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BSN III-A GROUP 2 S.Y.

2012-2013

Systemic Lupus Erythematosus


Definition: SLE is a multisystem, chronic, remitting and relapsing, rheumatic disease that may assume several forms. It is serious inflammatory disease of unknown etiology occurs mainly in young women and produces symptoms referable to multiple organ systems. SLE diffusely

involves the vascular and connective tissues of multiple organs producing inflammation and biochemical and structural changes. Usually the most important abnormalities occur in the viscera; however, pathologic changes exactly like those with rheumatoid arthritis may also occur in the joints, facia, tendons and bursae. The rheumatic symptoms are commonly less severe than with classisc rheumatoid arthritis. Also, the prognosiss of SLE is poorer than that of rheumatoid arthritis because of the greater visceral pathology. Commonly death results from failure of a vital organ, e.g., renal failure (MSN-Luckmann & Sorensen). Incidence: The overall prevalence of SLE is estimated to be 100 per 100,000 persons. It occurs 10 times more frequently in women than in men and approximately three times more frequently in African-American population than in Caucasians (Ruddy et.al.,2001)-(MSN-Brunner & Suddarth). Pathophysiology: SLE is a result of disturbed immnue system that causes an exaggerated production of autoantibodies. This immunoregulatory disturbance is brought about by some combination of genetic, hormonal (as evidenced by the usual onsset during the childbearing years), and

environmental factors (sunlight, thermal burns). Certain medications, such as Hydralazine (Apresoline), Procainamide (Pronestyl), Ioniazid (INH), Chlorpromazine (Thorazine), and some antiseizure medications have been implicated in chemical or drug induced SLE. The SLE, the increase in autoantibody production is thought to result from abnormal suppresor T-cell function, leading to immune complex deposition and tissue damage. Inflammtion stimulates antigens, which in turn stimulate additional antibodies, and the cycle repeats (MSNBrunner & Suddarth). Clinical Manifestations: The clinical pattern and prognosis with SLE are highly variable. The illness may develop rapidly with an acute fulminant course which may produce death within a few weeks, or it may develop insidiously and become a chronic illness subject to remissions and exacerbations. The chronic pattern is more common and with proper steroid theraphy the patient may live for many years. Acute clinical findings may inculde fever; prostration; delirium; convulsions; psychosis;coma; musculoskeletal aches and pains; butterfly rash on the face; pleural effusion; basilar pneumonia; generalized lymphadenophathy; pericarditis; tachycardia; gallop rhythm; hepatosplenomegaly; and nepritis. Clinical findings which may occur with chronic SLE are variable, depending upon the organ systems involved, but may include fever; malaise; weight loss; cutaneous discoid SLE lesions; erythema of exposed surfaces; generalized lymphadenophathy; severe hemolytic anemia; thrombocytopenic purpura; hypersplenism; pericarditis; tachycardia; gallop rhythm; peripheral vascular syndromes (e.g., Raynauds phenomenon, gangrene); ulcerative lesions of the mucous

membranes; abdominal pains; nausea; vomitiing; anorexia; bloody stools; hepatic dysfunction; hepatomegaly; focal glomerulonephritis; myalgia; arthralgia; neuritis; hemiplegia; pshycosis; convulsions; and coma (MSN-Luckmann and Sorensen). Assesment and Diagnostic Findings: Diagnosis o SLE is based on complete history, physical examination, and blood tests. In addition to the general assesment performed for any patient with a rheumatic disease, assesment for known or suspected SLE has special features. The skin is inspected for erythematous rashes. Cutaneous erythematous plaques with an adherent scale may be observed on the scalp, face, or neck. Areas of hyperpigmentation or depigmentation may be noted, depending on the phase and type of the disease. The patient should be questioned about skin changes (because these may be transitory) and specifically about sensitivity to sunlight or artificial ultraviolet light. The scalp should be inspected for alopecia and the mouth and throat for ulcerations reflecting gastrointestinal involvement. Cardiovascular assesment includes auscultation for pericardial friction rub, possibly associated with myocarditis and accompanying pleural effusions. The pleural effusions and infiltrations, which reflect respiratory insufficiency, are demonstrated by abnormal lung sounds. Papular, erythematous, and purpuric lesions developing on the fingertips, elbows, toes, and extensor surfaces of the forearms or lateral sides of the hand that may become necrotic vascular involvement. Joint swelling, tenderness, warmth, pain on movement, stiffness, and edema may be detected on physical examination. The joint movement is often symmetric and similar to that found in RA.

Typically, assesment reveals classic symptoms, including fever, fatigue, and weight loss and possibly arthritis, pleurisy, and pericarditis. Interactions with the patient and family may provide further evidence of systemic involvement. The neurologic assesment is directed at identifying and describing any central nervous system changes. The patient and family members are asked about any behavioral changes, including manifestations of neuroses or psychosis. Signs of depression are noted, as are reports of siezures, chorea, or other cental nevous system manifestations. No single laboratory test confirms SLE; rather, blood testing reveals moderate to severe anemia, thrombocytopenia, leukocytosis, or leukopenia and positive antinuclear antibodies. Other diagnostic immunologic tests support but do not confirm the diagnosis. Hematuria may be found in urinalysis. Medical Management: Treatment of SLE includes management of acute and chronic disease. Although SLE can be life-threatening, advances in its treatment have led to improved survival and reduced morbidity. Acute disease requires interventions directed at controlling increased disease activity or exacerbations that may involve any organ system. Disease activity is a composite of clinical and laboratory features that reflect active inflammation secondary to SLE. Management of the more chronic condition involves periodic monitoring and recognition of meaningful clinical changes requiring adjustment in therapy (Ruddy et al.,2001). The goals of treatment include preventing progressive loss of organ function, reducing the likelihood of acute disease, minimizing disease-related disabilities, and preventing complications

from therapy. Management of SLE involves regular monitoring to assess disease activity and therapeutic affectiveness. Pharmacologic Therapy: Medication therapy for SLE is based on the concept that local tissue inflammation is mediated by exaggerated or heightened immune responses, which can vary widely in intensity and require different therapies at different times. The NSAIDs used for minor clinical manifestations are often used along with corticosteroids in an efforts to minimize corticosteroids requirements. Corticosteroids are the single most important medication available for treatment. They are used topically for cutaneous manifestations, in low oral doses for minor disease activity, and in high doses in major disease activity. Intravenous administration of corticosteroids is an alternative to traditional high-dose oral use. Antimalarial medications are effective for managing cutaneouis, musculoskeletal, and mild systemic features of SLE. Immunosuppressive agents (alkilating agents and purine analog) are used because of their effect on immune function. These medications are generally reserved for patients who have serious forms of SLE and who have not responded to conservative therapies (Kimberly, 2001; National Institutes of Health, 1998; Ruddy et al.,2001). Nursing Management: The disease or its treatment may produce dramatic changes in appearance and considerable distress for the patient. The changes and the unpredictable course of SLE necessitate expert assessment skills and nursing care and sensitivity to the psychological reactions of the patient. Patients may be benifit from participation in support groups by receiving disease information, daily management tips, and social support. Because sun and ultraviolet light exposure can increase

disease activity or cause an exacerbation, patient should be taught to avoid exposure or to protect themselves with sunscreen and clothing. Because of the increase risk for involvement of multiple organ systems, patient should understand the need for routine periodic screenings as well as health promotion activities. A dietary consultation may be indicated to ensure that the patient is knowledgeable about dietary recommendations, given the increased risk for cardiovascular disease, including hypertension and artherosclerosis. The nurse instructs the patient about the importance of continuing prescribed medications and addresses the changes aand side effects that are likely with their use. The patient is reminded of the importance of monitoring because of the increased risk for systemic involement, including renal and cardiovascular effects. Nursing Diagnoses: Fatigue related to increased disease activity, pain, inadequate, sleep/rest, deconditioning, inadequate nutrition, and emotional stress/depression. Goal: Incorporates as part of daily activities strategies necessary to modify fatigue. Nursing Interventions
1. Provide instruction about fatigue.

a. Describe relatationship of disease activity to fatigue. b. Describe comfort measures while providing them. c. Develop and encourage a sleep routine (warm bath and relaxation technique to promote sleep.) d. Explain imprtance of rest for relieving systemic, articular, and emotional stress. e. Explain how to use energy conservation techniques.

Rationale 1. The patients understanding of fatigue will affect his or her actions. a. The amount of fatigue is directly related to the activity of the disease. b. Reelief of discomfort can relieve fatigue. c. Effective bedtime routine promotes restorative sleep. d. Different kinds of rest are needed to relieve fatigue and are based on patient need and response. e. A variety of measures can be used to conserve energy.

f. Identify physical and emotional factors that can cause fatigue. 2. Facilitate development of appropriate activity/rest schedule. 3. Encourage adherence to the treatment program. 4. Refer to and encourage a conditioning program. 5. Encourage adequate nutrition, including source of iron from food and supplements.

f. Awareness of the various causes of fatigue provides the basis for measures to modify the fatigue. 2. Alternating rest and activity conserves energy while allowing most productivity. 3. Overall control of disease activity can decrease the amount of fatigue. 4. Deconditioning resulting from lack of mobility, understanding, and disease activity contributes to fatigue. 5. A nutritious diet can help counteract fatigue.

Acute pain related to inflammation and increased disease activity, tissue damage, or lowered tolerance level. Goal: Improvement in comfort level; incorporation of pain management techniques into daily life. Nursing Interventions Provide variety of comfort measure Apllication of cold and heat Massage, position changes, rest Foam mattress, supportive pillow, splints d. Relaxation techniques, diversional activities 2. Administer anti-inflammatory, analgesic, and slow acting antirheumatic medications as prescribed. 3. Individualize medication schedule to meet patients need for pain management. 4. Encourage verbalization of feelings about pain and chronicity of disease. 5. Teach pathophysiology of pain and rheumatic disease, and assist patient to recognize that pain often leads to unproven methods of treatment. 6. Assist in identification of pain that leads to use of unproven methods of treatment. 7. Assess for subjective changes in pain. 1. a. b. c. Rationale 1. Pain may respond to non-pharmacologic interventions such as joint protection, exercise, relaxation and thermal modalities.

2. Pain of rheumatic disease responds to individual or combination medication regimens. 3. Previous pain experiences and management strategies may be different from those needed for persistent pain. 4. Verbalization promotes coping. 5. Knowledge of rheumatic pain and appropriate treatment may help patient avoid unsafe, ineffective therapies. 6. The impact of pain on an individuals life often leads to misconceptions about pain and pain management techniques. 7. The individuals description of the pain sensation is a more reliable indicator that objective measurements such as change in

vital signs, body movement, and facial expression.

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