Infective Endocarditis Treatment & Management
- Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD more...
The major goals of therapy for infective endocarditis (IE) are to eradicate the infectious agent from the thrombus and to address the complications of valvular infection. The latter includes both the intracardiac and extracardiac consequences of IE. Some of the effects of IE require surgical intervention. Emergent care should focus on making the correct diagnosis and stabilizing the patient with acute disease and cardiovascular instability. General measures include the following:
Treatment of congestive heart failure
Hemodialysis (may be required in patients with renal failure)
In most cases, the etiologic microbial agent is not known while the patient is in the ED. Three sets of blood cultures should be drawn over a few hours, and then empiric antibiotic therapy tailored to the patient’s history and circumstances may be administered (see Antibiotic Therapy, below).
No special diets are recommended for patients with endocarditis; however, if the patient has congestive heart failure, administer a sodium-restricted diet. Activity limitations are determined by the severity of the illness, complications (eg, stroke), and the presence of significant congestive heart failure.
Mild congestive heart failure resulting from valvular insufficiency or myocarditis may be managed with standard medical therapy. Often, this is progressive, and despite achieving a microbiological cure, it requires valvular surgery.
Antibiotics remain the mainstay of treatment for IE.
In the setting of acute IE, institute antibiotic therapy as soon as possible to minimize valvular damage. Three to 5 sets of blood cultures are obtained within 60-90 minutes, followed by the infusion of the appropriate antibiotic regimen. By necessity, the initial antibiotic choice is empiric in nature, determined by clinical history and physical examination findings.
Empiric antibiotic therapy is chosen based on the most likely infecting organisms. Native valve endocarditis (NVE) has often been treated with penicillin G and gentamicin for synergistic coverage of streptococci. Patients with a history of intravenous (IV) drug use have been treated with nafcillin and gentamicin to cover for methicillin-sensitive staphylococci. The emergence of methicillin-resistant S aureus (MRSA) and penicillin-resistant streptococci has led to a change in empiric treatment with liberal substitution of vancomycin in lieu of a penicillin antibiotic.
Prosthetic valve endocarditis (PVE) may be caused by MRSA or coagulase-negative staphylococci (CoNS) ; thus, vancomycin and gentamicin may be used for treatment, despite the risk of renal insufficiency. Rifampin is necessary in treating individuals with infection of prosthetic valves or other foreign bodies because it can penetrate the biofilm of most of the pathogens that infect these devices. However, it should be administered with vancomycin or gentamicin. These latter 2 agents serve to prevent the development of resistance to the rifampin.
Substitution of linezolid for vancomycin should be considered in patients with unstable renal function because of the difficulty of achieving therapeutic trough levels in this situation.
Linezolid or daptomycin are options for patients with intolerance to vancomycin or resistant organisms. Organisms with a minimum inhibitory concentration (MIC) to vancomycin of equal to or greater than 2 mcg/mL should be treated with alternative agents. Appropriate regimens should be devised in consultation with a specialist in infectious disease.
In the case of subacute IE, treatment may be safely delayed until culture and sensitivity results are available. Waiting does not increase the risk of complications in this form of the disease.
Eradicating bacteria from the fibrin-platelet thrombus is extremely difficult because (1) the high concentration of organisms present within the vegetation (ie, 10-100 billion bacteria per gram of tissue), (2) their position deep within the thrombus, (3) their location in both a reduced metabolic and reproductive state, and (4) the interference of fibrin and white cells with antibiotic action. For all of these reasons, bactericidal antibiotics are considered necessary for cure of valvular infection.
IV administration is preferred because more reliable therapeutic levels are achieved with this route. Orally administered antibiotics have been used as suppressive therapy for incurable valvular infections (ie, inoperable PVE).
Treat all patients in a hospital or skilled nursing facility to allow adequate monitoring of the development of complications and the response to antibiotic therapy.
American Heart Association guidelines for treatment
The American Heart Association (AHA) has developed guidelines for treating IE caused by the most frequently encountered microorganisms. (Go to updated guidelines [October 2007].) Antibiotic doses are predicated on normal renal function.
Adult NVE caused by penicillin-susceptible S viridans, S bovis, and other streptococci (MIC of penicillin of ≤0.1 mcg/mL) should be treated with one of the following regimens:
Administer penicillin G at 12-18 million U/d IV by continuous pump or in 6 equally divided doses for 4 weeks
Administer ceftriaxone at 2 g/d IV for 4 weeks. It may be given intramuscularly (IM) for short periods if venous access problems develop; ceftriaxone allows once-a-day outpatient IV therapy for clinically stable patients.
Administer penicillin G and gentamicin at 1 mg/kg (based on ideal body weight) every 8 hours for 2 weeks; short-course therapy with ceftriaxone and gentamicin for 2 weeks is a cost-effective regimen and is effective in selected patients; short-course therapy is recommended for those with uncomplicated NVE caused by sensitive S viridans and of less than 3 months’ duration
In patients who are allergic to penicillin, use vancomycin at 30 mg/kg/d IV in 2 equally divided doses for 4 weeks; the vancomycin dose should not exceed 2 g/d unless serum levels are monitored and can be adjusted to attain a peak vancomycin level of 30-45 mcg/mL 1 hour after completion of the intravenous infusion of vancomycin
For NVE caused by relatively resistant streptococci (MICs of penicillin of 0.1-0.5 mcg/mL), the following regimens are recommended:
Administer penicillin G at 18 million U/d IV, either by continuous pump or in 6 equally divided doses, for 4 weeks
Administer cefazolin at 6 g/d IV in 3 equally divided doses for 4 weeks
Both of the above regimens are combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for the first 2 weeks of therapy
For patients who are allergic to penicillin, administer vancomycin at 30 mg/kg/d IV in 2 equally divided doses (usually, do not exceed 2 g/d unless serum levels are monitored) for 4 weeks; peak vancomycin levels of 30-45 mcg/mL should be attained 1 hour after completion of the intravenous infusion
IE caused by nonresistant enterococci, resistant S viridans (MICs of penicillin G of >0.5 mcg/mL), or nutritionally variant S viridans and PVE caused by penicillin-G–susceptible S viridans or S bovis should be treated as follows:
Administer penicillin G at 18-30 million U/d IV, either by continuous pump or in 6 equally divided doses daily, combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for 4-6 weeks
Alternatively, administer ampicillin at 12 g/d by continuous infusion or in 6 equally divided doses daily, combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for 4-6 weeks
In patients who are allergic to penicillin, administer vancomycin at 30 mg/kg/d in 2 equally divided doses (usually, do not exceed 2 g/24 h unless serum levels are monitored). This may be combined with gentamicin for 4-6 weeks of treatment. A peak vancomycin level of 30-45 mcg/mL should be attained 1 hour after completion of the intravenous infusion.
Enterococcal PVE generally responds as well as disease involving native valves. Six weeks of treatment is recommended for patients with symptoms of enterococcal IE of more than 3 months’ duration, with relapsed infection, or with PVE.
A combination of an inhibitor of cell wall synthesis (ie, penicillin, vancomycin) with an aminoglycoside (ie, gentamicin, streptomycin) is necessary to achieve bactericidal activity against the enterococci. Tobramycin or amikacin does not act synergistically with antibiotics active against the bacterial cell wall.
Increasing numbers of enterococci have aminoglycoside-inactivating enzymes that make them relatively resistant to the usual synergistic combinations. These aminoglycoside-resistant strains have an MIC of 2000 mcg/mL or more for streptomycin and 500 mcg/mL or more for gentamicin. Of gentamicin-resistant enterococcal strains, 25% are susceptible to streptomycin.
Continuously infused ampicillin (serum level of 16 mcg/mL) is probably the best therapy for aminoglycoside-resistant enterococci. Alternative choices are imipenem, ciprofloxacin, or ampicillin with sulbactam. Vancomycin does not appear to be as useful as the aforementioned antibiotics.
Enterococcus faecalis may become resistant to the penicillins because of their production of beta-lactamases. These strains can be treated with ampicillin combined with sulbactam or with vancomycin combined with gentamicin.
High peak levels of gentamicin are not necessary to establish synergistic bactericidal activity against enterococci. Peak gentamicin levels of 3-5 mcg/mL, with a trough of less than 2 mcg/mL, frequently can be obtained with a dose of gentamicin of 1 mg/kg IV every 8 hours. Once-a-day gentamicin dosing should not be used because a prolonged postantibiotic effect against gram-positive organisms does not occur, and synergistic killing requires the simultaneous presence of an agent active in the cell wall and an aminoglycoside.
A study indicates that gentamicin usage, even for synergy, is associated with decreasing renal function. However, overall mortality does not appear to be increased. Certainly, gentamicin therapy should be continued to achieve synergy against enterococci, but the practice of administering gentamicin for 5 days in the treatment of S aureus IV drug abuse (IVDA) IE should be questioned.
Vancomycin-resistant isolates of Enterococcus faecium and Enterococcus faecalis (ie, vancomycin-resistant enterococci [VRE]) produce some of the most challenging nosocomial infections. Presently, no therapy has been proven highly effective for IE caused by strains of VRE.
Quinupristin/dalfopristin (ie, Synercid) may suppress E faecium bacteremia but frequently is not bactericidal. Other options for therapy include linezolid, a combination of ampicillin and imipenem, and chloramphenicol. In one small series, the combination of ampicillin and ceftriaxone was found to be useful against VRE. Often, the valve must be replaced to achieve a cure.
NVE caused by methicillin-sensitive S aureus (MSSA) should be treated as follows:
Administer nafcillin or oxacillin at 2 g IV every 4 hours for 4-6 weeks
Administer cefazolin at 2 g IV every 8 hours for 4-6 weeks
For patients who are allergic to penicillin, administer vancomycin at 30 mg/kg (usually, do not to exceed 2 g/24 h unless serum levels are monitored) for 4-6 weeks; a peak vancomycin level of 30-45 mcg/mL should be attained 1 hour after completion of the intravenous infusion.
Vancomycin therapy is associated with a significant failure rate (up to 35%) in the treatment of MSSA and MRSA bloodstream infection (BSI)/IE. It appears that vancomycin should not be used to treat infections with staphylococci with an MIC of greater than 1.5-2 mcg/mL. In these cases, alternative agents such as linezolid or daptomycin should be used.
PVE caused by MSSA should be treated as follows:
Administer nafcillin or oxacillin at 2 g IV every 4 hours for 6 weeks or longer
Alternatively, administer cefazolin at 2 g IV every 8 hours for 6 weeks or longer
Each of these options should be combined with rifampin at 300 mg orally every 8 hours for 6 weeks or longer and with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for the first 2 weeks
PVE caused by MRSA should be treated with vancomycin at 30 mg/kg (not to exceed 2 g/d unless serum levels are monitored) for 6 weeks or longer combined with rifampin and gentamicin as outlined above; a peak vancomycin level of 30-45 mcg/mL should be attained 1 hour after completion of the IV infusion; a significant concern is that MRSA may become resistant to vancomycin.
Treatment with linezolid appears to result in outcomes superior to those with vancomycin against many types of infections caused by MRSA and MSSA. The use of linezolid should be strongly considered instead of vancomycin in patients who are seriously ill. Another advantage of linezolid is that its dose does not need to be adjusted in patients with renal failure.
White blood cell counts, red blood cell counts, and platelet counts need to be monitored frequently while the patient is on linezolid. The risk of developing serotonin syndrome is low. After the fourth week of therapy, the risk of hematological and neuropathic complications rapidly increases.
Daptomycin (6 mg/kg/24 h) has been approved for the treatment of S aureus BSI and right-sided IE. Higher doses of daptomycin (12 mg/kg/24 h) are more effective, with little increase in adverse effects. Patients who have received vancomycin have a higher rate of resistance to daptomycin.
HACEK microorganisms should be treated as follows:
Administer ceftriaxone at 2 g/d IV for 4 weeks
Alternatively, administer ampicillin at 12 g/d by continuous pump or in 6 equally divided doses daily; this may be combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for 4 weeks
Culture-negative NVE is usually treated with vancomycin and gentamicin. In patients who have previously received antibiotics, initial therapy should consist of either ampicillin-sulbactam plus gentamicin (3 mg/kg/d) or vancomycin plus gentamicin and ciprofloxacin. Because of the increased risk of renal failure with gentamicin, the latter regimen is preferred.
Patients with culture-negative PVE are usually given vancomycin and gentamicin, targeting possible enterococcal or CoNS infections. In patients with suspected PVE who have previously received antibiotics, enteric therapy should consist of vancomycin, gentamicin, cefepime, and rifampin. Because of the risk of developing resistance to rifampin, many clinicians would start this antibiotic only after the blood cultures results become negative.
Treatment of other microorganisms is as follows:
For P aeruginosa, administer ceftazidime, cefepime, or imipenem, combined with high-dose tobramycin at 8 mg/kg/d in 3 divided doses, to attain peak blood levels of 15-20 mcg/mL, for 6 weeks
For enteric gram-negative rods (eg, E coli, Proteus mirabilis), administer ampicillin, ticarcillin-clavulanic acid, piperacillin, piperacillin-tazobactam, ceftriaxone, or cefepime combined with gentamicin or amikacin for 4-6 weeks
For Streptococcus pneumoniae, administer ceftriaxone at 2 g/d IV or vancomycin (if penicillin allergy or high-level penicillin G resistance [MIC of 2 mcg/mL or more]) for 4 weeks
For diphtheroids, administer penicillin G at 18-24 million U/d in 6 divided doses or vancomycin combined with gentamicin for 4 weeks
For Q fever ( C burnetii infection), administer doxycycline combined with rifampin, trimethoprim-sulfamethoxazole, or a fluoroquinolone for 3-4 years
PVE is especially difficult to treat because the microorganisms adhere to the foreign body and may make them impervious to the bactericidal action of agents active in the cell wall. All patients with PVE require at least 6 weeks of antimicrobial therapy. Rifampin is the key drug in the treatment of PVE, as it is one of the only antimicrobial agents that penetrate the biofilm laid down by S aureus and CoNS. Because of the risk of these organisms developing resistance to rifampin, many clinicians withhold the addition of rifampin until blood cultures have cleared.
Penicillin-sensitive S viridans PVE should be treated with 2 weeks of penicillin G or ceftriaxone combined with gentamicin, followed by 4 weeks of penicillin G or ceftriaxone.
If the S viridans PVE is caused by an organism with a penicillin MIC of 0.2 mcg/mL or more, penicillin G or ceftriaxone combined with gentamicin combination therapy should be administered for 4-6 weeks. If the combination therapy is administered for only 4 weeks, penicillin G or ceftriaxone should be continued for an additional 2 weeks. Vancomycin is substituted for penicillin or ceftriaxone if the patient has a history of severe, immediate penicillin hypersensitivity, such as urticaria, anaphylaxis, or angioedema.
Enterococcal PVE therapy is complicated by the multiple types of enterococcal antimicrobial resistance, including beta-lactamase production (rare), different types of aminoglycoside-inactivating enzymes (more common), and VRE (increasingly common). If the enterococci are highly resistant to both gentamicin and streptomycin, ampicillin should be administered for 8-12 weeks by continuous infusion.
No effective therapy is known for VRE PVE.
Patients with PVE must be monitored carefully for signs of valve dysfunction, congestive heart failure, and heart block. They should also be monitored for clinical response to therapy, conversion of positive blood culture results, renal function status, and serum blood levels of vancomycin and aminoglycosides.
Valve replacement surgery should be performed promptly if any of the following occurs: moderate-to-severe congestive heart failure, valve dysfunction, perivalvular or myocardial abscess formation, the presence of an unstable valve that is becoming detached from the valve ring, more than one embolic episode with persistent vegetations observed on transtracheal echocardiogram, or the presence of vegetations larger than 1 cm in diameter.
If PVE does not respond to antimicrobial therapy and blood cultures results remain positive or if a relapse of bacteremia occurs after infection, the prosthetic valve should be replaced. In the presence of microorganisms that have no microbicidal agent (eg, VRE, fungi) or in the presence of other recalcitrant organisms (eg, P aeruginosa, S aureus, enteric gram-negative rods, Brucella species, C burnetii), past clinical experience shows that early replacement of the prosthetic valve improves the chances for cure.
Fungal endocarditis is rare and primarily occurs after prosthetic valve surgery and in individuals who abuse intravenous drugs. Candida species and Aspergillus species are the organisms most frequently encountered. Currently available antifungal agents have not been successful in eliminating fungal IE. The only cures for proven fungal IE have resulted when surgical excision of the infected valves was combined with amphotericin B therapy.
Empiric therapy of IVDA IE should be aimed at S aureus. Whether to use vancomycin or oxacillin/nafcillin depends on the incidence of MRSA in the community. Generally, gram-negative organisms occur infrequently, and delay in covering them initially is acceptable.
Some clinicians obtain peak and trough blood samples during the course of antimicrobial therapy of IE in order to run serum bactericidal tests. These tests are performed by incubating serial 2-fold dilutions of serum that contains antimicrobials with an inoculum of 100,000 colony-forming units per milliliter of the target microorganism that has been previously isolated from the patient’s blood for 24-48 hours.
Peak antimicrobial concentrations that inhibit and kill the bacteria at a 1:32 or greater dilution in serum are a consistent predictor of a favorable clinical response. Antimicrobial dosages are adjusted to try to attain this goal. However, many clinicians feel that the serum bactericidal test does not have a reproducible result, and these clinicians rely on standardized tests of antimicrobial susceptibility (ie, MICs) and serum antimicrobial assays of peak and trough levels to determine whether sufficient amounts of antimicrobial agents are being administered.[71, 72, 73, 74, 75, 76]
Management of S aureus Bacteremia
Management of S aureus bacteremia in the presence of an intravascular catheter includes promptly removing the catheter, initiating appropriate antibiotic therapy, monitoring of blood culture results in 24-48 hours, and performing transesophageal echocardiography (TEE).
If the follow-up blood culture and TEE findings are negative and no evidence of metastatic infection is found, then 2 weeks of antistaphylococcal therapy is appropriate.
If the follow-up blood culture findings are positive and the TEE results indicate the presence of IE, then the patient is treated for 4-6 weeks with antistaphylococcal antibiotics.
If the follow-up blood culture results are positive and the TEE findings show no evidence of IE, then metastatic infection, such as a splenic abscess or osteomyelitis, must be considered while appropriate antibiotic therapy is continued and while the extracardiac source of infection is sought.
It is important to recognize that, in up to one third of cases, a cause of persistent BSI is not identified. A good deal of these may be explained by endotheliosis. For the time being, the duration of antibiotic therapy for each case of S aureus catheter-related BSI must be individualized. The author and others would treat cases that meet the criteria of continuous bacteremia for a total of 4 weeks despite a negative TEE result.[77, 78, 79]
Although thrombosis is a key element of IE, anticoagulation with warfarin (Coumadin, Jantoven) is controversial. Indeed, evidence indicates patients who are anticoagulated have worse outcomes than those who are not anticoagulated. Patients who are treated with anticoagulation appear to have a higher rate of intracerebral bleeding. If an established reason for anticoagulation (eg, deep venous thrombosis, presence of a mechanical prosthetic valve) exists, a standard regimen of anticoagulation should be followed.
Indications for Surgery
Approximately 15-25% of patients with IE eventually require surgery.
Indications for surgical intervention in patients with NVE are as follows:
Congestive heart failure refractory to standard medical therapy
Fungal IE (except that caused by Histoplasma capsulatum)
Persistent sepsis after 72 hours of appropriate antibiotic treatment
Recurrent septic emboli, especially after 2 weeks of antibiotic treatment
Rupture of an aneurysm of the sinus of Valsalva
Conduction disturbances caused by a septal abscess
Kissing infection of the anterior mitral leaflet in patients with IE of the aortic valve
Congestive heart failure in a patient with NVE is the primary indication for surgery. A second relapse, during or after completion of treatment, requires replacement of the valve.
Paravalvular abscess and intracardiac fistula almost always require surgical intervention. Patients with culture-negative NVE who remained febrile for more than 10 days should be considered surgical candidates. Persistent hypermobile vegetations, especially those with a history of embolization beyond 7 days of antibiotic therapy, should be treated with surgery. Cardiac surgery should be considered in patients with multiresistant organisms (eg, enterococci).
The indications for surgery in patients with PVE are the same as those for patients with NVE, with the addition of the conditions of valvular dehiscence and early PVE. Orally administered antibiotics have been used as suppressive therapy for incurable valvular infections (ie, inoperable PVE).
Surgery is often required for treatment of metastatic infections (eg, cerebral and other types of aneurysms and macroabscesses of the brain and spleen). Many cerebral abscesses may not be accessible. If this is the case, they can be monitored because 30% may heal when treated medically.
Occasionally, local debridement and the administration of appropriate antibiotics may be sufficient to cure an uncomplicated pacemaker pocket infection. However, most studies indicate that complete removal of the system is necessary for cure in most cases. Many patients in whom this is not possible eventually die of complications from relapsing infection. This aggressive approach is especially necessary when dealing with pacemaker IE.
The AHA 2010 guideline update on CIED infections and their management recommends complete removal of infected CIED and leads for the following patients:
All patients with definite CIED infection, as shown by valvular and/or lead endocarditis or sepsis
All patients with CIED pocket infection, as shown by abscess formation, device erosion, skin adherence, or chronic draining sinus without involvement of the transvenous section of the lead system
All patients with valvular endocarditis without definite involvement of the lead(s),device, or both
Patients with occult staphylococcal bacteremia
The guideline update states that complete removal is reasonable in patients with persistent occult gram-negative bacteremia despite appropriate antibiotic therapy.
Removal of the device and leads is not indicated in the following cases:
A superficial or incisional infection that does not involve the device, leads, or both
Relapsing bloodstream infection due to a non-CIED source and for which long-term suppressive antimicrobials are required
After removal of the infected device, placing a temporary transvenous pacer is best. Immediate insertion of a permanent pacemaker at a new site can be safely accomplished.
The AHA 2010 guideline update on CIED infection recommends careful evaluation of each patient to determine if a CIED is still needed. Replacement device implantation should not be ipsilateral to the extraction site. The guideline suggests the contralateral side, the iliac vein, and epicardial implantation as preferred alternative locations.
The AHA 2010 guideline recommends that if blood cultures were positive before the device extraction, blood cultures should be taken after the device removal, and new device placement should be delayed until blood cultures have been negative for at least 72 hours. If valvular infection is present, placement of new transvenous lead should be delayed for at least 14 days after CIED system removal.
In the past, removal of the intracardiac leads that had been in place for several months often necessitated open heart surgery. The use of laser technology to dissolve the pacemaker lead adhesions has proven successful, with a 94% success rate. The risk of dislodging vegetations during removal of infected leads is negligible. Patients whose leads cannot be removed are started on permanent antibiotic suppression.[80, 81]
The AHA 2010 CIED guideline update states that long-term suppressive antimicrobial therapy should be considered for patients with CIED infection who are not candidates for CIED removal. Such therapy should not be administered to patients who are candidates for CIED removal.
Prevention of Infective Endocarditis
Approximately 15-25% of cases of IE are a consequence of invasive procedures that produce a significant bacteremia. Because only 50% of those who developed valvular infection following a procedure were identified as being candidates for antibiotic prophylaxis, only approximately 10% of cases of IE can be prevented by the administration of preprocedure antibiotics. Maintaining good oral hygiene is probably more effective in the overall prevention of valvular infection because gingivitis is the most common source of spontaneous bacteremias.
Consider prophylaxis against IE in patients at higher risk. Patients at higher risk include those with the following conditions:
Presence of prosthetic heart valve
History of endocarditis
Cardiac transplant recipients who develop cardiac valvulopathy
Congenital heart disease with a high-pressure gradient lesion
The presence of a coronary artery stent is not considered to place the patient at high risk for endocarditis.
Any procedure involving manipulation of gingival tissue or the periapical region of teeth, or perforation of the oral mucosa
Any procedure involving incision in the respiratory mucosa
Procedures on infected skin or musculoskeletal tissue including incision and drainage of an abscess
Prophylaxis is no longer routinely recommended for gastrointestinal or genitourinary procedures.
Prevention of vascular catheter infections is an important prophylactic approach in preventing nosocomial infective endocarditis (NIE). Protective factors include the insertion and maintenance of catheters by an infusion therapy team, the use of topical disinfectants and antibiotics, and the practice of coating catheters with antimicrobial agents.
No double-blind studies have been performed to support the use of systemically administered antibiotics for the prevention of pacemaker or intracardiac defibrillator infections. However, awaiting definitive studies, the authors recommend prophylactic antibiotics, as with any implantable device. Of course, strict sterile technique must be followed. Antibiotic prophylaxis is not recommended for prevention of CIED infection in patients with pacemakers or intracardiac defibrillators during invasive procedures not directly related to device manipulation. Pacemaker infection due to transient bacteremias is uncommon.
There appeared to be no dramatic increase in rates of hospitalization following the changes to the recommendations for antibiotic prophylaxis in 2007.
For more information, see Antibiotic Prophylactic Regimens for Endocarditis.
American Heart Association guidelines for prophylaxis
The AHA periodically compiles recommendations for IE prophylaxis (Go to updated guidelines, October 2007). It is important to remember that these are not standards but guidelines and thus may be modified in particular circumstances. The guidelines remain unproven by randomized controlled clinical trials. Indeed, many examples of failure of these recommendations have been noted, even when they are applied appropriately.
The 3 major steps in the pathogenesis of IE that are vulnerable to antibiotic prophylaxis are the following:
- Killing of the pathogen in the bloodstream before it can adhere to the valve
- Preventing adherence to the valve/fibrin-platelet thrombus
- Eradicating any organisms that have attached to the thrombus
Successful antibiotic prophylaxis requires identifying those patients who are at risk, prioritizing the procedures that require prophylaxis, and selecting an appropriate antibiotic regimen. In general, bactericidal antibiotics are used. However, bacteristatic agents are probably effective in most circumstances.
Although the 2007 guidelines are a marked improvement because they prioritize the cardiac conditions and procedures that require antibiotic prophylaxis and emphasize the importance of promoting good oral hygiene, they offer little direction in dealing with the ever-growing problem of antibiotic-resistance patterns of S viridans and enterococci.
The importance of antibiotic prophylaxis of calcific valvular disease in elderly patients also needs to be more fully discussed. Calcific valvular disease is the most common underlying cardiac risk factor for the development of IE in this age group.
The author’s preference is to administer parenteral prophylactic antibiotics to patients with prosthetic valves because of the severe consequences of PVE.
The United Kingdom’s NICE 2008 guidelines on prophylaxis against IE differ from the AHA recommendations. The NICE guidelines do not recommend antibiotic prophylaxis for IE in patients undergoing dental procedures; however, they agree with the AHA guidelines in not recommending prophylaxis for those undergoing procedures in the upper and lower gastrointestinal tracts, the genitourinary tract, or the upper and lower respiratory tracts.
Subsequent to the 2008 NICE guidelines recommending abolition of all IE antibiotic prophylaxis, prescriptions for such prophylaxis dropped almost 80% without any apparent cases of IE. However, the authors of this article recommend continuing to follow the current AHA guidelines, especially in the presence of an intracardiac prosthetic device.
Failure to consider the diagnosis, especially in patients with a history of IV drug use and a low-grade fever, is a medicolegal pitfall. Many malpractice suits are caused by a failure to diagnose and a delay in diagnosis accompanied by a poor outcome for the patient.
As a rule for primary care clinics, do not administer antimicrobial agents to febrile patients with heart murmurs without first obtaining at least 2 sets of blood cultures.
The perception that most IE is preventable is wrong. Frequent episodes of transient bacteremia occur with chewing and other activities of daily life. Proving that a failure to give prophylaxis before dental and surgical procedures resulted in IE is difficult. However, this does not prevent legal action alleging IE as a consequence of failing to give the antimicrobial prophylaxis recommended by the AHA.
When a central venous line is needed, not inserting the line when a patient is known to be bacteremic is advisable. If no alternative to placing the line is available, bactericidal antimicrobial agents should be administered to try to prevent the development of IE.
In general, both a cardiologist and an infectious diseases specialist should be involved in the care of patients with IE. Consulting a cardiothoracic surgeon may be necessary. Personnel in the clinical microbiology laboratory must have the skill to isolate the organism, properly identify it, and perform susceptibility testing appropriate for the growth characteristics and requirements of the organism (with determination of the MIC of clinically relevant antimicrobial agents). To obtain the best possible information, the attending physician should work closely with the microbiology laboratory personnel.
Monitoring for posttreatment bacteremia
Patients should have blood cultures taken after 3-4 days of treatment to document eradication of the bacteremia. Blood cultures during treatment are essential if persistent fever or other signs develop that suggest failing treatment.
Failure to sterilize the bloodstream, despite adequate serum levels of appropriate antibiotics, should prompt a search for metastatic infection (eg, abscesses, especially splenic, or mycotic aneurysm).
Fever lasting longer than 10 days into therapy with an indicated antibiotic regimen should be of concern and should prompt a search for suppurative complications. Approximately 30% of patients have a return of fever after the initial response. This is usually caused by an intracardiac abscess or metastatic infection. Causes of unresponsive fever include myocardial or septal abscesses, large vegetations that resist sterilization, and metastatic infection. Occasionally, fever in patients with uncomplicated IE may take as long as 3 weeks to abate.
Monitoring for complications
Patients should be monitored for the development of the following complications:
Valvular dysfunction, usually insufficiency of the mitral or aortic valves
Myocardial or septal abscesses
Congestive heart failure
Organ dysfunction resulting from immunological processes
Complications, such as congestive heart failure resulting from valvular insufficiency and embolization, may occur after bacteriologic cure has been achieved. (Note that the diagnosis of developing congestive heart failure or valvular insufficiency is based on clinical findings, not solely on echocardiographic measurements.) The onset of valve dysfunction or moderate-to-severe congestive heart failure should lead to an evaluation for immediate valve replacement.
Monitoring for relapse
Relapse of IE usually occurs within 2 months of finishing clinically effective therapy. Infection with S aureus, enterococci, and gram-negative organisms (especially P aeruginosa) is associated with a high rate of relapse. Enterococcal infection of the mitral valve has the greatest potential for relapse.
Recurrent IE occurs most often in individuals who abuse IV drugs. Valvular infections in these patients recur at a rate of 40%. Those with pretreatment symptoms of IE of more than 3 months’ duration are at greater risk for relapse. Other significant risk factors for recurrence include a previous episode of IE, the presence of a prosthetic valve, and congenital heart disease.
In general, infected vascular catheters should be removed and should not be replaced over a guidewire. Surgically implanted devices, such as Broviac or Hickman catheters, do not necessarily need to be removed unless evidence of IE, a tunnel infection, or suppurative thrombophlebitis is present or if the infecting organism is a Corynebacterium species, a Pseudomonas species, a fungus, S aureus, or a Mycobacterium species. If bacteremia persists longer than a few days, the catheter must be removed.[88, 89]
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|Causative Organism(s)||Clinical Features of IE|
|Streptococcus intermedius group||
|Group D streptococci||
|Nonenterococcal group D||
|Group B streptococci||
|Group A, C, and G streptococci||
|Coagulase-negative S aureus||
|HACEK (ie, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)||
|Multiple pathogens (polymicrobial)||