Endocarditis
Endocarditis: Excerpt from Handbook of Diseases
Also called infective endocarditis and bacterial endocarditis, endocarditis is an infection of the endocardium, heart valves, or a cardiac prosthesis, resulting from bacterial or fungal invasion. This invasion produces vegetative growths on the heart valves, the endocardial lining of a heart chamber, or the endothelium of a blood vessel that may embolize to the spleen, kidneys, central nervous system, and lungs.
In endocarditis, fibrin and platelets aggregate on the valve tissue and engulf circulating bacteria or fungi that flourish and produce friable verrucous vegetations. Such vegetations may cover the valve surfaces, causing ulceration and necrosis; they may also extend to the chordae tendineae, leading to their rupture and subsequent valvular insufficiency.
Untreated endocarditis is commonly fatal, but with proper treatment, about 70% of patients recover. The prognosis is worst when endocarditis causes severe valvular damage, leading to insufficiency and heart failure, or when it involves a prosthetic valve.
Causes
Endocarditis occurs most commonly in I.V. drug abusers, patients with prosthetic heart valves, and those with mitral valve prolapse (especially males with a systolic murmur). These conditions have surpassed rheumatic heart disease as the leading risk factor.
Other predisposing conditions include coarctation of the aorta; tetralogy of Fallot; subaortic and valvular aortic stenosis; ventricular septal defects; pulmonary stenosis; Marfan syndrome; degenerative heart disease, especially calcific aortic stenosis; and, rarely, syphilitic aortic valve. Some patients with endocarditis have no underlying heart disease.
Infecting organisms
Organisms that cause infection differ among patient 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, and enterococci. Although many other bacteria occasionally cause the disorder, fungal causes are rare in this group. The mitral valve is involved most commonly, followed by the aortic valve.
In patients who are I.V. drug abusers, Staphylococcus aureus is the most common infecting organism. Less frequently, streptococci, enterococci, gram-negative bacilli, or fungi cause the disorder. Most often the tricuspid valve is 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 due to staphylococcal infection. Gram-negative aerobic organisms, fungi, streptococci, enterococci, or diphtheroids may also cause the disorder. The course of the infection is commonly fulminating and associated with a high mortality rate. “Late” cases (those that develop after 60 days) present similarly to those of native valve endocarditis.
Signs and symptoms
Early clinical features of endocarditis are usually nonspecific and include malaise, weakness, fatigue, weight loss, anorexia, arthralgia, night sweats, chills, valvular insufficiency and, in 90% of patients, an intermittent fever that may recur for weeks. A more acute onset is associated with highly pathogenic organisms such as S. aureus.
Endocarditis commonly causes a loud, regurgitant murmur that’s typical of the underlying heart lesion. A suddenly changing murmur or the discovery of a new murmur in the presence of fever is a classic physical sign of endocarditis.
In about 30% of patients, embolization from vegetating lesions or diseased valvular tissue may produce the following features of splenic, renal, cerebral, or pulmonary infarction or peripheral vascular occlusion:
❑ splenic infarction: pain in the left upper quadrant, radiating to the left shoulder; abdominal rigidity
❑ renal infarction: hematuria, pyuria, flank pain, decreased urine output
❑ cerebral infarction: hemiparesis, aphasia, or other neurologic deficits
❑ pulmonary infarction (most common in right-sided endocarditis, which usually occurs in I.V. drug abusers and after cardiac surgery): cough, pleuritic pain, pleural friction rub, dyspnea, hemoptysis
❑ peripheral vascular occlusion: numbness and tingling in an arm or a leg, finger, or toe or signs of impending peripheral gangrene.
Other signs include splenomegaly; petechiae of the skin (especially common on the upper anterior trunk) and the buccal, pharyngeal, or conjunctival mucosa; and splinter hemorrhages under the nails. Rarely, endocarditis produces 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’s lesions (purplish macules on the palms or soles).
Diagnosis
Three or more blood cultures in 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 infection or infections that are difficult to diagnose such as Haemophilus parainfluenzae. Other abnormal but nonspecific laboratory test results include:
❑ normal or elevated white blood cell count
❑ abnormal histiocytes (macrophages)
❑ elevated erythrocyte sedimentation rate
❑ normocytic, normochromic anemia (in 70% to 90% of endocarditis cases)
❑ positive serum rheumatoid factor (in about one-half of all patients with endocarditis after the disease is present for 3 to 6 weeks).
Echocardiography may identify valvular damage. Transesophageal echocardiography allows visualization of cardiac structures. Electrocardiography may show atrial fibrillation and other arrhythmias that accompany valvular disease.
Treatment
The goal of treatment is to eradicate the infecting organism. Antimicrobial therapy should start promptly and continue over 4 to 6 weeks. Selection of an antibiotic is based on identification of the infecting organism and on sensitivity studies. While awaiting test results or if blood cultures are negative, empiric antimicrobial therapy is based on the likely infecting organism.
Supportive treatment includes bed rest, aspirin for fever and aches, and sufficient fluid intake. Severe valvular damage, especially aortic or mitral insufficiency, may necessitate corrective surgery if refractory heart failure develops or in cases in which an infected prosthetic valve must be replaced.
Special considerations
❑ Before giving antibiotics, obtain a patient history of allergies.
CLINICAL TIP: Administer antibiotics on time to maintain consistent antibiotic blood levels.
❑ Observe for signs of infiltration and inflammation, possible complications of long-term I.V. drug administration, at the venipuncture site. To reduce the risk of these complications, rotate venous access sites.
❑ Watch for signs of embolization (hematuria, pleuritic chest pain, left upper quadrant pain, and paresis), a common occurrence during the first 3 months of treatment. Tell the patient to watch for and report these signs, which may indicate impending peripheral vascular occlusion or splenic, renal, cerebral, or pulmonary infarction.
❑ Monitor the patient’s renal status (blood urea nitrogen levels, creatinine clearance, and urine output) to check for signs of renal emboli or evidence of drug toxicity.
❑ Observe for signs of heart failure, such as dyspnea, tachypnea, tachycardia, crackles, neck vein distention, edema, and weight gain.
❑ Provide reassurance by teaching the patient and his family about this disease and the need for prolonged treatment. Tell them to watch closely for fever, anorexia, and other signs of relapse about 2 weeks after treatment stops. Suggest quiet diversionary activities to prevent excessive physical exertion.
❑ Make sure a susceptible patient understands the need for prophylactic antibiotics before, during, and after dental work, childbirth, and genitourinary, GI, or gynecologic procedures.
❑ Teach the patient how to recognize symptoms of endocarditis, and tell him to notify the physician immediately if they occur.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
More About Pericarditis
More Medical Textbooks Online about Pericarditis
Review other book chapters online related to Pericarditis:
Medical Books Excerpts
- Myocarditis
- "Professional Guide to Diseases (Eighth Edition)" (2005)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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» Next page: Myocarditis (Handbook of Diseases)
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