Printer Friendly

Prevention of infective endocarditis in the pediatric congenital heart population.

Infective endocarditis (IE) or subacute bacteria] endocarditis (SBE) is a major area of concern for the child with a congenital heart defect (CHD). IE constitutes less than 0.2% to 0.5% of all pediatric admissions, yet it remains an important cause of morbidity and mortality (about 10%) in children with cardiac malformation (Curran, Moulton, & Mavroudis, 1994; Dajani, 1993; Newberger, 1992). Although a relatively rare problem considering the number of patients at risk, IE continues to have a disproportionate influence on clinical practice and is one of the most feared complications of structural heart disease (Kaplan & Shulman, 1989).

Nurses working with the pediatric congenital heart population need to remain diligent by giving high priority to infective endocarditis discharge teaching in both the pre and post repair congenital heart patient. Knowing the information children and families need and understanding the updated recommendations from the American Heart Association (Dajani et al., 1997) can enable nurses to improve quality of patient education in children requiring endocarditis prophylaxis.


Infective endocarditis (IE) is an inflammatory process of valve, endocardium, or endothelium, resulting from infection from a bacterial or fungal agent, occurring almost exclusively in individuals with pre-existing anatomic abnormalities of the cardiovascular system (Curran et al., 1994; Dajani, 1993; Hazinski, 1992; Newberger, 1992). At one time, convention dictated that IE be classified as acute or subacute. Although many clinicians continue to use this terminology, classifying the disease based upon the microorganisms involved is more meaningful. For example, A-hemolytic streptococci almost always causes a prolonged subacute form of the illness; staphylococcus aureus, streptococcus pneumonlae, or B-Hemolytic streptococci are usually associated with a more virulent or "acute" clinical illness (Kaplan & Shulman, 1989). Because the newer classification is based on microbiologic etiology rather than description, a general term of HE is the more widely accepted term today (Friedman & Stark, 1990).


The incidence of IE in children ranges from 0.22 to 0.78 cases per 1000/year hospital admissions and appears to be rising (Dajani, 1993). Over the past two decades, the incidence of IE has gradually increased principally due to improvements in congenital heart surgery, the patient population at greatest risk for developing the disease (Curran et al., 1994; Dajani, 1993; Kaplan & Shulman, 1989; Newberger, 1992). However, it must also be noted that the use of indwelling catheters, immunosuppression medications, improved care of critically ill neonates, and widespread IV drug abuse among older children have led to an increase in the incidence of IE in structurally normal hearts (Curran et al., 1994; Wells, 1989).

Reported mortality rates for IE have decreased significantly from the pre-antibiotic era rate of virtually 100% to the 20% rate today (Curran et al., 1994; Dajani, 1993). But the ultimate consequences, including morbidity and mortality, which are principally related to the complications of the infection (Curran et al., 1994), and the expenses associated with prolonged and often intense medical and surgical therapy, remain formidable (Kaplan & Shulman, 1989).

Although the incidence of HE varies with specific cardiac lesions, virtually any congenital heart defect may predispose a child to develop IE (Dajani, 1993; Friedman & Stark, 1990; Newberger, 1992). The children at highest risk are those with cyanotic heart disease (e.g., tetralogy of Fallot, pulmonary atresia [PA], tricuspid atresia [TA]), ventricular septal defect [VSD] with aortic regurgitation or obstruction, aortic stenosis [AS], patent ductus arteriosus [PDA], and coarctation, as well as children with prosthetic heart valves, systemic-pulmonary shunts, and those who have recently undergone cardiac surgery (Kaplan & Shulman, 1989; Curran et al., 1994; Newberger, 1992).

Clinicians recognize that endocarditis can affect children of all ages with underlying cardiovascular disease. Although relatively uncommon, IE can occur in infants and young children, but most cases appear to occur among older children. An extensive review of the literature in the pediatric age group revealed that almost half of the children with endocarditis were 10 years of age or older (Curran et al., 1994; Kaplan & Shulman, 1989).

Reports in the literature indicate a wide disparity regarding IE in children. Most large studies are retrospective and do not report the total number of admissions to institutions during study periods. Studies conducted from 1952-1982 by various children's hospitals in North America found large discrepancies in the numbers of children admitted for IE (Friedman & Stark, 1990). Much has been written about the epidemiology of IE, yet documentation of epidemiologic trends has been somewhat imprecise. This has been related to two deficiencies: (a) the lack of adequate data about the size and specific characteristics of the population at risk, and (b) the lack of conclusive documentation of the diagnosis. Furthermore, because relatively few cases are seen in any one institution, many authors have combined their clinical experience over several decades. This frequently has resulted in obscuring epidemiologic trends (Kaplan & Shulman, 1989).

In reviewing the following studies, the reported overall risk in the congenital heart population for developing IE ranges from 0.9%-9.7%. Shah, Singh, Rose, and Keith (1966) determined the lifetime risk of developing IE in an unrepaired simple VSD was 12%-13%. Steeg, Marmer, Varmer, and Blumenthal (1970) found the risk was 3.2% over the first decade of life. In a large cooperative study on the natural history of VSD, AS, and pulmonary stenosis (PS), Gersony and Hayes (1977) reported a risk of 9.7% of patients developing IE by the age of 30. However, if the patient underwent surgical repair, the incidence was much lower, except in patients with AS in which the risk slightly increased to 1.4% (Friedman & Stark, 1990).

In a study of 266 children, tetralogy of Fallot accounted for the largest percentage of patients with CHD who developed IE (Kaplan, 1977). Similar findings are reported in studies from South Africa (Rose, 1978), New York City (Blumenthal, Griffiths, & Morgan, 1960), and France (Bayer, 1982). VSD was the second most common lesion, accounting for 16% of the group, followed by AS (8%), PDA (7%), and TGA (4%) ((Friedman & Stark, 1990). However, other studies reported that VSD (Yokochi, Sakamoto, Mikajima, & Ichinose, 1986; Johnson & Rhodes, 1982) and aortic valve disease (Auger, Marquis, Dyrda, & Martineau, 1981) were more common pre-disposing factors. The most common lesions found in patients with CHD who developed IE after surgery were tetralogy of Fallot and transposition of the great arteries (TGA) with PS (repaired with a systemic-pulmonary shunt) (Curran et al., 1994; Friedman & Stark, 1990).

A smaller study from Yale-New Haven hospitals found a higher incidence of IE in patients with CHD who had not undergone surgery than in those who had (Stanton, Baltimore, & Clemens, 1984). Acyanotic lesions were more common in the nonsurgery group; cyanotic lesions predated in the postoperative group. Dacron[R] patches and Gore-Tex[R] were more common sites of infection than prosthetic valves (Friedman & Stark, 1990). Commenting on the above studies, Friedman and Stark (1990) suggest that the large differences in findings are due to the complexity of the disease.


In most instances of endocarditis, two pre-existing conditions are present: (a) a congenital lesion of the heart or great vessels, and (b) an infective agent in the blood stream (Dajani, et al., 1990; Kaplan, & Shulman, 1989; Newberger, 1992). Furthermore, certain cardiac conditions are more often associated with endocarditis than others (Dajani et al., 1990). For instance, lesions leading to a high velocity of blood flow through a heart valve, septal defect, or blood vessel are associated with increased susceptibility to endocarditis (Newberger, 1992).

Virtually all vegetations occur in areas where there is a pressure gradient. The pressure gradient causes a hydrodynamic effect, which leads to turbulence against either the vascular endothelium or endocardium and results in tissue damage (Kaplan & Shulman, 1989). Vegetation usually forms on the low pressure side of the defect, where endothelial damage is established by the jet effect of the defect (Friedman & Stark, 1990) The turbulent blood flow results in tissue damage with disposition of platelets, fibrin, and thrombus formation. Circulating bacteria get trapped in this thrombus, becoming the focus of the IE (Curran et al., 1994, Dajani, 1993; Friedman & Stark, 1990: Hazinski, 1992; Newberger, 1992) Growth (if the fibrin and platelet deposition results in the formation of a nonbacterial thrombotic vegetation (NBTV), which Is essential in the pathogenesis endocarditis. Transient bacteria that occurs as a normal part of daily life may cause colonization of the NBTV. As the NBTV grows, adherence of the bacteria occurs and an infected vegetation develops (Friedman & Stark, 1990.)

Transient bacteremias occur frequently in human beings, particularly during surgical or dental procedures and instrumentation involving mucosal surfaces or contaminated tissues (Dajani, 1993). Blood-borne bacteria may lodge on damaged or abnormal heart valves, on the endocardium, or on endothelium near congenital anatomic defects, resulting in IE (Dajani et al., 1990). The ability of microorganisms to adhere to endocardial epithelial cells or to intravascular fibrin-platelet deposits is the critical first step in the development of IE. Those bacteria that most frequently cause IE can be shown experimentally to adhere more readily to normal aortic valve leaflets than do other organisms (Dajani, 1993). Moreover, specific products of these adherent bacteria enhance their ability to colonize the endocardium and fibrinplatelet deposits (Dajani, 1993). Additionally, endocarditis producing streptococci and staphylococci are potent stimulators of platelet aggregation, an action that enhances the formation of vegetation (Dajani, 1993).

Specific dental and surgical procedures are much more likely to initiate a bacteremia that results in IE, with dental procedures constituting the most frequent antecedent event prior to IE (Dajani et al., 1990; Newberger, 1992; Zales & Wright, 1997). Among the most potentially dangerous inducers of bacteremia is extraction of an abscessed tooth and dental cleaning, where a subsequent bacteremia may reach 80%. In one study, 155 strains off bacteria were isolated from 100 patients undergoing extraction or cleaning (Kaplan & Shulman, 1989).

In addition to dental procedures, other surgical procedures followed by bacteremia have been associated with IE. Such procedures include cardiac surgery, tonsillectomy, bronchoscopy, ventriculoatrial shunts for hydrocephalus, urologic surgery, placement of urinary and dialysis catheters, and a very minute percentage of cardiac catheterization (Dajani et al, 1990; Newberger, 1992).

Infectious foci outside the heart may be the origin of bacteremia leading to IE. Among such lesions are infections of the skin (boils), pneumonia, acute pyelonephritis, sinusitis, osteomyelitis, sepsis, burns, and those resulting from IV drug abuse (Newberger, 1992).

Although bacteremia is common following many invasive procedures, only a limited number of bacterial agents cause IE (Dajani et al., 1990). Approximately 80%-90% of reported cases of endocarditis are caused by gram-positive bacteria, principally streptococcus viridans and staphylococcus aureus (Curran et al., 1994; Dajani, 1993; Dajani et al., 1990; Friedman & Stark, 1990; Hazinski, 1992; Kaplan & Shulman, 1989; Newberger, 1992; Zales & Wright, 1997). Although streptococcus is most commonly responsible for IE (Hazinski, 1992), currently in the pediatric age group, staphylococcus aureus now accounts for approximately one fifth of all cases, essentially among patients without preexisting heart disease (Newberger, 1992). However, fungi, chlamydia, rickettsiae, and viruses may also be causative agents of IE in all patients (Dajani, 1993).

Clinical Manifestations/Diagnosis

Clinical presentation of patients with IE is highly variable and may simulate many other diseases. The spectrum of presentation varies from acute sepsis to nonspecific changes. IE should be suspected in any child with an underlying cardiac condition who presents with either unexplained fever or deterioration in cardiac function (Dajani, 1993).

Fever is the most common finding (present in about 65%-87% of cases), along with nausea, vomiting, irritability, malaise, anorexia, abdominal pain, arthritic symptoms, splenomegaly, appearance of a new murmur, petechiae, and fatigue. Patients with IE may also present with other serious complications such as congestive heart failure, stroke, or pulmonary or renal infarction (Curran et al., 1994; Dajani, 1993; Friedman & Stark, 1990; Kaplan & Shulman, 1989; Newberger, 1992; Zales & Wright, 1997).

Clinical presentation may vary with the causative organism. Streptococcus viridans and staphylococcus epidermis may present with only mild symptoms. Staphybcoccus aureus and streptococcus pneumoniae may be more acute, leading to a virulent picture. The clinical presentation also may vary with the site of infection. Acute aortic valve IE may lead to severe aortic insufficiency with congestive heart failure, while mitral valve endocarditis may lead to only mild mitral valve dysfunction but systemic embolization (Zales & Wright, 1997).

The diagnosis of IE requires first that the clinician have a high index of suspicion. Diagnosis of IE includes (a) pathologic evidence (CHD, cardiac surgery, echocardiogram), (b) at least two sets of blood cultures obtained by separate venipuncture positive for the same organism with no source of bacteremia other than the heart, or (c) or when IE is highly suspected based on presenting symptoms. Any patient with CHD who has a fever without an obvious cause should be suspected of having IE, and blood cultures should be part of the initial work-up. Serial blood cultures, two to six specimens obtained over 48 hours, have been shown to confirm the diagnosis in 95% of cases (Zales & Wright, 1997). Children with CHD are at increased risk for IE; therefore, even when an obvious source for a prolonged fever (e.g., pneumonia, UTI) has been identified, clinicians should still obtain blood cultures to exclude the possibility of bacteremia leading to simultaneous IE (Curran et al., 1994).


A good prognosis for the child with IE is clearly linked to establishing a prompt diagnosis and initiation of antibiotic therapy (Zales & Wright, 1997). Empiric antibiotic therapy with penicillin and an aminoglycoside should be initiated after three blood cultures have been obtained if there is a strong suspicion of IE. If possible, antibiotic therapy should be based on the cultural sensitivities. The effectiveness of therapy should be confirmed by tests of serum bactericidal activity (CBC w/diff, ESR) and the demonstration of adequate serum antibiotics. The duration of therapy depends on the patients response and the organism involved (Curran et al., 1994). Selection of the appropriate antimicrobial agent(s) is critical for the successful management of IE.

Several general principles provide a basis for the current recommendations for treatment. Preferred regimens include (a) parental therapy, especially in infants and children; (b) prolonged course, usually 4-6 weeks or longer; (c) bactericidal agents; and (d) synergistic combinations, when applicable (Dajani, 1993). The need for surgery for patients with IE generally indicates a failure of medical therapy. Persistent infection, despite antibiotic therapy, has been cited as the most common indication for surgery, followed by resulting valvular or other structural abnormalities after IE eradication (Curran et al., 1994).


The American Heart Association (AHA) issued new guidelines for the prevention of IE in 1997 (Dajani et al., 1997). These recommendations were formulated and prepared by an ad hoc writing group appointed by the AHA with liaisons representing the American Dental Association, the Infectious Diseases Society of America, the American Academy of Pediatrics, and the American Academy of GI Endoscopy.

Although the efficacy of currently recommended antibiotic prophylaxis has never been studied in man (Dajani, 1993; Friedman & Stark, 1990; Newberger, 1992), epidemiologic data provide several justifications for endocarditis prophylaxis (Dajani, 1993; Kaplan & Shulman, 1989). The updated AHA recommendations reflect analyses of relevant literature regarding procedure-related endocarditis, in vitro susceptibility data of pathogens causing endocarditis, results of prophylactic studies in animal models of endocarditis, and retrospective analyses of human endocarditis cases in terms of antibiotic prophylaxis usage patterns and apparent porophylaxis failures (Dajani et al., 1997). Because it is impossible to predict which child will develop IE or which particular procedure will be responsible, prophylactic antibiotics are recommended for children at risk for developing IE who are undergoing those procedures most likely to produce bacteremia with organisms that commonly cause IE (Dajani et al., 1990).

Major changes in the updated recommendations include the following: (a) an emphasis that most cases of IE are not attributable to an invasive procedure; (b) stratification of cardiac conditions into high, moderate, and negligible risk categories based on potential outcome if endocarditis develops; (c) clarification regarding procedures that may cause bacteremia and for which prophylaxis is recommended; (d) development of an algorithm to more clearly define when prophylaxis is recommended for patients with mitral valve prolapse; (e) reduction of the initial amoxicillin dose for oral/dental procedures to 2 g, with a follow-up antibiotic dose no longer recommended; (f) elimination of erythromycin as the recommended antibiotic for penicillin-allergic individuals, with clindamycin and other alternatives offered; and (g) simplification of the prophylactic regimens for GI/GU procedures. These changes were instituted to more clearly define when prophylaxis is or is not recommended, improve practitioner and patient compliance, reduce cost and potential GI side-effects, and approach more uniform world-wide recommendations (Dajani et al., 1997). Tables 1-5 provide IE recommendations and nonrecommendations for cardiac conditions and dental and surgical procedures from these most recent American Heart Association guidelines. The guidelines are meant to aid practitioners, bid are not intended as the standard of care for all cases or as a substitute for clinical judgment. They serve only to supplement practitioners in the exercise of their clinical judgment. it is impossible to make recommendations for all clinical situations in which IE may develop.
Table 1. Cardiac Conditions for Which Prophylaxis Is or
Is Not Recommended

Endocarditis Prophylaxis Recommended
High Risk Category

Prosthetic cardiac valves, including bioprosthetic and
  homograft valves
Previous bacterial endocarditis
Complex cyanotic congenital heart disease (e.g. single
  ventricle states, transposition of the great arteries,
  tetralogy of Fallot)
Surgically constructed system ic-pulmonary shunts or

Moderate Risk Category

Most other congenital cardiac malformations (other than
  above or below)
Acquired valvar dysfunction (e.g., rheumatic heart disease)
Hypertrophic cardiomyopathy
Mitral valve prolapse with valvar regurgitation and/or
  thickened leaflets

Endocarditis Prophylaxis Not Recommended
Negligible Risk Category (No Greater Risk than
the General Population)

Isolated secundum atrial septal defect
Surgical repair of atrial septal defect, ventricular septal
  defect, or patent ductus arteriosus (without residua
  beyond 6 months)
Previous coronary artery bypass graft surgery
Mitral valve prolapse without valvar regurgitation
Physiologic, functional, or innocent heart murmurs
Previous Kawasaki disease without valvar dysfunction
Previous rheumatic fever without valvar dysfunction
Cardiac pacemakers (intravascular and epicardial) and
  implanted defibrillators

Note: Adapted from statement "Prevention of Bacteria Endocarditis" by the American Heart Association Healthcare Professionals Scientific Publications, Journal of the American Medical Association, June 11, 1997 pp 1794-1801.
Table 2. Dental Procedures for Which Prophylaxis Is or Is
Not Recommended

Endocarditis Prophylaxis Recommended(*)

Dental extractions
Periodontal procedures including surgery, scaling, and
  root planing, probing, recall maintenance
Dental implant placement and reimplantation of avulsed
Endodontic (root canal) instrumentation or surgery only
  beyond the apex
Subgingival placement of antibiotic fibers/strips
Initial placement of orthodontic bands but not brackets
Intraligamentary local anesthetic injections
Prophylactic cleaning of teeth or implants where
  bleeding is anticipated

Endocarditis Prophylaxis Not Recommended

Restorative dentistry(**) (operative and prosthodontic)
  with/without retraction cord(***)
Local anesthetic injections (nonintraligamentary)
Intracanal endodontic treatment; post placement and buildup
Placement of rubber dams
Postoperative suture removal
Placement of removable prosthodontic/orthodontic
Taking of oral impressions
Fluoride treatments
Taking of oral radiographs
Orthodontic appliance adjustment
Shedding of primary teeth

(*) Prophylaxis is recommended for patients with high and moderate risk cardiac conditions.

(**) This includes restoration of decayed teeth (filling cavities) and replacement of missing teeth.

(***) Clinical judgment may indicate antibiotic use in selected circumstances that may create significant bleeding.

Note: Adapted from statement "Prevention of Bacterial Endocarditis" by the American Heart Association Healthcare Professionals Scientific Publications, Journal of the American Medical Association, June 11, 1997, pp. 1794-1801.
Table 3. Other Procedures for Which Prophylaxis Is Or Is Not

     Endocarditis Prophylaxis Recommended

Respiratory Tract

Tonsillectomy and/or adenoidectomy
Surgical operations that involve respiratory mucosal
Bronchoscopy with rigid bronchoscope

Gastrointestinal Tract(*)

Sclerotherapy for esophageal varices
Esophageal stricture dilation
Endoscopic retrograde cholangiography with biliary obstruction
Biliary tract surgery
Surgical operations that involve intestinal mucosa

Genitourinary Tract

Prostatic surgery
Urethral dilation

     Endocarditis Prophylaxis Not Recommended

Respiratory Tract

Endotracheal intubation
Bronchoscopy with flexible bronchoscope, with or without biopsy'
Tympanostomy tube insertion

Gastrointestinal Tract

Transesophageal echocardiography(**)
Endoscopy with or without gastrointestinal biopsy(**)

Genitourinary Tract

Vaginal hysterectomy
Vaginal delivery(**)
Cesarean section
In uninfected tissue:
  urethral catheterization
  uterine dilatation and curettage
  therapeutic abortion
  sterilization procedures
  insertion or removal of intrauterine devices


Cardiac catheterization, including balloon angioplasty
Implantation of cardiac pacemakers, implanted defibrillators,
  and coronary stents
Incision or biopsy of surgically scrubbed skin

(*) Prophylaxis is recommended for high-risk patients; optional for medium risk patients.

(**) Prophylaxis is optional for high-risk patients.

Note: Adapted from statement "Prevention of Bacterial Endocarditis by American Heart Association Healthcare Professionals Scientific Publications, Journal of the American Medical Association, June 11, 1997, pp. 1794-1801.
Table 4. Prophylactic Regimens for Dental, Oral Respiratory
Tract, or Esophageal Procedures (No Follow-up Dose Recommended)

Situation                    Agent                 Regimen(*)

Standard general
prophylaxis               Amoxicillin           Adults: 2.0 g;
                                                Children 50 mg/kg
                                                PO 1 hour before

Unable to take oral       Ampicillin            Adults: 2.0 g IM
medications                                     or IV; Children:
                                                50 mg/kg IM or IV
                                                within 30 minutes
                                                before procedure

Penicillin-allergic       Clindamycin           Adults: 600 mg,
                                                Children: 20 mg/kg
                                                PO 1 hour before


                          Cephalexin(**) or     Adults: 2.0 g;
                          Cefadroxil(**)        Children 50
                                                mg/kg PO 1 hour
                                                before procedure

                          Azithromycin or       Adults: 500 mg;
                          Clarithromycin        Children: 15 mg/kg
                                                PO 1 hour before

Penicillin-allergic and   Clindamycin           Adults: 600 mg;
unable to take                                  Children: 20 mg/kg
medications                                     IV within 30
                                                minutes oral
                                                before procedure


                          Cefazolin(**)         Adults: 1.0 g;
                                                Children: 25 mg/kg
                                                IM or IV within
                                                30 minutes before

(*) Total children's dose should not exceed adult dose.

(**) Cephalosporins should not be used in individuals with immediate type hypersensitivity reaction (urticaria, angioedema, or anaphylaxis) to penicillins.

Note: Adapted from statement "Prevention of Bacterial Endocarditis" by the American Heart Association Healthcare Professionals Scientific Publications, Journal of the American Medical Association, June 11, 1997, pp 1794-1801.

Table 5. Prophylactic Regimens for Genitourinary/Gastrointestinal (Excluding Esophageal) Procedures
Situation                          Agent(s)(*)

High-risk patients                 Ampicillin

High-risk patients allergic        Vancomycin
to ampicillin/amoxicillin          plus

Moderate-risk patients             Amoxicillin

Moderate-risk patients             Vancomycin
allergic to

Situation                  Regimen(**)

High-risk patients         Adults: ampicillin 2.0 g IM/IV
                           1.5 mg/kg (not to exceed 120 mg)
                           within 30 min of starting
                           procedure. 6 hours later,
                           ampicillin 1 g IM/IV or
                           amoxicillin 1 g PO; Children:
                           ampicillin 50 mg/kg IMAV (not to
                           exceed 2.0 g), plus gentamicin 1.5
                           mg/kg within 30 minutes of
                           starting procedure. Six hours later,
                           ampicillin 25 mg/kg IM/IV or
                           amoxicillin 25 mg/kg PO.

High-risk patients         Adults: 1.0 g IV over
allergic to                1-2 hours plus gentamicin 1.5
ampicillin/amoxicillin     mg/kg IVAM (not to exceed 120mg).
                           Complete dose within 30 minutes
                           of starting procedure; Children:
                           vancomycin 20 mg/kg IV over 1-2
                           hours gentamicin 1.5 mg1kg IV/IM.
                           Complete dose within 30 minutes
                           of starting procedure.

Moderate-risk patients     Adults: amoxicillin 2.0 g PO 1
                           hour before procedure; 2.0 g
                           IV/IM within 30 minutes of starting
                           procedure. Children: amoxicillin
                           50 mg/kg PO 1 hour before procedure,
                           OR Ampicillin 50 mg/kg IM/IV within
                           30 minutes of starting procedure.

Moderate-risk patients     Adults: vancomycin 1.0 g IV over
allergic to                1-2 hours. Complete infusion within
ampicillin/amoxicillin     30 minutes of starting the procedure.
                           Children: vancomycin 20 mg/kg IV over
                           1-2 hours. Complete dose within
                           30 minutes of starting the procedure.

(*) No second dose of vancomycin or gentamicin is recommended,

(**) Total children's dose should not exceed adult dose.

Note: Adapted from statement "Prevention of Bacterial Endocarditis' by the American Heart Association Healthcare is Scientific Publications, Journal of the American Medical Association, JUne 11, 1997, pp, 1794-1801

Practitioners must exercise their own clinical judgment in determining the choice of antibiotics and number of doses administered in individual cases or special circumstances (Dajani et al., 1990; Dajani et al., 1997). In addition to prophylactic regimen for genitourinary procedures, antibiotic therapy should be direct against the most likely pathogen. In patients who have prosthetic heart valves, a previous history of IE, or surgically constructed systemic-pulmonary shunts or conduits, physicians may choose to administer prophylactic antibiotics even for low-risk procedures that involve the lower respiratory, genitourinary, or gastrointestinal tracts (Dajani et al., 1990).

There are special situations in which the above recommendations may not apply. Surgical procedures through infected tissues require antimicrobial therapy directed against the most likely pathogen. Children who are receiving penicillin prophylaxis for prevention of rheumatic fever recurrence may have A-streptococci in their oral cavities that are relatively resistant to penicillins. In such cases, an agent other than amoxicillin should be selected for IE prophylaxis. Finally, prophylaxis is recommended for patients who undergo open heart surgery, but such prophylaxis should be aimed primarily against staphylococcus. A first-generation cephalosporin or vancomycin is a reasonable choice, but should only be used postoperatively and for a short duration (Dajani, 1993),

Nursing's Role in Patient Education

Patient education has become an integral part of health care delivery and is now considered a necessary component of the health care experience rather than a luxury (Rosenblum, 1994). Nurses involved in direct patient care are expected to balance the competing roles of patient/family educator, direct care provider, patient care planner, and supervisor of professional and non-professional staff (Hamric & Spross, 1989).

Similarly, educational responsibilities are a traditional part of the advanced practice nurse (APN) role, and commonly is considered to be an element of expert practice. Because the education focus of the staff nurse and APN is primarily on the child and family, the educator subrole of the APN tends to overlap with the functions of the staff nurse (Hamric & Spross, 1989). However, one characteristic separates the APN from other educators: the ability to perform several roles requiring multiple skills and competencies, often teaching children/families, staff, and students simultaneously. The APN's education role includes formal and informal teaching of staff nurses and graduate and undergraduate students in nursing and other disciplines. The informal teaching strategies are sometimes augmented by the development of structured educational resources such as patient education pamphlets and unit-based classes. This is important in that the APN may act as a consultant to determine patient teaching needs and then provide the teaching while acting as a role model for staff nurses and students (Hamric & Spross, 1989).

Stafford commented in an account of the APN role that "Every nurse is a teacher; not to teach is not to nurse" (Hamric & Spross, 1989). Because IE prophylaxis is such an important element of patient education in the pediatric congenital heart population, both staff nurses and APNs are in advantageous positions to provide a quality teaching plan to patients and their families.

Discussion of the Teaching Plan

A teaching plan outline is provided in Table 6; an in-depth discussion of the plan follows.
Table 6. Teaching Plan Outline

I. Teaching Plan: Incorporate patient education into plan of care.
  A. Assessment of patient/parent knowledge about IE prophylaxis.
    1. Assess knowledge of CHD, pathophysiology, diagnosis,
       treatment, and prevention protocols.
    2. Determine educational level, reading/listening
       comprehension, and ability to process information.

  B. Intervention
    1. Give preprinted booklet or handout (with AHA guidelines)
       on IE prevention to patients/parents prior to a teaching
       session for review.
    2. Negotiate a time for teaching session with patients/parents.
    3. Review information/answer questions
      a. Encourage good oral hygiene (Brush twice/day with soft,
         nylon bristle brush, brushing between the gums as well
         as teeth themselves, dental floss).
      b. Dental check-ups every 6 months.
      c. Remember, patients/pa rents should always inform all
         doctors or dentists of their heart condition, so they
         can prescribe antibiotics before procedures.
      d. Give extra copies of booklet to patients/pa rents to give
         to all their physicians to attach to patients chart.
         Physicians and dentists will then have a resource to
         prescribe the appropriate procedure specific antibiotics
         and dosages.

  C. Evaluation/Outcomes
    1. On follow-up visits, ask patients/pa rents details regarding
       IE prophylaxis, e.g., details regarding last dental visit.
    2. Congenital heart patients will practice IE prophylaxis
       for a lifetime, decreasing the risk of developing IE.

I. Teaching Plan: Incorporate patient education into a plan of care. Health care accrediting agencies such as the Joint Commission on the Accreditation of Healthcare Organizations (JCAHO) have recently mandated that patient education be included in patient care planning (JCAHO, 1992).

A. Assessment of patient/parent knowledge about IE prophylaxis: Studies have found that a recurring theme of the child who is hospitalized is a parent's need for information. Specifically, parents express the need to understand very complex information about treatment plans, the seriousness of their child's illness, expected length of stay, purpose and nature of procedures their child will experience, expected outcomes, and how they can participate in their child's care. Research findings indicate that providing information reassures, confirms, informs, and assists parental coping (Snowdon & Kane, 1995).

Assessment of knowledge level in patient teaching is directly related to compliance. Parents/children's reading ability must be evaluated: What level of education have parents experienced, and can they read? Comprehension of the information involves understanding the meaning of what is read, not just recognizing the words. Listening comprehension is an important aspect of learning: Does the parent understand what is being read, the verbal instruction? Inherent in comprehension is cultural literacy. Cultural literacy means that an individual posses the background information and perspective necessary to read and communicate verbally with understanding. The individual must understand the undertones of a comment or conversation, the intonation of voice, and terminology. Cultural literacy involves knowing how to communicate. And finally, do parents/children possess the ability to process information? Process is one's ability to use reading, language, and comprehension skills to develop a whole picture--being able to use one's external and internal resources (i.e., life experiences) to derive a logical connection of a concept, situation, or instructions (Fuszard, 1995).

B. Intervention:

1. Give parents printed instructions. Studies of pediatric discharge programs have focused largely on the structure and context with which information is provided to parents, and the relationship between providing information and compliance with treatment regimens. One such study suggests that the majority of parents do not comply with prescribed regimens when only verbal information is presented to them (Snowdon & Kane, 1995). Discharge instructions frequently consist of preprinted general guidelines for all parents of hospitalized children. Thus discharge teaching does not account for the family's individual need, but rather focuses on very general information (Snowdon & Kane, 1995).

2. Negotiate a time for a teaching session after review of instructions by parents/patients. Amount of time required for patient education should be individualized based on the nurse's assessment of knowledge level, language barriers, level of comprehension, reading ability, etc.

3. Review information/answer questions: A comprehensive explanation of the need for good oral hygiene enables parents to understand and feel involved in their child's care. Explain that individuals who are at risk for developing IE should establish and maintain the best possible oral health to reduce sources of bacterial seeding (Dajani et al., 1990). In general, dental or surgical procedures that induce bleeding from the gingiva or from mucosal surfaces of the oral, respiratory, and GI/GU tracts require IE prophylaxis. Such procedures include tooth extraction, professional dental cleaning, gum surgery, tonsillectomy/adenoidectomy, bronchoscopy with rigid scope, esophageal dilatation, and others (Dajani, 1993). Refer to a preprinted booklet or handout for the updated AHA recommendations. Reinforce the need to communicate to dentists and other physicians of the child's CHD. Give copies of the printed material to the child's physicians, providing them with a ready resource to aid in prescribing the appropriate procedure-specific antibiotics and dosages.

C. Evaluation/Outcomes: To evaluate the prevention plan, when parents/children return for follow-up visits, ask questions about the last dental visit what was done, and if they are practicing IE prophylaxis. The desired outcome is that parents/children will comply with the recommended IE prophylaxis for a lifetime, decreasing the risk of IE.


Because of the high morbidity and mortality associated with IE, any measure that can prevent the disease is advisable. Prophylactic antibiotics are recommended for children who are at risk to develop IE when undergoing procedures that may induce bacteremia with organisms likely to cause IE (Dajani, 1993).

Nurses can make a difference in the prevention of IE in the Pediatric congenital heart population. By delivering a comprehensive and thorough teaching plan, pediatric congenital heart patients can move forward on a continuum of health and well-being.


Auger, R, Marquis, G., Dyrda, I., & Martineau, J.P. (1981). Infective endocarditis update: Experience from a heart hospital. Acta Cardiology, 36005), 105-123.

Bayer, A.S. (1982). Staphylococcal bacteremia and endocarditis: State of the art. Archives of Internal Medicine, 142,1169.

Blumenthal, S., Griffiths, S.P., & Morgan, B.C. (1960). Bacterial endocarditis in children with heart disease: A review based on the literature and experience with 58 cases. Pediatrics, 26, 993.

Curran, R.D., Moulton, A.L., & Mavroudis, C. (1994). Infective Endocarditis. In C. Mavroudis & C. Backer (Eds.), Pediatric cardiac surgery (pp. 604-6161. St. Louis, MO: The C.V. Mosby Company.

Dajani, A.S. (1993). Endocarditis. In I.H. Gessner & B.E. Victories (Eds.), Pediatric cardiology. A problem oriented approach (pp. 221-228). Philadelphia: W.B. Saunders Company.

Dajani, A.S., Bisno, A.L., Chung, K.J., Durack, M.B., Freed, M., Gerber, M.A., Karchmer, A.W., et al. (1990). Prevention of bacterial endocarditis: Recommendations by the American Heart Association. Journal of the American Medical Association, 265(22), 2919-2922.

Dajani, A.S., Taubert, K., Wilson, W., Bolger, A.F., Bayer, A., Ferried, P., Gewitz, M.H., at al. (1997). Prevention of bacterial endocarditis. Healthcare Professionals Scientific Publications: Guidelines prepared by the American Heart Association. Journal of the American Medical Association, 277, 1794-1801.

Friedman, R.A., & Stark, J.R. (1990). Infective endocarditis. In A. Gerson, J.T. Bricker & D.G. McNamara (Eds.), the science and practice of pediatric cardiology (pp. 1561-1574). Philadelphia: Leo & Febiger.

Fuszard, B. (1995). Teaching patients with low literacy skills. Innovative teaching strategies in nursing (pp. 232-234). Baltimore: Aspen Publishers, Inc.

Gersony, W.M., & Hayes, C.J. (1977). Bacterial endocarditis in patients with pulmonary stenosis, aortic stenosis, or ventricular septal defect. Circulation, 56, 84.

Hamric, A.B., & Spross, J.A. (1989l. The clinical nurse specialist in theory and practice (2nd ad.). Philadelphia: W.B. Saunders Company.

Hazinski, MA (1992). Nursing care of the critically ill child (2nd ad.). St. Louis, MO: Mosby Year Book.

Johnson, C.M., & Rhodes, K.H. (1982). Pediatric endocarditis. Mayo Clinic Proceedings, 57, 86.

Kaplan, E.L. (1977). Infective endocarditis in the pediatric age group: An overview. In Infective endocarditis: An American Heart Association symposium, 51-54.

Kaplan, E.L., & Shulman, S.T. (1989). Endocarditis, In F.H. Adams, G.C. Emmanouilides, & T.A. Riemenschnsider (Eds.), Heart disease in infants, children, and adolescents (pp. 718-730). Baltimore: Williams and Wilkins.

Newberger, J.W. (1992). Infective endocarditis. In D.C. Fyler (Ed.), Nadas' pediatric cardiology (pp. 369-375). St. Louis: Mosby Year Book.

Rose, A.G. (1978). Infective endocarditis complicating congenital heart disease. South Africa Medical Journal, 53,739.

Rosenblum, R.K. (1994). Developing a pediatric patient-family education program. Pediatric Nursing, 20(4), 359-362. Shah, P., Singh, W.S.A., Rose, V., & Keith, J.D. (1966). Incidence of bacterial endocarditis in ventricular septal defects. Circulation, 34, 127.

Snowdon, A.W., & Kane, D.J. (1995). Parental needs following the discharge of a hospitalized child. Pediatric Nursing, 21(5), 425-428.

Stanton, B.F., Baltimore, R.S., & Clemens, J.D. 11984). Changing spectrum of infective endocarditis in children. American Journal of Disabled Children, 138, 720.

Steeg, C.N., Marmer, E.L., Varmer, A.D., & Blumenthal, S. (1970). The risk of infective endocarditis in patients with ventricular septal defect: Ar "life table" analysis. Circulation, 3(42), 113.

Wells, W.J. (1989). Surgical problems of endocarditis in children. Journal of Cardiac Surgery, 4, 313.

Yokochi, K., Sakamoto, H., Mikajima, T., & Ichinose, E. (1986). Infective endocarditis in children: A current diagnostic trend and the embolic complications. Japan Circulation Journal, 50, 1294.

Zales, V.R., & Wright, K.L. (February, 1997). Endocarditis, pericarditis, myocarditis. Pediatric Annals: A Journal of Continuing Pediatric Education, 202), 116-121.

Margaret M. Estlow, MSN, RN, PNP, C, is a Clinical Nurse Level III, Pediatric Cardiac Med/Surg Unit, Deborah Heart & Lung Center, Browns Mills, NJ.
COPYRIGHT 1998 Jannetti Publications, Inc.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1998 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Estlow, Margaret M.
Publication:Pediatric Nursing
Date:May 1, 1998
Previous Article:Leading change is leading creativity.
Next Article:Caring for children awaiting heart transplantation: psychosocial implications.

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters