Bacterial endocarditis is a relatively
uncommon, life-threatening
infection of the
endothelial surface of the
heart, including the heart
valves. Despite advances in antimicrobial
therapy and the diagnosis and treatment
of complications, bacterial endocarditis
continues to be responsible for substantial
morbidity and mortality.
While anyone can contract endocarditis,
the infection usually develops in individuals
with underlying structural cardiac
defects. It can occur whenever these persons
develop bacteremia with the organisms
likely to cause endocarditis. Bacteremia
may occur spontaneously (i.e.,
caused by organisms introduced through
food chewing or tooth brushing), or it
may develop as a complication of a focal
infection, such as a periodontal or periapical
infection, a urinary tract infection,
pneumonia or cellulitis. Selected surgical
and dental procedures and instrumentations,
especially those involving mucosal
surfaces or contaminated tissue, can cause
a transient bacteremia that rarely persists
for more than a few minutes.
For endocarditis to develop, two independent
events are normally required: an
area of endothelium must be damaged, and
a bacteremia caused by adherent organisms
must occur. If endothelium is damaged but
a bacteremia does not occur, bacterial
endocarditis will not develop. Conversely, if
a bacteremia occurs, normal undamaged
heart endothelium is not conducive to bacterial
colonization. In congenital or
acquired cardiac lesions, endothelium can
be damaged by an abnormally high-velocity
jet-stream--like flow that results in turbulent,
rather than laminar, blood flow.
A model was developed to delineate the
hemodynamic mechanisms for the development
of endocarditis.[1] This model
showed that endothelial damage and bacterial
deposition occur in the low-pressure
area immediately distal to an obstruction,
such as coarctation of the aorta, a regurgitant
mitral or aortic valve, or a ventricular
septal defect. Thus, endothelium on the
ventricular side of a regurgitant aortic
valve would be damaged, and the right
ventricular wall (or right heart valves)
would be damaged from the jet-stream--like
blood flow created by a ventricular
septal defect. Endothelium can also be damaged
by direct trauma caused by a device (e.g.,
an indwelling cardiac catheter) or by intracardiac
surgery.
Trauma to the endothelium of a cardiac
valve or to the endocardium can induce thrombogenesis
(deposition of fibrin and platelets),
which leads to a nonbacterial, thrombotic
endocardial lesion. This lesion is more susceptible
to bacterial colonization than is normal,
undamaged endothelium.
Although bacteremia is a frequent problem
after many invasive procedures, only certain bacteria
commonly cause endocarditis. Vegetation
can develop following a bacteremia with one of
these organisms. This vegetation is composed of
fibrin, platelets, red blood cells, a few white blood
cells and the infecting microorganisms.
The incidence of endocarditis following
most procedures is low in patients with underlying
cardiac disease. According to the
American Heart Association (AHA),[2] a reasonable
approach to endocarditis prophylaxis
should consider the following points:
1. The degree to which the patient's underlying
condition creates a risk of endocarditis.
2. The apparent risk of bacteremia with the
procedure.
3. The potential adverse effects of the prophylactic
antimicrobial agent to be used.
4. The cost-benefit aspects of the recommended
prophylactic regimen.
It is not always possible to predict which
patients will develop bacterial endocarditis and
which procedure will be responsible. In fact,
most cases of endocarditis are not attributable
to a specific invasive procedure. Nonetheless,
certain bacteria are known to be associated
with endocarditis in at-risk patients. Consequently,
recommendations for the prevention
of endocarditis have been issued by various
organizations throughout the world. The AHA
developed the recommendations that are most
widely followed in the United States. These
recently revised guidelines serve as a point of
reference for the discussion in this article.[2]
The AHA recommendations are designed to
assist in the rational use of prophylaxis for the
prevention of bacterial endocarditis. The
guidelines take into account both the patient's
underlying cardiac condition and the risk of an
endocarditis-producing bacteremia during a
surgical or dental procedure. The recommendations
are not intended to be the standard of
care for all patients or to serve as a substitute
for clinical judgment. Physicians and dentists
must use their own judgment in selecting an
antibiotic and determining the number of
doses that are to be administered in individual
patients or in special circumstances.
Even with appropriate antibiotic prophylaxis,
endocarditis may occur. Consequently,
physicians and dentists should maintain a high
index of suspicion regarding any unusual clinical
events that occur following procedures in
which antibiotic prophylaxis was administered.
Particular attention should be given to unexplained
fever, night chills, weakness, myalgia,
arthralgia, lethargy or malaise in a patient who
has had a dental or surgical procedure.
Cardiac Conditions and Endocarditis Prophylaxis
Endocarditis is associated with some cardiac
conditions more often than with others.[3]
Furthermore, when enclocarditis develops in
patients with underlying cardiac conditions,
disease severity and ensuing morbidity can be
variable. Thus, endocarditis prophylaxis is recommended
for use in patients who are at
higher risk for endocarditis than persons in
the general population. Prophylaxis is particularly
important for patients in whom endocardial
infection would be most likely to cause
severe morbidity or even mortality.
Cardiac conditions for which prophylaxis is
or is not recommended are listed in Table 1.[2]
These conditions are stratified into high-,
moderate- and negligible-risk categories
based primarily on the potential outcome if
enclocarditis occurs. The negligible-risk category
includes cardiac conditions in which
endocarditis develops no more often than in
the general population.
Consequently, they are listed in the moderate-risk
category. On the other hand, patients in
whom regurgitation has not been documented
are at no higher risk for endocarditis than persons
in the general population and therefore
do not need prophylaxis.
A detailed discussion of the pathophysiology
of mitral valve prolapse is found in the AHA
guidelines.[2] A clinical approach to determining
the need for endocarditis prophylaxis in the
patient with suspected mitral valve prolapse is
presented in Figure 1.[2] Details about the role of
echocardiography in the diagnosis of mitral
valve prolapse are provided elsewhere.[13]
[Figure 1 ILLUSTRATION OMITTED]
Although endocarditis can occur in anyone,
including persons with no underlying cardiac
defects, the negligible-risk category includes
cardiac conditions in which the risk of endocarditis
is no higher than in the general population.
Patients with these cardiac conditions
do not require endocarditis prophylaxis.
Procedures That Can Cause Bacteremia
Bacteremias commonly occur during activities
of daily living, such as routine tooth
brushing or food chewing. With respect to
endocarditis prophylaxis, significant bacteremias
are caused only by the organisms
commonly associated with endocarditis and
attributable to identifiable procedures.
Prophylaxis is recommended for procedures
that are known to induce significant bacteremias
with the organisms commonly associated
with endocarditis and attributable to
identifiable procedures. Invasive procedures
performed through surgically scrubbed skin
are not likely to produce such bacteremias.
Dental and Oral Procedures
Both the incidence and the magnitude of
bacteremias of oral origin are proportional to
the degree of oral inflammation and infection.[14,15]
Therefore, it is important that patients
at risk for endocarditis maintain good
oral health to reduce potential sources of bacterial
seeding. Oral maintenance includes regular
brushing (with manual or powered
toothbrushes) and flossing at home, as well as
regular visits to the dentist. Some authorities
recommend the use of an antiseptic mouth
rinse, such as chlorhexidine (Peridex) or povidone-iodine
(Betadine), immediately before
dental procedures to help reduce the incidence
and magnitude of bacteremia.[2,14]
Dental and oral procedures for which anti-microbial
prophylaxis is or is not recommended
are listed in Table 2.[2] In general, prophylaxis
is recommended for procedures
associated with significant bleeding from hard
or soft tissues, including periodontal surgery,
scaling and professional teeth cleaning. Prophylaxis
is also recommended for tonsillectomy
or adenoidectomy. Antimicrobial prophylaxis
is not recommended for procedures in which
significant bleeding is not anticipated.
or removal of an intrauterine device, and
prophylaxis may be warranted.
Recommended Prophylactic Regimens
Prophylactic regimens are directed at the
organisms most likely to result in bacteremia
during a procedure. Enclocarditis prophylaxis
is most effective when an antibiotic is given
perioperatively in a dose sufficient to ensure
an adequate serum concentration of the drug
during and after the procedure. To reduce the
likelihood of microbial resistance, prophylactic
antibiotic therapy should be used only during
the perioperative period.
The antimicrobial regimens listed in Table 4[2]
are designed to be initiated shortly (hours to
days) before a procedure. A follow-up dose is
recommended in only a few situations.
Table 4
Endocarditis Prophylactic Regiments for Dental, Oral,
Respiratory Tract and Esophageal Procedure
Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P,
et al. Prevention of bacterial endocarditis.
Recommendations by the American Heart Association.
JAMA 1997;277:1794-801.
The Council on Scientific Affairs of the American
Dental Association has approved the American
Heart Association guidelines as they relate to
dentistry. The American Society for Gastrointestinal
Endoscopy has approved the guidelines as they
relate to gastroenterology.
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KATHRYN A. TAUBERT, PH.D., is senior scientist in the Department of Science
and Medicine at the American Heart Association, Dallas, as well as adjunct
associate professor of physiology at the University of Texas Southwestern
Medical School, also in Dallas. Dr. Taulbert received her doctorate in medical
physiology from the University of Texas Southwestern Medical School and
completed a postdoctoral fellowship in the Department of Cardiology at Dallas
Veterans Affairs Hospital.
ADNAN S. DAJANI, M.D., is professor of pediatrics at Wayne State University
School of Medicine, Detroit, where he is also director of infectious disease
at Children's Hospital of Michigan. Dr. Dajani received his medical degree
from the American University of Beirut, Lebanon. He completed a residency in
pediatrics at Case Western Reserve University, Cleveland, and a fellowship in
pediatric infectious diseases at the University of North Carolina, Chapel Hill.
Address correspondence to Kathryn A. Taubert, Ph.D., Department of Science
and Medicine, American Heart Association, 7272 Greenville Ave., Dallas, TX
75231. Reprints are not available from the authors.
COPYRIGHT 1998 American Academy of Family Physicians
COPYRIGHT 2000 Gale Group