CHAPTER 20 Care of Patients with Immune Function Excess

What should you INTERPRET and how should you RESPOND to a patient experiencing excess IMMUNITY and loss of protection as a result of a severe allergic reaction?

Perform and interpret physical assessment, including: • Taking vital signs, especially respiratory rate and depth and blood pressure • Auscultating all lung fields • Monitoring oxygen saturation by pulse oximetry • Assessing cognition • Assessing for the use of accessory muscles • Assessing for the presence of thick or excessive secretions • Assessing the patient's ability to cough and clear the airway Respond by: • Removing or discontinuing the offending agent • Ensuring a patent airway • Notifying the Rapid Response Team • Applying oxygen, and assessing the patient's responses to this intervention • Maintaining IV access, changing IV tubing, hanging normal saline • Keeping the patient's head elevated between 10 and 45 degrees • Preparing to administer IV diphenhydramine and epinephrine • Staying with the patient

Anaphylaxis: Health Promotion and Maintenance

Prevention and early intervention are critical. Teach the patient with a history of allergic reactions to avoid allergens whenever possible, to wear a medical alert bracelet, and to alert health care personnel about specific allergies. Some patients must carry an emergency anaphylaxis kit (e.g., a kit with injectable epinephrine, sometimes called a "bee sting kit") or an epinephrine injector, such as the EpiPen or Twinject automatic injector. The EpiPen device is a spring-loaded injector that delivers 0.3 mg of epinephrine per 2-mL dose directly into the subcutaneous tissue or intramuscularly. The medical records of patients with a history of anaphylaxis should prominently display the list of specific allergens. Ask the patient about drug allergies before giving any drug or agent. If he or she has a known allergy, be sure to document in the medical record the allergen and the typical response produced and communicate the allergy and its response to other members of the health care team. Skin tests should be performed before giving any substance that has a high incidence of causing anaphylactic reactions, such as iodine-containing dyes. Be aware of common cross-reacting agents. For example, a patient who is allergic to penicillin is also likely to react to cephalosporins because both have a similar chemical structure. People who have an allergy to bananas, avocados, and some nuts are more likely to have a latex allergy, although this is not universal. Take precautionary measures if a drug or agent must be used despite a history of allergic reactions. Start an IV, and place intubation equipment and a tracheostomy set at the bedside. The patient is often premedicated with diphenhydramine (Benadryl, Allerdryl ) or a corticosteroid. The allergy-causing substance is given first intradermally, then subcutaneously, and then intramuscularly in increasing doses at 20- to 30-minute intervals.

Sjögren's Syndrome

Sjögren's syndrome (SS) is a group of problems that often appear with other autoimmune disorders. Problems include dry eyes, dry mucous membranes of the nose and mouth (xerostomia), and vaginal dryness. These problems are caused by autoimmune destruction (excess IMMUNITY) of the lacrimal, salivary, and vaginal mucus-producing glands. Often, the patient with SS also has rheumatoid arthritis or fibromyalgia. Most patients with SS are women 35 to 45 y. An exact triggering agent has not been identified, viral infection is strongly suspected, especially 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 digestion of carbohydrates, promotes tooth decay, and increases the risk for oral and nasal infections. Vaginal dryness increases the risk for infection and causes painful sexual intercourse.

Allergic Rhinitis: Allergy Testing

Skin testing can show which specific allergens are the cause of a type I reaction. Skin testing is performed as scratch testing or intradermal testing. Patch testing is often reserved for contact dermatitis. A scratch or prick test can show an immediate hypersensitivity reaction to an allergen and is used in routine allergy testing for type I reactions. Allergens introduced through a scratch or prick cause a localized reaction (wheal) when the test result is positive. Results are usually determined after 15 to 20 min.

Allergy Testing: Patient Preparation

Systemic glucocorticoids and antihistamines are discontinued 2 weeks before the test to avoid suppressing the test response. Nasal sprays to reduce mucous membrane swelling are permitted, except for sprays that contain an antihistamine.

Allergic Rhinitis: Avoidance Therapy

Teach the patient to avoid direct or close contact with these agents. Some allergens, such as foods or drugs, may be easy to avoid. Other allergens, such as pollen, mold, or dust mites, may require environmental changes. Teach patients that airborne allergens can be reduced by air-conditioning and air-cleaning units. Removing cloth drapes, upholstered furniture, and carpeting also reduces airborne allergens. Covering mattresses and pillows with plastic or an ultra-mesh cover reduces exposure to dust mites and mold, as does laundering bed linens weekly. Simple interventions, such as keeping pets out of the bedroom and thorough cleaning of the room to remove animal hair and dander, may reduce symptoms. Frequent bathing of the pet 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 fur, feathers, or dander may need to be removed.

Allergy Testing: Procedure

The best site for scratch testing is the inside of the forearm or on the back. Gently clean the skin with soap and water, and remove surface oils with alcohol. Small drops of sera containing different known allergens are placed on the skin. The skin is scratched or pricked through the drop with a skin testing needle. Control drops are also applied to determine how a person reacts to substances that do not normally stimulate a reaction (negative control) and to substances that normally should stimulate an excess IMMUNITY reaction (positive control). Allergen-tested areas are examined and then compared with the control areas. Areas with erythema and wheal formation are positive for that antigen. Ensure that emergency equipment is available during testing. This includes manual resuscitation bag, oxygen, suction equipment, IV infusion set, and drugs for anaphylaxis (epinephrine and diphenhydramine).

Allergic Rhinitis: Physical Assessment/Clinical Manifestations

The patient with allergic rhinitis has rhinorrhea (a "runny" nose), a "stuffy" nose, and itchy, watery eyes. He or she may breathe through the mouth, and the voice has a nasal sound. Drainage from the nose is usually clear or white. The nasal mucosa appears swollen and pink. The patient may have a headache or feel pressure over the frontal and maxillary sinuses. Placing a penlight directly on the skin over the sinuses and observing for a glow (transillumination) often shows reduced glow when rhinitis is present. With postnasal drip, the patient has a dry, scratchy throat and pharyngitis. He or she often feels as though a cold is present that has lasted longer than a week. Fever is rare unless an infection occurs.

Sjögren's Syndrome: Patient-Centered Collaborative Care

Usually has blurred vision, burning and itching of the eyes, and thick mattering in the conjunctiva. Difficulty swallowing food is common, as are changes in taste. Ask about nosebleeds (epistaxis) and frequent upper respiratory infections. Examination reveals enlarged lymph nodes. If rheumatoid arthritis (RA) accompanies SS, the patient has swollen, painful joints and limited joint mobility. Laboratory assessment may show increased amounts of general antinuclear antibodies, anti-SS-A or anti-SS-B antibodies, and elevated levels of IgM rheumatoid factor. No cure for SS. Drugs used to modulate the immune system in patients with SS include low-dose chemotherapy with methotrexate (Rheumatrex) or cyclophosphamide (Cytoxan). Both drugs have serious long-term side effects, especially on liver and bone marrow function. Other immunosuppressive drugs used to manage SS are corticosteroids, cyclosporine (Gengraf, Neoral, Sandimmune), and hydroxychloroquine (Plaquenil). The monoclonal antibody rituximab (Rituxan) has been beneficial for patients with severe inflammatory manifestations of SS. A variety of artificial tears and artificial saliva can help reduce the dry eye and dry mouth manifestations. Teach patients to use humidifiers in the home to increase environmental moisture. Use of water-soluble vaginal lubricants and moisturizers can increase patient comfort and reduce vaginitis. Some patients relieve dry mouth with drugs that increase salivation, such as systemic pilocarpine (Salagen). A drug that increase tears production is cyclosporine (Restasis) eyedrops. Another intervention for dry eyes is to block the tear outflow channel with small plugs or close it surgically.

Gender Health Considerations

Virtually all autoimmune disorders, especially rheumatic disorders, occur much more commonly among women than men. The risk for autoimmune disease among women compared with men ranges from 5 : 1 to 20 : 1.

Allergy Testing: Follow-up Care

Wash the solution from the skin. Topical steroids and oral antihistamines may be given to reduce itching and increase patient comfort. If an antihistamine that causes sedation is given, another person must drive the patient. Intradermal testing is reserved for substances that are strongly suspected of causing allergy but did not test positive with scratch testing. Intradermal testing increases the risk for an adverse reaction, including anaphylaxis. Ensure that emergency equipment is present. Small amounts of testing sera (0.1 mL) are injected intradermally on the upper arm, and the area is observed for erythema and wheal formation. The degree of allergy is estimated by the size of the response. Preparation and follow-up care are the same as for scratch testing. Oral food challenges are used for patients who have allergic rhinitis when the allergen is eaten rather than inhaled. This type of testing is used to identify specific allergens if skin testing is not conclusive and if keeping a food diary has failed. The test requires the patient to eliminate suspected foods for 7 to 14 days before testing. After this time, the patient is directed to eat a specific suspected food for at least 1 day and to monitor for manifestations of allergy. When many food allergies are present, the patient may have to eat only one food type per day of testing. Oral food challenges are not performed using foods that have previously caused a serious or anaphylactic reaction

Allergic Rhinitis: Drug Therapy

This therapy involves the use of steroidal and nonsteroidal agents (to reduce inflammation), vasoconstrictors, antihistamines, mast cell stabilizers, and drugs that inhibit the release or action of leukotrienes. Decongestants are available as systemic oral drugs or nasal sprays. These drugs do not clear the allergen or prevent the release of mediators such as histamine. They work by causing vasoconstriction in the inflamed tissue, thereby reducing the edema. Decongestants often contain ephedrine, phenylephrine, or pseudoephedrine. Secretions are reduced when vasoconstricting drugs are combined with an anticholinergic drug, such as scopolamine or atropine. Side effects include dry mouth, increased blood pressure, and sleep difficulties. Antihistamines block histamine from binding to the receptor. This action prevents vasodilation and capillary leak. Many antihistamines also decrease secretions. Some antihistamines, such as diphenhydramine (Benadryl, Allerdryl image) and chlorpheniramine (Allergy, Aller-Chlor, Chlor-Trimeton), often induce sedation. Others, such as desloratadine (Clarinex), cetirizine (Zyrtec), and fexofenadine (Allegra), are less sedating. Corticosteroids decrease INFLAMMATION and excess IMMUNITY by preventing the synthesis of mediators. Corticosteroid nasal sprays (topical intranasal steroids) can prevent the symptoms of rhinitis. Systemic corticosteroids can produce severe side effects and are used only on a short-term basis. Mast cell stabilizing drugs include nasal sprays, such as cromolyn sodium (Nasalcrom), that prevent mast cell membranes from opening when an allergen binds to IgE. Thus these drugs prevent the symptoms of allergic rhinitis; not for acute! Leukotriene antagonists may be used to manage and prevent allergic rhinitis. Zileuton (Zyflo) prevents leukotriene synthesis. Zafirlukast (Accolate) blocks the leukotriene receptor.

Type I: Rapid Hypersensitivity Reactions

Type I, or rapid hypersensitivity, also called atopic allergy, is the most common type of hypersensitivity. This type results from the increased production of the immunoglobulin E (IgE) antibody class. Acute INFLAMMATION occurs when IgE responds to an antigen, such as pollen, and causes the release of histamine and other vasoactive amines from basophils, eosinophils, and mast cells. Examples of type I reactions include anaphylaxis and allergic asthma. Atopic allergies such as hay fever and allergic rhinitis; and allergies to substances such as latex, bee venom, peanuts, iodine, shellfish, drugs, and thousands of other environmental allergens. Allergens can be contacted in these 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) • Contacted (latex, pollens, foods, environmental proteins) Reactions occur just in the areas exposed to the antigen, such as the mucous membranes of the nose and eyes, causing symptoms of rhinorrhea, sneezing, and itchy, red, watery eyes. Other reactions may involve all blood vessels and bronchiolar smooth muscle causing widespread blood vessel dilation, 349decreased cardiac output, and bronchoconstriction. This condition is known as anaphylaxis.

Key Points: Safe and Effective Care Environment

• Ensure that only latex-free products are used for a patient who has a known latex allergy. • Verify that all allergies are documented in a prominent place in the patient's medical record. • Keep emergency equipment and drugs (epinephrine, Benadryl, cortisol) in or near the room of a patient with known severe allergies or a history of anaphylaxis.

Key Points: Psychosocial Integrity

• Explain all diagnostic procedures, restrictions, and follow-up care to the patient scheduled for tests related to hypersensitivities. • Stay with the patient in anaphylaxis. • Reassure patients who are in anaphylaxis that the appropriate interventions are being instituted.

Key Points: Physiological Integrity

• Identify patients at risk for hypersensitivity reactions, especially anaphylaxis. • Communicate a patient's allergies to all members of the health care team. • Immediately assess the respiratory status and airway of patients who show any manifestations of an allergic reaction. • Immediately discontinue the IV drug or solution of a patient having an anaphylactic reaction to that drug or solution. Do not discontinue the IV, but change the IV tubing and hang normal saline. • Hold the dose of any prescribed drug when a patient develops angioedema. • Give oxygen to any patient in anaphylaxis.

Type IV: Delayed Hypersensitivity Reactions

Type IV reaction, the reactive cell is the T-lymphocyte (T-cell). Antibodies and complement are not involved. Sensitized T-cells (from a previous exposure) respond to an antigen by releasing chemical mediators and triggering macrophages to destroy the antigen. A type IV response typically occurs hours to days after exposure. It consists of edema, induration, ischemia, and tissue damage at the site. An example of a small type IV reaction is a positive purified protein derivative (PPD) test for tuberculosis (TB). In a patient previously exposed to TB, an intradermal injection of this agent causes sensitized T-cells to clump at the injection site, release lymphokines, and activate macrophages. Induration and erythema at the injection site appear after about 24 to 72 hours. Examples of type IV reactions include contact dermatitis, poison ivy skin rashes, local response to insect stings, tissue transplant rejections, and sarcoidosis. Patch testing for type IV hypersensitivity involves applying test chemicals that contain the allergen(s) to which the patient has been exposed. The patches remain in place for 48 hours. After removal, the skin areas in contact with the chemical are examined for localized redness, swelling, and blisters. Removal of the offending antigen is the major focus of management. The reaction is self-limiting in 5 to 7 days, and the patient is treated symptomatically. Monitor the reaction site and sites distal to the reaction for circulation adequacy. Diphenhydramine (Benadryl) is not useful for type IV reactions because histamine is not the main mediator. Because IgE does not cause this type of reaction, desensitization does not reduce the response. Corticosteroids can reduce the discomfort and help resolve the reaction.

Allergic Rhinitis: Complementary and Alternative Therapies

Use of aromatherapy. Possible mechanisms of action include competition and desensitization. Some patients with pollen allergies report decreased problems after eating unprocessed honey.

Action Alert

Use only latex-free products in the care of a patient with a known latex allergy.

Allergic Rhinitis: Laboratory Assessment

A white blood cell (WBC) count and differential indicate the presence of excess IMMUNITY with an allergic response by an increase in eosinophils. A patient with severe seasonal allergic rhinitis may have an eosinophil count as high as 12% (normal being 1% to 2%). Some patients have an increased total WBC count, but the percentage of neutrophils remains normal (55% to 70%). If an acute infection occurs with allergic rhinitis, both the total WBC count and the neutrophils increase. Tests indicating an allergic reaction include serum immunoglobulin E (IgE) levels measured by enzyme-linked immunosorbent assay (ELISA) and the radioallergosorbent test (RAST). A normal level of IgE for adults is about 39 IU/ mL (or less than 100 IU/mL). This level increases greatly with allergies. The radioimmunosorbent test (RIST) shows the blood level of IgE directed against a specific antigen and can determine specific allergies.

Critical Rescue

Administer epinephrine as quickly as possible. Most deaths from anaphylaxis are related to delay in epinephrine administration.

Allergic Rhinitis

Allergic rhinitis, or hay fever, is triggered by IMMUNITY and INFLAMMATION reactions to airborne allergens, especially plant pollens, molds, dust, animal dander, wool, food, and air pollutants. Some acute episodes are "seasonal". Chronic rhinitis, or perennial rhinitis, occurs intermittently (with no predictable seasonal pattern) or continuously when a person is exposed to certain allergens. In "nonallergic rhinitis," the same manifestations are present although no allergic cause is identified and the immune system not involved. On first exposure to an allergen (an antigen that causes allergic sensitization), the person responds by making antigen-specific IgE. This IgE binds to the surface of basophils and mast cells. These cells have many granules containing vasoactive amines (including histamine) that are released. Once the antigen-specific IgE is formed, the person is sensitized to that allergen. In a type I allergic reaction, the already sensitized person is re-exposed. 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 the cell membrane. The membrane opens and releases the vasoactive amines. Histamine causes capillary leak, nasal and conjunctival mucus secretion, and itching (pruritus), often occurring with erythema (redness). The secondary phase results from the release of other cellular proteins. These other proteins draw more white blood cells to the area and stimulate a more general inflammatory reaction through actions of leukotriene and prostaglandins. The resulting inflammation increases the clinical manifestations and continues the response.

Genetic Considerations

Although allergic tendencies are inherited, specific allergies are not inherited.

Anaphylaxis

Anaphylaxis, the most life-threatening example of a type I hypersensitivity reaction, occurs rapidly and systemically. It can be fatal. The major factor in fatal outcomes for anaphylaxis is a delay in the administration of epinephrine. Drugs and dyes are more common causes of anaphylaxis in acute care settings; food and insect stings/bites are common causes in community settings.

Allergic Rhinitis: History

Ask the patient to describe the onset and duration of problems in relation to possible allergen exposure. Ask about work, school, and home environments and about possible exposures through hobbies, leisure time, or sports activities. Because a tendency toward type I allergic responses can be inherited, ask about family history.

Anaphylaxis: Interventions

Assess respiratory function first. Emergency respiratory management is critical during an anaphylactic reaction. The upper airways and lower airways are affected by bronchoconstriction that quickly impairs airflow and leads to hypoxemic arrest. Immediately establish or stabilize the airway. If an IV drug is suspected to be causing the anaphylaxis, stop the drug immediately but do not remove the venous access because restarting an IV may be very difficult. Change the IV tubing and hang NS. Epinephrine (1 : 1000) 0.3 to 0.5 mL is the first-line drug for anaphylaxis. It is given IM or IV. This drug constricts blood vessels, improves cardiac contraction, and dilates the bronchioles. The same dose may be repeated every 5 to 15 minutes. Antihistamines such as diphenhydramine (Benadryl, Allerdryl) 25 to 100 mg are second-line drugs and are given IV or IM for angioedema and urticaria. If needed, an endotracheal tube may be inserted or an emergency tracheostomy. If the patient can breathe independently, give oxygen to reduce hypoxemia. Start oxygen therapy via a high-flow non-rebreather facemask at 90% to 100%. Monitor pulse oximetry. Use suction to remove excess mucus and other secretions. Continually assess the respiratory rate and depth, and assess breath sounds continually for bronchospasm, wheezing, crackles, and stridor. Bed to 45 degrees unless severe hypotension. For bronchospasms, the patient may be given an inhaled beta-adrenergic agonist such as metaproterenol (Alupent) or albuterol (Proventil) via high-flow nebulizer. Oral steroids are continued (at lower doses) after the anaphylaxis is under control to prevent the late recurrence.

Autoimmunity

Autoimmunity is a process whereby antibodies or lymphocytes are directed against healthy normal cells and tissues. (Antibodies directed against self tissues or cells are known as autoantibodies.) For unknown reasons, the immune system fails to recognize certain body cells or tissues as self and thus triggers immune reactions. The responses, both antibody- and cell-mediated responses, are directed against normal body cells. Examples of diseases that have an autoimmune cause include systemic lupus erythematosus (SLE), polyarteritis nodosa, scleroderma, rheumatoid arthritis, autoimmune hemolytic anemia, rheumatic fever, and Hashimoto's thyroiditis (Table 20-3). Other diseases, such as type 1 diabetes mellitus, may have multiple causes, one of which is autoimmune. There is no cure. Anti-inflammatory drugs and immunosuppressive drugs are commonly used along with symptomatic treatment to suppress the excess IMMUNITY.

Drug Alert

Because effects are systemic, teach patients with high blood pressure, glaucoma, or urinary retention to consult with a health care professional before taking any decongestant.

Chart 20-2 Key Features Anaphylaxis PG 352 IGGY

Clinical Criteria 1 Onset within minutes to hours of skin or mucous membrane problems involving swollen lips, tongue, soft palate, uvula; widespread hives; pruritus; or flushing along with any one of these new onset symptoms: • Respiratory distress or ineffectiveness: ▪ Dyspnea ▪ Bronchospasms ▪ Wheezes ▪ Stridor ▪ Hypoxia ▪ Cyanosis ▪ Peak expiratory rate flow lower than the patient's usual • Hypotension or any indication of reduced perfusion resulting in organ dysfunction: ▪ Loss of consciousness ▪ Incontinence ▪ Hypotonia ▪ Absent deep tendon reflexes Clinical Criteria 2 Onset within minutes to hours of two or more of these symptoms after a patient has been exposed to a potential allergen: • Skin or mucous membrane problems involving swollen lips, tongue, soft palate, uvula; widespread hives; pruritus; or flushing • Respiratory distress or ineffectiveness as evidenced by any dyspnea, bronchospasms, wheezes, stridor, hypoxia, cyanosis, or peak expiratory rate flow lower than the patient's usual • Hypotension or any indication of reduced perfusion resulting in organ dysfunction, such as loss of consciousness, incontinence, hypotonia, or absent deep tendon reflexes • Persistent GI problems such as nausea or vomiting, cramping, abdominal pain Clinical Criteria 3 Onset within minutes to hours of hypotension with systolic blood pressure lower than 90 mm Hg or 30% lower than the patient's baseline systolic pressure.

Allergic Rhinitis: Desensitization Therapy

Commonly called "allergy shots," may be needed when allergens are identified and cannot be avoided easily. It involves subcutaneous injections of very dilute solutions of the identified allergen or allergens. A 0.05-mL dose of this solution is injected subcutaneously. Usually an increasing dose is given weekly until the patient is receiving a 0.5-mL dose. The patient is then started on the lowest dose of the next higher concentration of allergen solution. The process is repeated with increasing concentrations of allergen solutions until the patient is receiving the maximum dose of the greatest concentration (usually 1 : 100), depending on his or her response. The recommended full course of treatment is about 5 years. Desensitization appears to reduce allergic responses by competition. In theory, the very small amounts of allergen first injected are too low to bind to the IgE already present but are enough to induce immunoglobulin G (IgG) production against that allergen. IgG is not attached to either mast cells or basal cells, and allergens that bind to IgG do not trigger allergic responses. IgG then clears the allergen from the body. By gradually increasing the allergen injection, large amounts of IgG are produced against the allergen. When the patient is then exposed to the allergen in the environment, the IgG binds to it and clears it from the body before IgE can bind to it. IgG is successful in the competition to bind the allergen.

Goodpasture's Syndrome

Goodpasture's syndrome is an autoimmune disorder in which autoantibodies attack the glomerular basement membrane and neutrophils. The two organs with the most damage are the lungs and the kidneys. A person with the disorder may have lung and/or kidney problems. Lung damage is manifested as pulmonary hemorrhage. Kidney damage shows as glomerulonephritis that may rapidly progress to complete kidney failure. Most common in adolescent males or young men.

Hypersensitivities/Allergies

Hypersensitivity or allergy is excessive INFLAMMATION occurring in response to the presence of an antigen (foreign protein or allergen) to which the patient usually has been previously exposed. It can cause problems that range from uncomfortable (e.g., itchy, watery eyes or sneezing) to life threatening (e.g., allergic asthma, anaphylaxis, bronchoconstriction, or circulatory collapse). Hypersensitivity reactions are classified into four basic types, determined by differences in timing, pathophysiology, and manifestations (Table 20-1).

Critical Rescue

Immediately call the Rapid Response Team if you suspect anaphylaxis, because most anaphylactic deaths are related to treatment delay. If the patient is not treated immediately, he or she may lose consciousness. Dysrhythmias, shock, and cardiopulmonary arrest may occur within minutes as intravascular volume is lost and the heart becomes hypoxic.

Type II: Cytotoxic Reactions

In a type II (cytotoxic) reaction, the body makes autoantibodies directed against self cells that have some form of foreign protein attached to them. The autoantibody binds to the self cell and forms an immune complex. The self cell is then destroyed along with the attached protein. Clinical examples of type II reactions include immune hemolytic anemias, immune thrombocytopenic purpura, hemolytic transfusion reactions, Goodpasture's syndrome, and drug-induced hemolytic anemia. Management of type II reactions begins with discontinuing the offending drug 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 kidney failure can be life threatening.

Type III: Immune Complex Reactions

In a type III reaction, excess antigens cause immune complexes to form in the blood (Fig. 20-4). These circulating complexes usually lodge in small blood vessel walls of the kidneys, skin, and joints. The complexes trigger INFLAMMATION, and tissue or vessel damage results. Mostly connective tissue disorders are caused by type III reactions. For example, the manifestations of rheumatoid arthritis are caused by immune complexes that lodge in joint spaces followed by tissue destruction, scarring, and fibrotic changes. Systemic lupus erythematosus (SLE) has immune complexes lodged in the vessels (vasculitis), the glomeruli (glomerulonephritis), the joints (arthralgia, arthritis), and other organs and tissues. Serum sickness is a group of manifestations that occurs after receiving serum or certain drugs. Immune complexes are deposited in blood vessel walls of the skin, joints, and kidneys. Common causes of serum sickness are penicillin, other antibiotics, and some animal serum-based drugs. Other agents known to cause serum sickness include antilymphocyte globulin and antithymocyte globulin, used to treat organ transplant rejection. The patient with serum sickness has fever, arthralgia (achy joints), rash, malaise, lymphadenopathy (enlarged lymph nodes), and possibly polyarthritis and nephritis about 7 to 12 days after receiving the agent. Serum sickness is usually self-limiting, and manifestations subside after several days. Management is symptomatic; antihistamines are given for itching and aspirin for arthralgias. Prednisone is given if manifestations are severe.

Anaphylaxis: Assessment

Initial manifestations may be subtle, such as sudden severe abdominal cramping and diarrhea. A set of three criteria, listed in Chart 20-2, is used for diagnosis of anaphylaxis. A patient is considered to have anaphylaxis whenever any one of these three criteria is met. A patient having an anaphylactic reaction first has feelings of uneasiness, apprehension, weakness, and impending doom. Often he or she is anxious and frightened. These feelings are followed, often quickly, by generalized itching and urticaria (hives). Erythema and sometimes angioedema (diffuse swelling) of the eyes, lips, or tongue occur next (Fig. 20-3). Intensely itchy skin wheals or hives may appear and sometimes merge to form large, red blotches. Mediators cause INFLAMMATION, bronchoconstriction, mucosal edema, and excess mucus production. Respiratory symptoms include congestion, rhinorrhea, dyspnea, and increasing respiratory distress with audible wheezing. On auscultation, crackles, wheezing, and reduced breath sounds are heard. Patients may have laryngeal edema as a "lump in the throat," hoarseness, and stridor (a crowing sound). Distress increases as the tongue and larynx swell and more mucus is produced. Stridor increases as the airway begins to close. Increasing bronchoconstriction can lead to reduced chest movement and impaired airflow. Respiratory failure may follow from laryngeal edema, suffocation, or lower airway constriction causing hypoxemia (poor blood oxygenation). The patient is usually hypotensive and has a rapid, weak, irregular pulse from extensive capillary leak and vasodilation. He or she is faint and diaphoretic with increasing anxiety and confusion.

Latex Allergy

Latex allergy is a type I hypersensitivity reaction in which the specific allergen is a processed natural latex rubber protein. When the allergen enters the body through inhalation or direct contact with blood vessels (e.g., as might occur during surgery), interaction with IgE occurs, leading to a type I reaction. Latex allergen contact is limited to the skin or mucous membranes, causing contact dermatitis, a type IV hypersensitivity reaction. Others may have a "mixed" allergic response to latex, with symptoms of both type I and type IV People at greatest risk are those with a high exposure to natural latex products, such as patients with spina bifida, people who routinely use latex condoms, and health care workers who use latex gloves, especially gloves that are powdered. Document all food allergies because some have cross-reactivity for latex allergy. Avoiding products that contain natural latex proteins can prevent reactions and initial sensitivity. Most surgical gloves, tubing, and vial closures are now being made from synthetic substances that do not contain latex proteins. Interventions for the patient who has a type I or a type IV reaction to latex are the same as for reactions caused by other allergens.

Goodpasture's Syndrome: Patient-Centered Collaborative Care

Often is not diagnosed until serious lung or kidney problems are present. Manifestations include shortness of breath, hemoptysis (bloody sputum), decreased urine output, weight gain, generalized edema, hypertension, and tachycardia. Chest x-rays show areas of consolidation. The most common cause of death is uremia as a result of kidney failure. Interventions focus on reducing damage from excess IMMUNITY and performing some type of renal replacement therapy. Drug therapy is the mainstay of treatment for Goodpasture's syndrome. High-dose corticosteroids are most often used. Other drug therapy to suppress the autoimmune response is the same as that for Sjögren's syndrome (SS). Additional therapy involves plasmapheresis (filtration of the plasma to remove some proteins) to remove the autoantibodies. If the lungs and kidneys do not have permanent damage, patients undergoing plasmapheresis have shown clinical improvement. Some patients using plasmapheresis need infusions of intravenous immunoglobulin (IVIG) to maintain antibody protection against infection. Depending on the level of kidney function remaining, the patient may need ongoing renal replacement therapy. Peritoneal dialysis or hemodialysis may be used. Kidney transplantation is an option for some patients with Goodpasture's syndrome. After transplantation, kidney function is normal and a few patients have been completely disease-free. In others, the kidney problems are improved but the lung destruction continues. Some of the drugs used to prevent kidney rejection also suppress the autoimmune response.

TABLE 20-1 Mechanisms and Examples of Types of Hypersensitivities

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TABLE 20-2 Common Agents That Cause Anaphylaxis

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Chart 20-4 Common Examples of Drug Therapy Anaphylaxis

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TABLE 20-3 Known or Probable Autoimmune Disorders

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Chart 20-3 Best Practice for Patient Safety & Quality Care Emergency Care of the Patient with Anaphylaxis

• Immediately assess the respiratory status, airway, and oxygen saturation of patients who show any symptom of an allergic reaction. • Call the Rapid Response Team. • Ensure that intubation and tracheotomy equipment is ready. • Apply oxygen using a high-flow, non-rebreather mask at 90% to 100%. • Immediately discontinue the IV drug or infusing solution of a patient having an anaphylactic reaction to that drug or solution. Do not discontinue the IV, but change the IV tubing and hang normal saline. • If the patient does not have an IV, start one immediately and run normal saline. • Be prepared to administer epinephrine IV (preferred) or IM. ▪ Epinephrine 1 : 1000 concentration, 0.3 to 0.5 mL IV push or IM ▪ Repeat drug administration as needed every 5 to 15 minutes until the patient responds • Keep the head of the bed elevated about 10 degrees if hypotension is present; if blood pressure is normal, elevate the head of the bed to 45 degrees or higher to improve ventilation. • Raise the feet and legs. • Stay with the patient. • Reassure the patient that the appropriate interventions are being instituted.

What might you NOTICE if the patient is experiencing excess IMMUNITY and loss of protective response in the form of a severe allergic reaction?

• Possible skin rash, blisters, wheals, especially on the skin at the IV site • Swelling of the face, lips, tongue (angioedema) • Difficulty breathing, hoarseness, stridor, wheezing • Cyanosis • Increasing anxiety

Chart 20-1 Patient and Family Education: Preparing for Self-Management Care and Use of Automatic Epinephrine Injectors

• Practice assembly of injection device with a non-drug-containing training device provided through the injection device manufacturer. • Keep the device with you at all times. • When needed, inject the drug into the top of your thigh, slightly to the outside, holding the device so that the needle enters straight down. • You can inject the drug right through your pants; just avoid seams and pockets where the fabric is thicker. • Use the device when any symptom of anaphylaxis is present and call 911. It is better to use the drug when it is not needed than to not use it when it is needed!!! • Whenever you need to use the device, get to the nearest hospital for monitoring for at least the next 4 to 6 hours. • Have at least two drug-filled devices on hand in case more than one dose is needed. • Protect the device from light and avoid temperature extremes. • Carry the device in the case provided by the manufacturer. • Keep safety cap in place until you are ready to use the device. • Check the device for: ▪ Expiration date—If the date is close to expiring or has expired, obtain a replacement device.* ▪ Drug clarity—If the drug is discolored, obtain a replacement device. ▪ Security of cap—If the cap is loose or comes off accidently, obtain a replacement device.

Key Points: Health Promotion and Maintenance

• Urge all patients with severe allergies or those who have a history of anaphylaxis to wear a medical alert bracelet. • Teach the patient and family about the manifestations of allergic reactions and when to seek medical help. • Teach the patient who has a known drug allergy about which other drugs are likely to stimulate the same reactions. • Teach the patient who carries an automatic epinephrine injector how to care for, assemble, and use the device. Obtain a return demonstration.