Prevention of Infective Endocarditis: Revised Guidelines from the American Heart Association and the Implications for Dentists

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Prevention of Infective Endocarditis: Revised Guidelines from the American Heart Association and the Implications for Dentists Clinical P RACTIC E Prevention of Infective Endocarditis: Revised Guidelines from the American Heart Association and the Implications for Dentists Contact Author David K. Lam, DDS; Ahmed Jan, DDS; George K.B. Sándor, MD, DDS, PhD, FRCD(C), FRCSC, FACS; Dr. Sándor Email: george.sandor@ Cameron M.L. Clokie, DDS, PhD, FRCD(C) utoronto.ca ABSTRACT Infective endocarditis is a rare but life-threatening microbial infection of the heart valves or endocardium, most often related to congenital or acquired cardiac defects. The American Heart Association (AHA) recently updated its recommendations on prophylaxis during dental procedures. The revisions will have a profound impact on both the patient and the dental practitioner. The purpose of this paper is to review the pathogenesis and clinical presentation of infective endocarditis and discuss the 2007 AHA guidelines and their implications for dentists. For citation purposes, the electronic version is the definitive version of this article: www.cda-adc.ca/jcda/vol-74/issue-5/449.html nfective endocarditis is an uncommon but American Dental Association, the Infectious potentially life-threatening microbial in- Diseases Society of America and the American Ifection of the heart valves or endocardium, Academy of Pediatrics, to review input from most often related to congenital or acquired national and international experts on the cardiac defects. High morbidity and mortality disease. The recommendations of this group rates remain associated with the infection culminated in the 2007 AHA guidelines on despite advances in diagnosis, antimicrobial prophylaxis for infective endocarditis, which therapy, surgical techniques and manage- will have a profound impact on both patients ment of associated complications. Since the and dental practitioners. American Heart Association (AHA) pro- The purpose of this paper is to review duced guidelines on the prevention of in- the pathogenesis and clinical presentation of fective endocarditis in 1997,1 many groups infective endocarditis and discuss the new have questioned the efficacy of antimicrobial guidelines on prophylaxis and their implica- prophylaxis in patients who undergo dental tions for dentists. procedures and have suggested that this rec- ommendation be revised.2–6 Pathogenesis of Infective Endocarditis The AHA appointed a writing group, in- Turbulent blood flow produced by certain cluding experts in the prevention and treat- types of congenital or acquired heart disease ment of infective endocarditis from the may traumatize the endothelium and result JCDA • www.cda-adc.ca/jcda • June 2008, Vol. 74, No. 5 • 449 ––– Sándor ––– Table 1 Diagnosis of infective endocarditis7 sites.6 Mediators of bacterial adherence serve as virulence Major criteria factors in the pathogenesis of infective endocarditis. Some streptococci in the viridans group contain a lipoprotein Positive blood culture receptor antigen I (LraI) that acts as a major adhesin Echocardiogram evidence of endocardial involvement to the fibrin platelet matrix of nonbacterial thrombotic New valvular regurgitation endocarditis.6,9 Minor criteria Predisposing heart condition Microbial Proliferation within a Vegetation Intravenous drug use Once attached to an anatomic focus, these microor- Fever ganisms stimulate further deposition of fibrin and plate- lets on their surface. Thus buried, the microorganisms Vascular phenomena (emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, Janeway can multiply rapidly, apparently uninhibited by host de- 6 lesions) fenses. More than 90% of the microorganisms in mature Immunologic phenomena (glomerulonephritis, Osler’s valvular vegetations are unresponsive to antibiotics as 6,10 nodes, Roth’s spots, rheumatoid factor) they are metabolically inactive. Isolated blood culture or serologic evidence of active Thus, infective endocarditis arises from complex infection interactions between the bloodstream microbial patho- Echocardiogram findings consistent with endocarditis gen and the matrix molecules and platelets at sites of but not diagnostic of the disease endocardial cell damage. Clinical Presentation of Infective Endocarditis Signs and Symptoms in the deposition of platelets and fibrin on the damaged The classic symptoms of infective endocarditis include endocardium or endothelial surface. This may result in fever, anemia, positive blood cultures and heart murmur.7 the formation of sterile vegetations, a condition known as However, diagnosis must always involve a high level of 6,7 nonbacterial thrombotic endocarditis. Invasion of the clinical suspicion, as these classic findings may not al- bloodstream by microbes that can colonize this damaged ways be present (Table 1). Other symptoms may include site may result in infective endocarditis. fatigue, weight loss, night sweats, anorexia and arth- ralgia. Emboli may result in chest pain, abdominal pain, Odontogenic Sources of Transient Bacteremia blindness, paralysis and hematuria. Petechiae may occur In 1909, Horder discovered an association between on skin or mucosal tissues and linear hemorrhages may dental health and infective endocarditis, when he noted be visible under the nails. Osler’s (subcutaneous) nodes, that “infection is grafted upon a previously sclerosed endocardium... the source of the infecting agent, in most Janeway lesions (flat, nontender, red spots on palms and of the cases, is the mouth.”8 Oral mucosal surfaces are soles that blanch on pressure) and retinal hemorrhages populated by a dense endogenous microflora. Trauma to may also be noted. these surfaces, particularly the gingival crevice around Laboratory Findings teeth, releases these microbial species transiently into the • Leukocytosis with neutrophilia bloodstream. • Increased erythrocyte sedimentation rate Transient bacteremia caused by the viridans group • Positive C-reactive protein of streptococci and other oral microflora commonly oc- • Increased levels of serum immunoglobulins curs during dental extractions, other procedures and • Blood cultures positive for pathogen even during routine daily activities.6,7 The frequency and intensity of the resulting bacteremias is related to the • Positive rheumatoid factor nature and magnitude of the tissue trauma, the density Electrocardiogram Findings of microbial flora and the degree of inflammation or • Prolonged PR interval (caused by abscess) infection at the trauma site. The species entering the • Silent myocardial infarction (caused by emboli in bloodstream depends on the endogenous microflora that coronary artery) colonize the traumatized site. Echocardiography Microbial Adherence • Vegetations The focus of infection is determined by the ability of • Valvular perforations various microbial species to adhere to specific anatomic • Other abnormalities (e.g., abscesses, pericarditis) 450 JCDA • www.cda-adc.ca/jcda • June 2008, Vol. 74, No. 5 • ––– Infective Endocarditis ––– Box 1 Cardiac conditions with the highest risk of adverse important than prophylactic antibiotics for a dental pro- outcome from infective endocarditis and for which cedure in reducing the risk of infective endocarditis. prophylactic dental procedures are recommended6 Revised AHA Guidelines on Prophylaxis for Infective • Prosthetic cardiac valve Endocarditis • Previous infective endocarditis In its 2007 guidelines,6 the AHA concluded that • Congenital heart diseasea bacteremia resulting from daily activities is much more - Unrepaired cyanotic congenital heart disease, likely to cause infective endocarditis than bacteremia including palliative shunts and conduits associated with a dental procedure. Moreover, they con- - Completely repaired congenital heart defect with cluded that only an extremely small number of cases of prosthetic material or device, whether placed by infective endocarditis might be prevented by antibiotic surgery or by catheter intervention, during the prophylaxis even if prophylaxis is 100% effective. Thus, b first 6 months after the procedure antibiotic prophylaxis is not recommended based solely - Repaired congenital heart disease with residual on an increased lifetime risk of acquisition of infective defects at the site or adjacent to the site of a pros- endocarditis. thetic patch or prosthetic device (which inhibit As a result, the revised guidelines were greatly simpli- endothelialization) fied. The major changes include the following: infective • Cardiac transplantation with subsequent cardiac endocarditis prophylaxis for dental procedures is recom- valvulopathy mended only for patients with underlying cardiac condi- aExcept for the conditions listed here, antibiotic prophylaxis is no longer recom- tions associated with the highest risk of adverse outcome mended for any other form of congenital heart disease. from infective endocarditis (Box 1). Antibiotic prophyl- bProphylaxis is recommended because endothelialization of prosthetic material occurs within 6 months after the procedure. axis is no longer recommended for those with any other form of congenital heart disease. Prophylaxis is recommended for all dental procedures that involve manipulation of gingival tissue or the peri- Prophylaxis for Infective Endocarditis during apical region of teeth or perforation of the oral mucosa Dental Procedures only for patients at highest risk of adverse outcome from Rationale for Prophylaxis infective endocarditis (Box 1). Prophylaxis is no longer The 1997 AHA guidelines1 recommended antimi- needed for routine anesthetic injections through non- crobial prophylaxis to prevent
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