Subacute Bacterial Endocarditis: Making the Diagnosis Illustration by Kevin A

Subacute Bacterial Endocarditis: making the diagnosis Illustration by Kevin A. Somerville/Phototake ©

Abstract: The presentation of endocarditis varies from patient to patient, making it a difﬁ cult infection to diagnose correctly. While some patients will develop symptoms acutely over days, it may take weeks or months for symptoms to develop as in the case of subacute bacterial endocarditis.

By Kristen Luttenberger, RN, MSN, CCRN, APN; and Mary DiNapoli, RN, MSN, APN-c

G was a 42-year-old man in optimal health who The records indicated normal S1S2 heart sounds with no men- worked full-time and was an active weight lifter, tion of murmur, rub, or gallop. Without any kind of signiﬁ cant R hunter, and ﬁ sherman. RG presented to the internist medical history noted, RG was sent home with a differential with complaints of malaise, shortness of breath, and low-grade diagnosis of bronchitis and viral syndrome and was prescribed fever for weeks. Upon exam, RG had “scattered crackles,” a an oral antibiotic and inhaler. A week later, family members temperature of 100.4º F, slight shortness of breath on exertion, brought RG to the ED due to the inability to walk from bilateral and diaphoresis. Otherwise, the physical exam was normal. lower extremity edema.

Key words: Bacterial endocarditis, subacute bacterial endocarditis, prosthetic valve endocarditis

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Within the next few hours in the ED, RG became confused. pursue a protracted course of weeks to months, cures may The labs returned with a blood urea nitrogen of 45 mg/dL, cre- be produced with antibiotics alone, and a later mortality atinine of 3.3 mg/dL, aspartate aminotransferase-321 units/L, ensues (up to a year) if not treated.9 alanine aminotransferase-408 units/L, total bilirubin-2.4 ABE is characterized by more dramatic symptoms such mg/dL, and negative blood cultures masked by the weeklong as a continuous bacteremia, temperatures spiking over 102º therapy of oral antibiotics. RG developed multisystem organ F, frequent septic embolic complications (metastatic focus), failure from septic shock involving his kidneys, liver, and an acute and virulent organism attacking both damaged heart. A case of subacute bacterial endocarditis (SBE) turned and normal heart valves (more often normal), and a new acute, and a previously unknown bicuspid aortic valve from murmur with valvular destruction.6,8 Due to the dangers birth was the cause. of septic embolic phenomena, myocardial abscesses, valve Although this case ended well with an aortic valve re- destruction, sepsis, and diffi culty curing with antibiotics, placement, mitral valve repair, and a relatively full recovery, ABE is usually treated as a medical emergency requiring car- the lesson for NPs is that the vague symptoms of SBE can be diac valvular replacement. If untreated, an earlier mortality easily misdiagnosed leading to catastrophic results. ensues.8,9 (See Clinical differences between SBE and ABE). Nosocomial endocarditis (NE) is considered a hospital- ■ Defi nitions acquired form of ABE. It has similar characteristics in that it The history of endocarditis dates as far back 1723 where is acute, temperatures over 102º F, and affects normal heart Lazaire Riviere fi rst described gross autopsy fi ndings of the valves. NE is usually related to an intracardiac device placed disease.1 Then it was the Gulstonian lectures of 1885 where in the hospital setting such as temporary central venous cath- Sir William Osler (hence “Osler nodes”) drew a distinction eters, pulmonary artery catheters, and pacemakers. The im- between “simple” and “malignant” forms of the disease. The portance of the skin prep for the introduction of percutaneous “simple” form of endocarditis correlates to what now has central devices cannot be emphasized enough because MSSA become SBE and the “malignant” form is now characterized (methicillin-sensitive S. aureus) and MRSA (methicillin-resis- as an acute onset and fulminant course referred to as acute tant S. aureus) are the usual pathogens of cause.6 Sherwood infective endocarditis (IE) or acute bacterial endocarditis et al. compared outcomes of MSSA endocarditis with MRSA (ABE).2 It is worthy to note that many studies of diagnosis endocarditis and found no signifi cant difference.10 and treatment of endocarditis do not differentiate between Similarly, there is prosthetic valve endocarditis (PVE), acute and subacute disease process, and many principles which involves an infection of a prosthetic cardiac valve of diagnosis and management are identical.3 Some physi- or relating structure. In this situation patients would cian researchers also argue that the distinction between have bacteremia and cardiac vegetation on the prosthetic subacute and acute is not useful for clinical management structure. PVE is frequently caused by coagulase-negative and is arbitrary. The opinion is that the focus of diagnosis staphylococci (CoNS), which is a normal skin fl ora.8,11 The and clinical relevance should be on the causative organism importance of skin prep must be emphasized, along with involved (such as Staphylococcus aureus bacterial endocar- the practitioner’s ability to recognize the possibility of en- ditis).4,5 Some types of endocarditis are also not caused by docarditis in prosthetic valve patients with positive blood bacteria (that is, Haemophilus parainfl uenzae, fungi, culture cultures of CoNS. CoNS may not just be a skin contaminant negative), so using the word “bacteria” in diagnosis may be in these patients. misleading. Nonbacterial thrombotic endocarditis (NBTE) is char- In the literature, clear-cut definitions of SBE versus acterized with small sterile thrombi on the leafl ets of the ABE have been published by Burke A. Cunha, MD, Chief, cardiac valves that do not elicit any infl ammatory reaction Infectious Disease Division, Winthrop-University Hospital, but can become systemic emboli producing infarcts. NBTE Mineola, N.Y.6-8 In Dr. Cunha’s work, he characterizes SBE is usually seen in debilitated patients in a hypercoagulable by fever less than 102º F, a heart murmur, a continuous state, such as cancer or sepsis, and has been referred to as ma- bacteremia with possible aseptic emboli phenomenon, pri- rantic endocarditis in the past. Finally there is Libman-Sacks marily caused by viridian streptococci from the oral cavity, endocarditis, which is occasionally encountered in systemic an avirulent organism causing endocarditis in patients with lupus erythematosus (SLE). These vegetations are sterile preexisting valvular heart disease, and a variety of peripheral and may be encountered with a valvulitis in this disorder.9 manifestations. The majority of organisms responsible for SBE are avirulent/noninvasive pathogens of viridans strep- ■ Epidemiology tococci, which include S. sanguis, S. intermedius, S. sanguinis, Endocarditis accounts for approximately 1 case per 1000 S. anginosus, S. salivarius, S. mutans, and others.6-8 SBE may U.S. hospital admissions, with a range of 0.16 to 5.4 cases

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per 1,000 admissions.4 The American Heart As- sociation (AHA) places the annual incidence of Clinical differences between SBE and ABE IE in the United States at 10,000 to 20,000 new Symptoms SBE ABE 12 cases. Although the primary causes of endo- Anorexia + – carditis have varied, the incidence of the disease Myalgias/arthralgias +/– + has remained relatively the same over the past 30 Fatigue + – years. However, this epidemiology may possibly Dyspnea/cough – + vary due to changes in the diagnostic criteria Pleuritic chest pain/ hemoptysis – + of endocarditis and changes in defi nitions over Lumbar back pain + + time.4 Weight loss +/– – Endocarditis is more common in men and Headache +/– + the incidence increases with age due to the cur- Mental status changes +/– + rent, low incidence of acute rheumatic heart Acute confusional states – + disease.13,14 It is also more commonly involved Unexplained stroke + – with the mitral valve only (40%), followed by the Sudden unilateral blindness + – aortic valve only (36%), and followed by multi- Left upper quadrant pain Splenic Splenic abscess abscess valvular disease.15-17 Signs Rheumatic heart disease was the most com- Fever (° F) <102 >102 mon cause of endocarditis in the preantibiotic New heart murmur – +/– era. Nowadays about 75% of patients who de- Splenomegaly + – velop endocarditis have some type of underlying Petechiae + + structural heart disease (that is, congenital or Osler nodes + – calcifi cation). These include mitral regurgita- Janeway lesions – + tion; aortic valve disease, including stenosis and Splinter hemorrhages + +/– 17-19 regurgitation; and congenital heart disease. Roth spots + – Prosthetic valves (1% to 4% 1st year), prior his- Heart failure – + tory of endocarditis, invasive medical procedures, Laboratory tests drug use, healthcare-associated infections, soci- Anemia + – etal hazards as in body piercings, and some sys- Marked leukocytosis – + temic medical conditions (that is, HIV, end-stage Hematuria, proteinuria, RBC casts + – kidney disease, diabetes mellitus) are also among Microscopic hematuria + +/– risk factors.4,17 The majority of the time a right- Elevated ESR (mm/hour) >50 <50 sided heart valve involvement is a good indica- Elevated RF titer + – tion of I.V. drug abuse (tricuspid valve-78% of Elevated VDRL titer + – cases, mitral-24%, and aortic-8%).4 S. aureus has CSF Aseptic Purulent meningitis meningitis been identifi ed as the most common pathogen profi le profi le 20,21 worldwide in endocarditis, and embolic risk Heart block (ECG) – + has been found to be the highest among the fi rst CXR (septic pulmonary emboli) – + days following the initiation of antibiotics and Brain CT/MRI Usually nega- Possible cere- in cases where the vegetation is very large and tive, possible britis micro- mobile ( greater than 15 mm).22 microembolic abscesses or stroke hemorrhage purulent ■ Pathophysiology meningitis Endocarditis is the infl ammation of the part of Legend: + commonly present the heart that lines the cardiac chambers called +/– uncommonly present the endothelial layer and the endocardium, which – rarely, if ever, present is the origin of the large vessels in direct prox- CSF = cerebrospinal fl uid; MRI: magnetic resonance imaging; RBC = red blood cell. imity to the heart. This inflammation can be Adapted from: Cunha BA, D’Elia AA, Pawar N, Schoch P. Viridans streptococcal (Strepto- attributable to infectious or noninfectious causes coccus intermedius) mitral valve subacute bacterial endocarditis (SBE) in a patient with and mainly refers to the inflammation of the mitral valve prolapse after a dental procedure: the importance of antibiotic prophylaxis. Heart Lung. 2010;39(1):64-72. heart valves themselves. The heart valves consist www.tnpj.com The Nurse Practitioner • March 2011 33

of three normal membranous layers called the fi brosa, the endocarditis). Although not completely understood, the spongiosa, and the laminosa, which are all covered on both absence of white blood cells may likely relate to the dense sides by endothelial cells. There are also different types of nature of the vegetation tissue where the bacteria causing these endothelial cells called microvascular endothelial cells, endocarditis is buried in a nongrowing state deep in the veg- arteriolar endothelial cells, aortic endothelial cells, and ve- etation.25 Specifi cally the vegetations of SBE are associated nous endothelial cells. The function of these endothelial cells with less valvular destruction and have granulation tissue includes regulating vascular tone, permeability, coagulation, indicative of healing at their bases. There lie many dangers in fi brinolysis, and an infl ammatory response to defend against regard to the vegetation. They can erode into the underlying an invading microorganism. When these cells are invaded myocardium and produce a ring abscess. Or, they can em- by an organism, endothelial cell injury and dysfunction bolize causing infection at the sites where the emboli lodge, results with alterations in vascular permeability, leukocyte stroke, or a variety of other dangerous organ infarctions.9,23 and platelet activation and adhesion, and homeostasis. The Even in these modern times of medicine, there is still entire infl ammatory cytokine cascade begins similar to sep- very little known about the specifi c role of the endothe- sis.23 Specifi cally to SBE, Presterl et al. found the decreased lium in the pathogenesis of endocarditis and induction response of patient monocytes to the pathogens may con- of endocardial infl ammation. Studies continue to analyze tribute to the low-grade infl ammatory response and to the the ability of bacteria to attach to the endothelial cells by course of streptococcal endocarditis.24 The destructive na- means of cell-envelope glycopolymer found on certain ture of endocarditis is a result of pathogens exerting a brisk specifi c bacteria such as teichoic acid, lipoteichoic acid, and infl ammatory response. Monocyte attraction, ulceration, fi bronectin.23 Banks et al. identifi ed two bacterial proteins tissue destruction, and fi brotic scarring eventually affect (involving S. Sanguis endocarditis) as being responsible for valve function and myocardial hemodynamics. In addition the majority of the cytokine induction. They hypothesized to this immune response, the type of pathogen itself largely that these proteins, or the receptors to which they bind, may impacts the course and severity of endocarditis.23 be therapeutic targets and may allow the development of Many researchers view the hallmark of endocarditis as adjunctive therapies to prevent endocardial damage during the presence of friable, bulky, potentially destructive vegeta- the treatment of endocarditis.26 tions containing fi brin, infl ammatory cells, and bacteria or other organisms on the heart valves.9 Vegetations develop ■ Presentation due to the previously mentioned infl ammatory activation History of the endothelium, which disrupts the endothelial cell bar- The presentation of endocarditis varies from patient to pa- rier in many ways. When viewed under a microscope, white tient, making it diffi cult sometimes to diagnose correctly as blood cells that the body uses to fi ght infection are uncom- in the previous case study. While some patients will develop mon. This fi nding explains why antibiotics are needed for symptoms acutely over days, others’ symptoms develop over many weeks to kill the infecting organism (see Bacterial weeks or months as in SBE. Most patients complain of fever and nonspecifi c constitutional symptoms, such as fatigue, malaise, and weight loss, along with 50% complaining of Bacterial endocarditis frank arthritis to diffuse myalgias.27 It is important to note that patients who report muscular skeletal symptoms that have been misdiagnosed as rheumatic disorders may be inap- propriately treated with steroids.8 These patients may actually have SBE. With the use of corticosteroids for nonspecifi c symptoms, SBE can be easily masked and therefore the diagnosis of endocarditis can be delayed. Other chief complaints may include dyspnea, headache, backache, chills, chest pain, and anorexia.1 The presentation of ABE varies from SBE in that they are resulting from either embolic or intracardiac suppura- tive complications. ABE’s onset is abrupt, and causes rapid progressive destruction of the infected valve. The infected

Source: Rubin R, Strayer D, eds. Rubin’s Pathology: Clinicopathologic valve is destroyed by the bacteria that rapidly multiply Foundations of Medicine. 5th ed. Philadelphia, PA: Wolters Kluwer/ within the friable vegetations. The complications that de- Lippincott Williams & Wilkins. 2008:462. velop include severe dyspnea and fatigue resulting from

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heart failure (HF), neuropsychiatric complications that to make a defi nitive diagnosis. (See Modifi ed Duke criteria result from central nervous system (CNS) involvement, and for the diagnosis of IE). overall signs of a septic picture.1 In the review of symptoms, questions should include any Lab tests history of abrupt onset or a protracted course of fl ulike symp- The criterion standard test for diagnosing SBE is the doc- toms. Because it is well known that bacteremia can result from umentation of a continuous bacteremia based on blood various invasive procedures, the patients should be questioned culture results. The growth of Gram-positive bacteria is on any history of periodontal disease and/or dental work, the most common pathogens causing endocarditis. Staphy- preexisting heart anomalies, or history of gastroinstinal and lococcal endocarditis is the most severe form of the disease, urinary tract procedures. The potential for invasive procedures occurring in 3 to 4 cases per 10,000 hospital admissions, and to produce a bacteremia varies greatly; however, healthcare- in 10% to 25% of endocarditis cases.29 Streptococcus viridans associated bacteremias (mostly associated with intravascular is also one of the more common organisms causing SBE, and lines) have more than doubled in the last few years.1 most commonly occurs in the setting of preexisting valvular disease. Exceptions to positive blood cultures are observed ■ Physical exam on patients with PVE and right-sided IE.1 False-negative Due to the sometimes vague symptoms of SBE, an extremely culture results are also seen with prior use of antibiotics. thorough physical exam needs to be performed. Fever is In diagnosing SBE, three to fi ve sets of blood cultures are present in nearly 50% of patients in most studies; however, needed for confi rmation of diagnosis. Other lab work should elderly patients and patients with renal failure or heart fail- include complete blood cell count with differential to evalu- ure may be less likely to have a febrile response.27 Embolic phenomena may be present, such as petechiae, splinter Embolic phenomena may be present, hemorrhages, and Osler nodes, all of such as petechiae, splinter hemorrhages, which are seen on the skin of the hands and feet, as well as the conjunctiva and and Osler nodes. palate.5 Osler nodes have been traditionally reported as painful red-purple raised cutaneous nodules in association with SBE, which ate anemia, possible leukocytosis with a left-sided shift, along may exemplify more pathogenesis of an immunologic phe- with elevated erythrocyte sedimentation rate (ESR), RF titer, nomenon. Although some crossover is hypothesized among and Venereal Disease Research Laboratories (VDRL) titers. the two types of skin lesions, the painless Janeway lesions Hematuria may also be present in urinalysis. are believed to be more associated with ABE, and be more a product of the septic microemboli.28 Eighty-fi ve percent CXR of patients have a new, audible murmur, either systolic or A chest X-ray with an anterior/posterior and lateral view diastolic, and any evidence of heart failure is a late sign. may be abnormal, with consolidation, atelectasis, pleural Splenomegaly is also a fi nding that is commonly present effusions, or evidence of HF. Septic pulmonary emboli may on physical exam in SBE. Finally, a neurologic exam should be present in ABE. be included for any signs of major vessel embolism, visual fi eld defects, or altered mental status, and also to serve as a Imaging studies baseline for any changes in the future. Purulent meningitis Primarily performed in the diagnostic workup of SBE, a may be observed in patients with ABE compared with the 2-D transthoracic echocardiogram (TTE) can detect 85% aseptic type observed in SBE.1 of vegetations.1 Transesophageal echocardiograms (TEE) are indicated when the patient has a mechanical prosthetic ■ Diagnosis valve or to visualize any myocardial abscesses. Immunos- The diagnosis of SBE is usually through the gold standard cintigraphy with Tc-Fab-1 fragments in combination with of positive blood cultures, along with presenting clinical TEE improves diagnostic accuracy with TTE/TEE in patients symptoms. In the diagnosis of this disease, the most widely with SBE.30 ECGs are done to detect whether there is any accepted clinical criteria is the Duke criteria, which have an conduction delays that may be present. Multislice computed estimated 76% to 100% sensitivity, and 88% to 100% speci- tomography (CT) scans of the chest for valvular images and fi city, with a negative predictive value of at least 92%.27 This also of the head (for those who show CNS symptoms) are criterion relies on blood culture and echocardiogram data also helpful in the diagnostic workup. www.tnpj.com The Nurse Practitioner • March 2011 35

■ Complications in left-sided SBE, whereas pulmonary embolism is frequent The mortality in non-I.V. drug users with acute/subacute in right-sided and pacemaker lead SBE.22 These embolic endocarditis with S. aureus is approximately 40%.31 Valve re- events are a frequent and sometimes life-threatening com- placement may be required, especially when the aortic valve plication of SBE, and are associated with higher mortality is involved in ABE.32 Complications occur when vegetations and morbidity. Sepsis and multisystem organ failure may embolize to blood vessels and organs causing mycotic an- also result in severe cases of ABE that have either gone too eurysms, infarcts, abscesses, and arteritis.33 Cerebral arteries far without ample treatment (late diagnosis) or are not and the spleen are the most frequent sites of embolization responding to present treatment.

■ Modifi ed Duke criteria for the diagnosis of IE Treatment The primary goals of therapy for IE are to MAJOR CRITERIA eliminate the infectious agent and address Blood culture positive the complications, if any, of the valvular in- • Typical organism (x-hemolytic streptococcus, S. bovis, HACEK organ- fection. In heart failure, which results from isms [Haemophilus species, Actinobacillus actinomycetemcomitans, insuffi ciency of the valve affected, medical Cardiobacterium hominis, Eikenella corrodens, and Kingella species]., or community-acquired S. aureus or enterococcus management is the treatment of choice. If without a primary focus ) from two separate blood cultures the disease is progressive, despite achieving • Persistent bacteremia with any organism (two positive cultures >12 a cure with antibiotic therapy, valve surgery hours apart or three positive cultures or a majority of four or more is the end choice of treatment. cultures >1 hour apart • Bacteremia with S. aureus, regardless of whether the bacteremia was Traditionally, antibiotic therapy has been nosocomially acquired or whether a removable focus of infection is found the standard of care and the main choice of Evidence of endocardial involvement treatment for SBE. In SBE, treatment may • Echocardiographic fi ndings: mobile mass attached to valve or valve be safely delayed until results of the cultures apparatus, or abscess, or new partial dehiscence of prosthetic valve and sensitivities are available, if the patient • New valvar regurgitation is clinically stable without evidence of HF or Serology end-organ complications. I.V. administra- • Single positive blood culture for Coxiella burnetii or antiphase tion of antibiotics for 4 to 6 weeks has been 1 immunoglobulin G antibody titer >1:800 the preferred, traditional route because of MINOR CRITERIA the more reliable therapeutic levels that are • Predisposing condition: I.V. drug use or predisposing cardiac condition achieved. Definitive treatment with anti- • Temperature >38° C biotics is guided by the responsible patho- • Vascular phenomena: arterial embolism, septic pulmonary emboli, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, gen that has been isolated from the culture Janeway lesions specimens. When the correct organism or • Immunologic phenomena: glomerulonephritis, Osler nodes, Roth pathogen has been clearly identifi ed, the cul- spots, rheumatoid factor ture sensitive treatment regimen can begin. • Echocardiogram fi ndings consistent with endocarditis but not meeting major criteria The standard therapy for endocarditis that • Microbiologic evidence: positive blood cultures not meeting major criteria is caused by enterococci includes penicillin or serologic evidence of active infection consistent with endocarditis or ampicillin plus gentamicin. When the en- Defi nite Infective Possible Infective Rejected Infective docarditis is caused by S. aureus, the choice Endocarditis Endocarditis Endocarditis of antibiotics is nafcillin plus gentamicin or • Pathologically • Findings that • Firm alternative diagnosis vancomycin or daptomycin plus gentamicin. proven infective fall short of • Resolution of infective Another alternative is cefazolin plus genta- endocarditis defi nite infective endocarditis syndrome micin. These types of combination therapies • Clinical criteria endocarditis but with antibiotic therapy meeting either 2 not rejected of 4 days or less are the most appropriate empirical coverage major criteria, or • No pathologic evidence for patients with native valve endocarditis 1 major and three of infective endocarditis (NVE). If MRSA is suspected and/or con- minor criteria, or at surgery or autopsy fi rmed, the drugs of choice are vancomycin 5 minor criteria with antiobiotic therapy of 4 days or less and gentamicin, as well as with patients who are penicillin allergic. In those cases where Adapted with permission from Li JS, Sexton DJ, Mick N, et al. Proposed modifi cations to the Duke patients have a PVE, the treatment of choice criteria for the diagnosis of infective endocarditis. Clin Infect Dis. 2000; 30(4):633-638. is vancomycin, gentamicin, and rifampin.1,5

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Patients should have blood cultures taken after 3 to 4 tions with a high to moderate risk of SBE. These condi- days of treatment to document the eradication of the bac- tions include prosthetic heart valves, history of bacterial teremia and are especially important if persistent fever or endocarditis, complex cyanotic congenial heart disease, other signs develop that suggest failing treatment. Failure congenital malformations, acquired valvular heart disease, to eradicate the bacteremia or fever lasting longer than 10 mitral valve prolapsed with regurgitation, and hypertrophic days should prompt a search for superlative complications cardiomyopathy. These cardiac conditions all required pro- (for example, abscesses or metastatic infections).1 phylactic antibiotics depending on type of procedure being Patients with IE/SBE may eventually require surgery. In performed.12,37 patients who have a NVE, the primary indicator for surgery In April 2007, the AHA revised the guidelines about the is heart failure. This is especially indicated when during role of antimicrobials in the prevention of IE.12 These new antibiotic therapy, or after completion of antibiotics, there guidelines were based on in vitro studies, clinical experi- is a second relapse of symptoms. Patients with paravalvular ence, and experimental animal model, rather than random- abscess or persistent hypermobile vegetations should be ized controlled clinical trials. They recommended a more treated with surgery,1 especially in those with history of narrowed range in cardiac conditions and medical/dental embolization and fevers after 7 days of antibiotic therapy. procedures when antibiotic prophylaxis is indicated. The Mitral valve repair using Carpentier techniques in patients AHA concluded that antibiotic prophylaxis may prevent with active endocarditis offers very good long-term re- only a small number of SBE cases for those patients who sults with a low rate of recurrence or reoperation.34 Early undergo invasive procedures and also that there is a greater surgery for NVE is associated with an in-hospital mortality benefi t compared with medical therapy alone.35 If early Future considerations for the treatment surgical intervention is necessary then of endocarditis include improvements in antibiotic therapy is still required for 4 to 8 weeks after the procedure. cardiac imaging technology. Finally, in an attempt to decrease length of stay and prolonged parenteral therapy, I.V.–to-oral switch programs have been used suc- risk in the adverse reactions of the antibiotic rather than cessfully to treat ABE/SBE caused by a variety of organisms.36 the proven benefi t from prophylaxis. The recommendation Most patients in need of long-term I.V. antibiotics require a is to use antibiotic prophylaxis for those individuals only peripherally inserted central catheter line that necessitates at high risk for SBE. These include individuals with pros- additional patient education and monitoring. thetic heart valves, a history of infectious endocarditis, an unrepaired congenital heart disease, a repaired congenital ■ Prognosis heart defect with prosthetic material or a device, any re- When IE/SBE is left untreated, the end result is usually fatal. paired congenital heart defect with residual defects near However, with aggressive medical and possibly surgical treat- the prosthetic device, or cardiac valvulopathy in a trans- ment, the outcomes for patients are dramatically different. planted heart.12,38 The AHA also created a wallet card that For the appropriately managed NVE patient the cure rates specifi cally details the dosage/antibiotics for those patients are as follows: S. viridans and S. bovis infection-98%, en- at risk for endocarditis. terococci and S. aureus infection who abuse I.V. drugs-90%, community-acquired S. aureus infection in individuals who ■ Conclusions do not abuse I.V. drugs-60% to 70%, infection with aerobic Future considerations for the treatment of endocarditis Gram-negative organisms-40% to 60%, and infections with include improvements in cardiac imaging technology for fungal organisms-less than 50%. For appropriately managed the diagnosis of the presence of vegetation. Agents that PVE, the cure rates are 10% to 15% lower for all previously prevent the formation or promote the dissolution of the mentioned organisms in NVE, surgery is required more vegetation are also being examined, along with the ongoing frequently, and approximately 60% of early CoNS PVE cases improvement in antibiotics. This improvement includes the and 70% of late CoNS PVE cases are curable.1 investigation of involving cell wall-specifi c enzymes and antibacterial antibodies that act as adjuncts to antibiotics ■ Prevention in facilitating bacteriologic clearance.4 In 1997, the AHA guidelines recommended prophylactic SBE can have serious consequences, and the potential antibiotics for the prevention of SBE for cardiac condi- for malpractice litigation due to failure to diagnose or www.tnpj.com The Nurse Practitioner • March 2011 37

delayed diagnosis accompanied by a poor outcome for the 16. McDonald JR, Olaison L, Anderson DJ, et al. Enterococcal endocarditis: 107 cases from the International Collaboration on Endocarditis Merged patient. There have been documented case studies of failure Database. Am J Med. 2005;118(7):759-766. of the current AHA recommendations even when they 17. McDonald JR. Acute infective endocarditis. Infect Dis Clin North Am. are applied appropriately.7 Therefore, NPs must follow 2009;23(3):643-664. 18. Michel PL, Acar J. Native cardiac disease predisposing to infective the revised 2007 AHA guidelines, keeping in mind that they endocarditis. Eur Heart J. 1995;16(suppl B):2-9. may need modiﬁ cation in particular circumstances based 19. Weinberger I, Rotenberg Z, Zacharovitch D, Fuchs J, Davidson E, Agmon on the individual clinical setting and risk of developing SBE. J. Native valve infective endocarditis in the 1970s versus 1980s: underlying cardiac lesions and infecting organisms. Clin Cardiol. 1990;13(2):94-98. Overall, the key to maximizing treatment success is knowl- 20. Murdoch DR, Corey GR, Hoen B, et al. Clinical presentation, etiology, and edge of this disease process and early diagnosis. SBE is outcomes of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. complex, and the clinical team must have an understanding 2009;169(5):463-473. of the epidemiology, microbiology, and natural history of 21. Fowler VG Jr, Miro JM, Hoen B, et al. Staphylococcus aureus endocarditis: a endocarditis, as well as a grasp of the AHA guiding prin- consequence of medical progress. JAMA. 2005;293(24):3012-3021. 22. Habib G. Embolic risk in subacute bacterial endocarditis: determinants and ciples of prophylaxis, diagnosis, and medical and surgical role of transesophageal echocardiography. Curr Card Rep. 2003;5:129-136. management. 23. Presterl E, Rokita E, Graninger W, Hirschi AM. 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