RN Expert Guides: Cardiovascular Care, 1st Edition (2008)

Chapter 6. Inflammatory Disorders

ENDOCARDITIS

Endocarditis is an infection of the endocardium, heart valves, or cardiac prosthesis that results from bacterial or fungal invasion.

In patients with infective endocarditis, fibrin and platelets cluster on valve tissue and engulf circulating bacteria or fungi. This produces vegetation, which, in turn, may cover the valve surfaces, causing deformities and destruction of valvular tissue. It may also extend to the chordae tendineae, causing them to rupture, which leads to valvular insufficiency.

Sometimes vegetation forms on the endocardium, usually in areas altered by rheumatic, congenital, or syphilitic heart disease. It may also form on normal surfaces. Vegetative growth on the heart valves, endocardial lining of a heart chamber, or the endothelium of a blood vessel may embolize to the spleen, kidneys, central nervous system, and lungs.

Endocarditis can be classified as native valve endocarditis, endocarditis in I.V. drug users, or prosthetic valve endocarditis. It can be acute or subacute. Untreated, endocarditis is usually fatal. With proper treatment, however, about 70% of patients recover. The prognosis is worse when endocarditis causes severe valvular damage—leading to insufficiency and left-sided heart failure—or when it involves a prosthetic valve.

Pathophysiology

In endocarditis, bacteremia—even transient bacteremia after dental or urogenital procedures—introduces the pathogen into the bloodstream. This infection causes fibrin and platelets to aggregate on the valve tissue and engulf circulating bacteria or fungi that flourish and form on fragile, wartlike vegetative growths on the heart valves, the endocardial lining of a heart chamber, or the epithelium of a blood vessel. (See Degenerative changes in endocarditis.) Such growths may cover the valve surfaces, causing ulceration and necrosis. They may also extend to the chordae tendineae, leading to rupture and subsequent valvular insufficiency. Ultimately, they may embolize to the spleen, kidneys, central nervous system, and lungs.

DEGENERATIVE CHANGES IN ENDOCARDITIS

This illustration shows typical growths on the endocardium produced by fibrin and platelet deposits on infection sites.

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are I.V. drug abusers

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have mitral valve prolapse (especially with a systolic murmur)

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have rheumatic heart disease.

Other predisposing conditions include:

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coarctation of the aorta

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tetralogy of Fallot

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subaortic and valvular aortic stenosis

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ventricular septal defects

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pulmonary stenosis

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Marfan's syndrome

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degenerative heart disease, especially calcific aortic stenosis

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rarely, a syphilitic aortic valve.

However, some patients with endocarditis have no underlying heart disease.

Infecting organisms differ among these groups. In patients with native valve endocarditis who aren't I.V. drug abusers, causative organisms usually include (in order of frequency) streptococci, especially Streptococcus viridans, staphylococci, or enterococci. Although other bacteria occasionally cause the disorder, fungal causes are rare in this group. The mitral valve is the most common valve involved, followed by the aortic valve.

In patients who are I.V. drug abusers, Staphylococcus aureus is the most common infecting organism. Less common causes of the disorder are streptococci, enterococci, gram-negative bacilli, or fungi. The tricuspid valve is the most common valve involved, followed by the aortic valve and then the mitral valve.

In patients with prosthetic valve endocarditis, early cases (those that develop within 60 days of valve insertion) are usually caused by staphylococcal infection. However, gram-negative aerobic organisms, fungi, streptococci, enterococci, or diphtheroids may also cause the disorder. The course is usually sudden and severe and is associated with a high mortality rate. Late cases (occurring after 60 days) show signs and symptoms similar to native valve endocarditis.

Complications

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Heart failure

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Death

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Aortic root abscess

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Myocardial abscesses

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Pericarditis

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Cardiac arrhythmia

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Cerebral emboli

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Brain abscesses

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Septic pulmonary infarcts

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Arthritis

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Glomerulonephritis

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Acute renal failure

Assessment findings

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The patient may report a predisposing condition and complain of nonspecific signs and symptoms, such as weakness, fatigue, weight

loss, anorexia, arthralgia, night sweats, and an intermittent fever that may recur for weeks.

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Inspection may reveal petechiae of the skin (especially common on the upper anterior trunk) and the buccal, pharyngeal, or conjunctival mucosa, and splinter hemorrhages under the nails.

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Rarely, you may see Osler's nodes (tender, raised, subcutaneous lesions on the fingers or toes), Roth's spots (hemorrhagic areas with white centers on the retina), and Janeway lesions (purplish macules on the palms or soles).

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Clubbing of the fingers may be present in patients with longstanding disease.

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Auscultation may reveal a murmur in most patients, except those with early acute endocarditis and I.V. drug abusers with tricuspid valve infection. The murmur is usually loud and regurgitant, which is typical of the underlying rheumatic or congenital heart disease. A murmur that changes suddenly or a new murmur that develops in the presence of fever is a classic sign of endocarditis.

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Percussion and palpation may reveal splenomegaly in longstanding disease. In patients who have developed left-sided heart failure, your assessment may reveal dyspnea, tachycardia, and bibasilar crackles.

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In 12% to 35% of patients with subacute endocarditis, embolization from vegetating lesions or diseased valve tissue may produce typical characteristics of splenic, renal, cerebral, or pulmonary infarction, or peripheral vascular occlusion:

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- Splenic infarction causes pain in the left upper quadrant, radiating to the left shoulder, and abdominal rigidity.

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- Renal infarction causes hematuria, pyuria, flank pain, and decreased urine output.

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- Cerebral infarction causes hemiparesis, aphasia, and other neurologic deficits.

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- Pulmonary infarction causes cough, pleuritic pain, pleural friction rub, dyspnea, and hemoptysis. These signs and symptoms are most common in patients with right-sided endocarditis, which typically occurs among I.V. drug abusers and after cardiac surgery.

o

- Peripheral vascular occlusion causes numbness and tingling in an arm, leg, finger, or toe, or signs of impending peripheral gangrene.

Diagnostic test results

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Three or more blood cultures during a 24- to 48-hour period identify the causative organism in up to 90% of patients. The remaining

10% may have negative blood cultures, possibly suggesting fungal or difficult-to-diagnose infections such as Haemophilus parainfluenzae.

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Other abnormal but nonspecific laboratory results include:

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- abnormal histiocytes (macrophages)

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- normocytic, normochromic anemia (in patients with subacute infective endocarditis)

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- elevated erythrocyte sedimentation rate and serum creatinine level

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- positive serum rheumatoid factor in about half of patients with endocarditis after the disease is present for 6 weeks

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- proteinuria and microscopic hematuria.

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An electrocardiogram reading may show atrial fibrillation and other arrhythmias that accompany valvular disease.

Treatment

The goal of treatment is to eradicate all infecting organisms from the vegetation. Therapy should start promptly and continue over 4 to 6 weeks. Selection of an anti-infective drug is based on the infecting organism and sensitivity studies. Although blood cultures are negative in 10% to 20% of the subacute cases, the practitioner may want to determine the probable infecting organism.

Supportive treatment includes bed rest, aspirin for fever and aches, and sufficient fluid intake. Severe valvular damage, especially aortic insufficiency or infection of a cardiac prosthesis, may require corrective surgery if refractory heart failure develops or if an infected prosthetic valve must be replaced.

Nursing interventions

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Stress the importance of bed rest. Assist the patient with bathing if necessary. Provide a bedside commode because using a commode puts less stress on the heart than using a bedpan. Offer the patient diversionary, physically undemanding activities.

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To reduce anxiety, allow the patient to express his concerns about the effects of activity restrictions on his responsibilities and routines. Reassure him that the restrictions are temporary.

·

Before giving an antibiotic, obtain a patient history of allergies. Administer the prescribed antibiotic on time to maintain a consistent drug level in the blood.

 

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Observe the venipuncture site for signs of infiltration or inflammation, a complication of long-term I.V. administration. To reduce the risk of this complication, rotate venous access sites.

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Assess cardiovascular status frequently, and watch for signs and symptoms of left-sided heart failure, such as dyspnea, hypotension, tachycardia, tachypnea, crackles, and weight gain. Check for changes in cardiac rhythm or conduction.

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Administer oxygen and evaluate arterial blood gas levels, as needed, to ensure adequate oxygenation.

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Monitor the patient's renal status (including blood urea nitrogen levels, creatinine clearance, and urine output) to check for signs of renal emboli and drug toxicity.

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Make sure the susceptible patient understands the need for a prophylactic antibiotic before, during, and after dental work, childbirth, and genitourinary, GI, or gynecologic procedures. (See Teaching the patient with endocarditis.)

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH ENDOCARDITIS

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Teach the patient about the anti-infective medication that he'll continue to take. Stress the importance of taking the medication and restricting activity for as long as recommended.

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Tell the patient to watch for and report signs of embolization and to watch closely for fever, anorexia, and other signs of relapse that could occur about 2 weeks after treatment stops.

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Discuss the importance of completing the full course of antibiotics, even if he's feeling better. Make sure susceptible patients understand the need for prophylactic antibiotics before, during, and after dental work, childbirth, and genitourinary, GI, or gynecologic procedures.

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Teach the patient to brush his teeth with a soft toothbrush and rinse his mouth thoroughly. Tell him to avoid flossing his teeth and using irrigation devices.

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Teach the patient how to recognize symptoms of endocarditis. Tell him to notify the practitioner immediately if such symptoms occur.

ff2-b01382759RED FLAG

Watch for signs and symptoms of embolization (hematuria, pleuritic chest pain, left upper quadrant pain, or paresis), a common occurrence during the first 3 months of treatment. Tell the patient to watch for and report these signs and symptoms, which may indicate impending peripheral vascular occlusion or splenic, renal, cerebral, or pulmonary infarction.

MYOCARDITIS

Myocarditis—a focal or diffuse inflammation of the myocardium—is typically uncomplicated and self-limiting. It may be acute or chronic and can occur at any age. In many patients, myocarditis fails to produce specific cardiovascular symptoms or electrocardiogram (ECG) abnormalities. Recovery usually is spontaneous and without residual defects.

Pathophysiology

Damage to the myocardium occurs when an infectious organism triggers an autoimmune, cellular, and humoral reaction. The resulting inflammation may lead to hypertrophy, fibrosis, and inflammatory changes of the myocardium and conduction system. The heart muscle weakens and contractility is reduced. The heart muscle becomes flabby and dilated, and pinpoint hemorrhages may develop.

Causes of myocarditis include:

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bacterial infections, such as diphtheria, tuberculosis, typhoid fever, tetanus, and staphylococcal, pneumococcal, and gonococcal infections

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fungal infections, including candidiasis and aspergillosis

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helminthic infections such as trichinosis

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hypersensitive immune reactions, including acute rheumatic fever and postcardiotomy syndrome

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parasitic infections, especially South American trypanosomiasis (Chagas' disease) in infants and immunosuppressed adults; also toxoplasmosis

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radiation therapy; large doses of radiation to the chest in treating lung or breast cancer

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toxins, such as lead, chemicals, and cocaine, and alcoholism

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viral infections (most common cause in the United States and western Europe), such as coxsackievirus A and B strains and, possibly, poliomyelitis, influenza, Epstein-Barr virus, human immunodeficiency virus, cytomegalovirus, measles, mumps, rubeola, rubella, and adenoviruses and echoviruses.

Complications

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Recurrence of myocarditis

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Chronic valvulitis (when it results from rheumatic fever)

 

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Dilated cardiomyopathy

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Arrhythmias and sudden death

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Heart failure

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Pericarditis

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Ruptured myocardial aneurysm

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Thromboembolism

Assessment findings

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The history commonly reveals a recent upper respiratory tract infection with fever, viral pharyngitis, or tonsillitis.

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The patient may complain of nonspecific signs and symptoms, such as fatigue, dyspnea, palpitations, persistent tachycardia, and persistent fever, all of which reflect the accompanying systemic infection.

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Occasionally, the patient may complain of a mild, continuous pressure or soreness in the chest. This pain is unlike the recurring, stress-related pain of angina pectoris.

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Auscultation usually reveals S3 and S4 gallops, a muffled S1, possibly a murmur of mitral insufficiency (from papillary muscle dysfunction) and, if the patient has pericarditis, a pericardial friction rub.

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If the patient has left-sided heart failure, you may notice pulmonary congestion, dyspnea, and resting or exertional tachycardia disproportionate to the degree of fever.

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If myofibril degeneration occurs, it may lead to right-sided and left-sided heart failure, with cardiomegaly, jugular vein distention, dyspnea, edema, pulmonary congestions, persistent fever with resting or exertional tachycardia disproportionate to the degree of fever, and supraventricular and ventricular arrhythmias.

Diagnostic test results

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Endomyocardial biopsy can be used to confirm a myocarditis diagnosis.

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Cardiac enzyme levels, including creatine kinase (CK), CK-MB, serum aspartate aminotransferase, and lactate dehydrogenase, are elevated.

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White blood cell count and erythrocyte sedimentation rate are elevated.

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Antibody titers, such as antistreptolysin-O titer, are elevated in patients with rheumatic fever.

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ECG typically shows diffuse ST-segment and T-wave abnormalities, as in patients with pericarditis, conduction defects (prolonged PR

interval), or other ventricular and supraventricular ectopic arrhythmias.

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Cultures of stool, throat, pharyngeal washings, blood, or other body fluids may identify the causative bacteria or virus.

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Echocardiography may show a weak heart muscle, an enlarged heart, or fluid surrounding the heart.

Treatment

An antibiotic is prescribed to treat the bacterial infections. An antipyretic is used to reduce fever and help decrease the stress on the heart. The patient will be placed on bed rest to reduce oxygen demands and to reduce the heart's workload. Activity restrictions will help minimize myocardial oxygen consumption. The patient will be given supplemental oxygen therapy. His sodium intake will be restricted, and he'll be given a diuretic to decrease fluid retention. An angiotensin-converting enzyme inhibitor will also be prescribed. For patients with heart failure, digoxin (Lanoxin) will be used to increase myocardial contractility. (Administer digoxin carefully because some patients may show a paradoxical sensitivity to even small doses.)

An antiarrhythmic, such as quinidine (Quinaglute) or procainamide (Pronestyl), is used to treat arrhythmias. Use these drugs cautiously because they may depress myocardial contractility. A temporary pacemaker may be inserted if complete atrioventricular block occurs.

Anticoagulation is used to prevent thromboembolism. A corticosteroid and an immunosuppressant, while controversial, are sometimes used to combat life-threatening complications, such as intractable heart failure.

Nonsteroidal anti-inflammatory drugs are contraindicated during the acute phase (first 2 weeks) because they increase myocardial damage. Cardiac assist devices or transplantation may be used as a last resort in severe cases that resist treatment.

Nursing interventions

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Stress the importance of bed rest. Assist the patient with bathing if necessary. Provide a bedside commode because using a commode puts less stress on the heart than using a bedpan. Offer the patient diversionary, physically undemanding activities.

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Assess cardiovascular status frequently, watching for signs and symptoms of left-sided heart failure (such as dyspnea, hypotension,

and tachycardia). Check for changes in cardiac rhythm or conduction.

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Administer oxygen and evaluate arterial blood gas levels, as needed, to ensure adequate oxygenation.

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Observe the patient for signs and symptoms of digoxin toxicity (such as anorexia, nausea, vomiting, blurred vision, and cardiac arrhythmias) and for complicating factors that may potentiate toxicity, such as electrolyte imbalance and hypoxia.

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Administer a parenteral anti-infective as indicated. (See Teaching the patient with myocarditis.)

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH MYOCARDITIS

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Teach the patient about anti-infectives. Stress the importance of taking the prescribed drug and restricting activities for as long as the practitioner orders.

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Teach the patient to check his pulse for 1 full minute before taking a cardiac glycoside at home. Direct him to withhold the dose and notify the practitioner if his heart rate falls below the predetermined rate (usually 60 beats/minute).

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During recovery, recommend that the patient resume normal activities slowly and avoid competitive sports.

PERICARDITIS

Understanding pericarditis, pages 344 and 345.)

The prognosis depends on the underlying cause, but typically the prognosis is good in patients with acute pericarditis, unless constriction occurs.

Pathophysiology

Pericardial tissue damaged by bacteria or other substances results in the release of chemical mediators in inflammation (prostaglandins, histamines, bradykinins, and serotonins) into the surrounding tissue, thereby initiating the inflammatory process. Friction occurs as the inflamed pericardial layers rub against each other. Histamines and other chemical mediators dilate vessels and increase vessel permeability. Vessel walls then leak fluids and protein (including fibrinogen) into tissues, causing extracellular edema. Macrophages already present in the tissue begin to phagocytize the invading bacteria and are joined by neutrophils and monocytes. After several days, the area fills with an exudate composed of necrotic tissue and dead and dying bacteria, neutrophils, and macrophages. Eventually, the contents of the cavity autolyze and are gradually reabsorbed into healthy tissue.

UNDERSTANDING PERICARDITIS

Pericarditis occurs when a pathogen or other substance attacks the pericardium, leading to the following events.

Inflammation

Pericardial tissue damaged by bacteria or other substances releases chemical mediators of inflammation (such as prostaglandins, histamines, bradykinins, and serotonins) into the surrounding tissue, starting the inflammatory process. Friction occurs as the inflamed pericardial layers rub against each other.

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Vasodilation and clotting

Histamines and other chemical mediators cause vasodilation and increased vessel permeability. Local blood flow (hyperemia) increases. Vessel walls leak fluids and proteins (including fibrinogen) into tissues, causing extracellular edema. Clots of fibrinogen and tissue fluid form a wall, blocking tissue spaces and lymph vessels in the injured area. This wall prevents the spread of bacteria and toxins to adjoining healthy tissues.

Initial phagocytosis

Macrophages already present in the tissues begin to phagocytize the invading bacteria but usually fail to stop the infection.

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Enhanced phagocytosis

Substances released by the injured tissue stimulate neutrophil production in the bone marrow. Neutrophils then travel to the injury site through the bloodstream and join macrophages in destroying pathogens. Meanwhile, additional macrophages and monocytes migrate to the injured area and continue phagocytosis.

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Exudation

After several days, the infected area fills with an exudate composed of necrotic tissue and dead and dying bacteria, neutrophils, and macrophages. This exudate, which is thinner than pus, forms until all infection ceases, creating a cavity that remains until tissue destruction stops. The contents of the cavity autolyze and are gradually reabsorbed into healthy tissue.

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Fibrosis and scarring

As the end products of the infection slowly disappear, fibrosis and scar tissue may form. Scarring, which can be extensive, can ultimately cause heart failure if it restricts movement.

A pericardial effusion develops if fluid accumulates in the pericardial cavity. Cardiac tamponade results when fluid accumulates rapidly in the pericardial space, compressing the heart, preventing it from filling during diastole, and resulting in a drop in cardiac output.

Chronic constrictive pericarditis develops if the pericardium becomes thick and stiff from chronic or recurrent pericarditis, encasing the heart in a stiff shell and preventing it from properly filling during diastole. This causes an increase in left- and right-sided filling pressures, leading to a drop in stroke volume and cardiac output.

Common causes of pericarditis include:

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aortic aneurysm with pericardial leakage (less common)

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bacterial, fungal, or viral infection (infectious pericarditis)

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drugs, such as hydralazine (Apresoline) or procainamide (Procan SR)

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high dose radiation to the chest

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hypersensitivity or autoimmune disease, such as acute rheumatic fever (most common cause of pericarditis in children), systemic lupus erythematosus, and rheumatoid arthritis

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idiopathic factors (most common in acute pericarditis)

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myxedema with cholesterol deposits in the pericardium (less common)

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neoplasms (primary or metastases from lungs, breasts, or other organs)

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previous cardiac injury, such as a myocardial infarction (MI; Dressler's syndrome), trauma, or surgery (postcardiotomy syndrome), that leaves the pericardium intact but causes blood to leak into the pericardial cavity

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uremia.

Complications

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Pericardial effusion (major complication of acute pericarditis)

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Cardiac tamponade

Assessment findings

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The patient's history may include an event or disease that can cause pericarditis, such as a chest trauma, an MI, or a recent bacterial infection.

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The patient with acute pericarditis typically reports sharp, sudden pain, usually starting over the sternum and radiating to the neck, shoulders, back, and arms. The pain is usually pleuritic, increasing with deep inspiration and decreasing when the patient sits up and leans forward. This decrease occurs because leaning forward pulls the heart away from the diaphragmatic pleurae of the lungs.

Pericarditis can mimic the pain of an MI. However, the patient may have no pain if he has slowly developing tuberculous pericarditis or postirradiation, neoplastic, or uremic pericarditis.

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The patient may also report dyspnea.

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Auscultation almost always reveals a pericardial friction rub, which is a grating sound heard as the heart moves. You can hear it best during forced expiration, while the patient leans forward or is on his hands and knees in bed. The rub may have up to three components that correspond to atrial systole, ventricular systole, and the rapid-filling phase of ventricular diastole.

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Occasionally, the friction rub is heard only briefly or not at all. If acute pericarditis has caused very large pericardial effusions, heart sounds may be distant.

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Palpation may reveal a diminished or an absent apical impulse.

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Chronic constrictive pericarditis causes the membrane to calcify and become rigid. It also causes a gradual increase in systemic venous pressure and symptoms similar to those of chronic right-sided heart failure (such as fluid retention, ascites, and hepatomegaly).

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Tachycardia, an ill-defined substernal chest pain, and a feeling of fullness in the chest may indicate pericardial effusion.

ff2-b01382759RED FLAG

Pallor, clammy skin, hypotension, paradoxical pulse (a drop in systolic blood pressure of 15 mm Hg or greater during slow inspiration), jugular vein distention, and dyspnea indicate cardiac tamponade.

Diagnostic test results

Laboratory results indicate inflammation and may identify the disorder's cause. They include:

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normal or elevated white blood cell count, especially in patients with infectious pericarditis

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elevated erythrocyte sedimentation rate

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slightly elevated CK-MB level with associated myocarditis

 

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culture of pericardial fluid obtained by open surgical drainage or pericardiocentesis (which sometimes identifies a causative organism in patients with bacterial or fungal pericarditis).

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Other pertinent laboratory data include a blood urea nitrogen level to check for uremia, an antistreptolysin-O titer to detect rheumatic fever, and a purified protein derivative skin test to check for tuberculosis.

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Electrocardiography shows characteristic changes in patients with acute pericarditis. Such changes include elevated ST segments in the limb leads and most precordial leads. Downsloping PR segments and upright T waves are present in most leads. The QRS complexes may be diminished when pericardial effusion is present. Rhythm changes may also occur, including atrial ectopic rhythms (such as atrial fibrillation) or sinus arrhythmias. In chronic constrictive pericarditis, there may be low-voltage QRS complexes, T-wave inversion or flattening, and P mitral (wide P waves) in leads I, II, and V6.

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Echocardiography indicates pericardial effusion when it shows an echo-free space between the ventricular wall and the pericardium.

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Chest X-rays may be normal with acute pericarditis. The cardiac silhouette may be enlarged with a water bottle shape caused by fluid accumulation if pleural effusion is present.

Treatment

Appropriate treatment aims to relieve symptoms, manage underlying systemic disease, and prevent or treat pericardial effusion and cardiac tamponade.

In patients with idiopathic pericarditis, postmyocardial infarction pericarditis, or postthoracotomy pericarditis, treatment consists of bed rest as long as fever and pain persist and administration of a nonsteroidal drug, such as aspirin or indomethacin (Indocin), to relieve pain and reduce inflammation. If symptoms continue, the practitioner may prescribe a corticosteroid. Although corticosteroids provide rapid, effective relief, they must be used cautiously because the disorder may recur when drug therapy stops. If an infectious cause is suspected, the patient may be started on antibacterial, antifungal, or antiviral therapy.

When infectious pericarditis results from disease of the left pleural space, mediastinal abscesses, or septicemia, the patient requires an antibiotic, surgical drainage, or both. If cardiac tamponade develops, the practitioner may perform emergency pericardiocentesis and may inject an antibiotic directly into the pericardial sac.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH PERICARDITIS

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If surgery is necessary, teach the patient how to perform deep-breathing and coughing exercises before he undergoes the procedure.

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Tell the patient to resume his daily activities slowly and to schedule rest periods into his daily routine as instructed by the practitioner.

Recurrent pericarditis may require partial pericardectomy, which creates a window that allows fluid to drain into the pleural space. In patients with constrictive pericarditis, total pericardectomy may be necessary to permit the heart to fill and contract adequately. Treatment must also include management of rheumatic fever, uremia, tuberculosis, and other underlying disorders.

Nursing interventions

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Stress the importance of bed rest. Assist the patient with bathing if necessary. Provide a bedside commode because using a commode puts less stress on the heart than using a bedpan. Offer the patient diversionary, physically undemanding activities.

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Place the patient in an upright position to relieve dyspnea and chest pain.

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Provide an analgesic to relieve pain and oxygen to prevent tissue hypoxia.

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Because cardiac tamponade requires immediate treatment, keep a pericardiocentesis set handy if you suspect pericardial effusion.

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Assess cardiovascular status frequently, watching for signs of cardiac tamponade.

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To reduce anxiety, allow the patient to express his concerns about the effects of activity restrictions on his responsibilities and routines. Reassure him that the restrictions are temporary.

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Before giving an antibiotic, obtain a patient history of allergies. Administer the prescribed antibiotic on time to maintain a consistent level in the blood.

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Observe the venipuncture site for signs of infiltration or inflammation, a possible complication of long-term I.V. administration. To reduce the risk of this complication, rotate venous access sites.

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Provide appropriate postoperative care, similar to that given after cardiothoracic surgery. (See Teaching the patient with pericarditis.)

RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE

A systemic inflammatory disease of childhood, acute rheumatic fever develops after infection of the upper respiratory tract with group A beta-hemolytic streptococci.

Rheumatic fever principally involves the heart, joints, central nervous system, skin, and subcutaneous tissues. It commonly recurs.

The term rheumatic heart disease refers to the cardiac involvement of rheumatic fever—its most destructive effect. Cardiac involvement develops in up to 50% of patients and may affect the endocardium, myocardium, or pericardium during the early acute phase. It may later affect the heart valves, causing chronic valvular disease.

Long-term antibiotic therapy can minimize the recurrence of rheumatic fever, reducing the risks of permanent cardiac damage and valvular deformity.

Although rheumatic fever tends to be familial, this tendency may reflect contributing environmental factors. For example, in lower so-cioeconomic groups, incidence is highest in children ages 5 to 15, probably resulting from malnutrition and crowded living conditions. Rheumatic fever usually strikes during cool, damp weather in winter and early spring. In the United States, it's most common in the northern states.

Pathophysiology

Carditis may affect the endocardium, myocardium, or pericardium during the early acute phase. Later, the heart valves may be damaged, causing chronic valvular disease.

The extent of damage to the heart depends on where the disorder strikes. Pericarditis causes a pericardial friction rub and, occasionally, pain and effusion. Myocarditis produces characteristic lesions called Aschoff bodies in the acute stages as well as cellular swelling and fragmentation of interstitial collagen, leading to formation of a progressively fibrotic nodule and interstitial scars. Endocarditis causes valve leaflet swelling, erosion along the lines of leaflet closure, and blood, platelet, and fibrin deposits, which form beadlike vegetation. It usually affects the mitral valve in females and the aortic valve in males; in both, it affects the tricuspid valves occasionally and the pulmonic valve rarely.

Complications

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Destruction of the mitral and aortic valves

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Pancarditis (pericarditis, myocarditis, and endocarditis)

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Heart failure

Assessment findings

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Nearly all affected patients report having a streptococcal infection a few days to 6 weeks earlier.

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They usually have a recent history of low-grade fever that spikes to at least 100.4° F (38°C) late in the afternoon, unexplained epistaxis, and abdominal pain.

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Most patients complain of migratory joint pain (polyarthritis). Swelling, redness, and signs of effusion typically accompany such pain, which usually affects the knees, ankles, elbows, and hips.

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If the patient has pericarditis, he may complain of sharp, sudden pain that usually starts over the sternum and radiates to the neck, shoulders, back, and arms. The pain is usually pleuritic, increases with deep inspiration, and decreases when the patient sits up and leans forward. (This position pulls the heart away from the diaphragmatic pleurae of the lungs.) The pain may mimic that of a myocardial infarction.

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A patient with heart failure caused by severe rheumatic carditis may complain of dyspnea, right upper quadrant pain, and a hacking, nonproductive cough.

Inspection may reveal skin lesions such as erythema marginatum, a nonpruritic, macular, transient rash. The lesions are red with blanched centers and well-demarcated borders. Lesions typically appear on the trunk and extremities.

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Near tendons or the bony prominences of joints, you may notice subcutaneous nodules that are firm, movable, nontender, and about 1/8″ to ¾″ (0.3 to 2 cm) in diameter. They occur around the elbows, knuckles, wrists, and knees, and less commonly on the scalp and backs of the hands. These nodules persist for a few days to several weeks and, like erythema marginatum, commonly accompany carditis.

 

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You may notice edema and tachypnea if the patient has left-sided heart failure.

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Palpation may reveal a rapid pulse rate, and auscultation may reveal a pericardial friction rub (a grating sound heard as the heart moves) if the patient has pericarditis. You can hear it best during forced expiration, with the patient leaning forward or on his hands and knees.

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Murmurs and gallops may also occur. With left-sided heart failure, you may hear bibasilar crackles and a ventricular or an atrial gallop. The most common murmurs include:

o

- a systolic murmur of mitral insufficiency (a high-pitched, blowing, holosystolic murmur, loudest at apex, possibly radiating to the anterior axillary line)

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- a midsystolic murmur caused by stiffening and swelling of the mitral leaflet

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- occasionally a diastolic murmur of aortic insufficiency (a lowpitched, rumbling, almost inaudible murmur).

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Valvular disease may eventually cause chronic valvular stenosis and insufficiency, including mitral stenosis and insufficiency and aortic insufficiency. In children, mitral insufficiency remains the major effect of rheumatic heart disease.

Diagnostic test results

No specific laboratory tests help determine the presence of rheumatic fever, but the following test results support the diagnosis:

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Jones criteria revealing either two major criteria or one major criterion and two minor criteria, plus evidence of a previous group A streptococcal infection, are necessary for diagnosis. (See Jones criteria for diagnosing rheumatic fever.)

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C-reactive protein is positive (especially during the acute phase).

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Cardiac enzyme levels may be increased in patients with severe carditis.

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Antistreptolysin-O titer is elevated in almost all patients within 2 months of onset. (Rising anti-DNase B test results can also detect recurrent streptococcal infection.)

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Throat cultures may continue to show the presence of group A streptococci; however, they usually occur in small numbers. Isolating them is difficult.

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Electrocardiography reveals no diagnostic changes, but some patients show a prolonged PR interval.

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Chest X-rays show normal heart size, except in patients with myocarditis, heart failure, and pericardial effusion.

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Echocardiography helps evaluate valvular damage, chamber size, ventricular function, and the presence of a pericardial effusion.

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Cardiac catheterization is used to help evaluate valvular damage and left ventricular function in patients with severe cardiac dysfunction.

JONES CRITERIA FOR DIAGNOSING RHEUMATIC FEVER

The Jones criteria are used to standardize the diagnosis of rheumatic fever. Diagnosis requires that the patient have either two major criteria or one major criterion and two minor criteria, plus evidence of a previous streptococcal infection.

Major criteria

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Carditis

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Migratory polyarthritis

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Sydenham's chorea

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Subcutaneous nodules

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Minor criteria

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Fever

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Arthralgia

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Elevated acute phase reactants

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Prolonged PR interval

Treatment

Effective management eradicates the streptococcal infection, relieves symptoms, and prevents recurrence, thus reducing the risk of permanent cardiac damage. During the acute phase, treatment includes penicillin or erythromycin (E-Mycin) (for patients with penicillin hypersensitivity). Salicylates, such as aspirin, relieve fever and minimize joint swelling and pain. If the patient has carditis or if salicylates fail to relieve pain and inflammation, the practitioner may prescribe a corticosteroid.

Supportive treatment requires strict bed rest for about 5 weeks during the acute phase for patients with active carditis, followed by a progressive increase in physical activity. The increase depends on clinical and laboratory findings and the patient's response to treatment.

After the acute phase subsides, a monthly I.M. injection of penicillin G benzathine (Bicillin) or daily doses of oral sulfadiazine (Sulfasalazine) or penicillin G may be used to prevent recurrence. Such preventive treatment usually continues for 5 to 10 years.

Heart failure requires continued bed rest, sodium restriction, digoxin (Lanoxin), an angiotensin-converting enzyme inhibitor, and a diuretic. Severe mitral or aortic valvular dysfunction that causes persistent heart failure requires corrective surgery, such as commissurotomy, valvuloplasty, or valve replacement. Corrective valvular surgery seldom is necessary before late adolescence.

Nursing interventions

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Before giving penicillin, ask the patient (or, if the patient is a child, his parents) if he has ever had a hypersensitivity reaction to it. Even if he hasn't, warn him that such a reaction is possible.

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Administer the prescribed antibiotic on time to maintain a consistent drug level in the blood.

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Stress the importance of bed rest. Assist with bathing as necessary. Provide a bedside commode because using a commode puts less stress on the heart than using a bedpan. Offer the patient diversionary, physically undemanding activities.

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Place the patient in an upright position to relieve dyspnea and chest pain if needed.

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Provide an analgesic to relieve pain and oxygen to prevent tissue hypoxia as needed.

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To reduce anxiety, allow the patient to express his concerns about the effects of activity restrictions on his responsibilities and routines. Reassure him that the restrictions are temporary.

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If the patient's status is unstable because of chorea, clear his environment of objects that could make him fall.

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After the acute phase, encourage the patient's family and friends to spend as much time as possible with the patient to minimize his boredom. Advise parents to secure a tutor to help their child keep up with schoolwork during the long convalescence.

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Help the parents overcome any guilt feelings they may have about their child's illness. Failure to seek treatment for streptococcal infection is common because the illness may seem no worse than a cold.

 

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See Teaching the patient with rheumatic fever and rheumatic heart disease.)

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE

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Explain all tests and treatments to the patient.

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Tell the patient to resume activities of daily living slowly and to schedule rest periods in his routine, as instructed by the practitioner.

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Tell the parents or patient to stop penicillin therapy and call the physician immediately if the patient develops a rash, fever, chills, or other signs or symptoms of an allergic reaction.

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Instruct the patient and family to watch for and report early signs and symptoms of left-sided heart failure, such as dyspnea and a hacking, nonproductive cough.

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Teach the patient and family about this disease and its treatment. Warn the parents to watch for and immediately report signs and symptoms of recurrent streptococcal infection: sudden sore throat, diffuse throat redness and oropharyngeal exudate, swollen and tender cervical lymph glands, pain on swallowing, temperature of 101° to 104° F (38.3° to 40°C), headache, and nausea. Urge them to keep the child away from people with respiratory tract infections.

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Help the patient's family understand the frustrations associated with chorea (such as nervousness, restlessness, poor coordination, weakness, and inattentiveness). Emphasize that these effects are transient.

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Make sure the patient and his family understand the need to comply with prolonged antibiotic therapy and follow-up care. Arrange for a visiting nurse to oversee home care if necessary.

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Explain that an antibiotic must be given prophylactically before any dental work or other invasive procedure.