Infective endocarditis: Perioperative management and surgical principles
2014; Elsevier BV; Volume: 147; Issue: 4 Linguagem: Inglês
10.1016/j.jtcvs.2013.11.022
ISSN1097-685X
AutoresKareem Bedeir, Michael J. Reardon, Basel Ramlawi,
Tópico(s)Cardiac Valve Diseases and Treatments
ResumoDespite advances in microbial prevention and elimination, the frequency of endocardial infection is still increasing and it remains to be a serious condition. The strategies and aggressiveness of medical and surgical algorithms for managing these patients are evolving and having a significant effect on morbidity and mortality. This review addresses the current understanding of the processes by which the most common and most threatening complications occur, and the current management strategies that cardiologists and cardiac surgeons should be aware of when treating these seriously ill patients. Despite advances in microbial prevention and elimination, the frequency of endocardial infection is still increasing and it remains to be a serious condition. The strategies and aggressiveness of medical and surgical algorithms for managing these patients are evolving and having a significant effect on morbidity and mortality. This review addresses the current understanding of the processes by which the most common and most threatening complications occur, and the current management strategies that cardiologists and cardiac surgeons should be aware of when treating these seriously ill patients. Despite major advances in diagnostic modalities and antimicrobial therapies, infective endocarditis (IE) remains an extremely ominous infection, with a 1-year mortality rate of up to 40%.1Hoen B. Alla F. Selton-Suty C. Beguinot I. Bouvet A. Briancon S. et al.Changing profile of infective endocarditis: results of a 1-year survey in France.JAMA. 2002; 288: 75-81Crossref PubMed Scopus (812) Google Scholar, 2Wallace S.M. Walton B.I. Kharbanda R.K. Hardy R. Wilson A.P. Swanton R.H. Mortality from infective endocarditis: clinical predictors of outcome.Heart. 2002; 88: 53-60Crossref PubMed Scopus (249) Google Scholar Management of these critically ill patients requires an understanding of the disease process in its various microbial, hemodymanic, embolic, and immunologic forms. At the time of diagnosis, patients have often progressed to complications through 1 aspect of the disease. An appreciation of the spectrum of the disease processes is crucial for providing a timely and effective intervention. In this article, the processes by which the most common and most threatening complications occur, as well as what every physician ought to know when treating these seriously ill patients are discussed. After bacteria seed the endocardium, erosions into various cardiac structures take place though an interplay of direct bacterial invasion, enhanced inflammatory response, and liquifactive enzyme release within cardiac tissues. This is particularly pronounced in IE caused by Staphylococcus aureus, especially in the aortic valve position. This is probably due to the less annular fibrous tissue support in the aortic position compared with the mitral position. Unfortunately, IE tends to occur more frequently in the aortic valve than any other valve, and the frequency of S aureus as the cause of IE has increased dramatically over the past 2 decades, from 2% in 1990 to 25% in 2009.3Habib G. Hoen B. Tornos P. Thuny F. Prendergast B. Vilacosta I. et al.Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer.Eur Heart J. 2009; 30: 2369-2413Crossref PubMed Scopus (1648) Google Scholar Congestive heart failure (CHF) through a sudden volume overload on the ventricles, whether caused by a sudden regurgitant lesion or shunt creation, can complicate IE. Sudden regurgitation usually occurs as a result of chordal rupture in native valve endocarditis (NVE), a valve leaflet perforation in NVE or in bioprosthetic valve IE, or valve dehiscence in prosthetic valve endocarditis (PVE). In NVE and PVE, CHF is the complication with the greatest independent impact on prognosis whether medically or surgically treated.4Hasbun R. Vikram H.R. Barakat L.A. Buenconsejo J. Quagliarello V.J. Complicated left-sided native valve endocarditis in adults: risk classification for mortality.JAMA. 2003; 289: 1933-1940Crossref PubMed Scopus (277) Google Scholar, 5Vikram H.R. Buenconsejo J. Hasbun R. Quagliarello V.J. Impact of valve surgery on 6-month mortality in adults with complicated, left-sided native valve endocarditis: a propensity analysis.JAMA. 2003; 290: 3207-3214Crossref PubMed Scopus (280) Google Scholar Early studies comparing antimicrobial therapy with surgery in patients with IE complicated by CHF demonstrated a clear superiority with surgery (23% vs 71% mortality rates).6Aksoy O. Sexton D.J. Wang A. Pappas P.A. Kourany W. Chu V. et al.Early surgery in patients with infective endocarditis: a propensity score analysis.Clin Infect Dis. 2007; 44: 364-372Crossref PubMed Scopus (174) Google Scholar, 7Croft C.H. Woodward W. Elliott A. Commerford P.J. Barnard C.N. Beck W. Analysis of surgical versus medical therapy in active complicated native valve infective endocarditis.Am J Cardiol. 1983; 51: 1650-1655Abstract Full Text PDF PubMed Scopus (145) Google Scholar, 8Richardson J.V. Karp R.B. Kirklin J.W. Dismukes W.E. Treatment of infective endocarditis: a 10-year comparative analysis.Circulation. 1978; 58: 589-597Crossref PubMed Scopus (275) Google Scholar Much less commonly, heart failure can be obstructive in nature when large vegetation obstructs a heart chamber outflow. A similar pathophysiology also leads to paraannular extension (PAE) of the infection. Given the similar pathophysiology, PAE is also more common with necrotizing organisms, and in the aortic position. In addition, PAE is one of the most frequent complications of IE, occurring in up to 100% of infected prosthetic valves and 40% of infected native valves.9Fernicola D.J. Roberts W.C. Frequency of ring abscess and cuspal infection in active infective endocarditis involving bioprosthetic valves.Am J Cardiol. 1993; 72: 314-323Abstract Full Text PDF PubMed Scopus (36) Google Scholar The infectious process around the valve weakens the annulus, and eventually leads to tissue destruction, valve dehiscence, abscess formation, and sometimes fistulization. This is associated with an increased occurrence of CHF and a higher mortality rate. A PAE-related fistula has been shown to lead to up to 40% mortality.10Thuny F. Beurtheret S. Mancini J. Gariboldi V. Casalta J.P. Riberi A. et al.The timing of surgery influences mortality and morbidity in adults with severe complicated infective endocarditis: a propensity analysis.Eur Heart J. 2011; 32: 2027-2033Crossref PubMed Scopus (157) Google Scholar, 11Prendergast B.D. Tornos P. Surgery for infective endocarditis: who and when?.Circulation. 2010; 121: 1141-1152Crossref PubMed Scopus (263) Google Scholar In addition to the local destruction that complicates IE, systemic embolization is the most common complication. Emboli usually consist of vegetations or friable necrotic and often infected tissues. Unlike local effects, this is more common in the mitral valve position. Although the embolic risk is high (embolic events occur in up to 50% of patients), this risk declines dramatically with initiation of antibiotic treatment, and even more after 2 weeks of effective continuation.3Habib G. Hoen B. Tornos P. Thuny F. Prendergast B. Vilacosta I. et al.Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer.Eur Heart J. 2009; 30: 2369-2413Crossref PubMed Scopus (1648) Google Scholar, 12Di Salvo G. Habib G. Pergola V. Avierinos J.F. Philip E. Casalta J.P. et al.Echocardiography predicts embolic events in infective endocarditis.J Am Coll Cardiol. 2001; 37: 1069-1076Abstract Full Text Full Text PDF PubMed Scopus (328) Google Scholar, 13Anguera I. del Rio A. Moreno A. Pare C. Mestres C.A. Miro J.M. Complications of native and prosthetic valve infective endocarditis: update in 2006.Curr Infect Dis Rep. 2006; 8: 280-288Crossref PubMed Scopus (9) Google Scholar, 14Steckelberg J.M. Murphy J.G. Ballard D. Bailey K. Tajik A.J. Taliercio C.P. et al.Emboli in infective endocarditis: the prognostic value of echocardiography.Ann Intern Med. 1991; 114: 635-640Crossref PubMed Scopus (338) Google Scholar The rate of systemic embolization is significantly higher in patients who have had a previous embolic event, those in the first 2 weeks of antibiotic therapy, those with left-sided IE especially in the mitral position, those with mobile vegetation that is large (10-15 mm) or increasing in size despite antibiotic therapy, and those patients infected with certain pathogens (S aureus, fungi, enterococci, and HACEK).3Habib G. Hoen B. Tornos P. Thuny F. Prendergast B. Vilacosta I. et al.Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer.Eur Heart J. 2009; 30: 2369-2413Crossref PubMed Scopus (1648) Google Scholar, 12Di Salvo G. Habib G. Pergola V. Avierinos J.F. Philip E. Casalta J.P. et al.Echocardiography predicts embolic events in infective endocarditis.J Am Coll Cardiol. 2001; 37: 1069-1076Abstract Full Text Full Text PDF PubMed Scopus (328) Google Scholar, 15Vilacosta I. Graupner C. San Roman J.A. Sarria C. Ronderos R. Fernandez C. et al.Risk of embolization after institution of antibiotic therapy for infective endocarditis.J Am Coll Cardiol. 2002; 39: 1489-1495Abstract Full Text Full Text PDF PubMed Scopus (331) Google Scholar No vascular bed is immune, but 65% of these pathogens usually affect the brain, 90% in the middle cerebral artery territory. Renal and splenic vascular beds are also commonly involved.16Heiro M. Nikoskelainen J. Engblom E. Kotilainen E. Marttila R. Kotilainen P. Neurologic manifestations of infective endocarditis: a 17-year experience in a teaching hospital in Finland.Arch Intern Med. 2000; 160: 2781-2787Crossref PubMed Scopus (322) Google Scholar When a septic embolus reaches its target, it ends up causing an infarction, an abscess usually with S aureus, or rarely a mycotic aneurysm when the intramural vasa vasora are involved. This is usually followed by wall attenuation and progressive aneurysmal dilatation of the affected vessel. Less virulent organisms usually have a less pronounced local effect. An indolent subacute course triggers an antibody response that puts the patient at risk of immune complex glomerulonephritis. Acute renal failure complicates up to 30% of patients with IE and is associated with a poor prognosis. This is especially true when it is compounded by septic renal embolism, prerenal failure caused by CHF, and the nephrotoxic effects of gentamicin and vancomycin, commonly used in high doses for treating these patients.17Conlon P.J. Jefferies F. Krigman H.R. Corey G.R. Sexton D.J. Abramson M.A. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis.Clin Nephrol. 1998; 49: 96-101PubMed Google Scholar An accurate diagnosis is crucial. Missing a diagnosis likely leads to a poor outcome or death, and overdiagnosing patients leads to exposure to high doses of potentially toxic antimicrobials that are unnecessary. Several defining criteria have been proposed including those by Pelletier and Petersdorf18Pelletier Jr., L.L. Petersdorf R.G. Infective endocarditis: a review of 125 cases from the University of Washington Hospitals, 1963-72.Medicine (Baltimore). 1977; 56: 287-313Crossref PubMed Scopus (393) Google Scholar and Von Reyn and colleagues19Von Reyn C.F. Levy B.S. Arbeit R.D. Friedland G. Crumpacker C.S. Infective endocarditis: an analysis based on strict case definitions.Ann Intern Med. 1981; 94: 505-518Crossref PubMed Scopus (660) Google Scholar; however, the more recent Duke criteria and their revisions in 2000 seem to be the most widely used.20Lamas C.C. Eykyn S.J. Suggested modifications to the Duke criteria for the clinical diagnosis of native valve and prosthetic valve endocarditis: analysis of 118 pathologically proven cases.Clin Infect Dis. 1997; 25: 713-719Crossref PubMed Scopus (156) Google Scholar, 21Li J.S. Sexton D.J. Mick N. Nettles R. Fowler Jr., V.G. Ryan T. et al.Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis.Clin Infect Dis. 2000; 30: 633-638Crossref PubMed Scopus (2872) Google Scholar Based on the latter, a diagnosis is made if any of the following is present: (1) pathologically tested tissue; (2) 2 major criteria; (3) 1 major plus 3 minor criteria; or (4) 5 minor criteria (Table 1). A high pretest probability justifies commencing treatment even if the diagnosis is not definite according to the criteria.Table 1Major and minor revised Duke criteriaMajorMinorPersistent positive blood culture with typical infective endocarditis microorganismPredisposing factor: known cardiac lesion, recreational drug injectionEvidence of endocardial involvement with echocardiogramFever >38°CEvidence of embolismImmunologic problemsPositive blood culture (that does not meet a major criterion) Open table in a new tab Cornerstone major criteria include blood cultures and echocardiographic findings. However, an accurate diagnosis is not always straightforward, given that 25% to 30% of patients in this era present with no previously known cardiac structural abnormality.22Murdoch D.R. Corey G.R. Hoen B. Miro J.M. Fowler Jr., V.G. Bayer A.S. et al.Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study.Arch Intern Med. 2009; 169: 463-473Crossref PubMed Scopus (1492) Google Scholar This is in part due to the more acute rather than subacute disease process taking place with the increased prevalence of S aureus as a causative agent. An accurate diagnosis has been made even more difficult by increasing rates of culture-negative IE. In the United States, 79% of cases with culture-negative IE were found to be due to early administration of antimicrobials or faulty culturing technique, emphasizing their relative importance and how seemingly trivial details may alter or complicate the diagnosis.23Houpikian P. Raoult D. Blood culture-negative endocarditis in a reference center: etiologic diagnosis of 348 cases.Medicine (Baltimore). 2005; 84: 162-173Crossref PubMed Scopus (335) Google Scholar Echocardiography should be done as soon as IE is suspected. The role of echocardiography goes beyond the diagnosis, and repeat echocardiography is recommended on clinical deterioration or when complications are suspected. Echocardiography guides the decision on whether to operate and when, as discussed later. However, the role of transthoracic echocardiography (TTE) in the assessment of left-sided IE is controversial, because of its significantly lower negative predictive values compared to transesophageal echocardiography (TEE).24Shively B.K. Gurule F.T. Roldan C.A. Leggett J.H. Schiller N.B. Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis.J Am Coll Cardiol. 1991; 18: 391-397Abstract Full Text PDF PubMed Scopus (346) Google Scholar, 25Erbel R. Rohmann S. Drexler M. Mohr-Kahaly S. Gerharz C.D. Iversen S. et al.Improved diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approach. A prospective study.Eur Heart J. 1988; 9: 43-53PubMed Google Scholar Although TEE has a near 100% negative predictive value with NVE, it is operator dependent and is far less sensitive for PVE and abscesses of the mitral valve associated with posterior annular calcification.3Habib G. Hoen B. Tornos P. Thuny F. Prendergast B. Vilacosta I. et al.Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer.Eur Heart J. 2009; 30: 2369-2413Crossref PubMed Scopus (1648) Google Scholar, 26Hill E.E. Herijgers P. Claus P. Vanderschueren S. Peetermans W.E. Herregods M.C. Abscess in infective endocarditis: the value of transesophageal echocardiography and outcome: a 5-year study.Am Heart J. 2007; 154: 923-928Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar In these situations, repeat TEE as well as a combination of TTE and TEE might mitigate the limitations caused by acoustic shadowing. Unfortunately, 15% of patients with proven IE were reported to have no echocardiographic findings.27Habib G. Management of infective endocarditis.Heart. 2006; 92: 124-130Crossref PubMed Scopus (154) Google Scholar Managing a patient with IE aims at 2 goals: eradication of infection and restoration of cardiac structures. Eradicating infection, whether medically or surgically, should abort the disease process, and thus prevent further local, hemodynamic, immunologic, or embolic complications. Structural restoration is primarily surgical and is aimed at repairing the damaged tissue in which healing would not be sufficient, and would otherwise have short-term or long-term hemodynamic implications. Once the diagnosis of IE is suspected, at least 3 sets of blood culture samples should be drawn from different sites and at 30-minute intervals.28Bonow R.O. Carabello B.A. Chatterjee K. de Leon Jr., A.C. Faxon D.P. Freed M.D. et al.2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.Circulation. 2008; 118: e523-e661Crossref PubMed Scopus (1152) Google Scholar, 29Lee A. Mirrett S. Reller L.B. Weinstein M.P. Detection of bloodstream infections in adults: how many blood cultures are needed?.J Clin Microbiol. 2007; 11: 3546-3548Crossref Scopus (319) Google Scholar This should be followed immediately by initiation of intravenous empirical antibiotic therapy as shown in Table 2. With no justification for delay, this empirical therapy should be qualitatively bactericidal and quantitatively in high doses for up to 6 weeks. Selecting the best antibiotic for a particular patient should be guided by the presence or absence of previous antibiotic use, whether this is a suspected case of NVE, early PVE or late PVE, and by consultation with the microbiological team regarding epidemiologic clues for pathogen trends and antibiotic resistance at that specific area or facility. A list of generally encountered epidemiologic clues that might guide antibiotic selection has been published previously.30Baddour L.M. Wilson W.R. Bayer A.S. Fowler Jr., V.G. Bolger A.F. Levison M.E. et al.Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America.Circulation. 2005; 111: e394-e434Crossref PubMed Google ScholarTable 2Empirical antimicrobial therapy with early PVE, late PVE, and NVEEarly PVE (<12 months after surgery)NVE and late PVE (≥12 months after surgery)Vancomycin plus rifampin (± gentamicin)Combination penicillins (ampicillin-sulbactam and amoxicillin-clavulanate) (± gentamicin)If intolerant to penicillins: vancomycin plus ciprofloxacin (± gentamicin) Open table in a new tab In general, the nature and pathogenesis of early PVE is different from other forms of IE. NVE and late PVE usually occur with distant blood stream pathogen access, which eventually leads to pathogen adherence at a point in the heart that has been previously predisposed, whether by disease causing a jet and Venturi effect on the low-pressure side or by an implanted prosthesis. On the other hand, early PVE is mostly caused by microbes that can adhere to the annulus-ring interface and to the perivalvular suture pathways when they are coated with fibronectin and fibrinogen before endothelialization takes place. Inoculation typically takes place within the first 60 days after surgery and is usually nosocomial. After this period, and up to 12 months, there is a transition in pathogenesis and causative organisms that ends with complete endothelialization. The mechanism, the microbiology, and the incidence of PVE beyond 12 months are similar to NVE. Both the American Heart Association (AHA)/American College of Cardiology (ACC) and the European Society of Cardiology (ESC) guidelines regard gentamicin as an optional addition to initial combination therapy, because of its presumed synergistic effect with cell-wall inhibitors. The ESC guidelines, however, recommend it for PVE.3Habib G. Hoen B. Tornos P. Thuny F. Prendergast B. Vilacosta I. et al.Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer.Eur Heart J. 2009; 30: 2369-2413Crossref PubMed Scopus (1648) Google Scholar, 28Bonow R.O. Carabello B.A. Chatterjee K. de Leon Jr., A.C. Faxon D.P. Freed M.D. et al.2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.Circulation. 2008; 118: e523-e661Crossref PubMed Scopus (1152) Google Scholar A valid argument against gentamicin has been proposed, given its proven renal toxicity against the background of doubtful benefit.31Cosgrove S.E. Vigliani G.A. Fowler Jr., V.G. Abrutyn E. Corey G.R. Levine D.P. et al.Initial low-dose gentamicin for Staphylococcus aureus bacteremia and endocarditis is nephrotoxic.Clin Infect Dis. 2009; 48: 713-721Crossref PubMed Scopus (222) Google Scholar, 32Fowler Jr., V.G. Boucher H.W. Corey G.R. Abrutyn E. Karchmer A.W. Rupp M.E. et al.Daptomycin versus standard therapy for bacteremia and endocarditis caused by.Staphylococcus aureus. N Engl J Med. 2006; 355: 653-665Crossref PubMed Scopus (1243) Google Scholar These studies recommended the use of daptomycin as a noninferior option for proven staphylococcal infection rather than standard therapy including gentamicin. However, the impact of gentamicin on creatinine clearance did not seem to lead to dialysis or otherwise adversely affect the patients' course in these studies. With the exception of staphylococcal infections, fever should resolve within a few days after starting therapy, and all patients should have surveillance blood cultures after 3 to 4 days of intravenous drug therapy. In a significant number of patients, cultures are negative, and this should never rule out IE. As mentioned earlier, previous antibiotic use is a common reason why cultures are not positive. Also slow-growing or atypical organisms (Q-fever and Bartonella) and fungal infection might be present.30Baddour L.M. Wilson W.R. Bayer A.S. Fowler Jr., V.G. Bolger A.F. Levison M.E. et al.Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America.Circulation. 2005; 111: e394-e434Crossref PubMed Google Scholar, 33Bonow R.O. Carabello B.A. Kanu C. de Leon Jr., A.C. Faxon D.P. Freed M.D. et al.ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons.Circulation. 2006; 114: e84-e231Crossref PubMed Scopus (1960) Google Scholar In most true cases of IE, blood cultures are positive and therapy should be modified accordingly. Lists of different drug regimens, doses, combinations, and durations of therapy for cultured organisms have been published previously.3Habib G. Hoen B. Tornos P. Thuny F. Prendergast B. Vilacosta I. et al.Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer.Eur Heart J. 2009; 30: 2369-2413Crossref PubMed Scopus (1648) Google Scholar, 30Baddour L.M. Wilson W.R. Bayer A.S. Fowler Jr., V.G. Bolger A.F. Levison M.E. et al.Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America.Circulation. 2005; 111: e394-e434Crossref PubMed Google Scholar Medical regimens should not be modified based only on qualitative microbial sensitivity. Minimum inhibitory concentrations (MIC) of specific drugs for specific pathogens should be followed. For example, S aureus exists in strains that are vancomycin intolerant and stop growing in the presence of the drug rather than die. These strains resurge after the treatment stops. Moreover, the high trough levels of vancomycin that are necessary for this growth inhibition are also enough to cripple the patient''s renal function. In this situation, the MIC should guide the substitution of vancomycin with less nephrotoxic alternatives such as daptomycin or teicoplanin.32Fowler Jr., V.G. Boucher H.W. Corey G.R. Abrutyn E. Karchmer A.W. Rupp M.E. et al.Daptomycin versus standard therapy for bacteremia and endocarditis caused by.Staphylococcus aureus. N Engl J Med. 2006; 355: 653-665Crossref PubMed Scopus (1243) Google Scholar, 34Huang J.H. Hsu R.B. Treatment of infective endocarditis caused by methicillin-resistant Staphylococcus aureus: teicoplanin versus vancomycin in a retrospective study.Scand J Infect Dis. 2008; 40: 462-467Crossref PubMed Scopus (12) Google Scholar Generally, antimicrobial combinations are preferred over monotherapy. This increases efficacy, reduces required drug doses and thus adverse effects, reduces the emergence of resistant strains, and shortens the duration of therapy. Aminoglycosides synergize with β-lactams and glycopeptides, and slow-growing or dormant pathogens residing within vegetation or biofilms justify the need for rifampicin for prolonged duration.3Habib G. Hoen B. Tornos P. Thuny F. Prendergast B. Vilacosta I. et al.Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer.Eur Heart J. 2009; 30: 2369-2413Crossref PubMed Scopus (1648) Google Scholar While antibiotic therapy is continued, close monitoring for treatment effectiveness and disease progression is key to the success of treatment. Fever and various indicators of ongoing inflammation have to be followed attentively, renal function and other side effects of the drugs should be anticipated, and complications of disease progression should be vigorously dealt with. The importance of close monitoring shou
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