Nursing Care of Patients With Immune Disorders PDF

4068_Ch19_339-361 15/11/14 1:29 PM Page 339 Nursing Care of Patients 19 With Immune Disorders SHARON M. NOWAK...

4068_Ch19_339-361 15/11/14 1:29 PM Page 339 Nursing Care of Patients 19 With Immune Disorders SHARON M. NOWAK KEY TERMS anaphylaxis (AN-uh-fih-LAK-siss) angioedema (AN-gee-oh-eh-DEE-mah) LEARNING OUTCOMES ankylosing spondylitis (ANG-kih-LOH-sing SPON- da-LEYE-tiss) 1. Explain the immunological mechanism for the four types histamine (HISS-tah-mean) of hypersensitivities. urticaria (UR-tih-KAIR-ee-ah) 2. Explain the pathophysiology of disorders of the immune system. 3. Identify the etiologies, signs, and symptoms of immune system disorders. 4. Plan nursing care for patients undergoing tests for immune system disorders. 5. Describe current medical treatment for immune system disorders. 6. List data collected when caring for patients with disorders of the immune system. 7. Explain factors that alter or influence the self-recognition portion of the immune system. 8. Plan nursing care for patients with disorders of the immune system. 9. Evaluate effectiveness of nursing interventions. 339 4068_Ch19_339-361 15/11/14 1:29 PM Page 340 340 UNIT FOUR Understanding the Immune System Disorders of the immune system can be divided into three cat- life threatening. The patient must ha ve had previous expo- egories. The first category is hypersensitivity reactions, which sure (sensitization) to the antigen. During this exposure, im- include conditions such as anaphylaxis, hemolytic transfusion munoglobulin E (IgE) antibodies are made and attach to reactions, measles, and transplant rejections. Autoimmune dis- mast cells throughout the body. When a subsequent exposure orders (e.g., rheumatoid arthritis, ulcerative colitis, and multiple occurs, the antigen causes IgE to trigger mast cells to release sclerosis) are the second category. The third category includes their contents. One of the substances released is histamine, the immune deficiencies, such as hypogammaglobulinemia and which causes vasodilation, changes in vascular permeability, acquired immunodeficiency syndrome (AIDS; see Chapter 20). an increase in mucous production, and contraction of various smooth muscles. If the second antigen exposure is localized, the reaction is HYPERSENSITIVITY REACTIONS mild and remains local. However, if the exposure is systemic, the reaction is massive and widespread. Respiratory allergies, The immune system is an adapti ve system that protects the such as allergic rhinitis and allergic asthma, with associated body. However, sometimes this system can cause injury to disorders of atopic dermatitis, tend to be reactions of a larger the body because of its e xaggerated response. One of these scale. Anaphylaxis, urticaria, and angioedema are the sever- occasions is when a hypersensitivity reaction occurs. In 1963, est forms of type I reactions. Gell and Coombs developed a system of classifying hyper- A type I reaction occurs when the patient has a positi ve sensitivity reactions as types I, II, III, and IV , according to reaction to a scratch test. A scratch test is done to identify the way the tissue is injured. specific allergens to which a patient is reactive. Tiny amounts Type I Hypersensitivity Reaction of a variety of common allergens are scratched onto the skin, An anaphylactic reaction, a type I reaction, is an immediate reaction that occurs on e xposure to a specif ic antigen WORD BUILDING (Fig. 19.1). The reaction can range from mild to severe and angioedema: angeion—vessel + oidema—swelling First Exposure Memory Antigens cell Plasma cell Helper T cell B cell Macrophage After Exposure Antibodies (immunoglobulins) Mast cell Second Exposure = Histamine = Prostaglandins Mast cell FIGURE 19.1 Type I hypersensitivity. 4068_Ch19_339-361 15/11/14 1:29 PM Page 341 Chapter 19 Nursing Care of Patients With Immune Disorders 341 which is then observed for indications of a reaction: redness, vesicles (blisters); these eventually break open, crust o ver, and edema, and pruritus. If these indicators occur, it is considered scale off. There is decreased sweating in these areas with the skin to be a local reaction. eventually thickening (lichenification) in the areas of dermatitis. Allergic Rhinitis DIAGNOSTIC TESTS. There are no tests to conf irm this diag- nosis. A detailed history and physical examination are used to Allergic rhinitis is the most common form of aller gy. When diagnose it and to exclude other diseases with similar symp- symptoms occur throughout the year, it is called perennial al - toms. Serum IgE levels will be elevated in these patients and lergic rhinitis. If the symptoms occur seasonally, it is called hay tend to correlate with the severity of the disease. If an infection fever. The causative antigens are environmental and airborne. is present, culture and sensitivity tests may be ordered to de- PATHOPHYSIOLOGY. Allergic rhinitis is the result of an termine the infecting organism and appropriate treatment. antigen–antibody reaction. Ciliary action decreases and mucous THERAPEUTIC MEASURES. Treatment focuses on the symp- secretions increase. Vasodilation and local tissue edema occur. toms of pruritus and dry and inflamed skin. Antipruritics are SIGNS AND SYMPTOMS. Signs and symptoms vary in inten- vital in reducing the itch–scratch c ycle that predisposes the sity and include sneezing, nasal itching, profuse watery rhin- patient to lesion infections. Luk ewarm soaks followed with orrhea (runny nose), and itchy red eyes. The nasal mucosa is application of emollients and oil-in-w ater lubricants such as pale, cyanotic, and edematous. Frequently there are dark cir- Alpha Keri oil tend to be the most effective for dryness. Top- cles under the eyes, called allergic shiners, caused by venous ical corticosteroids may be ordered for their anti-inflammatory congestion in the maxillary sinuses. properties. Topical calcineurin inhibitors such as tacrolimus and pimecrolimus also reduce the inflammatory response and DIAGNOSTIC TESTS. Skin testing may be performed to iden- relieve itching and rash when steroids are not effective. If skin tify the specific offending allergens to allow avoidance of the lesions become infected, topical or systemic antibiotics are allergen. However, skin testing does not always identify the prescribed. Dilute bleach soaks may also be used twice a week allergen, and has limited usefulness for allergens that cannot to reduce severity of symptoms, especially those of infection. be easily avoided once identified. The in vitro allergy test or For long-term management of symptoms, it is important to radioallergosorbent test (RAST), can be a beneficial alterna- identify and eliminate the triggers of the hypersensiti vity, tive to skin testing for some patients. while controlling environmental temperature and humidity. THERAPEUTIC MEASURES. Initial treatment involves eliminating the offending environmental stimuli. Antihistamines and nasal Anaphylaxis decongestants may be prescribed to relie ve symptoms. If the Anaphylaxis is a se vere systemic type I hypersensiti vity symptoms are severe, corticosteroids may also be given via in- reaction. Table 19.1 lists the numerous possible causes of halation or nasal spray. Rinsing the sinuses can be an inexpensive anaphylaxis. and effective way to reduce nasal congestion. Key to this inter- vention is to avoid introducing microorganisms into the nasal passage. The saline solution must be either sterile or made from WORD BUILDING distilled water or previously boiled then cooled water. anaphylaxis: ana—up + phylaxis—protection Rhinophototherapy uses light w aves to reduce the hyper- immune response seen in this disorder. The treatment is usually done three times a week for 3 weeks and relie ves symptoms such as sneezing, itching, and runny nose. Immunotherapy, referred to as aller gy shots, is reserv ed TABLE 19.1 SUBSTANCES THAT for patients with severe or debilitating symptoms (see Chapter COMMONLY TRIGGER ANAPHYLACTIC 18). This therapy continues until the patient no longer has REACTIONS symptoms when exposed to the environmental antigen. Antibiotics Aminoglycosides Atopic Dermatitis (Eczema) Amphotericin B Atopic dermatitis, often called eczema, is a familial, chronic Cephalosporins inflammatory skin response. Penicillins Sulfonamides PATHOPHYSIOLOGY. These skin lesions are not typical for Tetracyclines a type I hypersensitivity reaction, and a specific antigen can- not usually be identified as the cause. However, the patho- Anesthetics, Lidocaine physiology of atopic dermatitis is belie ved to be a type I Antiarrhythmics Procaine hypersensitivity reaction, mediated by IgE antibodies, be- Hormones Adrenocorticotropic hormone cause it is commonly found in patients with allergic rhinitis Estradiol or allergic asthma. Insulin SIGNS AND SYMPTOMS. Initially there is pruritus, edema, Vasopressin and extremely dry skin, which is followed by eruptions of tiny Continued 4068_Ch19_339-361 15/11/14 1:29 PM Page 342 342 UNIT FOUR Understanding the Immune System TABLE 19.1 SUBSTANCES THAT TABLE 19.2 ANAPHYLAXIS SUMMARY COMMONLY TRIGGER ANAPHYLACTIC REACTIONS—cont’d Signs and Generalized smooth-muscle Symptoms spasms Other Barbiturates Bronchial narrowing Medications Diazepam (Valium) Stridor Phenytoin (Dilantin) Wheezing Protamine Dyspnea Salicylates Laryngeal edema Abdominal cramping and Diagnostic Agents Contrast dyes diarrhea Medical Products Latex rubber Nausea and vomiting Increased capillary permeability Foods Beans Fluid shifts from blood Chocolate vessels to interstitium Eggs Hypotension Fruits (e.g., strawberries) Tachycardia Grains (e.g., wheat) Increased respiratory Nuts symptoms Shellfish Blood vessels dilate Food Additives Bisulfites Further decreasing circulating Monosodium glutamate (MSG) volume Diffuse erythema (redness) Proteins Horse serum Increased skin temperature Rabbit serum Apprehension Venoms Bees, wasps, hornets Drowsiness Fire ants Profound restlessness Snakes Headache Possible seizures Pollens Grass Ragweed Diagnostic Tests Testing to guide treatment Arterial blood gases Electrocardiogram (ECG) monitoring PATHOPHYSIOLOGY. IgE antibodies produced from previous History and physical exam antigen sensitization are attached to mast cells throughout the After recovery—allergen testing body. In this reaction, the antigen is introduced at a systemic for prevention level, which causes widespread release of histamine and other Therapeutic Intravenous (IV) access chemical mediators contained within the mast cells. The most Measures Epinephrine IV profound complications of an anaphylactic reaction are res- Vasopressive drugs IV piratory and cardiac arrest. Immediate treatment is needed to (dopamine) prevent death. Oxygen SIGNS AND SYMPTOMS. Anaphylaxis produces sudden and Antihistamines (oral, IV, life-threatening signs and symptoms (Table 19.2). Generalized injection) smooth muscle spasms occur, causing bronchial narrowing Corticosteroids (oral, IV, injection) and creating stridor, wheezing, dyspnea, and laryngeal edema, If severe respiratory which can lead to respiratory arrest. Cramping, diarrhea, nau- compromise: sea, and vomiting also result from these spasms. Capillary per- Tracheostomy or endotracheal meability increases, allowing fluid to shift from the vessels to intubation the interstitium. This causes hypotension, tachycardia, and an Mechanical ventilation increase in respiratory symptoms. The blood volume in the Complications Respiratory and cardiac arrest vessels decreases while the blood vessels dilate, resulting in a further decrease in circulating blood volume. The dilation also Priority Nursing Impaired Gas Exchange causes diffuse erythema (redness) and w armth of the skin. Diagnoses Anxiety Neurologic changes include apprehension, dro wsiness, pro- Ineffective Health Maintenance found restlessness, headache, and possible seizures. 4068_Ch19_339-361 15/11/14 1:30 PM Page 343 Chapter 19 Nursing Care of Patients With Immune Disorders 343 DIAGNOSTIC TESTS. There is no time for tests to be per - 3. What should the licensed practical nurse/licensed formed during an anaphylactic reaction other than those vocational nurse (LPN/LVN) do to help Mrs. needed to guide symptom treatment, such as arterial blood Barnes? gases or electrocardiogram (ECG) monitoring. Anaphylaxis 4. What members of the health team should the is diagnosed based on physical assessment and history from LPN/LVN anticipate collaborating with? the patient or significant other. After the patient’s recovery, Suggested answers are at the end of the chapter. allergen testing may be considered for future prevention. THERAPEUTIC MEASURES. Intravenous (IV) access is a prior- ity for administration of IV epinephrine, v asopressor drugs (dopamine), and fluids to increase blood pressure. Oxygen Urticaria therapy is started. If respiratory symptoms are se vere, a tra- PATHOPHYSIOLOGY AND ETIOLOGY. Urticaria (hives) is a cheostomy or endotracheal intubation may be needed, with type I hypersensitivity reaction. It is triggered by the antigen- mechanical ventilation. Antihistamines and corticosteroids stimulated reaction of IgE antibodies, which causes the may also be given. release of mast cell contents, especially histamine. The causes of urticaria are numerous. In addition to medications and foods, cold, local heat, pressure, and stress can also cause ur- ticaria. Many patients with underlying chronic conditions, EVIDENCE-BASED PRACTICE such as systemic lupus erythematosus (SLE), lymphoma, Clinical Question hyperthyroidism, or cancer, are susceptible to urticaria. What is the effectiveness of epinephrine auto- SIGNS AND SYMPTOMS. The lesions of urticaria are raised, injectors in relieving symptoms during anaphy- pruritic, nontender, and erythematous wheals on the skin.They laxis when they occur in the community? tend to be concentrated on the trunk and proximal extremities. Evidence After a review of the literature, no new recommen- DIAGNOSTIC TESTS. Diagnosis is based on physical e xami- dations could be made for the effectiveness of ep- nation and history. inephrine auto-injectors. So the use of epinephrine THERAPEUTIC MEASURES. Treatment depends on the degree auto-injectors in anaphylaxis is recommended of symptoms. In the most se vere cases, epinephrine may be based on the best currently available information. given to quickly resolve the urticaria. Corticosteroids may be Implications for Nursing Practice given orally, topically, or IV. Antihistamines and histamine Reinforce teaching to patients with prescribed (H2) blockers may aid in resolution by blocking the release epinephrine autoinjectors on the importance of of histamine. Patients suffering with the chronic form of ur- carrying the epinephrine autoinjector as directed ticaria might require IgE monoclonal antibody therapy such and refilling prescriptions as needed. as with omalizumab (Xolair). The use of acupuncture as an adjunctive measure is being studied. REFERENCE Sheikh, A., Simons, F. E. R., Barbour, V., & Worth, A. (2012). Angioedema Adrenaline auto-injectors for the treatment of anaphy- PATHOPHYSIOLOGY AND ETIOLOGY. There are two major laxis with and without cardiovascular collapse in the com- classifications of angioedema, acquired and hereditary. munity. Cochrane Database of Systematic Reviews, 8, Hereditary angioedema is considered rare and consists of CD008935. three types; acquired angioedema, the more common form, consists of six types. The underlying physiologic factor in the hereditary and most of the acquired types of angioedema is a defective or deficient C1inhibitor (C1-INH). This deficiency CRITICAL THINKING leads to a buildup of bradykinin, which leads to the sympto- Mrs. Barnes mology. Visit the U.S. Hereditary Angioedema Association at www.haea.org for more information. Mrs. Barnes, a 32-year-old woman, was brought into SIGNS AND SYMPTOMS. Depending on the location and e x- the emergency department after having been stung mul- tiple times by bees while gardening. She has numerous tensiveness of the edema, angioedema eruptions are usually red welts over her body that she says are itchy. She is nonpruritic and painless. Unlike the epidermal eruptions of ur- very anxious. Her temperature is 99.2°F (37.22°C), ticaria, angioedema eruptions are of the dermal and subcuta- blood pressure is 102/58 mm Hg, pulse is 102 beats per neous layers of the skin. There may also be mucous membrane minute, and respiratory rate is 26 per minute. edema. The eruptions usually last longer than with urticaria. DIAGNOSTIC TESTS. A comprehensive history and physical 1. What might be causing Mrs. Barnes’ symptoms? 2. What additional information is needed? examination confirm the diagnosis. Skin testing may be per- formed to determine the specific antigen. 4068_Ch19_339-361 15/11/14 1:30 PM Page 344 344 UNIT FOUR Understanding the Immune System THERAPEUTIC MEASURES. The most basic treatment involves Provide family with the information needed to distinguish avoiding the antigen. Symptoms may be relie ved with anti- between anxiety or panic and a serious physiological histamines and corticosteroids. For long-term treatment, im- problem so that they can make informed decisions regard- munotherapy for allergen desensitization may be indicated. ing obtaining emergency medical care. Treatment modalities for acute symptoms include a number Risk for Impaired Skin Integrity related to effects of allergic of newer Food and Drug Administration–approved medications: reaction To build up the patient’s C1-INH, there is Cinryze, a puri- Expected Outcome: The patient’s skin will remain intact. fied C1-INH and ecallantide (Berinert) a C1-esterase in- Assess and document skin and lesions to provide a basis hibitor, which prevents the breakdown of any C1 inhibitor for interventions and evaluation. present. Teach patient to keep fingernails short and clean to mini- Kalbitor, a brand of plasma kallikrein inhibitor helps mize the damage or risk for infection if scratching does symptoms. occur. Icatibant (Firazyr), a selective bradykinin B2 receptor an- Teach patient to apply clean, white cotton clothing (socks, tagonist, helps symptoms. gloves/mittens, undershirt) over affected area, especially Infusion of fresh frozen plasma reverses the angioedema at bedtime, to minimize scratching while allowing for air symptoms associated with angiotensin-converting enzyme movement with minimal irritation from dyes. inhibitor–induced angioedema, which tends to be resistant Teach patient to use gentle rubbing or pressure instead of to standard treatments. scratching to minimize the amount of skin trauma. Androgens, antifibrinolytics, and immunosuppressive therapy are useful in the long-term treatment of some of Ineffective Health Maintenance related to lack of knowledge of the acquired types of angioedema. methods to decrease inflammation and pruritus and reduce episodes of inflammation Nursing Process for the Patient With a Type I EXPECTED OUTCOME: The patient or caregiver will state un- Hypersensitivity Disorder derstanding and follow the mutually agreed-on plan of care. DATA COLLECTION. Gather information about the patient’ s Assess patient’s knowledge of disease and its causes to signs and symptoms. Immediately report an y sudden dysp- provide a basis for teaching and evaluation. nea, shortness of breath, anxiety, restlessness, or chest or back Assess patient’s values and beliefs regarding plan of care pain. Identify any allergies the patient may ha ve as well as to ensure that it corresponds to patient’s ideals, thereby signs and symptoms that occur with exposure to the allergen. improving compliance. Perform a thorough skin assessment, and carefully document Assess barriers to patient’s ability to carry out plan of care any lesions or rashes. Note any changes in rashes or lesions and plan interventions to decrease barriers to improve the or signs of infection, such as redness, warmth, and drainage. likelihood of the patient implementing the plan of care. Assess the patient’s knowledge of disease process, causes, Discuss methods of avoiding the allergen with the patient, treatment plan, and self-care. Note responses to treatments. such as wearing a mask when mowing the lawn or work- NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. ing outdoors, having heating ducts cleaned, covering heat Impaired Gas Exchange related to laryngeal edema registers with filters, and frequent home vacuuming and EXPECTED OUTCOME: The patient will maintain clear lung dusting to promote an understanding of preventive meth- fields and remain free of signs of respiratory distress at all ods and prevent allergen exposure and anaphylaxis. times. Teach patient to use medical identification for allergies so prompt medical attention can be given if the patient is un- Monitor respiratory rate, depth, and effort such as use of able to give information. accessory muscles, nasal flaring, or abdominal breathing Explain need to obtain a prescription for an epinephrine to identify problems early. autoinjector, and teach patient how to use it if antigen is Monitor the patient for restlessness, changes in mentation, environmental (e.g., insect sting or foods; see Chapter 18). level of consciousness, changes in voice, or dysphagia to The teaching plan for atopic dermatitis includes signs and identify problems and intervene early. symptoms of infection, use of humidification during the Position the patient in a high-Fowler’s or semi-Fowler’s winter months to prevent dryness, wearing cotton cloth- position to improve ventilation and decrease upper airway ing to minimize irritation, and cool soaks to decrease edema. pruritus. Anxiety related to dyspnea or pruritus Teaching for urticaria includes stress management and re- EXPECTED OUTCOME: The patient will state that anxiety is laxation techniques to relieve urticaria and to follow ther- controlled. apeutic regimen including prescribed medications and their correct usage to reduce symptoms. Stay with the patient and speak calmly to reduce fear or Document teaching and patient understanding. frustration. Teach patient to visualize the absence of anxiety, itching, EVALUATION. If interventions have been effective, there will or dyspnea to decrease anxiety. be no signs of respiratory distress, and lung f ields will be 4068_Ch19_339-361 15/11/14 1:30 PM Page 345 Chapter 19 Nursing Care of Patients With Immune Disorders 345 clear. The patient’s posture, facial expressions, gestures, and results in a massi ve amount of cellular debris that blocks concentration will reflect no anxiety. The skin will remain in- blood vessels throughout the body. This leads to ischemia and tact. If there are lesions, the y will be reduced and healing. necrosis of tissue and organs and can be life threatening. The patient will express knowledge of disorder and treatment ETIOLOGY. Occasionally, antibodies form after a bacterial plan. The patient will verbalize no barriers to attaining treat- or viral infection. Ho wever, prior sensitization is usually ment goals. from a previous blood transfusion or pre gnancy. ABO and Type II Hypersensitivity Reaction Rh blood type must be matched for transfusions. The ABO blood types are A, B, AB, and O (Fig. 19.3). People with A type II hypersensitivity reaction involves the destruction of a blood type O are universal donors because they do not have cell or substance that has an antigen attached to its cell mem- A or B antigens. Ho wever, those with type O blood can re- brane, which is sensed by either immunoglob ulin G (IgG) or ceive only type O blood. People with type AB blood are uni- immunoglobulin M (IgM) as being a foreign antigen (Fig. 19.2). versal recipients, because they do not make A or B antibodies. When an antigen marker is sensed as foreign, an antibody at- Those with blood types other than AB cannot receive AB taches to the antigen on the cell membrane, causing lysis of the blood because they have A or B antibodies. cell or accelerated phagoc ytosis (engulfing and ingestion). Rh antigens are present in people who are Rh +. A person When a cell is foreign, such as a bacterium, this process is ben- who is Rh + has the D antigen, which is the strongest antigen eficial. However, sometimes antigens on the surf ace of a red of the 50 possible antigens. Rh antibodies are present in those blood cell (RBC) can be sensed as foreign for the different ABO − − who are Rh after a sensitizing event. A person who is Rh does blood types, which results in the RBC being destroyed. − not have the D antigen. Those who are Rh + can receive Rh − Hemolytic Transfusion Reaction blood, but those who are Rh cannot receive Rh+ blood because of the formation of antibodies to the Rh + blood. If maternal PATHOPHYSIOLOGY. A hemolytic transfusion reaction is a and fetal blood Rh factors (RBC surface antigens) are different, type II hypersensitivity reaction in which incompatible sur - the mother becomes sensitized by the fetal Rh type, which can face antigens on RBCs are transfused. These antigens may be ABO or Rh incompatible. (ABO and Rh [Rhesus] are human blood group systems.) The recipient’s antibodies at- tach to the foreign antigens on the transfused RBCs, causing rapid lysis (destruction) of the RBC. The rapid RBC lysis Antibodies RBC Foreign antibodies attach to the normal self-marking cell membrane antigens RBC membrane degregates FIGURE 19.3 ABO blood types. From Venes, D. (Ed.). (2009). Taber’s cyclopedic medical dictionary (21st ed., p. 306). FIGURE 19.2 Type II hypersensitivity. Philadelphia: F.A. Davis. 4068_Ch19_339-361 15/11/14 1:30 PM Page 346 346 UNIT FOUR Understanding the Immune System affect future fetuses. For example, an Rh0(D)-negative pregnant DIAGNOSTIC TESTS. The direct Coombs’ test confirms this di- woman becomes sensitized by a Rh 0(D)-positive fetus. As a agnosis. In the laboratory , a small amount of the patient’ s result, the blood cells of future Rh0(D)-positive fetuses can be RBCs is washed to remove any unattached antibodies. Anti- destroyed by maternal antibodies crossing the placenta. human globulin is added to see if agglutination (clumping) of the RBCs results. If agglutination occurs, an immune reaction such as a hemolytic transfusion reaction is taking place. CRITICAL THINKING THERAPEUTIC MEASURES. To prevent production of anti- Rh0(D) antibodies, a Rh 0(D) immune globulin (RhoGAM) Blood Types injection is given to Rh 0(D)-negative patients accidentally 1. Who is the universal ABO Rh recipient? given Rh0(D)-positive blood or e xposed to Rh 0(D)-positive 2. Who is the universal ABO Rh donor? fetal blood by delivery, miscarriage, abortion, amniocentesis, − 3. Can someone with an A Rh blood type safely or intra-abdominal trauma. When antibodies do not form, receive O Rh+ blood? then a hemolytic reaction can be prevented. Suggested answers are at the end of the chapter. If a reaction occurs, medications are given to treat the re- action such as those listed in Table 19.4. NURSING PROCESS FOR THE PATIENT EXPERIENCING A HEMOLYTIC TRANSFUSION REACTION. SIGNS AND SYMPTOMS. A hemolytic transfusion reaction is Data Collection. Prevention of hemolytic reactions is crucial. usually accompanied by a rather sudden onset of lo w back Following strict institutional guidelines for blood transfusion (flank) or chest pain, hypotension, fe ver rising more than administration helps ensure the patient’s safety. After blood 1.8°F (1°C), chills, tachycardia, tachypnea, wheezing, dysp- is released from the hospital blood bank, tw o nurses, desig- nea, urticaria, and anxiety (Table 19.3). The patient also may nated per institutional policy, double-check specified data. At report a headache and nausea. the bedside, transfusion guidelines include double-checking the patient’s name and identification number on the chart, unit of blood, and patient’s identification bracelet, as well as TABLE 19.3 HEMOLYTIC TRANSFUSION checking the patient’s blood type in the chart, on the unit of REACTION SUMMARY blood, and paperwork with the unit of blood. Agency policy is followed for taking vital signs during a Signs and Low back or chest pain blood transfusion. Minimally, vital signs are taken before the Symptoms Hypotension start of the blood transfusion, 15 minutes into the transfusion, Fever rising more than 1.8°F (1°C) and when the transfusion is completed. It tak es only a small Chills amount of blood to trigger a hemolytic transfusion reaction, so Tachycardia it is critical to stay with the patient at the bedside during the Tachypnea, wheezing, dyspnea first 15 minutes of any blood transfusion. This enables detec- Urticaria tion of a blood transfusion reaction early for quick action to Anxiety minimize cell destruction and complications, including death. Headache If symptoms of a reaction are noted, the blood transfusion Nausea is immediately stopped, and agenc y policy for a suspected transfusion reaction is follo wed. A normal saline infusion Diagnostic Direct Coombs’ test with new tubing is started to keep the vein patent. The health Tests Small amount of patient’s RBCs are care practitioner (HCP) and blood bank are immediately no- washed tified. A nurse remains with the patient for reassurance and Antihuman globulin is added monitoring of symptoms and vital signs. If a blood incom- If agglutination (clumping) occurs, patibility is suspected, the unused blood and blood tubing are an immune reaction is occurring returned to the blood bank for testing. A series of blood and Therapeutic Depends on severity of reaction and urine specimens are collected and sent to the laboratory for Measures organs affected analysis. The HCP’s orders are followed to treat the patient’s Antihistamines symptoms. Corticosteroids Epinephrine Diuretics, to assist kidneys BE SAFE! Complications If severe: shock, acute renal failure Every unit of blood, even of the same blood type, Priority Fear is unique and can trigger a blood transfusion re- Nursing Ineffective Tissue Perfusion action. Careful monitoring with every transfusion Diagnoses Risk for Injury is necessary. 4068_Ch19_339-361 15/11/14 1:30 PM Page 347 Chapter 19 Nursing Care of Patients With Immune Disorders 347 TABLE 19.4 MEDICATIONS USED IN HEMOLYTIC TRANSFUSION REACTIONS Medication Class/Action Examples Nursing Implications Antihistamines Block histamine at histamine1 diphenhydramine (Benadryl) Take with or without food. receptors, thereby preventing or Avoid ethanol, central nervous system reversing the effects of histamine depressants, and over-the-counter (capillary permeability, itching, and antihistamines. bronchospasms). Avoid prolonged exposure to sunlight. Use caution with activities requiring mental alertness. Corticosteroids Hormones with marked anti- dexamethasone (Decadron) Take PO with food. inflammatory effects due to hydrocortisone (Solu-Cortef) Never stop taking suddenly. inhibition of prostaglandin synthesis methylprednisone Monitor weight. and accumulation of macrophages (Solu-Medrol) Assess for edema, shortness of breath, and leukocytes at site. prednisolone (Delta-Cortef) jugular vein distention, and signs and prednisone (Deltasone) symptoms of congestive heart failure. beclomethasone (Beconase) Monitor blood glucose level. Monitor for evidence of gastrointestinal bleeding. Sympathomimetics Marked stimulation of alpha, beta1, Epinephrine (Adrenalin, Use only 1:1000 solution for IV; 1:100 IV and beta2 receptors, causing EpiPen) will cause death. vasoconstriction, bronchodilation, Do not expose drug to heat, light, or air. and cardiac stimulation. Ophthalmic and nasal preparations may sting. May elevate blood glucose level. Nursing Diagnoses, Planning, and Implementation. Risk for Injury related to prolonged shock resulting in multiple Fear related to serious threat to health status organ failure, death EXPECTED OUTCOME: The patient will state reduced fear. EXPECTED OUTCOME: The patient will remain free of injury at all times. Allow patients to express their concerns to allow inaccu- rate information to be corrected. Use two methods to identify patient before giving blood Inform patients about procedures and treatments to reduce products to prevent incorrect identification and adminis- fear. tration of blood product. Remain with patient and allow significant others to visit to Remain with patient during first 15 minutes of transfusion offer emotional support. and then obtain vital signs to detect signs of reaction. Ineffective Tissue Perfusion, Cardiopulmonary and Peripheral, Give medications such as epinephrine or steroids, as or- related to arterial/venous blood flow exchange problems dered, to support affected tissues and organs. EXPECTED OUTCOME: The patient will have adequate tissue Give diuretics as ordered to assist kidney excretion of cel- perfusion as evidenced by palpable peripheral pulses, uri- lular debris from reaction. nary output of 30 mL per hour, and no respiratory distress. Deficient Knowledge related to lack of exposure to blood trans- fusions Assess and maintain airway, and provide oxygen to pro- EXPECTED OUTCOME: The patient will state understanding mote oxygenation. of blood transfusion options. Assess for pain and provide pain relief measures to reduce pain. Encourage patient to discuss autologous (self) blood do- Monitor vital signs and intake and output to detect nation option with HCP to avoid a transfusion reaction. changes for prompt treatment. This may be an option for patients having elective surgery. Position patient with head elevated if short of breath to After a hemolytic transfusion reaction, explain to patients aid breathing. the importance of informing future health care providers 4068_Ch19_339-361 15/11/14 1:30 PM Page 348 348 UNIT FOUR Understanding the Immune System about the reaction to ensure that specific blood tests are complexes form and lodge in small v essels, which leads to performed for less common antibodies if the patient is inflammation, tissue damage, and necrosis. Serum sickness ever typed for a blood transfusion again. occurs occasionally after administration of penicillin or sulfonamide. EVALUATION. If interventions have been effective, the patient states reduced fear, has normal organ and tissue function, and SIGNS AND SYMPTOMS. The signs and symptoms usually reports understanding of blood transfusion options to prevent occur 7 days to 3 weeks after the exposure. Most predominant transfusion reactions. is severe urticaria and angioedema. The patient may have a fever, malaise, muscle soreness, arthralgia, splenomegaly, and Type III Hypersensitivity Reaction occasionally nausea, vomiting, and diarrhea. Lymphadenopa- A type III hypersensitivity reaction involves immune complexes thy may occur, especially in the lymph nodes closest to the formed by antigens and antibodies, usually of the IgG type antigen entry site. (Fig. 19.4). The patient is sensitized with an initial exposure to DIAGNOSTIC TESTS. With serum sickness, there is often a the antigen, and a reaction occurs with a later exposure. The re- slight elevation in the white blood cell (WBC) count, sedimen- action is localized and evolves over several hours, with symp- tation rate, and C-reactive protein. IgG and IgM immunoglob- toms ranging from a red, edematous skin lesion to hemorrhage ulins increase substantially , while the complement assay and necrosis. The process involves formation of antigen–antibody decreases. Plasma cells are seen on the peripheral blood smear. complexes in the blood v essels as the antigen is absorbed through the vessel wall. Neutrophils are attracted to the area and THERAPEUTIC MEASURES. Because serum sickness tends to release enzymes that ultimately lead to blood vessel damage. be self-limiting within about 10 days, treatment is focused on symptoms. Antipyretics may be given for fever and analgesics Serum Sickness and anti-inflammatories for arthralgia. Antihistamines and PATHOPHYSIOLOGY AND ETIOLOGY. Serum sickness is a type epinephrine may be given for urticaria and angioedema. If III hypersensitivity immune reaction in which antigen–antibody symptoms persist, corticosteroids may be ordered. First Exposure Memory cell Macrophage Plasma T-helper B cell cell cell Second Exposure Antigen-antibody complexes Leading to occlusion in blood vessels and ischemia FIGURE 19.4 Type III hypersensitivity. 4068_Ch19_339-361 15/11/14 1:30 PM Page 349 Chapter 19 Nursing Care of Patients With Immune Disorders 349 NURSING PROCESS FOR THE PATIENT WITH SERUM SICKNESS. Antigens Data Collection. Symptoms are noted. Responses to pre- scribed medications are documented. The causative agent Sensitized may be identified through the history-taking process and is T cell important for the patient to determine to prevent a recurrence of the condition. Nursing Diagnoses, Planning, and Implementation Pain related to muscle and joint soreness EXPECTED OUTCOME: The patient will state pain is reduced Sensitized to acceptable level within 30 minutes of report of pain. T cell with antigen Monitor pain using a pain rating scale of 0 to 10 to iden- tify need for treatment. Provide analgesics as ordered to relieve symptoms. Risk for Deficient Fluid Volume related to fever and gastrointestinal fluid loss EXPECTED OUTCOME: The patient will maintain blood pres- sure, pulse, and urine output within normal limits. Observe for signs of hypovolemia, such as restlessness, weakness, muscle cramps, headaches, inability to concen- T-helper Cytoxic T-suppressor cell T cell cell trate, irritability, and postural hypotension to detect defi- ciencies to report to the HCP. Monitor intake and output to detect imbalances. Provide antiemetics as ordered to relieve nausea. Encourage oral replacement therapy with hypotonic glucose- Leukotrienes - Destroys electrolyte solutions, such as sports replacement drinks or attract more target cells macrophages ginger ale, because they increase fluid absorption and correct deficient fluid volume. FIGURE 19.5 Type IV hypersensitivity. Maintain IV fluids at ordered rate to replace lost fluids, but avoid fluid overload. EVALUATION. Goals are met if the patient reports less pain dramatically since the implementation of universal precautions and if vital signs and urine output are within normal limits. and the use of latex gloves began in 1987. Many times, latex Type IV Hypersensitivity Reaction gloves are worn when they are not needed, which increases exposure to the latex protein. Latex-free gloves are available. A type IV hypersensitivity reaction, also called a delayed reac- For patients who are allergic to latex, special protocols are fol- tion, occurs when a sensitized T lymphocyte comes in contact lowed using latex-free equipment. For information about latex with the particular antigen to which it is sensitized (Fig. 19.5). allergy, visit the American Academy of Allergy, Asthma, and The resulting necrosis is caused by the actions of macrophages Immunology at www.aaaai.org. Also visit the U.S. F ood and and the various T lymphocytes involved in the cell-mediated Drug Administration at www.fda.gov. immune response. SIGNS AND SYMPTOMS. Within a number of hours of expo- Contact Dermatitis sure, the area of contact becomes red and pruritic, with fragile PATHOPHYSIOLOGY. When a substance or chemical comes vesicles. Secondary infections may develop. (See earlier dis- in contact with the skin, it is absorbed and binds with special cussion of atopic dermatitis.) skin proteins called haptens. With the first contact, there is DIAGNOSTIC TESTS. Diagnosis is made by assessment of the no reaction or symptoms, but within 7 to 10 days, T memory skin and lesions through biopsy, culture or patch testing, and cells are formed. Therefore, on subsequent exposures, the T a detailed patient history. memory cells quickly become activated T cells, which secrete the chemicals that may cause symptoms. THERAPEUTIC MEASURES. Treatment consists of controlling symptoms. Oral or topical antihistamines and topical drying ETIOLOGY. Poison ivy and poison oak are the most common agents may be used. Topical corticosteroids may be used and irritants causing this reaction. Latex rubber also may cause con- are most effective if sparingly applied after a bath or shower. tact dermatitis and can trigger type I anaphylactic reactions. If symptoms are severe, systemic corticosteroids may be pre- Latex Allergy. Latex allergy is a serious problem for those who scribed. Tacrolimus (Protopic) and pimecrolimus (Abre va), work in health care. Anaphylactic reactions to late x can be which are classified as topical immunomodulators, may also fatal. Exposure to latex for those in health care has increased be prescribed when other treatments fail. 4068_Ch19_339-361 15/11/14 1:30 PM Page 350 350 UNIT FOUR Understanding the Immune System NURSING PROCESS FOR THE PATIENT WITH CONTACT DERMATITIS. TABLE 19.5 TRANSPLANT REJECTION Data Collection. Symptoms are assessed for planning of in- SUMMARY terventions. Identification of the causati ve agent is noted in the patient’s history. Patient recognition of the cause is Signs and Depend on: important to prevent a recurrence of the condition. Special Symptoms Involved transplanted tissue or protocols are used for patients aller gic to latex. Some fa- organ cilities may prepare special latex-free kits containing com- Severity of reaction mon supplies nurses use to care for patients. Ensure that Reflect failure of the organ or tissue latex allergy protocols are followed if a patient has a latex allergy to prevent possible development of life-threatening Diagnostic Biopsy anaphylaxis. Tests Scans Blood tests Nursing Diagnoses, Planning, and Implementation. Arteriography See Nursing Care Plan for the P atient With Contact Ultrasonography Dermatitis. Therapeutic Depends on type of transplant Transplant Rejection Measures Preventive preoperative preparation PATHOPHYSIOLOGY AND ETIOLOGY. Any form of trans- with medications, transfusions, or planted living tissue is sensed as foreign material by the im- radiation to minimize the risk of mune system. This is why lifelong immunosuppression is rejection needed to help prevent transplant rejection, which can occur Complications Total failure and loss of transplanted at any time. Lymphocytes become sensitized during an in- organ or tissue duction phase immediately after the tissue is transplanted. If Cause of death is most commonly immunosuppression is not effective, the sensitized lympho- due to infection, with immuno- cytes invade the transplanted tissue and destroy it via the re- suppression therapy a contributory lease of chemicals and macrophage acti vity, resulting in factor varying degrees of transplant rejection. Priority Grieving (actual or anticipatory) SIGNS AND SYMPTOMS. Various signs and symptoms occur Nursing Fear depending on the transplanted tissue or or gan involved and Diagnoses Deficient Knowledge the severity of the rejection (Table 19.5). Signs and symptoms Other diagnoses depend on which reflect failure of the organ or tissue, such as renal failure for organ is failing a rejected kidney. COMPLICATIONS. A total failure and loss of the transplanted tissue or organ can occur, or the tissue or organ can be dam- aged from immunological reactions and not function at full reduced medication side ef fects while improving patient capacity. The greatest cause of death follo wing a transplant outcomes. If rejection occurs, medications may be used to is infection. Immunosuppression therapy, which is needed to attempt to reverse the rejection. Supportive care is provided prevent tissue rejection after the transplant, is a major con- based on the failing organ, such as hemodialysis if a kidney tributory factor for severe infection development. Because rejection occurs. the immune system is suppressed, it is unable to ef fectively fight infections. NURSING CARE. Nursing care depends greatly on the type of transplant performed. Initially, the patient is in an intensi ve DIAGNOSTIC TESTS. Biopsy, scans, blood tests, arteriography, care unit under close observation and support. Observing for and ultrasonography are some tests that may be performed to signs of rejection is a priority throughout the patient’s hospi- aid in diagnosing a transplant rejection. talization. Another consideration for nursing care is the psy- THERAPEUTIC MEASURES. Depending on the type of trans- chological support of patient and family. Many patients wait plant, the body’s immunological system is prepared before a long time before a donor match is found. Once a matching surgery with medications, transfusions, or radiation to min- donor is found, there is usually great elation. Yet if a donor’s imize the risk of rejection. After the transplant, lifelong im- death made the transplant possible, the patient and f amily munosuppression is needed (although studies are ongoing may simultaneously feel a profound sadness for the donor’ s in which the same or gan donor’s bone marrow is trans- family. Patients need time to v erbalize feelings and under- planted at the same time as the or gan transplant such as a stand that these feelings are normal and diminish with time. kidney to reduce or elimination the need for antirejection Also, the fear of transplant rejection is al ways present and drugs). Improved specificity of immunosuppressants has must be discussed. 4068_Ch19_339-361 15/11/14 1:30 PM Page 351 Chapter 19 Nursing Care of Patients With Immune Disorders 351 NURSING CARE PLAN for the Patient With Contact Dermatitis Nursing Diagnosis: Risk for Impaired Skin Integrity related to effects of allergic reaction and pruritus Expected Outcome: The patient’s skin will remain intact. Evaluation of Outcome: Is patient’s skin intact? If not intact, is skin healing? Does patient express a plan for preventing impaired skin integrity? Intervention Identify and document skin and lesions. Rationale Provides a basis for intervention planning and evaluation of healing. Evaluation Are lesions present? Are lesions healing? Intervention Teach patient to keep fingernails short and clean. Rationale Short, clean nails cause less damage or infection if scratching occurs. Evaluation Does skin remain intact despite scratching? Intervention Teach patient to apply clean, white cotton clothing (socks, gloves/mittens, undershirt) over affected area, especially at bedtime. Rationale Cotton allows air movement. White cloth is less irritating than those with dyes. Scratching is decreased during sleep with the use of gloves/mittens or by covering affected area. Evaluation Are symptoms of skin irritation reduced? Intervention Teach patient to use gentle rubbing or pressure instead of scratching. Rationale Use of gentle rub- bing or pressure instead of scratching causes less skin trauma. Evaluation Does skin remain intact despite itchy sensation? Intervention Explain that tepid baking soda baths, colloidal oatmeal baths (e.g., Aveeno), and cool washcloths or cool baths reduce itching. Rationale These items help dry the vesicle and minimize the pruritus. Evaluation Is itching reduced? Nursing Diagnosis: Ineffective Health Maintenance related to lack of knowledge of methods to decrease inflam- mation and reduce episodes of inflammation Expected Outcome: The patient or caregiver will follow the mutually agreed-on plan of care. Evaluation of Outcome: Can patient express knowledge of etiology, signs and symptoms, and treatment plan? Does patient discuss any emotional, social, financial, or material blocks to attaining treatment goals? Intervention Identify patient’s knowledge of disease and causes. Rationale Provides a basis for the teaching plan. Evaluation Does patient state baseline knowledge? Intervention Ask patient’s values and beliefs regarding plan of care. Rationale Patients are more compliant if their belief system fits into plan of care. Evaluation Does patient’s belief system work with plan of care? Intervention Identify barriers to patient’s ability to carry out plan of care and plan interventions to decrease barriers. Rationale Barriers can prevent patient from carrying out plan of care. Evaluation Are barriers identi- fied? Are solutions to barriers planned? Intervention Teach patient to wear medical alert identification for allergen. Rationale With allergen identifica- tion, prompt medical care can be given in case patient is unable to give information. Evaluation Does patient agree to use allergen identification? Intervention Discuss methods of avoiding allergen with patient. Rationale Understanding prevention methods can help prevent allergen exposure. Evaluation Can patient state methods to help prevent allergen exposure? Continued 4068_Ch19_339-361 15/11/14 1:30 PM Page 352 352 UNIT FOUR Understanding the Immune System NURSING CARE PLAN for the Patient With Contact Dermatitis—cont’d Intervention Teach patient to wash with a brown soap (e.g., Fels-Naptha) or, if unavailable, any soap when con- tact with the offending agent is suspected. Rationale This removes offending agent. Evaluation Does patient state understanding of need to wash off agent with exposure? Intervention Teach patient not to scratch skin. Rationale Scratching can spread the dermatitis, as well as cause infection. Evaluation Does patient avoid scratching? Education. Rejection can take place weeks, months, or years Pernicious Anemia after a transplant (with decreasing risk). The patient and family PATHOPHYSIOLOGY. Antibodies that destroy gastric parietal need to be educated about specif ic signs and symptoms of re- cells lead to decreased production of intrinsic factor. Other in- jection. Also, because infection is a major complication of long- trinsic factor antibodies (type I and type II) alter the binding term immunosuppressant medications, the patient and f amily sites, which ultimately decreases the ability of intrinsic factor need to know signs and symptoms of infection and when to no- to assist in the absorption of vitamin B12 in the ileum. Intrinsic tify the HCP of problems. Steroid use may mask the symptoms factor plays a role in vitamin B12 absorption in the small bowel, of infection, so small indicators such as a lo w-grade fever so a vitamin B12 deficiency may result, causing decreased pro- should be reported promptly. Education regarding prescribed duction of RBCs. Intrinsic f actor is involved in most vitamin medications is a must because the long-term success of a trans- B12 absorption, but evidence has demonstrated that there is a plant depends on compliance with immunosuppressant therapy. route independent of intrinsic factor for some absorption of vi- Avoidance of people with colds or infections is also important tamin B12. This has important treatment implications. to reduce the immunosuppressed patient’s risk of infection. ETIOLOGY. There tends to be a f amilial tendency toward the autoimmune form of pernicious anemia. Causes of the acquired AUTOIMMUNE DISORDERS form of pernicious anemia (non–immune-related) include any type of gastric or small-bo wel resections coupled with no or In autoimmune disorders, the immune system no longer rec- inadequate vitamin B12 or intrinsic factor replacement. ognizes the body’s normal cells as self. Instead, antigens on these normal body cells are recognized as foreign material, SIGNS AND SYMPTOMS. The patient experiences increasing and the body launches an immune response to destroy them. weakness, loss of appetite, glossitis (inflammation or infec- A number of f actors either cause or influence this break- tion of the tongue), and pallor. Irritability, confusion, and down of self-recognition, including viral infections, drugs, and numbness or tingling in the extremities (peripheral neuropa- cross-reactive antibodies. Some microbes stimulate production thy) occur because the nervous system is affected. of antibodies but are so closely related to normal cell antigens DIAGNOSTIC TESTS. On microscopic e xamination of the that the antibodies also attack some normal cells. Hormones patient’s RBCs, macrocytic (enlarged cells) anemia is diag- also may influence this breakdown of self-recognition. nosed. Macrocytic anemia and low vitamin B 12 levels are in- Some autoimmune disorders are discussed next, whereas dicators of pernicious anemia and folic acid def iciency. To others are discussed in chapters related to the body system determine if the diagnosis is pernicious anemia, intrinsic factor most affected. Table 19.6 lists additional autoimmune disor- antibodies and parietal cell antibodies can be tested. Methyl- ders and the chapters in which they are discussed. malonic acid levels (when vitamin B12 low), and homocysteine, will be elevated, whereas serum cobalamin will be decreased. A Schilling test can be done b ut is used less today than in the past because it is a complicated test. For the Schilling TABLE 19.6 AUTOIMMUNE DISORDERS test, radioactive vitamin B 12 is administered to the patient. The patient’s urine is then collected for 24 hours (48 hours Disorder Refer to for patients with renal disease), and the amount of radioac- Idiopathic thrombocytopenic purpura Chapter 28 tive vitamin B12 excreted in the urine is measured. If intrinsic factor is decreased, gastric absorption of vitamin B12 is also Multiple sclerosis Chapter 50 decreased, so that more vitamin B12 is excreted in the urine. Myasthenia gravis Chapter 50 Gastric secretion analysis is done to measure le vels of hy- drochloric acid (HCl) because low or absent HCl may indi- Rheumatoid arthritis Chapter 46 cate pernicious anemia. Ulcerative colitis Chapter 34 Further studies such as radioimmunoassay (RIA) or enzyme- linked immunosorbent assay (ELISA) may be performed to 4068_Ch19_339-361 15/11/14 1:30 PM Page 353 Chapter 19 Nursing Care of Patients With Immune Disorders 353 confirm an autoimmune etiology and specify which antibody hormone receptors on the thyroid gland and stimulate the thy- is present, type I or type II. roid gland to secrete thyroid hormones. The thyroid gland en- larges as a result of this o verstimulation (hyperthyroidism). THERAPEUTIC MEASURES. Corticosteroids may correct the It becomes inf iltrated with lymphoc ytes and phagoc ytes, problem if it is immunologically caused. Otherwise, vitamin causing inflammation and further enlargement. Then different B12 therapy is needed, usually for life. autoantibodies appear that destroy thyroid cells, which slows NURSING CARE. Vitamin B12 is administered as ordered. secretion activity, causing hypothyroidism. Care related to fatigue and safety are important. Ambulation, ETIOLOGY. The exact cause is unknown, although it occurs frequent rest periods, and providing assistance with activities in females eight times more often than in males. It is also of daily living (ADLs) as indicated by the patient’ s activity more common in people aged 30 to 50 years and patients with tolerance are helpful for the patient with anemia. Down syndrome and Turner syndrome. Education. The patient and family need education regarding oral or parenteral medication therap y. If vitamin B 12 injec- SIGNS AND SYMPTOMS. Initial signs and symptoms are tions are prescribed, the patient must understand that this is those of hyperthyroidism, such as restlessness, tremors, chest a lifelong need to pre vent the return of symptoms. P atients pain, increased appetite, diarrhea, moist skin, heat intoler - should not miss injections, periodic vitamin B 12 testing, or ance, and weight loss. follow-up appointments. These manifestations may go unrecognized and progress quickly into hypothyroidism. At this point, an enlarged thy- Idiopathic Autoimmune Hemolytic Anemia roid gland (goiter) may be seen. Signs and symptoms may include fatigue, bradycardia, hypotension, dyspnea, anorexia, PATHOPHYSIOLOGY. In this disorder, autoantibodies, for no constipation, dry skin, weight gain, sensitivity to cold, facial known reason, are produced that attach to RBCs and cause puffiness, and a slowing of mental processes. them to either lyse or agglutinate (clump).When lysis occurs, fragments of the destro yed RBCs circulate in the blood. If DIAGNOSTIC TESTS. Immunofluorescent assay, a test that de- agglutination occurs, occlusions in the small blood v essels tects antigens on cells using an antibody with a fluorescent are followed by tissue ischemia. tag, detects antithyroid antibodies. Serum TSH levels are el- evated, whereas triiodothyronine (T3) and thyroxine (T4) lev- SIGNS AND SYMPTOMS. Clinical manifestations vary from els are low. A thyroid scan is also done. mild fatigue and pallor to severe hypotension, dyspnea, pal- pitations, headaches, and jaundice. Problems concentrating THERAPEUTIC MEASURES. Thyroid hormone replacement and thinking frequently occur. therapy of thyroxine is the primary means of treatment. Life- long thyroid hormone therapy is needed. DIAGNOSTIC TESTS. The RBC count, hemoglobin (Hgb), and hematocrit (Hct) are low, and microscopic e xamination re- NURSING CARE. If the patient has a goiter, a soft diet may be veals fragmented RBCs. Lactate dehydrogenase (LDH) and needed for comfort. Frequent rest periods may be needed, as serum bilirubin levels are elevated because of RBC destruc- well as slowly increasing patient activity. Antiembolic stock- tion and tissue ischemia. ings may help prevent venous stasis during the lo w-energy, THERAPEUTIC MEASURES. Supportive measures such as sup- decreased-activity phase. Daily weights and monitoring intake plemental oxygen may be started. F olic acid may be pre- and output when cardiac status is compromised are important scribed to increase production of RBCs. IV immunoglobulin, to detect abnormalities such as fluid retention. Because weight immunosuppressant medications, and corticosteroids may be gain and facial puffiness alter patients’ self-image, patients useful in obtaining remission. In more se vere cases, blood need an opportunity to v erbalize their feelings to help them transfusions and erythrocytapheresis (a process in which ab- adjust to this disease process. normal RBCs are removed and replaced with normal RBCs) Education. Patients taking thyroid hormone replacement ther- may be instituted. F or severe cases a splenectomy may be apy should avoid foods high in iodine. The diet should also performed in an attempt to stop the destruction of RBCs. consist of large amounts of fiber to combat constipation. Dur- ing the hyperthyroidism phase, a diet high in protein and car- NURSING CARE. The patient’s signs and symptoms should be bohydrates encourages weight gain. Education re garding monitored and reported as needed. Frequent rest periods should prescribed medications is also needed. Cholestyramine, fer- be planned into the patient’ s daily routine to pre vent fatigue. rous sulfate, sucralfate, iron-containing multivitamins, cal- Blood products are administered as ordered to replace RBCs. cium carbonate and all other antacids interfere with the Education. The patient and family are instructed on the med- absorption of levothyroxine from the gastrointestinal tract. ical regimen, and their understanding is verified. Therefore, levothyroxine should not be taken within a mini- mum of 4-hour period from these medications. Hashimoto’s Thyroiditis PATHOPHYSIOLOGY. Autoantibodies for thyroid-stimulating Lupus Erythematosus hormone (TSH) form in Hashimoto thyroiditis. Ho wever, There are four types of lupus. Neonatal is the rarest form instead of inactivating TSH, the autoantibodies bind with and is passed on from a mother who has lupus to her fetus. 4068_Ch19_339-361 15/11/14 1:30 PM Page 354 354 UNIT FOUR Understanding the Immune System Drug-induced lupus erythematosus (DILE) af fects approxi- ETIOLOGY. The cause of SLE is unkno wn, but the disorder mately 10% of total lupus patients and rarely af fects major tends to occur in f amilies. Identified chromosomal markers organs. Research has identif ied about 80 prescription med- indicate a genetic link. Environmental factors may also play a ications that have caused DILE (Box 19-1). A small percent- critical role in the development of SLE. Infections, high stress age of lupus patients have the type that affects only the skin, levels, various hormones and drugs (especially antibiotics such a condition called discoid lupus erythematosus (DLE). This as sulfa and penicillin), and ultraviolet light have all been linked form is not life threatening and does not af fect any internal to triggering SLE. Exacerbation of symptoms, also called a organs. Most patients with