Antibiotic Prophylaxis Disputed for Infective Endocarditis
By Barbara A. Biedrzycki, RN, MSN, AOCN, CRNP
Summary—Experts estimate that 4000 to 15,000 new cases of infective endocarditis (see definitions, p. 10) occur annually in the United States. Bacteremias result from many etiologies, including dental or surgical procedures. Prevention is critical to this relatively uncommon yet deadly disease, and it has been the rationale for antibiotic prophylaxis for four decades. Through the examination of epidemiological and outcomes measurement data, researchers conclude that the relatively low incidence of endocarditis and the lack of data supporting the efficacy of prophylactic antibiotic use call for reconsideration of existing policies recommending antibiotic prophylaxis.1 Although prophylaxis was examined in dental patients, the implication applies to patients preparing for any type of surgery.
Infective endocarditis is not a reportable disease, and the incidence rate cannot be accurately determined; however, based on data from developed countries, it is estimated that 4000 to 15,000 new cases occur in the United States each year. Bacteremias may occur during dental and surgical procedures, and the current standard regimen for prophylactic antibiotics to prevent infective endocarditis in susceptible patients is amoxicillin 2 g orally one hour before the procedure.2 A study reported in Annals of Internal Medicine suggests that clinicians and practitioners may want to take another look at practice standards and protocols.
Study subjects were recruited over a 27-month period from a population-based network of 54 hospitals in eight counties in the Philadelphia metropolitan statistical area and the county of New Castle, DE. Patients with the diagnosis of infective endocarditis were identified by hospital staff and invited to participate in a study to explore the dental and cardiac risks for infective endocarditis focusing on the indications for antibiotic prophylaxis.1
Risk of Infective Endocarditis
Individuals at greatest risk of infective endocarditis include:
• those with pre-existing heart disease, including the relatively high risk associated with prosthetic heart valves, previous infective endocarditis, cyanotic congenital heart disease, aortic valve disease, mitral regurgitation, mitral regurgitation and stenosis, patent ductus arteriosus, ventricular septal defect, and coarctation of the aorta;
• the elderly, possibly related to underlying degenerative or calcified valve lesions;
• intravenous drug users who might inject bacteria directly or have secondary infections from the skin flora or local infected injection sites. More than 50% of drug-related endocarditis is caused by a strain of Staphylococcus aureus from the drug users’ skin or mucosal bacterial flora;
• post-cardiac surgery patients, especially those with valve replacements (while S. epidermis infections usually occur from inoculation during or immediately after surgery, streptococci may infect the prosthesis at any time, unrelated to surgery);
• and patients on hemodialysis who have an increased risk due to their arteriovenous shunts, which serve as a ready portal of entry for bacteremias. Two to 6% of patients receiving long-term hemodialysis develop endocarditis, and they have a high mortality rate of 53%.2
After obtaining informed consents from both the case patient and the physician, the study proceeded by securing medical records to identify echocardiographic and microbiology reports. Three of the researchers reviewed this information to determine whether the data supported a case of infective endocarditis. Concurrence by at least two of the three researchers determined the inclusion of a case. There was agreement on 379 cases.1
Study controls were enrolled through the Wakesberg random-digit dialing method. Excluding those younger than 18, intravenous drug users, and those who developed endocarditis in the hospital, case and controls were matched for age, sex, and neighborhood of residence. Ninety-two cases were excluded: 65 for intravenous drug use and 27 for nosocomial infection. Ninety-five percent of the remaining 287 cases completed a structured telephone interview to elicit data, including:
• demographic characteristics;
• diagnostic and therapeutic medical and dental procedures in the year before the study date;
• potential host risk factors, including pre-existing cardiac lesions, pre-existing local infections, risk factors for oral and dental disease, diabetes mellitus, immune deficiencies, family history of endocarditis, alcoholism, malignant conditions, and autoimmune disease;
• previous antibiotic use;
• and other recent illnesses.
Medical and dental records were requested (1,381), and 92% (1,265) were reviewed to validate procedures and diagnoses. Major study variables included:
• dental flora infection—if organism was viridans streptococci, nutritionally variant streptococci, Actinobacillus species, Cardiobacterium hominis, anerobes, alpha-hemolytic streptococci (not group D), unspecified streptococci, or Haemophilus, Eikenella, Kingella, or Neisseria species;
• any valvular heart abnormality—mitral valve prolapse, congenital heart disease, history of rheumatic fever with heart involvement, prosthetic heart valve, previous episode of endocarditis, or other heart disease;
• and dental treatments—both invasive (dental hygiene, extractions, periodontal treatment, endodontic treatment, mouth or gingival surgery, treatment of tooth abscess) and noninvasive (simple restorations, prosthetic and restorative dentistry, fluoride treatments).1
Case and control patients were similar in age, sex, ethnicity, education, occupation, and dental insurance status. No significant relationship was found in these demographic data variables. A significant relationship (P=0.001) did exist with case patients whose care was paid for by a government program in which:
• 272 (95%) had multiple positive blood cultures;
• and 12 of 15 cases with negative blood cultures received antibiotic prior to obtaining blood cultures.
Among case and control patients with cardiac valvular abnormalities, researchers found no statistically significant increased risk from dental procedures when infected with dental flora (P > 0.3) or effect from prophylaxis antibiotics (P > 0.2).
The only significant relationship identified among dental procedures and endocarditis was tooth extraction two months prior to hospital admission (P = 0.03). This variable could not be included in the full model study because there was an inadequate sample with only six case patients and no controls having a tooth extraction.1 (See table below.)
Implications for Practice
While antibiotic prophylaxis for at-risk patients has been a widely accepted practice for more than four decades, this study challenges its premise. The researchers concluded "only a few cases of infective endocarditis could be prevented by antibiotic prophylaxis for dental procedures even if 100% efficiency was assumed."1
By this strong statement they recommend that policies for antibiotic prophylaxis be reviewed and updated based on this scientific evidence of low incidence and questionable efficacy. The logic of the principles that created the framework for the widely accepted guidelines for antibiotic prophylaxis for dental procedures is upturned by research documenting outcomes.
It is generally accepted that dental procedures have the potential to induce bacteremia. It is known that endocarditis has high morbidity and mortality rates and that prophylactic antibiotics prevent endocarditis in animal experiments. In addition, some express concern that malpractice claims may be propagated when there is a failure to give prophylactic antibiotics.3
Now there is scientific epidemiologic and outcomes measurement data on which to base future practice. The benefits of reducing overuse of prophylactic antibiotics are plentiful, including decreased risk for adverse reactions such as anaphylaxis, fewer side effects, lower cost, and less potential for drug-resistant organisms.3
Already researchers note viridans streptococci, the most frequent bacterial organism inducing infective endocarditis, have become more resistant.4 This research may stimulate questions about the scientific basis of other widely accepted guidelines and tenets of medical practice. Advanced practice nurses need to realize that guidelines are just that: principles by which to determine a course of action. Guidelines are not necessarily a standard of care, nor do they provide a substitute for clinical judgment.
Practitioners need to look beyond the words of the guidelines, to their scientific foundation, and then add intrinsic, holistic nursing framework to plan and provide the best possible care and treatment.
1. Strom BL, Abrutyn E, Berlin JA. Dental and cardiac risk factors for infective endocarditis. Ann Int Med 1998;129:761-769.
2. Durack D. 1998. Infective Endocarditis. In: Alexander RW, Schlant RC, Fuster V, eds. Hurst’s The Heart. New York City: McGraw-Hill; 1998:2205-2237.
3. Durack DT. Antibiotics for prevention of endocarditis during dentistry: Time to scale back? (editorial). Ann Int Med 1998;129:829-831.
4. Doern GV, Ferraro MJ, Brueggemann AB, et al. Emergence of high rates of antimicrobial resistance among viridans group streptococci in the United Sates. Antimicrob Agents Chemother 1996;40:891-894.