Infective Endocarditis
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[edit] Infective Endocarditis
Burke A. Cunha
Diane H. Johnson
Natalie C. Klein
[edit] EPIDEMIOLOGY AND ETIOLOGY
Infective endocarditis (IE) is defined as an infection of the valvular and nonvalvular endothelial surfaces of the heart. Although most frequently caused by bacteria, other microorganisms such as fungi, rickettsiae, mycoplasmas, or chlamydiae may also cause endocarditis.
Endocarditis is classified as acute or subacute depending on the clinical course of the untreated illness. Subacute bacterial endocarditis (SBE) usually occurs on previously damaged valves, and is due to relatively avirulent organisms (e.g., viridans streptococci). The course of illness is indolent and characterized by night sweats, fevers, and malaise. Acute bacterial endocarditis (ABE) occurs on normal and damaged heart valves and also in association with intravenous drug use or intravascular catheters or devices. ABE is caused by virulent microorganisms such as Staphylococcus aureus, Streptococcus pneumoniae, or Pseudomonas aeruginosa. The clinical course is fulminant with rapid valvular destruction and a high incidence of metastatic disease. IE should be viewed as subacute or acute. This clinical classification explains difference in signs, symptoms, laboratory abnormalities, and differing pathogens associated with SBE vs. ABE. Isolation of the organism in culture-positive endocarditis serves as a guide for antimicrobial therapy[1][2][3] (Box 69-1).
| Box 69-1 - Culture-positive and Culture-negative Endocarditis |
Culture-positive
|
[edit] PATHOPHYSIOLOGY
The left side of the heart is more frequently involved in infection, with the mitral valve affected more frequently than the aortic valve. Rheumatic heart disease, congenital heart disease (e.g., bicuspid valves, ventricular septal defects, coarctation of the aorta), and degenerative disease such as calcific aortic stenosis all predispose a person to the development of IE.[4][5]
After the endothelial surface of the valve or cardiac structure is damaged by high velocity or turbulent blood flow, a sterile platelet or fibrin clot is formed that results in marantic or nonbacterial thrombotic endocarditis. When a transient bacteremia occurs, the platelet or fibrin thrombus may become colonized. As the bacteria multiply, there is further disposition of fibrin and platelets that protect the pathogens from the host defenses. Portions of this vegetation may break off and embolize systemically. The valve may be damaged or destroyed, and the endocardium can be invaded by myocardial abscesses, resulting in the development of heart block or dysrhythmias.[4][6]
[edit] CLINICAL MANIFESTATIONS
The classic signs and symptoms of SBE are fever, anemia, splenomegaly, a cardiac murmur, and embolic phenomena. The clinical manifestations of IE depend on whether the patient has SBE or ABE.
The history of valvular disease, recent medical or dental procedures, infections, or intravenous drug abuse (IVDA) is important to obtain. The source of viridans streptococcal SBE is usually the mouth. The symptoms of SBE typically begin within 2 weeks of the initial bacteremia.[7] Nonspecific symptoms such as fever, weight loss, night sweats, low back pain, arthralgias, or malaise may be present in SBE due to relatively avirulent organisms (e.g., viridans streptococci).
Infection with more virulent pathogens such as S. aureus results in ABE.[4] Fever ≥102° F is the most common physical finding and is present in nearly all patients with ABE. Little or no fever may be due to recent antibiotic use. Fever may also be absent in elderly or debilitated patients, in patients with congestive heart failure or renal failure, or in IVDAs.[1][8] Heart murmurs are present in over 80% of patients, but may be absent in right-sided or mural endocarditis.[9] The physical examination may have findings of congestive heart failure in ABE. Splenomegaly is present in the minority of patients, but is most common in those with SBE.[10] Peripheral manifestations of endocarditis such as petechia or splinter hemorrhages are seen in about 15% of persons with IE. Osler's nodes (tender nodular lesions of the fingers and toes) and Janeway lesions (painless hemorrhagic macules on the palms and soles) are uncommon. Clubbing may occur in ABE secondary to S. aureus, and chronic acute clubbing may complicate SBE. Roth's spots, which are pale, retinal lesions surrounded by hemorrhage, are seen in less than 5%.[11][12] Low back pain, myalgias, and arthralgias are common in patients with IE, but very severe low back pain suggests enterococcal endocarditis. Up to one third of patients may have a monoarticular or polyarticular septic arthritis with ABE. Focal neurologic deficits may occur as a result of systemic septic embolization in ABE or immunologic-mediated bland embolus (aseptic meningitis) in SBE.[13]
Laboratory abnormalities in patients with IE are nonspecific. The majority of patients have a normochromic, normocytic anemia; leukocytosis with a left shift is variably present. The erythrocyte sedimentation rate (ESR) is elevated, and positive Venereal Disease Research Laboratories (VDRL) and elevated rheumatoid factors are often present in SBE. Urinalysis findings in SBE consist of microscopic hematuria or proteinuria.[8][3] Blood cultures are positive in almost all patients with infectious endocarditis. Since the bacteremia is continuous, all cultures should be positive. Blood culture positivity is related to volume of blood cultured by one or more venipunctures from one or more sites. In SBE and ABE, blood cultures should be obtained prior to initiating therapy. The most common reason for negative blood cultures is prior antibiotic use. Infection with fastidious organisms such as the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella) is rare. Legionella species and the nutritionally deficient streptococci may also result in negative cultures. The microbiologist should be alerted and specimens held for at least 3 weeks when a diagnosis of culture-negative IE is suspected.[8] Most patients with low-grade fevers, leukocytosis, and cardiac murmurs with or without vegetations by echocardiography do not have culture-negative endocarditis. Those who do will also have peripheral manifestations.
[edit] DIAGNOSIS
In addition to positive blood cultures with known endocarditis pathogens, echocardiography has been used to support the diagnosis of IE. Two-dimensional transthoracic echocardiography (TTE) has a sensitivity of approximately 50%, and is poor for detecting small vegetations and those on prosthetic valves. The larger the vegetation, the more likely the risk for systemic embolization. Transesophageal echocardiography (TEE) is more sensitive than TTE, but is invasive, not innocuous, and more expensive. TEE can detect small vegetations (<5 mm), perivalvular abscesses, and those on prosthetic valves.[1] Echocardiography of the heart should be obtained on all patients with suspected IE. However, vegetations without positive blood cultures do not signify IE, or even culture-negative IE.[14][15] Echocardiography should be obtained for baseline purposes in case of subsequent hemodynamic deterioration or congestive heart failure (CHF), or to rule out IE. The most common problem is that of interpreting the significance of viridans streptococci in blood cultures. High-grade bacteremia always represents SBE, but low culture positivity (e.g., one of three positive blood cultures for viridans streptococci) is never associated with SBE.
[edit] MANAGEMENT
[edit] Antibiotic Therapy
Empiric antimicrobial therapy is based on the presumptive organism causing infection.[16] Bacteriocidal antibiotics given in endocarditis doses for 4 to 6 weeks sterilize the vegetation. Current recommendations for treatment of IE in Table 69-2 are the consensus of the American Heart Association based on published studies and collective clinical experience of this group of experts.[16] The treatment of ABE is always urgent, but the start of SBE therapy is not time-critical. For native valve SBE, a β-lactam with or without gentamicin for viridans streptococci is appropriate empiric therapy. Nafcillin or vancomycin combined with gentamicin, directed against S. aureus, is adequate empiric therapy for endocarditis in IVDAs.[16] For prosthetic valve endocarditis (PVE), a combination of vancomycin and gentamicin covering Staphylococcus epidermidis and S. aureus is adequate initial therapy. Once the organism is isolated, therapy may need to be changed based on organism or susceptibility testing[16](Tables 69-1 and 69-2). After initiating appropriate therapy, fever should decrease within 72 hours and repeat blood cultures should be sterile.
Table 69-1 Clinical Differentiation of Acute vs. Subacute Endocarditis
| ABE | SBE | |
|---|---|---|
| Symptoms | ||
| Anorexia | − | + |
| Myalgias/arthralgias | + | ± |
| Fatigue | − | + |
| Dyspnea/cough | + | − |
| Pleuritic chest pain/hemoptysis | + | − |
| Lumbar back pain | + | + |
| Weight loss | − | ± |
| Headache | + | ± |
| Mental status changes | + | ± |
| Acute confusional states | + | − |
| Unexplained stroke | − | + |
| Sudden unilateral blindness | − | + |
| Left upper quadrant pain | Splenic abscess | Splenic infarct |
| CVA tenderness (renal abscess) | + | − |
| Signs | ||
| Fever | >102° F | <102° F |
| New heart murmur | ± | − |
| Splenomegaly | − | + |
| Petechiae | + | + |
| Osler's nodes | − | + |
| Janeway lesions | + | − |
| Splinter hemorrhages | ± | + |
| Roth's spots | − | + |
| Congestive heart failure (LVF) | + | − |
| Laboratory Tests | ||
| Anemia | − | + |
| Marked leukocytosis | + | − |
| Microscopic hematuria | ± | + |
| Hematuria, proteinuria, RBC casts | − | + |
| Elevated ESR | ≤50 mm/hr | ≥50 mm/hr |
| Elevated RF titer | − | + |
| Elevated VDRL titer | − | + |
| Circulating immune complexes | − | + |
| Synovial fluid analysis | Septic arthritis | Aseptic arthritis |
| Cerebrospinal fluid (CSF) | Purulent meningitis profile | Aseptic meningitis profile |
| Heart block | + | − |
| Chest x-ray | Pneumonia (septic pulmonary emboli) | − |
| Brain CT/MRI | Positive if cerebritis, microabscesses or hemorrhage (pyogenic arteritis) | Negative unless mycotic aneurysms or embolic CVAs |
| Mycotic aneurysms (abdominal CT/MRI) | − | + |
| +, Commonly present; ±, uncommonly present; −, rarely, if ever, present. | ||
Table 69-2 Suggested Empiric Therapy for Native Valve Endocarditis
| Rights were not granted to include this data in electronic media. Please refer to the printed book. |
Patients with continued fevers for more than 7 days on appropriate antibiotics, or who have persistently positive blood cultures, may have myocardial or metastatic abscesses. The most common sites for septic emboli are the spleen, liver, kidney, and lung, but emboli in the brain, bones or joints, or meninges may also occur. A computed tomography (CT) scan of the abdomen, pelvis and brain, or bone, or indium or gallium scan may be helpful in the diagnosis. Fever that abates after initiation of antibiotics but later recurs is usually due to recurrent septic emboli, noninfectious emboli phenomenon such as splenic infarct, or drug fever.
[edit] Surgical Indications
For most patients, medical therapy with 4 to 6 weeks of antibiotics is curative. However, valvular replacement may be necessary for certain complications: intractable heart failure, recurrent systemic emboli, inability to eradicate infection due to large vegetation or resistant organism, fungal endocarditis, myocardial abscess, or prosthetic valve dysfunction.
[edit] Prophylaxis
Although there are no randomized, controlled human studies to demonstrate that antibiotic prophylaxis prevents endocarditis, the use of prophylactic antibiotics in individuals with underlying cardiac abnormalities undergoing bacteremia-inducing procedures is common practice. Current guidelines from the American Heart Association are not universally agreed on.[17][18] Oral prophylaxis directed against viridans streptococci is now preferred to parenteral regimens (i.e., a single dose of amoxicillin, 2 gm (PO), given 1 hour before dental or upper respiratory tract surgical procedures is recommended for prophylaxis, with no further doses necessary). For the penicillin-allergic patient, a single dose of clindamycin, cephalexin, or azithromycin is an alternative approach.
Prophylactic regimens for gastrointestinal or genitourinary procedures are IV/IM ampicillin and gentamicin for high-risk patients, or amoxicillin alone for moderate-risk patients. These are directed against enterococci, the sole cause of SBE acquired from a source below the waist (Table 69-3).
Table 69-3 Prophylactic Antibiotic Regimens
| Procedure | Antibiotic | Alternative |
|---|---|---|
| Dental, upper respiratory tract, or esophagus | Amoxicillin 2 gm | Clindamycin 600 mg or cephalexin 2 gm or azithromycin 500 mg |
| Gastrointestinal (GI) or genitourinary (GU) | ||
| High risk✢ | Ampicillin 2 gm (IV/IM) plus gentamicin 1.5 mg/kg (IV) within 30 minutes prior to procedure and 6 hours later ampicillin 1 gm (IV) or amoxicillin 1 gm (PO) | Vancomycin 1 gm (IV) slowly over 1 hour and gentamicin 1.5 mg/kg (IM) or slowly (IV) |
| GI or GU | ||
| Moderate risk† | Amoxicillin 2 gm (PO) 1 hr before procedure, or ampicillin 2 gm (IV/IM) within 30 minutes prior to procedure | Vancomycin 1 gm (IV) slowly over 1 hour |
✢Prosthetic valves, previous bacterial endocarditis, complex cyanotic congenital heart disease, surgically constructed systemic pulmonary shunts.
†Other congenital cardiac malformations, acquired valvular dysfunction, hypertrophic cardiomyopathy, mitral valve prolapse with murmur, and/or thickened leaflets.
[edit] REFERENCES
- ↑ 1.0 1.1 1.2 BA Cunha, VM Gill, JM Lazar: Acute infective endocarditis. Infect Dis Clin North Am 1996; 10:811 - 833.
- ↑ SL Harris: Definitions and demographic characteristics. D Kaye Infective endocarditis. ed 2. New York: Raven; 1992:1 - 18.
- ↑ 3.0 3.1 WM Scheld, MA Vande: Endocarditis and intravascular infection. GL Mandell JE Bennett R Dolin Principles and practices of infectious diseases. ed 4. New York: Churchill Livingstone; 1995:740 - 783.
- ↑ 4.0 4.1 4.2 M Korzeniowski, D Kaye: Endocarditis. SL Gorbach JG Bartlett NR Blacklow Infectious diseases. ed 2. Philadelphia: WB Saunders; 1998:663 - 674.
- ↑ LL Pelletier, RG Petersdorf: Infective endocarditis: a review of 125 cases from the University of Washington Hospital 1963-1972. Medicine (Baltimore) 1977; 56:287.
- ↑ PM Sultan, TA Drake, MA Sande: Pathogenesis of endocarditis. Am J Med 1995; 78 (Suppl B):110.
- ↑ L Weinstein, JT Schlessinger: Pathoanatomic pathophysiologic and clinical correlations in endocarditis. N Engl J Med 1974; 291:832 - 836.
- ↑ 8.0 8.1 8.2 D Kaye: Infective endocarditis ed 2. New York: Raven; 1992:
- ↑ GJ Garvey, HC Neu: Infective endocarditis—an evolving disease: a review of endocarditis at the Columbia-Presbyterian Medical Center 1968-1973. Medicine 1978; 57:105 - 127.
- ↑ MS Terpenning, BP Buggy, CA Kaufman: Infective endocarditis: clinical features in young and elderly patients. Am J Med 1987; 83:626 - 634.
- ↑ LM Bush, CC Johnson: Clinical syndrome and diagnosis. D Kaye Infective endocarditis. ed 2. New York: Raven; 1992:99 - 113.
- ↑ L Weinstein, J Brusch: Clinical manifestations of native valve endocarditis. L Weinstein J Brusch Infective endocarditis. New York: Oxford; 1996:
- ↑ PE Hermans: The clinical manifestations of infective endocarditis. Mayo Clin Proc 1982; 57:15.
- ↑ DT Durack, AS Lukes, DR Bright,et al.: New criteria for the diagnosis of infective endocarditis. Am J Med 1994; 96:200 - 209.
- ↑ AS Lukes, DR Bright, DT Durack: Diagnosis of infective endocarditis. Infect Dis Clin North Am 1993; 7:1 - 9.
- ↑ 16.0 16.1 16.2 16.3 WR Wilson, AW Karchmer, AS Dajani,et al.: Antibiotic treatment of adults with infective endocarditis due to streptococci, enterococci, staphylococci and HACEK microorganisms. JAMA 1995; 274:1706 - 1713.
- ↑ AS Dajani, KA Taubert, W Wilson,et al.: Prevention of bacterial endocarditis: recommendations by the American Heart Association. JAMA 1997; 277:1794 - 1801.
- ↑ DT Durack: Antibiotics for prevention of endocarditis during dentistry: time to scale back?. Ann Intern Med 1998; 129:829 - 831.
