemically. It affects multiple organs within seconds to minutes of exposure to an allergen. Anaphylaxis is not common, and the episodes can vary in severity and symptom. It can be fa­tal. Many substances can trigger anaphylaxis in a susceptible person (Table).



Typically, a client experiencing an anaphylactic reaction first complains of feelings of uneasiness, apprehension, weakness, and impending doom. The nurse notes that the client is anx­ious and frightened. These feelings are followed, often quickly, by a generalized pruritus and urticaria (hives). The nurse sees erythema and sometimes angioedema (diffuse swelling) of the eyes, lips, or tongue.



Antibiotics (penicillin, cephalosporins, tetracycline, sulfon-amides, streptomycin, vancomycin, chloramphenicol, am-photericin B, others)

Adrenocorticotropic hormone, insulin, vasopressin, protamine

Allergen extracts, muscle relaxants, hydrocortisone, vaccines, local anesthetics (lidocaine, procaine)

Whole blood, cryoprecipitate, immune serum globulin

Radiocontrast media












Legumes, nuts










Hymenoptera: bees,

       wasps, hornets

Fire ants


Snake venom



   Anaphylaxis caused by these substances is probably a result of direct mast cell degran­ulation rather than an IgE-mediated hypersensitivity event.

   Intensely praritic skin wheals or hives commonly appear, and these sometimes merge together in a large, red blotch.

Histamine and other biochemicals cause bronchoconstriction, mucosal edema, and excess mucus production. On respira­tory assessment, the nurse notes congestion, rhinorrhea, dys­pnea, and increasing respiratory distress with audible wheezing.

On auscultation the nurse detects crackles, wheezing, and diminished breath sounds. Clients may experience laryngeal edema as a "lump in the throat," hoarseness, and stridor (a crowing sound). Distress increases as the tongue and larynx become more edematous and excess mucous secretion con­tinues. The nurse may note increasing stridor and anxiety as the airway begins to close. Respiratory failure may follow quickly as a complication of laryngeal edema, suffocation, or lower airway bronchoconstriction causing hypoxemia (insuf­ficient oxygenation of blood) and hypercapnia (increased carbon dioxide in the blood).

The client is usually hypotensive and has a rapid, weak, and irregular pulse. These findings are due to vasodilation and in­creased capillary permeability with a resultant leakage of intravascular fluids. The nurse notes faintness and diaphoresis, increasing anxiety, confusion and, if the client is not treated immediately, loss of consciousness. Dysrhythmias, shock, and cardiac arrest may occur within minutes as intravascular vol­ume is lost. Abdominal cramping, diarrhea, or vomiting is less common. Respiratory failure or shock and cardiac dysrhyth­mias account for 70% of deaths from anaphylaxis.


NIC interventions for clients with anaphylaxis are listed in Chart.

EMERGENCY RESPIRATORY MANAGEMENT. Emer­gency respiratory management is critical for clients experi­encing an anaphylactic reaction, because the severity of the reaction and consequences increases with time. An airway must be established or stabilized immediately. The nurse may need to initiate cardiopulmonary resuscitation. Epinephrine (1:1000) 0.3 to 0.5 mL should be given subcutaneously as soon as possible after the appearance of symptoms of sys­temic anaphylaxis. This drug constricts the blood vessels, in­creases myocardial contraction, and dilates the bronchioles. The same dose may be repeated every 15 to 20 minutes if needed. Other commonly administered drugs are listed in Chart.

Antihistamines such as diphenhydramine (Allerdryl, Be­nadryl) 25 to 100 mg are usually given intravenously, intra­muscularly, or orally to treat angioedema and urticaria. This agent blocks the histamine receptor site (H,) in vascular and bronchiolar smooth muscle. If necessitated by the extent of upper airway narrowing, the physician may insert a small endotracheal tube or perform an emergency tracheostomy.


If the client can breathe independently, the nurse admin­isters oxygen to minimize hypoxemia. Oxygen is started via nasal cannula at 2 to 6 L/min or via face mask at 40% to 60% before arterial blood gas results are obtained. The nurse monitors pulse oximetry to determine oxygenation ade­quacy, with the goal of maintaining an oxygen saturation greater than 90%. If pulse oximetry readings are not satis­factory, arterial blood gases may be tested to determine the effectiveness of therapy. Suction is used to remove excess mucous secretions if indicated. The client's rate, rhythm, and depth of respirations, as well as the presence of bronchospasm and abnormal breath sounds, are assessed contin­ually. The nurse or other assistive nursing personnel elevates the client's bed to 45 degrees unless contraindicated because of hypotension.

For severe bronchospasm, the client is given amino­phylline 6 mg/kg IV over 20 to 30 minutes. If the client is tak-400 with diphenhydramine (Allerdryl, Benadryl). The sub­stance is given first intradermally, then subcutaneously, and then intramuscularly in increasing doses at 20- to 30-minute intervals so the initial dose by the next route does not exceed the final dose by the previous route. When carefully per­formed, this procedure is fairly safeing aminophylline regularly, no more than 3 mg/kg is given. Maintenance aminophylline (0.3 to 0.5 mg/kg/hr) is initiated. The client may be given an inhaled beta-adrenergic agonist such as metaproterenol (Alupent) or albuterol (Proventil) via high flow nebulizer every 2 to 4 hours. Corticosteroids are added to emergency interventions, but they are not effective immediately. To prevent the late recurrence of symptoms, ta­pered doses of oral steroids are started after the anaphylaxis is under control.

The nurse's primary role in caring for the client with ana­phylaxis is to assess for changes in any body system or for ad­verse effects of drug therapy. For severe anaphylaxis, the client is admitted to a critical care unit for cardiac, pulmonary arterial, and capillary wedge pressure monitoring. The nurse carefully observes for fluid overload from the rapid adminis­tration of medications and IV fluids and reports changes to the physician immediately. The client may be discharged from the hospital when respiratory and cardiovascular sys­tems have returned to baseline.

PREVENTION. Because of the rapid onset of life-threatening symptoms and the potentially fatal outcome of this condition, sometimes even with appropriate medical in­tervention, preventing anaphylaxis is critical. The nurse teaches the client with a history of allergic reactions to avoid allergens whenever possible, wear a medical alert bracelet, and alert health care personnel about specific allergies. Some clients must carry an emergency anaphylaxis kit (e.g., a bee sting kit with injectable epinephrine) or an epinephrine injec­tor such as the EpiPen automatic injector (Dey Laboratories, Napa, CA). The EpiPen device is an easy-to-use, spring-loaded injector that delivers 0.3 mg of epinephrine per a 2-mL dose (Figure).

The medical record of clients with a history of anaphylactic symptoms should prominently display the list of allergens to which they are sensitive. A careful history is obtained be­fore administering any drug or therapeutic agent. Skin tests should be performed before administering any substance with a highly associated incidence of anaphylactic reactions, such as iodine-containing dyes. Physicians and nurses must be aware of common cross-reacting agents. For example, a client with a history of penicillin sensitivity is also likely to react to cephalosporins because both have a similar chemical struc­ture. Clients with an allergy to bananas are also likely to have a latex sensitivity.

Precautionary measures must be taken if an agent must be used despite a history of allergenic reactions. An IV solution is started, and intubation equipment and a tracheostomy set are placed at the bedside. The client is often premedicated


The client is a 52-year-old woman with type 1 diabetes who comes to an urgent care center. She fell 1 day ago and scraped her left shin. She now has a large, red, and indurated area around the abrasion. She is diagnosed with cellulitis and is to begin her first dose of penicillin intravenously because of her diabetes. The client explains that she is allergic to peni­cillin. When asked what type of reaction she has to penicillin, the client says she gets a severe rash over most of her body. The physician changes the order to cephalothin (Keflin) to be given intravenously for the first dose, followed by oral cephalexin (Keflex).

With the client in an examination room, you start an IV with normal saline and hang a 50-mL piggyback containing 1 g cephalothin and normal saline. The piggyback line is placed in the port closest to the IV needle.

Approximately 5 minutes after the infusion begins, the client says she is having a hard time catching her breath. She feels dizzy and scared. You find her pulse to be thready and too rapid to count. Her lips are dusky, and she begins to wheeze.

  What should you do with the IV?

  What is your next response?

  Why should you or should you not start oxygen on this

  Would epinephrine be helpful in this situation? Why or why
not? Where, how much, and by what route would you ad­
minister it?

  Would diphenhydramine (Benadryl) be helpful in this situa­
tion? Why or why not?

  What is the explanation for this reaction to cephalothin?


Latex Allergy


Latex allergy or hypersensitivity is a type I hypersensitivity reaction in which the specific allergen is a protein found in processed natural latex rubber products. When the allergen enters the body through inhalation or direct contact with blood vessels (such as might occur during surgery), interac­tion with immunoglobulin E (IgE) occurs and causes clini­cal manifestations of type I hypersensitivity reactions, in­cluding anaphylaxis. For some people, contact with the latex allergen is limited to the skin or mucous membranes. This causes contact dermatitis, a type IV delayed hypersensitivity reaction. Others may have a "mixed" hypersen­sitivity response to the latex allergen and experience symp­toms of both type I and type IV hypersensitivities. Others may express only one or the other type of reaction.

The incidence of latex hypersensitivity is increasing (Becker, 2000; Floyd, 2000). The individuals most at risk are those with a high exposure to natural latex products, such as health care workers (Karvonen, 1999), clients with spina bifida, and people who routinely use latex condoms.


The nurse questions all clients regarding the use of and known reactions to natural latex products. In addition, the nurse and other health care workers need to consider their own exposure and risk for hypersensitivities to natural latex products.

Avoiding products containing natural latex proteins can prevent reactions and initial sensitivity. More elastomeric products such as surgical gloves, tubing, and vial closures are now being made from synthetic substances containing no la­tex proteins. One such product is the thermoplastic elastomer glove, ElastyLite. It is essential that latex-free products be used in the care of a client with a known latex allergy. Inter­ventions for the client experiencing a type I or type IV hyper­sensitivity reaction to latex are the same as for hypersensitiv­ities caused by other allergens.



In a type II (cytotoxic) reaction, the body makes special au-toantibodies directed against self-cells or tissues that have some form of foreign protein attached to them. The autoanti-body binds to the self-cell and forms an antigen-antibody complex, or immune complex (Figure). The self-cell is then destroyed by phagocytosis or complement-mediated ly­sis. Clinical examples of type II reactions in­clude Coombs'-positive hemolytic anemias, thrombocytopenic purpura, hemolytic transfusion reactions (when an individual receives the wrong blood type during a transfu­sion), hemolytic disease of the newborn, Goodpasture's syn­drome, and drug-induced hemolytic anemia.


Treatment of type II cytotoxic reactions begins with discon­tinuing the offending drag or blood product. Plasmapheresis  (filtration of the plasma to remove specific substances) to re­move autoantibodies may be beneficial. Otherwise, treatment is symptomatic. Complications such as hemolytic crisis and renal failure can be life threatening.



In a type III reaction, soluble immune complexes are formed, usually with antigen excess (Figure). These circulating immune complexes are usually deposited in the walls of small blood vessels. Common sites include the kidneys, skin, joints, and other small blood vessels. The deposited immune complex activates complement, resulting in tissue or vessel damage.

There are many immune complex disorders (mostly con­nective tissue disorders) in which the type III reaction is the major mechanism of disease. For example, the clinical mani­festations of rheumatoid arthritis are caused by immune com­plexes that lodge in joint spaces; this is followed by tissue de­struction and, later, scarring and fibrous changes. Similarly, the clinical manifestations of systemic lupus erythematosus re­sult from the deposition of immune complex in the vessels (vasculitis), glomeruli (nephritis), joints (arthralgia, arthritis), and other organs and tissues. In this disorder, the immune complex is composed of cellular deoxyribonucleic acid (DNA) and anti-DNA antibodies.

Serum sickness is a complex of symptoms that occurs after the administration of a foreign serum or certain drugs. It is caused by the collection of immune complexes deposited in the walls of blood vessels in the skin, joints, and kidney. The most common causes of serum sickness today are penicillin and related drags and some animal serum antitoxins. Serum sickness used to be quite common when vaccines were madewith horse or rabbit serum, but now most vaccines are made with human serum or antigen fragments. Currently used agents that can cause serum sickness are antilymphocyte globulin and antithymocyte globulin, which are used to sup­press the immune response in organ transplantation.


The client with serum sickness has symptoms of fever, arthralgia (achy joints), rash, lymphadenopathy (enlarged lymph nodes), malaise, and possibly polyarthritis and nephri­tis. These symptoms usually appear approximately 7 to 12 days after receiving the causative agent. The nurse alerts the client to the possibility of serum sickness and what symptoms to look for. When administering a foreign serum to a client, the nurse is also prepared for a type I anaphylactic reaction and has emergency equipment and medications close at hand. Serum sickness is usually self-limiting, and symptoms subside after several days. Treatment is usually symptomatic; antihistamines are given for pruritus, and aspirin is given for arthralgias. Prednisone is given if symptoms are severe.




In a type IV reaction, the reactive cell is the T-lymphocyte. Antibodies and complement are not involved. Sensitized T-lymphocytes (from a previous exposure) respond to an anti­gen by producing and releasing certain lymphokines (chemi­cal mediators), and they recruit, retain, and activate macrophages to destroy the antigen. Unlike with a type I hy­persensitivity reaction, which occurs immediately, a type IV response typically occurs hours to days after exposure. A type IV reaction is characterized by an accumulation of lympho­cytes and macrophages, which causes edema, ischemia, and tissue destruction at the site.

An example of a small type IV reaction is a positive puri­fied protein derivative (PPD) test for tuberculosis. In a client previously exposed to tuberculosis, an intradermal injection of this agent causes sensitized T-cells to accumulate at the in­jection site, release lymphokines, and recruit and activate macrophages. Induration and erythema at the site of the in­jection appear after approximately 24 to 48 hours.

Other clinical examples of type IV hypersensitivity reac­tions include contact dermatitis, poison ivy skin rashes, a lo­cal response to insect stings, allograft (tissue transplant) re­jections, and granulomatous diseases in which the antigen is unknown (e.g., sarcoidosis).



Removal of the offending antigen is the major focus of man­agement. The reaction is self-limiting in 5 to 7 days, and the client is treated symptomatically. Nursing responsibilities in­clude monitoring the reaction site and sites distal to the reac­tion for circulation adequacy. Diphenhydramine (Benadryl) is of minimal benefit for type IV reactions because histamine is not the main mediator. In addition, IgE does not appear to play a role in this type of reaction, and therefore desensitization does not diminish the response. Corticosteroids or other anti-inflammatory agents can reduce the discomfort and help resolve the reaction more quickly.

Identification of Allergen

Patch testing can be used to identify the allergen. This type of testing involves skin contact with substances to which the client is potentially allergic. Contact with a specific allergen results in a delayed hypersensitivity reaction that develops in 48 to 96 hours.

Test chemicals are applied to uninvolved skin under occlusive tape patches. After the patches are removed, the skin ar­eas in contact with the chemical are examined closely for in­dications of localized erythema, swelling, and vesicular (blister) eruption. For a positive patch test result to have clin­ical relevance, a history of exposure to substances containing the chemical is required.

CLIENT PREPARATION. To prevent suppression of the inflammatory response to an allergen, systemic corticos­teroids or antihistamines are discontinued for at least 48 hours before the test. Topical steroid therapy may be continued as long as the agent is not applied on the area to be tested. To al­lay the client's anxiety, the nurse explains that patch testing does not involve pricking the skin with needles. The client is informed that testing will involve three separate visits to the allergist or dermatologist: one to apply the test patches, a sec­ond for an initial reading, and a third for detection of any de­layed hypersensitivity reactions.

PROCEDURE. The upper back is the preferred site for the application of test patches. After the client has disrobed, the back is inspected for evidence of rash and the presence of hair. If a rash is present, alternative test sites are the flanks, the lower back, and the upper arms. Any hair in the area is shaved to prevent poor contact and subsequent false-negative results. Removing skin oils with alcohol allows better adhesion of the patches.

Small quantities of chemicals and solutions in standard­ized concentrations are placed in separate metal chambers that are backed with hypoallergenic adhesive tape. The tape is carefully applied to the skin so each chemical is held in con­tact with the skin surface. Each chamber is marked for later identification. As many as 60 or more chemicals may be tested simultaneously.

The nurse instructs the client to keep the test sites dry at all times. Baths are substituted for showers until testing is complete. The client is instructed to use caution when wash­ing the hair to avoid getting the patches wet. Excessive physical activity that results in sweating is discouraged. Reapplying patches that come loose can interfere with an accurate interpretation of true allergic reactions. Thus the nurse reinforces the necessity of removing loose or nonad-herent test patches for later reapplication by the allergist or nurse.

The initial reading is performed 2 days after application. The tape containing the chemical-filled chambers is peeled away from the skin, and each area of contact is marked with indelible ink for future reading. The nurse documents any ini­tial allergic or irritant reactions in the client's medical record. The final reading occurs in 2 to 5 days.

FOLLOW-UP CARE. If a potential allergen is identified, the client is given a list of items containing that chemical. These items are to be avoided.




(Benadryl, Allerdryl-


25-50 mg q4-6h

Instruct client not to drive or

operate heavy machinery.



Do not give during an acute asthma attack.





Telachlor, Teldrin,


2-8 mg 1 -3 times/day

Avoid alcoholic beverages.


Same as for diphenhydramine.







10 mg q/d

Give every other day to clients

with renal or hepatic dysfunction.






5-10 mg qd

Reduce dose for clients with

renal or hepatic dysfunction




60 mg bid or 180 mg qd

Same as for loratadine.




(may be given as a "taper" or "short-term burst")



5-40 mg/day

Not recommended unless symptoms are severe


Drug can cause significant sedation.

Sedation decreases the voluntary muscle contractions needed for breathing.

Drug potentiates the effects of alcohol.

Renal or hepatic dysfunction re­duces drug clearance.

Same as for loratadine.


Systemic side effects are com­mon and serious:

  GI ulceration

  Poor wound healing

  Decreased immune function

  Increased risk for infections

  Weight gain


  Personality changes

  Fluid retention

Same as for prednisilone.



The client is a 25-year-old man who was stung by a wasp on the right hand yesterday while hiking. He experi­enced no problem except for pain at the site. When he woke up today, however, his right hand was twice the size of his left hand, and it was red, nontender, and very warm. He wonders if he has an infection.

  What additional assessment data should you obtain?

  Why should you or should you not start oxygen on this

  Would epinephrine be helpful in this situation? Why or why
not? Where, how much, and by what route would you ad­
minister it?

  Would diphenhydramine (Benadryl) be helpful in this situa­
tion? Why or why not?




This relatively new category of hypersensitivity reactions in­volves inappropriate stimulation of a normal cell surface recep­tor by an autoantibody, resulting in a continuous "turned-on" state for the cell. The classic example of a stimulatory reaction is Graves' disease, a form of hyperthyroidism. In Graves' dis­ease an autoantibody binds to thyroid-stimulating hormone (TSH) receptor sites on the thyroid gland. This binding contin­ually stimulates the thyroid cells to produce thyroid hormones, causing the client to have symptoms of severe hyperthyroidism. These symptoms occur even though the thy­roid gland itself is completely normal. In a sense, the tissue re­sponding to the autoantibody is "out of control" from the body's normal feedback system of checks and balances.

COLLABORATIVE MANAGEMENT For type V reactions involving only one organ, management focuses on removing enough of the responding (stimulated) tissue to return the function to normal. With Graves' disease, thyroid tissue is usually either surgically removed or de­stroyed with radiation. If more than one tissue is being stim­ulated by the autoantibodies or if the tissue is widespread, the focus of treatment is on reducing the production of autoanti­bodies through immunosuppression.


Autoimmunity is a process whereby a person develops and ex­presses an inappropriate immune response. In this response, antibodies and/or lymphocytes are directed against healthy normal cells and tissues. For unknown reasons, certain cells or tissues of the body are recognized as non-self-cells or are no longer tolerated as self-cells, and immune reactions occur. The resulting antibody-mediated and cell-mediated responses are similar to normal immune responses against non-self-cells, but they are inappropriate and sometimes excessive.






Systemic lupus erythematosus

DNA, DNA proteins

Rheumatoid arthritis

IgG, possibly cartilage

Progressive systemic sclerosis

DNA proteins

Mixed connective tissue


DNA proteins




Autoimmune hemolytic anemia


Autoimmune thrombocytopenic




Diabetes mellitus, Type 1

Islet cells, insulin, insulin receptor





Glomerular basement



Goodpasture's syndrome

Glomerular basement

membranes, pulmonary

basement membranes



Graves' disease

Thyroid-stimulating hormone receptor


Hashimoto's thyroiditis

Thyroid cell surface

Idiopathic Addison's disease

Adrenal cell

Myasthenia gravis

Acetylcholine receptor, acetylcholine

Pernicious anemia


Intrinsic factor, parietal

cell, B12 complexes



Stratum corneum

Reiter's syndrome

Possibly collagen, conjunctival cells


Sjogren's syndrome

Salivary gland cells, vaginal mucous cells,

lacrimal gland cells




Uveal tract cells (eye)


Unknown, possibly collagen or endothelial cells


IgG, Immunoglobulin G.


The causes of alterations in self-tolerance are not known, but there are multiple theories.

Autoimmunity research is ongoing, and there are few con­firmed, established data. Not only is the cause of autoimmunity uncertain, but there is also a lack of consensus regarding which diseases are truly autoimmune. Examples of diseases generally believed to be autoimmune include systemic lupus erythemato­sus, polyarteritis nodosa, rheumatoid arthritis, autoimmune he­molytic anemia, rheumatic fever, and Hashimoto's thyroiditis (Table). Other diseases, such as type I diabetes mellitus, may have multiple causes, one of which is autoimmune.

Connective tissue disorders, sometimes referred to as col­lagen disorders or rheumatic disorders, are characterized by changes in connective tissue. Many of these diseases are con­sidered autoimmune; autoantibodies have been detected for most of these disorders. Connective tissue disorders include systemic lupus erythematosus, rheumatoid arthritis, sclero-derma, and polyarteritis nodosa. Most of these tissue disor­ders are characterized as organ-nonspecific autoimmuni-ties, which means that the autoantibodies and the tissue damage are not limited to a specific organ. In organ-specific autoimmunities, tissue damage occurs in a specific organ.

Cost of Care

  Drug therapy with nonsteroidal anti-inflammatory drugs
(NSAIDs) remains a standard for autoimmune disorders that
are associated with chronic inflammation or chronic pain
(e.g., fibromyalgia, rheumatoid arthritis, and systemic lupus

  Aspirin is the oldest and most widely used NSAID.

  Side effects of chronic aspirin therapy include gastrointesti­
nal ulceration and bleeding, increased bleeding tendency,
and liver toxicities.

  Newer NSAIDs, especially the COX-2 selective inhibitors,
have main effects similar to aspirin and were thought to
have fewer side effects.

  The cost for 50 tablets of newer NSAIDs, especially the
COX-2 selective inhibitors, ranges from 10 to 30 times more
than the cost of aspirin.

  Recent studies using large sample sizes indicate that all
NSAIDs, including COX-2 selective drugs, have serious side
effects when taken chronically.

  The major side effect for which hospitalization and interven­
tion may be required is gastrointestinal ulceration. In addi­
tion, some NSAIDs are known to significantly reduce kidney
function to the point that intervention is necessary.

  The major benefit to the use of NSAIDs other than aspirin
may be solely in the convenience of once- or twice-per-day

Implications for Nursing

There may be little advantage to using the newer, more ex­pensive NSAIDs for inflammation and pain. The nurse must caution any client using NSAIDs for more than just a couple of days that these drugs are not harmless. Teaching priorities in­clude administration of the drugs with meals, prophylactic use of antacids or H2 histamine blockers, and the clinical manifes­tations of gastrointestinal, liver, or kidney function changes.

Management of autoimmunities depends on the organ or organs affected. Anti-inflammatory drugs and immunosuppressive drugs are commonly used along with symptomatic treatment.

WOMEN'S HEALTH CONSIDERATIONS Virtually all autoimmune disorders, especially rheumatic disorders, occur much more commonly among women than men (Cotran, Kumar, & Collins, 1999; Workman, 2000). The risk for autoimmune disease among women compared to men ranges from 5:1 to 20:1. In addition, most autoimmune disor­ders are more common among Caucasian women than among women of any other race.



Sjogren's syndrome (SS) is a group of problems that often ap­pear in association with other autoimmune disorders. Prob­lems include dry eyes (keratoconjunctivitis sicca), dry mucous membranes of the nose and mouth (xerostomia), and vaginal dryness. These problems are thought to be caused by autoimmune destruction of the lacrimal, salivary, and vaginal mucus-producing glands. Most commonly, the client with Sjogren's syndrome also has rheumatoid arthritis. Fibromyal­gia also is associated with SS.

Ninety percent of clients with Sjogren's syndrome are women between 35 and 45 years of age. SS is more common among clients with certain tissue types, specifically HLA-DRW52, HLA-DR3, and HLA-B8. Although an exact trig­gering agent has yet to be identified, viral infection is strongly suspected. The three viruses thought to be possible triggers for the autoimmune changes leading to Sjogren's syndrome are human immunodeficiency virus type 1 (HIV-1), human T-cell lymphotrophic virus type 1 (HTLV-1), and Epstein-Barr Virus (EBV).

Insufficient tears cause inflammation and ulceration of the cornea. Insufficient saliva decreases the digestion of carbohy­drates, promotes tooth decay, and increases the incidence of oral/nasal infections. Vaginal dryness increases the incidence of infection and may cause pain during sexual intercourse (dyspareunia).



The client with SS usually has blurred vision, burning and itching of the eyes, and thick mattering in the conjunctiva. Difficulty swallowing food is common, and the client often experiences changes in taste sensation. The nurse asks the client about the presence of nosebleeds (epistaxis) and fre­quent upper respiratory infections.

Physical examination reveals enlarged lymph nodes. If rheumatoid arthritis (RA) accompanies SS, the client has swollen, painful joints and limited joint mobility (see Chapter 21 for a complete discussion of RA). Laboratory assessment may show an increased presence of general antinuclear anti­bodies, anti-SS-A or anti-SS-B antibodies, and elevated levels of IgM rheumatoid factor.


IMMUNOMODULATION. Currently, there is no cure for SS. The intensity and progression of the disorder can be slowed by suppressing immune and inflammatory responses. The agents often used to modulate the immune system in clients with SS include low-dose chemotherapy with methotrexate (Rheumatrex) or cyclophosphamide (Cytoxan). Both agents can have serious long-term detrimental effects, especially on liver and bone marrow function. Other immunosuppressive agents that have shown benefit in managing SS are cortico-steroids, cyclosporine (Neoral, Sandimmune), and hydroxy-chloroquine (Plaquenil).

SYMPTOMATIC THERAPY. A variety of artificial tears and artificial saliva can help reduce symptoms of dry eye and dry mouth. Clients are instructed to use humidifiers in the home to increase the environmental moisture content. The use of water-soluble vaginal lubricants and moisturizers can in­crease comfort and reduce the incidence of vaginitis. Some clients have obtained significant relief from dry mouth with the use of systemic pilocarpine (Salagen). This agent is acholinergic agonist that mimics the effects of the parasympa-thetic nervous system, including increased salivation.

A nonpharmacologic intervention for dry eyes is to block the tear outflow channel (nasal punctum). The punctum can be blocked temporarily with small plugs or closed surgically. Either method allows the scant amount of tears produced to have longer contact with the eye.

Pain control is an issue for clients who have both SS and either rheumatoid arthritis or fibromyalgia. Nonsteroidal anti-inflammatory drugs (NSAIDs), rather than pure analgesics, are most commonly used to decrease inflammation and re­duce the associated pain. Many different types and strengths of NSAIDs are available by prescription and over-the-counter. The mechanism of action and side effects are similar for all NSAIDs, although the duration of action and cost can vary considerably.



Goodpasture's syndrome is an autoimmune disorder in which autoantibodies are made against the glomerular basement membrane and neutrophils. The two organs sustaining the most damage are the lungs and the kidney. Lung damage is manifested as pulmonary hemorrhage. Kidney damage mani­fests as glomerulonephritis, which may rapidly progress to complete renal failure. Unlike other autoimmune disorders, Goodpasture's syndrome is more common among males and generally occurs in adolescents or young adults (Cotran, Kumar, & Collins, 1999). The exact cause or triggering agent(s) is unknown.


The client with Goodpasture's syndrome usually is not diag­nosed until significant pulmonary and/or kidney problems are evident. Clinical manifestations include shortness of breath, hemoptysis (bloody sputum), decreased urine output, weight gain, generalized nondependent edema, hypertension, and tachycardia. A chest x-ray study reveals multiple areas of con­solidation. The most common cause of death is uremia as a re­sult of renal failure.

Spontaneous resolution of Goodpasture's syndrome has been known to occur but is rare. Interventions focus on re­ducing immune-mediated damage and in performing some type of renal supportive therapy.


DRUG THERAPY. The mainstay of drug therapy for Goodpasture's syndrome is high-dose corticosteroids. Addi­tional drug therapy to suppress the autoimmune response is the same as that for Sjogren's syndrome.

OTHER THERAPY. Additional therapy to modulate the immune responses with this autoimmune disorder involves plasmapheresis (filtration of the plasma to remove some pro­teins) to remove the autoantibodies. If the lungs and kidneys have not sustained permanent damage, clients undergoing plasmapheresis have shown clinical improvement. Some clients using plasmapheresis need supplemental administration of IV immunoglobulin (IVIG) to maintain antibody pro­tection against infection.

Renal Support Therapy

Depending on the level of remaining renal function, the client may need ongoing dialysis. Therapy usually begins with he-modialysis. For chronic therapy, peritoneal or hemodialysis may be instituted depending on the client's health status, abil­ity to self-manage the infusion and drainage systems, and lifestyle.

Renal transplantation is an option for some clients with Goodpasture's syndrome. After transplantation, renal function is normal. In rare instances, clients are disease free after transplantation. In others, the renal problems are improved but pulmonary destruction continues. Some of the drugs re­quired for immunomodulation for the transplanted kidney also suppress the autoimmune response.