Infective endocarditis: a review for nurses.

Infective Endocarditis

Infective Endocarditis A Review for Nurses Linda Josephson, MS, RN, CCRN-CMC

Infective endocarditis (IE) is a relatively uncommon condition that can present with a variety of noncardiac symptoms, making diagnosis of this condition challenging. Although IE is no longer uniformly fatal as it was in the preantibiotic era, it still has a high mortality rate. The major risk factor for IE, rheumatic fever, has decreased significantly in the industrialized west, but the incidence of IE remains as high as it was in the preantibiotic era. Today, IE has changed from a disease primarily of the young to one of the elderly. The increase in frequency of IE seems to be related to the fact that individuals are now living longer with chronic heart diseases and are having invasive medical procedures performed more often. The 2 main approaches to treating IE are the use of antibiotics and cardiac surgery. This article provides an overview of IE, epidemiology, pathogenesis, clinical manifestations, diagnosis criteria, and treatment options for IE. Keywords: cardiovascular diseases, infective endocarditis [DIMENS CRIT CARE NURS. 2014;33(6):327/340]

INFECTIVE ENDOCARDITIS: A CASE STUDY* AND REVIEW Mr Michael Kelleher is a 63-year-old man who presents to the emergency department of his local hospital with a chief complaint of difficulty speaking and weakness on his right side. These symptoms appeared when he awoke this morning. He has been brought to the hospital by his wife. Prior to going to bed last night, he had been in his usual state of health, with the exception of a flulike illness (Table 1). Michael has a medical history of well-controlled hypertension and type 2 diabetes mellitus. When asked about her husband’s state of health, Mrs Kelleher explains that he has not been feeling well for the past few weeks. His symptoms have been malaise, fatigue, and a low-grade fever. They had seen their primary doctor a week and half ago, and *Case study and name are fictitious.

DOI: 10.1097/DCC.0000000000000081

Mr Kelleher has been advised to rest, continue to take ibuprofen, and stay hydrated. In the emergency room, Michael is quickly triaged and sent for a noncontrast head computed tomography, which indicates that he has had an embolic stroke. However, because he awoke with the symptoms, it is not possible to determine a time for when the symptoms began, and he is not eligible for treatment with tissue thromboplastin.

Disposition Michael is admitted to the medical intensive care unit (ICU) with diagnosis of a new-onset embolic stroke and new-onset heart failure. Within 24 hours of his admission, Michael’s clinical condition has deteriorated. His heart failure is not improving with treatment, and he is not responding to diuresis. His renal function continues to worsen as his creatinine and November/December 2014

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TABLE 1 System

Neurological

Significant Findings From Michael’s Physical Examination Findings

Awake and alert; oriented to person, place, and time, but having difficulty speaking There is weakness of the right side, with the leg more affected than the arm

Cardiac

Heart rate is 94 beats/min; auscultation reveals a systolic murmur at the apex, which has not been documented before There is a left bundle-branch block seen on the electrocardiogram that also has not been documented before Blood pressure is 90/46 mm Hg with a mean arterial pressure of 58 mm Hg First troponin I is negative

Pulmonary

Respiratory rate is 24 with mild shortness of breath; pulse oximetry is 88% on room air Auscultation of lung fields reveals rales (crackles) one-third up bilaterally

Genitourinary

A urinary catheter is inserted, but only 50 mL of very concentrated urine is obtained

blood urea nitrogen levels increase (on admission, his creatinine was 1.5 mg/dL, and it is now 2.1 mg/dL; admission blood urea nitrogen was 45mg/dL, and now it is 75 mg/dL). A renal consult is placed, and a temporary dialysis catheter inserted. Shortly after this, Michael’s breathing, which has been tachypneic and labored, requiring increasing amounts of oxygen, worsens to the point that emergent endotracheal intubation and mechanical ventilation become necessary. Later that day, despite initiating continuous renal replacement therapy (CRRT), Michael’s heart failure does not improve. In the afternoon, Michael’s cardiac monitor shows a new onset of a high-grade atriovenous block, second-degree atriovenous block, Mobitz II, which is confirmed with a 12-lead electrocardiogram. The ICU attending physician asks for cardiac consult, and on recommendation of that consult, an emergent transesophageal echocardiogram (TEE) is done, and 2 sets of blood cultures are drawn. The TEE demonstrates vegetation on the mitral valve with a suspected perivalvular lesion around the mitral valve. After the 2 sets of blood cultures are drawn, broad-spectrum antibiotics are ordered, to cover the most likely causes of infective endocarditis (IE). A cardiac surgeon is consulted to evaluate Michael for potential replacement of the mitral valve and treatment of the perivalvular lesion. The cardiac surgeon sees Michael within a few hours, and surgery is planned for the next morning. The next day, Michael has open heart surgical re328

Dimensions of Critical Care Nursing

placement of the mitral valve and excision of the perivalvular lesion. He is then transferred to the surgical cardiac ICU for recovery from surgery. In the meantime, his blood cultures have come back with a preliminary result; all culture bottles show growth of Staphylococcus aureus. Michael’s physician has consulted infectious disease, and their recommendation is to continue Michael on his present course of intravenously administered (IV) antibiotics for the next 6 to 8 weeks (IV vancomycin). After his surgery, Michael begins to improve. He no longer has cardiac arrhythmias, and his temperature returns to normal for the first time in close to 3 weeks. He is now responding well to the CRRT, and his blood urea nitrogen and creatinine levels decrease. His lung compliance improves as shown by decreasing peak inspiratory pressures. Michael was able to be extubated on the second postoperative day, and CRRT stopped the next day. Two weeks after his admission, Michael is discharged to rehabilitation. Because of the placement of an artificial mitral valve, and now a history of IE, he remains at high risk for developing IE in the future. Michael will need to have antibiotics given prophylactically when he has high-risk procedures, including dental work done.

History of Infective Endocarditis Historically, IE was a difficult condition to understand and diagnose. Several centuries past between the first descriptions of IE that occurred in the medical literature and a rudimentary understanding of the pathogenesis of the disease occurred.1 Even today, recognition and diagnosis of IE can be difficult. In North America, it was William Osler who has been associated with an improved understanding and treatment of this condition.2 In 1885, Osler3 was asked to deliver the Gulstonian Lecture to the Royal College of Physicians in London. In that lecture, Osler presented a cogent description and summary of what was then known concerning the pathogenesis and treatment of IE.2,3 Osler’s presentation and summation of the condition have become a landmark event in the treatment of IE in North America. At the time of the lecture, the condition was known as malignant endocarditis. This was a reference to the severity and progressively worsening nature of the disease at that time. As the condition was later better understood, it was called bacterial endocarditis in recognition that bacterial infection was the cause of the endocarditis. Later, the name became infective endocarditis, reflecting the understanding that endocarditis can be caused by a number of organisms other than just bacteria.2 Osler described a triad of clinical findings pertinent to the presentation of IE: fever, heart murmur, and hemiplegia. In Osler’s day and prior to the advent of antibiotics, IE was an unvaryingly fatal condition.4,5 Even today, even with the advent of antibiotics, IE remains a difficult condition to treat. Its rate of occurrence is comparable to what it was in the preantibiotic era, and some authorities believe it may even

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exceed what it was in the preantibiotic era.4,5 However, changes in diagnostic criteria and tools make comparisons between contemporary occurrence and those in the past difficult.6

slower, it was no less deadly than the acute form was.4,5,10 This traditional classification of endocarditis is not as useful today as it has been in the past, and a more current classification that is based on the site and cause of the disease is in use.5

Epidemiology

NATIVE VALVE ENDOCARDITIS

The actual incidence of endocarditis is not precisely known, as this is not a reportable disease, and definitions have varied according to different authors, studies, and medical centers.6 A recent study using national statistics for hospital admissions estimated the incidence of IE for 2009 to be about 12.7 cases per 100 000 person-years. This is more than had previously been thought and indicates that IE is more common in the United States than has been realized. Furthermore, this study showed that the mean age for admission to hospitals due to IE was 60.8 years and that the number of patients admitted with IE who had intracardiac devices rose from 13.3% to 18.9%. Men are more prone to developing IE than are women; there is a male-to-female ratio of 1.7.1,4,6,10-12 Until the modern era, endocarditis was chiefly a disease of younger people, with rheumatic heart disease being the main causative factor. However, the successful use of antibiotics has resulted in a dramatic decrease in the occurrence of rheumatic fever in both the United States and Western Europe since the middle of the 20th century.7 Despite this decrease in rheumatic fever, the incidence of IE does not seem to have declined in the modern era. No longer a disease primarily of younger people, IE has undergone a ‘‘graying,’’ and older individuals are affected more frequently than are younger people. Endocarditis is now becoming a disease of the aged.8,9 The increased incidence of IE among older people is due to several factors. Our population is aging, and people are living longer with chronic heart conditions. Chronic heart diseases predispose individuals to the risk of developing endocarditis when bacteremia occurs. Also, this segment of the population is more apt to have invasive procedures done, and implanted devices placed, which is now a significant risk factor for the development of endocarditis. Another significant factor that has caused a change in the profile of patients affected by endocarditis is IV drug abuse. Individuals who abuse IV drugs are at greater risk for developing endocarditis. Individuals who use IV drugs tend to have valves on the right side of the heart affected, whereas endocarditis tends to develop on the left side for most other individuals.4,5,9,10-12

Native valve endocarditis (NVE) is the most common among patients who have a preexisting heart lesion. The most common type of preexisting heart lesion is mitral valve prolapse. If there is any degree of mitral valve regurgitation associated with the mitral valve prolapse, then the risk for IE increases to 52 per 100 000 person-years.4,6,8,9 Other underlying conditions that predispose to the development of IE are calcific aortic stenosis, which accounts for up to 50% of elderly patients who develop IE.9

Classification of Infective Endocarditis The traditional classification for endocarditis was either subacute or acute. Acute endocarditis had a more rapid onset and progression of the disease, with more severe symptoms; in contrast, subacute endocarditis had a more insidious onset and longer course of illness, with the symptoms not as severe. In the past, although the course of subacute endocarditis was

PROSTHETIC VALVE ENDOCARDITIS Prosthetic valve endocarditis (PVE) is the most severe form of IE with a high mortality rate of 20% to 40%. Prosthetic valve endocarditis accounts for 20% of all cases of IE, and the incidence is increasing, with about 5% of all valves, bioprosthetic and mechanical, becoming infected.9 Diagnosis of PVE is more difficult than NVE, because the symptoms tend to be more atypical and can be easily accounted for by other causes, especially in the early postoperative period. Prosthetic valve endocarditis that occurs within 60 days of surgery is considered to be early PVE. There is now research that indicates S aureus may be the most common causative organism of both early and late PVE. When PVE is associated with heart failure, intracardiac abscesses, or fistulas, it is considered to be complicated PVE, which is associated with a higher mortality rate. Patients with complicated PVE should be considered for early surgical treatment.4,9

NOSOCOMIAL INFECTIVE ENDOCARDITIS Nosocomial infective endocarditis has been defined as any IE that occurs within 48 hours after a patient has been admitted to the hospital or that occurs in association with a procedure that has been performed within 4 weeks of the manifestation of the IE.14-17 Insertion of central IV catheters, such as pulmonary artery catheters or transvenous pacing wires, has been associated with damage to the right-sided valves and infection of those valves.17 However, any bacteremia can result in IE, and IE has been associated with genitourinary and gastrointestinal procedures and surgical wound infections.9

PACEMAKER ENDOCARDITIS Pacemaker endocarditis (PE) is a relatively new category of endocarditis; it is caused by an infection due to an implantable device, such as a pacemaker or automatic implantable cardioverter defibrillator.18 Although a rare complication November/December 2014


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of having an implantable device inserted, it is nonetheless a serious one. Pacemaker endocarditis can result from infection of the generator pocket, infection of the leads, or infection of the distal portion of the lead that is in contact with the endocardium. This last instance is the least common of the PE and is the most difficult to treat.5,9 The majority of cases of PE are caused by staphylococci, both coagulase negative and positive.18

INTRAVENOUS DRUG USERS This group represents a distinctive subgroup of NVE. The risk for IE among this group is several times greater than that of patients with rheumatic heart disease or prosthetic valves.4,5,12 The majority of patients who are intravenous drug abusers and develop IE are men in their 20s and 30s.4,5,12 The microbiology for this group of patients is different than that for other groups and has a tendency to affect the valves of the right side of the heart. For this group of patients, S aureus is the main microorganism responsible for the infection.12 Intravenous drug abusers who have abnormal left-sided valves experience IE at about the same rate as the general population does. However, these infections are increasingly being caused by Pseudomonas aeruginosa, other gramnegative bacilli, fungi, and other atypical agents.4,12 Among intravenous drug abusers who are HIV positive, the clinical course and survival of IE do not seem to be very different from other groups, unless the CD4 count is less than 200/HL.4

Etiology Although there are a number of microorganism that can cause IE, the majority of cases of IE are due to a fairly

narrow range of bacteria. The majority of cases of IE are caused by staphylococci (both coagulase positive and negative), streptococci, and enterococci. These bacteria have the greatest ability to adhere to damaged valves and account for more than 80% of all cases of IE. Recent epidemiological studies indicate that S aureus has become the most common cause of IE, replacing Streptococcus viridans as the main cause of IE. Streptococcus viridans is now the second most common causative organism of IE.4,6,17,19 The causative microorganisms of IE differ somewhat based on the portal of entry.4,20 Native valve endocarditis tends to be caused by viridans streptococci, staphylococci, and the HACEK (Haemophilus parainfluenzae, Aggregatibacter aphrophilus, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) organisms that gain entry through the oral cavity, skin, and upper respiratory tract. Nosocomial endocarditis related to gastrointestinal manipulation is caused by Streptococcus bovis. Streptococcus bovis is also associated with polyps and colonic tumors. Infective endocarditis due to bloodstream infection caused by nosocomial factors tends to be associated with S aureus.4 Infective endocarditis caused by other nosocomial infections also tends to be caused by S aureus4,14,17 (Figure; Table 2).

STAPHYLOCOCCUS AUREUS This organism is the major cause of IE in all population groupsVit is the organism most responsible for IE, which is noted from large international series involving tertiary health care centers.4,21-23 Infection caused by S aureus is characterized as a toxic and severe febrile illness with frequent spread of infection from the heart to the periphery.

Figure. Factors leading to development of infective endocarditis. 330


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TABLE 2

Bacterial Causes of Different Types of Endocarditis Intravenous Drug Abuse

Causative Organism

Native Valve Endocarditis

Prosthetic Valve Endocarditis

Right Left Sided Sided

G12 mo

912 mo

S aureus

35%

77%

23%

25%

17%

Streptococci

32%

5%

15%

2%

28%

Enterococci

8%

2%

24%

10%

14%

Coagulase-negative staphylococci

4%

29%

12%

Gram-negative bacilli

3%

13%

13%

5%

Fungi

1%

12%

8%

2%

HACEK group

3%

Polymicrobials

6%

8%

10%

3%

5%

Culture negative

5%

3%

3%

8%

9%

5%

4%

Compiled from Karchmer,4 Habib et al,17 and Harrison et al.19 Abbreviation: HACEK, Haemophilus parainfluenzae, Aggregatibacter aphrophilus, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae.

Staphylococcus aureus is also responsible for infection of the valves and other cardiac tissues and frequently causes abscesses and fistula. Most patients with S aureus IE develop heart murmurs as a consequence of the damage that is done to the valve tissue by this organism. Staphylococcus aureus carries with it a high mortality rate, more than 40%.4,21-23

COAGULASE-NEGATIVE STAPHYLCOCCI In contrast to S aureus, which is a single species, this group of bacteria is made up of 13 different species. Coagulasenegative staphylococci have emerged as an important pathogen in nosocomial IE. In particular, Staphylococcus epidermidis is a frequent cause of IE in health careYassociated infections, implanted devices, PVE, and for about 8% to 10% of NVEs. Infective endocarditis caused by coagulase-negative staphylococci is often complicated and fatal.4

VIRIDANS STREPTOCOCCI These organisms are part of the normal flora of the human oropharynx, and in developed countries, they cause 18% to 30% of NVEs.4,6,19

STREPTOCOCOCCUS BOVIS (STREPTOCOCCUS GALLOLYTICUS) Now known as Streptococcus gallolyticus, this organism is a normal part of the gastrointestinal tract and causes 20%

to 40% of NVEs. When S gallolyticus is identified as the cause of IE, a colonoscopy is justified and should be done, because S gallolyticus is associated with the presence of polyps or malignant disease in the colon.4,6,19

OTHER STREPTOCOCCI Group A streptococci, or Streptococcus pyogenes, are an unusual cause of endocarditis. In intravenous drug abuse, it has been known to cause an IE similar to S aureus.12 Group B streptococcus (Streptococcus agalactiae), which is a normal part of the mouth, gastrointestinal tract, and genital tract, has the ability to infect both abnormal and normal valves. Group B streptococci cause a severe NVE that has a high incidence of systemic emboli and septic musculoskeletal complications. The $-hemolytic group of streptococci (groups A, B, C, and G) also are capable of infecting normal valve tissue, and infections by these bacteria result in an endocarditis that has frequent intracardiac and extracardiac complications.4,6,19

ENTEROCOCCI Most IEs caused by enterococci are due to Escherichia faecalis and Escherichia faecium. These bacteria are normally found in the gastrointestinal tract and often result in genitourinary infections. They cause both NVE and PVE in about 5% to 15% of the time.4,19

GRAM-NEGATIVE BACTERIA The HACEK organisms are a normal part of the upper respiratory tract and oropharyngeal flora. They are a group of gram-negative bacteria that are slow growing and prefer an enriched carbon dioxide atmosphere. These organisms all have an enhanced ability to cause IE. Together they account for 5% to 10% of the cases of IE. The HACEK group is the most common gram-negative cause of IE among individuals who do not use IV drugs. Because these bacteria are slow growing, they do not reproduce on regular agar plates. So they can cause a ‘‘culture-negative’’ endocarditis.4,16,19

Pathogenesis of Infective Endocarditis Endocarditis is the result of a complex interaction that occurs between the causative organism and the host. Usually the cardiac endocardium is resistant to infection, as long as it remains intact.1 The endocardium is most often damaged because of turbulent blood flow within the heart caused by a dysfunctional valve. Whether the valve is stenotic or regurgitant, it tends to cause turbulent blood flow, which is what leads to damage of the endocardium. Other causes of endocardial damage are due to the introduction of invasive devices such as catheters, sheaths, or pacing wires.4,17 When the endothelium becomes damaged, the body’s response is to deposit platelets and fibrin over the damaged area. These deposits are called nonbacterial thrombotic November/December 2014


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endocarditis (NBTE). The platelet-fibrin complex provides an advantageous environment for bacteria to become established in, as it provides some protection for the bacteria from the body’s defenses. The presence of damaged endothelium or NBTE does not necessarily mean that IE will occur. In order for the NBTE to progress to IE, it is necessary for a bacteremia to be present. Bacteremia can be caused by a variety of daily activities and health care procedures. Activities that involve the oral mucosa, the gums in particular, seem to cause the highest rate of bacteremia. The association between dental procedures and the occurrence of IE has been appreciated since 1909.5 However, it is not only dental procedures that can result in bacteremia. Activities such as tooth brushing or eating hard food can also cause bacteremia. The bacteremia that these activities cause tends to be very transient, lasting for less than 30 minutes, and the bacterial load is very small. But this does help to account for why some individuals may have IE caused by oral bacteria, with no history of dental procedures.4,5,17,19 Other common causes of bacteremia are medical and/or surgical procedures, which involve the genitourinary tract or gastrointestinal tract. If the mucosal surface being manipulated is diseased or infected, the risk of bacteremia is increased. Although the development of IE requires both the presence of NBTE and bacteremia, this combination being present does not always result in IE. In order for IE to occur, the organism must be able to persist and survive on the endothelium. This requires that the organism be resistant to the complement-mediated bactericidal activity of serum. In addition, the organism must be able to adhere to the NBTE. One of the compounds that enable an organism to do this is fibronectin, a molecule that has numerous binding sites and enables the organism to bind simultaneously to fibrin, collagen, and platelets. Fibronectin is produced by bacteria such as S aureus, S viridans, and some other strains of staphylococci and streptococci. What is less well understood is how some of the other virulent organisms causing IE are able to colonize intact valvular tissue.4,10 After adhesion has occurred, the organisms reproduce, a process that results in a complex of infected vegetation, microorganisms, and platelet-fibrin aggregation. As the organism continues to establish itself, additional fibrin and platelet aggregates are added to the lesion. This helps to create recesses within the lesion that protect the microbes from the body’s phagocytes.5 Consequently, a developing IE lesion consists of microorganisms, fibrin, platelets, red blood cells, and white blood cells. The microorganisms located on the surface of the lesion are continuously shed into the bloodstream and represent an ongoing source of bacteremia. This ongoing infection causes an inflammatory response, stimulating cytokines, and tumor necrosis factor, which are most likely involved in some of the systemic features of IE.4,5,17 332


Patients who are at increased risk for developing IE include individuals who have valvular disorders. Dysfunction of the valves creates turbulent blood flow that can cause damage to the endothelium of the heart and led to the creation of NBTA. Also, patients who have congenital heart defects or have an artificial valve are also more vulnerable to the development of IE. Rheumatic fever is a classic predisposing factor for the development of IE, and although this disease has decreased in incidence in the developed Western countries, it is still frequently seen in the developing world. Any patient who has had a previous history of IE remains at greater risk for developing the disease again. Intravenous drug abuse is also a risk factor for the development of IE. Intravenous drug abuse is the most commonly seen cause for development of IE involving the right-sided valves. Infection in this instance can be caused either by use of contaminated needles or from foreign substances that may be in the drug that is injected.

Clinical Manifestations Most of the signs and symptoms of IE are due to 4 mechanisms5 (Table 3): & infection of the endocardial layer of the heart and associated damage to the valves, and so on; & release of infected vegetation (septic emboli) that forms an emboli and blocks blood flow to organs and tissue; & continuous shedding of bacteria into the bloodstream that creates a continuous bacteremia and can stimulate inflammatory response from the host; and & the formation of immune complexes between the cells of the immune system and the causative organisms.

CHANGES TO THE ENDOCARDIAL LAYER OF THE HEART The infectious process destroys the tissue of the heart, particularly the leaflets of the valves. This disrupts the function of the valve and leads to varying degrees of heart failure. Acute mitral valve regurgitation can occur if the infectious process destroys the chordae tendineae, causing acute decompensated heart failure. The infectious process can also lead to the formation of abscesses and fistulae. Fistulae create openings between major blood vessels and cardiac chambers, or between the cardiac chambers themselves. This can result in intracardiac shunts and cause unoxygenated blood to be delivered to the tissues. Abscess development, especially around the aortic valve, can cause a wide variety of blocks or arrhythmias to develop if it disrupts the conduction system. It is also possible for an abscess to penetrate through to the pericardial space and cause a purulent pericarditis to form. As a rule, an infection involving the aortic valve progresses more rapidly than does an infection involving the mitral valve. However, the course of IE is highly variable and unpredictable.4,22,24,25

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TABLE 3

Clinical Manifestations of Infective Endocarditis (IE)

Process of IE

Cardiac involvement due to infectious process

Clinical Manifestation

& Valve dysfunction - MurmurV85% of patients with IE will have a cardiac murmur h May represent preexisting murmur - 10%-40% of patients will have a new or worsening cardiac murmur & Heart failure occurs in 30%-45% of patients & Shunting of unoxygenated blood if fistulae develop & Cardiac arrhythmias or blocks if abscess invades conduction system

Septic emboli

& Symptoms will vary according to the organ affected & Brain is the most common site of septic emboli & Septic emboli most apt to occur when - Vegetations 910 cm in diameter - Mitral valve involved - Left-sided valves affected - Causative organism is Staphylococcus aureus27,28 - Risk of embolization is greatly reduced after effective antibiotic treatment is started & Symptoms occurring due to septic emboli cause many patients to seek medical treatment & 40% of patients with IE have neurological symptoms due to emboli to brain

Formation of immune complexes

& Vegetation complexes continuously shed bacteria into the bloodstream & Causes ongoing bacteremia and can cause immune complexes to form & Immune complex can stimulate inflammatory response by the body and result in - Vasculitis - Nephritis

Peripheral manifestations of IE

& Roth spots: round, oval, white-centered hemorrhages found on the retina - Also seen in other conditions: hematologic malignancies, connective tissue diseases, vasculitis, diabetes32,33 & Osler nodes: reddened and painful nodules that are found on the pads of the fingers and toes - Exact cause unknown, may be due to septic microemboli or immune complexes - Osler nodes are found in other conditions such as bacteremia, typhoid fever, lupus32,33 & Janeway lesions: reddened, nontender, nonpainful nodules found on the palms of the hands and soles of the feet. - Believed to be caused by either necrotic microabscesses or septic microemboli from the endocardium32,33 & Splinter hemorrhages: small linear hemorrhages found under the nail - May be plum colored; then change to brown/black within a few days.32,33 - Splinter hemorrhages are not exclusive to IE, but can occur with mitral stenosis, psoriasis, vasculitis, meningococcemia, and trauma to the nails & All these signs, except splinter hemorrhage, are minor criteria on the Duke criteria4,11,32,33 & Some authorities believe that as many as 50% of patients with IE may have Q1 peripheral signs of IE4,9,32,33

SEPTIC EMBOLI As the infected lesion on the endocardium grows, part of the lesion can break off and travel to various organs. The part

of the lesion that breaks off is called a septic emboli, and it behaves in a way similar to a blood clot. Septic embolization is more common in November/December 2014


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& patients with left-sided valves involved, & patients with vegetations that are larger than 10 mm in diameter, & when the mitral valve is affected, and & when the causative organism is S aureus.27,28 Although any organ can be affected by septic emboli, the organs that are most often involved are the brain, spleen, bowel, and kidney; the brain is the organ that is affected most often. Septic emboli to the brain tend to present as a vascular cerebral insult would.4,17 Symptoms of embolicinfarcted events are often noted on presentation when the patient seeks medical care and are frequently the reason that the patient seeks medical attention. Once effective antibiotic therapy is started, the frequency of embolic events decreases from 13 per 1000 days to 1.2 per 1000 days. However, even after effective antimicrobial treatment has been completed, it is still possible for septic embolization to occur.4,19,29,30 Neurological symptoms occur in up to 40% of patients with IE and are associated with increased mortality.4,19,29,30 Embolic strokes are the most common and significant of the neurological complications of IE, with the middle cerebral artery being the most common site of a septic emboli. Other neurological symptoms that can occur are severe headache, seizure, and encephalopathy.4,31 If renal insufficiency occurs, it is usually due to decreased cardiac output that affects the function of the kidneys or from renal toxicity due to the antibiotics used to treat the IE. However, glomerulonephritis due to immune-complex deposits does occur in about 15% of patients. The immunecomplex depositions occur on the glomerular basement membrane interrupting filtration and causing renal dysfunction.4 Septic emboli to the kidney can also cause acute renal failure.

SHEDDING OF BACTERIA AND IMMUNE COMPLEXES As the infected lesion grows on the endocardial surface of the heart, it continually sheds bacteria into the bloodstream. This becomes a continued source of bacteremia that keeps the immune system activated and can result in the formation of immune complexes. These complexes can be deposited in various organs and in peripheral vascular tissue. The immune complexes can cause an inflammatory response and result in vasculitis, nephritis, and so on. Both of these mechanisms have been attributed to causing some of the classic peripheral manifestations of IE.4,32 The classic peripheral signs of IE are petechiae, splinter hemorrhage, Roth spots, Osler nodes, and Janeway lesions.

PERIPHERAL MANIFESTATIONS OF INFECTIVE ENDOCARDITIS With effective antibiotic treatment, these manifestations have become less frequent than in the preantibiotic era. Effective 334


treatment with antibiotics has helped to decrease the shedding of bacteria, decreasing the formation of immune complexes and the inflammation they can trigger.4,9,32,33 If the peripheral manifestations of IE are seen, it helps to confirm the diagnosis, but these signs have to be evaluated within the context of the whole clinical picture. For patients who are diagnosed with IE, it is worth looking to see if the patient has any peripheral signs associated with IE, as some authors believe that as many as 50% of patients may display at least one of peripheral signs.4,9,32,33

Modified Duke Criteria for Diagnosis of IE Infective endocarditis remains a disease that, although not rare, is not commonly seen either. It is a disease that presents with some subtleness and can be difficult to diagnosis.4,12,13,28 Osler’s description of endocarditis in 1885 was ‘‘Few diseases present greater difficulties in the way of diagnosis than malignant endocarditisI (such that) fully one-half the diagnosis was made postmortem.’’12 Although this comment was made in 1885, it remains relevant today as well (Table 4). Most of the signs and symptoms of IE are caused by a complication of the infectious process rather than the intracardiac infection itself.4 This can lead to a puzzling constellation of symptoms when the patient first seeks medical care. To be effectively diagnosed, clinicians have to be attentive to the possibility of IE being present. Infective endocarditis should be part of the differential diagnosis when the following conditions are present5: & febrile condition more than 1 week in patients with heart murmur, & febrile condition in IV drug addicts, & febrile conditions in patients with prosthetic valves or new onset of valvular dysfunction, and & young patients who present with a sudden neurological event. The current accepted criteria for determining if a patient has IE are the Duke criteria. This is a diagnostic strategy that was developed in 1994 by Durak and colleagues at Duke University.34 It replaces the older von Reyn criteria that had been used previously. The Duke criteria have a high sensitivity for identifying IE and have a negative predictive value of 92%.10 The Duke criteria are divided into major and minor criteria and establish 3 possible results based on the number of major and minor criteria that are present or not: definite IE, possible IE, and rejected IE. The major criteria of the Duke system utilize reliable data obtained from strict microbiological (blood cultures) and echocardiography (clinical) sources. In order to ensure the high specificity of the Duke criteria, some patients with positive blood cultures of common pathogens (such as S aureus and E faecalis, which can cause IE but also other infections) need to fulfill secondary criteria as well. Patients

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TABLE 4

Modified Duke Criteria Major Criteria: Definitions

I. Microbiological evidence A. Typical microorganism for infective endocarditis (IE) from 2 separate blood cultures (cx) B. Typical microorganism consistent with IE from 2 separate blood cx 1. Viridans streptococci, Streptococcus bovis, or HACEK group or 2. Community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus or C. Microorganisms consistent with IE from persistently positive blood culture: 1. Q2 blood samples drawn 12 h apart or 2. 3 or a majority of 94 separate blood cultures with first and last samples drawn 91 h apart II.Evidence of endocardial involvement A. Positive echocardiogram for IE 1. Oscillating intracardiac mass on valve or supporting structures, or in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation 2. Abscess or 3. New partial dehiscence of a prosthetic valve or B. New valvular regurgitation (worsening or changing of preexisting murmur is not sufficient) Minor Criteria: Definitions

III. Predisposition A. Heart diseasea

High risk: previous IE, aortic valve disease, rheumatic heart disease, prosthetic heart valves, coarctation of the aorta, and complex cyanotic congenital heart diseases. Moderate risk: mitral valve prolapse with valvular regurgitation or leaflet thickening, isolated mitral stenosis, tricuspid valve disease, pulmonary stenosis, and hypertrophic cardiomyopathy Low risk: secondary atrial septal defects, ischemia heart disease, previous coronary artery bypass graft, mitral valve prolapse with no murmur or thickening of the leaflets

B. Intravenous drug use 1. Fever Q38.0-C C. Vascular phenomena i. Major arterial emboli ii. Septic pulmonary infarcts iii. Myocotic aneurysms iv. Intracranial hemorrhage v. Conjunctival hemorrhages vi. Janeway lesions D. Immunologic phenomena 1. Glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor F. Microbiological evidence: positive blood culture 1 Positive blood culture not meeting major criterion as noted previously Excluding single positive cultures for coagulase-negative staphylococci and organisms that do not cause endocarditis or serologic evidence of active infection with organism consistent with IE a

Heart disease that is considered to predispose to IE is classified as high risk, moderate risk, and low risk.

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who have bacteremia caused by such classic IE organisms as S viridans and the HACEK group, which are seldom seen in patients without IE, are given greater significance in the diagnostic scheme. Bacteremias caused by staphylococci and enterococci have diagnostic significance primarily when they are community acquired and are without any apparent primary focus. The echocardiographic data that are given diagnostic weight within the Duke criteria are also very specific. Only 3 characteristics are included: mobile echodense masses attached to valvular leaflets or endocardial walls, periannular abscesses, or new dehiscence of a valvular prosthesis. The remaining 6 criteria are the minor ones and are frequent but nonspecific findings classically associated with IE.34-37 The effectiveness of the Duke criteria for reliably establishing the diagnosis of IE has been demonstrated in a number of clinical trials. The specificity of the originally proposed criteria has been demonstrated to be greater than 98% (this is the ability of the criteria to correctly identify those patients who do not have IE), and another study has found that the

TABLE 5

Duke criteria have good agreement with the clinical assessment by infectious disease clinicians.34 The original Duke criteria were shown to have some problems.19,34-36 Specifically, they tend to misclassify culture-negative cases and do not adequately account for the increasingly important role that endocardiography plays in diagnosing IE and the increased role of S aureus as a causative agent. To resolve some of these issues, a modified Duke criteria were proposed in 2000.33-36

TREATMENT OF INFECTIVE ENDOCARDITIS The mainstay of treatment for IE is appropriate therapy based on the causative organism (Table 5). Because the majority of cases of IE are due to bacteria, treatment with antibiotics is the most common and used to describe the general principles of treatment; however, other agents may be required to be used based on the causative organism. Some of the general principles of treating IE are as follows5,38,39: & Administration of IV antibiotics, in sufficiently highenough doses, over a long-enough time frame to destroy

Antibiotic Therapy for Infective Endocarditis (IE) Based on Organism and Native Valve Endocarditis (NVE) or Prosthetic Valve Endocarditis (PVE)

Organism

Native Valve Endocarditis

Drug/ Dose/Duration

Prosthetic Valve Endocarditis

Comments

Uncomplicated: 2 wk, complicated: 4 wk

Penicillin G 6 wk; gentamicin 2 wk

Relative penicillin-resistant Penicillin G 3 million units for streptococci 4-6 wk plus gentamicin 1 mg/kg for 2 wk

Penicillin G 3 million units for 4-6 wk plus gentamicin 1 mg/kg for 2 wk

Penicillin G for 6 wk and gentamicin for 4 wk

Penicillin-resistant streptococci

Penicillin G 3-4 million units/wk plus gentamicin 1 mg/kg both for 4-6 wk

Same regimen but 6 wk for complicated IE

Penicillin G and gentamicin for 6 wk

Methicillin-susceptible Staphylococcus aureus

Nafcillin or oxacillin for 6-8 wk, gentamicin may be added for the first 3-5 d

Nafcillin or oxacillin for 6-8 wk, Nafcillin or oxacillin with Begin therapy with susceptible antibiotics for 1-2 d and rifampin for 6 wk and gentamicin may be added then begin the rifampin gentamicin for 2 wk for the first 3-5 d.

Methicillin-resistant S aureus

Vancomycin 15 mg/kg for 4-6 wk, optional to add gentamicin for the first 3-5 d

Vancomycin 15 mg/kg for 4-6 wk, Vancomycin with rifampin If the staphylococcus is resistant to gentamicin, a 3rd agent for 6 wk, with gentamicin optional to add gentamicin for should be chosen for 2 wk the first 3-5 d

Right-sided staphylococcus for NVE

Nafcillin or oxacillin with gentamicin for 2 wk

Complications, or vegetations 91- to 2-mm diameter, are indications for longer therapy

Enterococci

Penicillin G 3-4 million units, plus gentamicin for 6-8 wk (1 mg/kg)

Same

Use longer time frame of 8 wk

Penicillin-resistant enterococci

Vancomycin 15 mg/kg and Same gentamicin 1 mg/kg for 4-6 wk

Use longer time frame than 6 wk

HACEK group

Ceftriaxone 2 g daily for 4 wk

Use for 6 wk

Penicillin-susceptible streptococci

336

Penicillin G 2-3 million units IV 4 wk. Gentamicin may be added 3-5 d to increase potency


Same

If penicillin allergyVceftriaxone 2g/d; for severe penicillin allergy, vancomycin 15 mg/kg 4 wk

If there is a relapse of the patient surgical treatment, is advised10,15,17,19,25

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&

&

&

&

the causative organisms. This is necessary because the vegetation structure of IE keeps the organisms isolated from the bloodstream. In order for the administration of antibiotics to be effective, the organism responsible for the infection must be reliably identified. In patients who are in critical conditionVhemodynamically compromisedVtreatment with empirical antibiotics should not be delayed. Three sets of blood cultures should be obtained, within 1 hour, from different venipuncture sites as able, prior to the start of antibiotic treatment.5 In patients who present with stable conditions, with subacute symptoms, treatment can usually be held until laboratory results of blood cultures can be obtained. This is important particularly if the patient has had previous treatment with antibiotics. By withholding treatment, blood cultures can be obtained without the confounding affects of antibiotics.5,17,19 All definite cases of IE according to the Duke criteria must be treated with antimicrobials. In cases where it is a possible diagnosis based on the Duke criteria, treatment decisions can be individualized based on clinician judgment. Organism-specific therapies: the susceptibility, of a particular microorganism to a given antibiotic, remains at the center of the treatment plan for the effective eradication of IE.5,17,19

Surgical Intervention Mortality and morbidity for patients with IE increase when cardiac and neurological complications occur. Effective treatment of such complications may require surgical intervention.4,19,30,39 The timing of when surgical intervention should occur is not conclusive. The risks versus benefits of surgery for the individual patient must be considered and individualized. The decision to take a patient to surgery is probably less complicated when multiple circumstances indicate that surgery is imperative. The following lists what is generally agreed to have good evidence for surgery that results in improved mortality for patients4,17,20,30,40-42: For NVE, early surgical intervention should be considered for patients with & heart failure; & aortic or mitral regurgitation in the presence of with elevated left ventricular pressures; & IE caused by fungal organisms or antibiotic-resistant bacteria; & heart block; or & abscess of the aortic valve, annulus, or penetrating lesions. Surgery is reasonable for recurrent emboli or vegetation that persists despite antibiotic therapy. Surgery may be considered if there is mobile vegetation if the endocarditis is

caused by fungal organism or microorganisms that are resistant to antibiotics. For PVE, early surgical intervention should be considered when the following are present: & heart failure, & dehiscence of a prosthetic valve or evidence of increasing obstruction or worsening regurgitation, & abscess formation, & surgery is reasonable for patients with PVE with persistent bacteremia or recurrent emboli despite appropriate antibiotic therapy, or & relapsing infection.

ACUTE HEART FAILURE A major reason that surgery is performed for patients with IE is moderate to severe congestive heart failure due to valvular regurgitation that does not respond to medical treatment. Aortic valve regurgitation tends to be less well tolerated than mitral valve regurgitation. Heart failure that is due to aortic valve regurgitation is less well tolerated than that due to mitral valve dysfunction, as the left atrium and pulmonary veins do not seem to accommodate the increased blood volume as well as the left ventricle does.30,40-42 For patients with congestive heart failure that does not respond to medical treatment, there is a high mortality rate of 60% to 90% within 6 months. However, if these patients are treated surgically, the mortality decreases to 20% to 40% for NVE and to 35% to 55% for PVE.4,19,30,40-42 Although the presence of heart failure is an increased surgical risk in itself, the risk of mortality is greater if surgery is not performed or if it is delayed. The development of acute heart failure is also related to the organism that causes the IE. Virulent pathogens such as S aureus, hemolytic streptococci, and Streptococcus pneumoniae carry an increased rate of causing acute heart failure.30

PERIVALVULAR INFECTION As infection spreads from the valves to the surrounding tissues, abscesses may form. The higher pressure on the left side of the heart can cause pressure on the weakened tissue of the abscess and can create a pseudoaneurysm. Blood as it flows through the heart washes the infected material and necrotic tissue out of the abscesses, creating craters around the valve. This process can result in a partial or complete separation of the valve from its annulus. Abscesses can also create a passage way from 1 heart chamber to another, forming a fistula. If the fistula is formed through to the pericardium, it is usually fatal.29,30

PERSISTENT SEPSIS If a patient with IE continues to demonstrate positive blood cultures despite appropriate antimicrobial therapy, or if the patient has ongoing fevers, this may demonstrate uncontrolled infection and warrant surgical treatment. Surgery is also November/December 2014


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justified when the patient has endocarditis caused by organisms that have had poor clinical outcomes. This would include endocarditis caused by yeasts, fungi, P aeruginosa, Brucella species, and Coxiella burnetti.4,19,30 Patients who present with IE due to S aureus should be considered for surgical intervention particularly if they demonstrate vegetations on transesophageal echocardiography and if they remain septic during the first week of antimicrobial therapy.12,22,26,27

PREVENTION OF SYSTEMIC EMBOLI Systemic embolization occurs in about one-fourth to one-half of all patients with IE. Some of the most common sites for embolization are the lungs, spleen, bowel, coronary arteries, and extremities.29 However, the brain remains the organ most at risk for embolization, with up to 65% of emboli reaching the central nervous system. It is the middle cerebral artery and its distributive branches that receive up to 90% of all the emboli that find their way to the cerebral circulation, and emboli here are associated with the highest mortality.4,31 In many instances, it is the effects of an embolization that cause patients to first seek medical care.20 Even after appropriate antimicrobial therapy is begun, however, embolization still remains a threat, although that threat decreases significantly after the first 2 weeks of antimicrobial therapy.29 Trying to determine which patients might have a repeat of embolization has been of great interest to researchers. ReTABLE 6

embolization carries a high mortality and morbidity risk. However, many of the studies that have tried to determine which patients are most at risk of re-embolization have yielded contradictory findings. Studies in the early 1990s were sometimes of poorer quality than later studies and did not have the advantage of using transesophageal echocardiography, but only transthoracic echocardiography, Some studies have found there is an increased risk of embolization related to the size of the vegetations; other studies found that it was associated with certain causative organisms, and still other studies associated the increased risk of embolization with the valve and side of the heart.17,19,29 In 2012, Kang et al42 reported on a prospective, randomized clinical trial that attempted to answer this question. In the study, patients who were randomized either received standard care as recommended by the American College of Cardiology/American Heart Association or received surgery within 48 hours of being randomized. The results of this trial, which included patients with severe valvular disease and large vegetations (910 mm) on either the aortic or mitral valve, showed that the patients in the early surgical group did not experience embolic events following the surgery. The trial randomized 37 patients to early surgery and 39 to standard therapy. This study helps to support the role of early surgery preventing embolization in IE for patients with large vegetations.42 Currently, it is recommended that

Conditions to Be Considered for Prophylactic IE Therapy

High Risk Definitely Require Prophylaxis Therapy

Prosthetic heart valves

Moderate Risk

Negligible Risk No Greater Risk Than the General Population

Mitral valve prolapse with regurgitation or thickened valve leaflets

Mitral valve prolapse without regurgitation or thickened valve leaflets

Patent ductus arteriosus

Pulmonary stenosis

Isolated atrial septal defect

Aortic regurgitation or stenosis

Bicuspid aortic valve or calcific aortic sclerosis with minimal hemodynamic abnormality

Arteriosclerotic plaques

Mitral regurgitation

Hypertrophic cardiomyopathy

Coronary artery disease

Mitral regurgitation and stenosis

Pure mitral stenosis

Cardiac pacemaker or implanted defibrillator

Ventricular septal defect

Tricuspid valve disease

Trivial valvular regurgitation on echocardiography without structural abnormality

Coarctation of the aorta

Degenerative valvular disease in elderly patients

Surgically repaired intracardiac lesion with residual hemodynamic abnormality or prosthetic device

Surgically repaired intracardiac lesions with minimal or no hemodynamic abnormality, less than 6 mo after the operation

Previous infective endocarditis Cyanotic congenital heart disease

Surgically constructed systemic-pulmonary shunts

Surgically repaired intracardiac lesions with minimal or no hemodynamic abnormality, 96 mo after the surgery (atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary stenosis) Prior coronary bypass graft surgery; prior Kawasaki disease or rheumatic fever without valvular dysfunction

Compiled from Newburger et al.20

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the decision, on when to do surgery to prevent embolization during IE, be based on the unique situation of the individual patients.4,19,29,30,38-40,42

PREVENTION OF INFECTIVE ENDOCARDITIS Infective endocarditis can be treated more effectively today than in the preantibiotic era, but IE still carries a significant mortality rate. The mortality rate for IE has been reported at between 9% and 30% globally.29 Even for those who survive IE, there can be long-term consequences. About one-third of patients who have IE must undergo cardiac surgery for treatment, and many of these patients will have a prosthetic valve placed. Patients with IE may experience neurological involvement due to a cerebral embolic event, which can have variable impact on their lives, depending on the location of the emboli and the extent of the damage it causes. These factors make it important that preventable cases of IE be avoided.4,19 There are few studies that have been done in populations at risk for IE. This creates difficulty in making recommendations on what procedures should have prophylaxis based on evidence. Not only should prophylaxis be effective, but also the consequences of antibiotic prophylaxis should be more beneficial than detrimental. Antibiotics can have injurious consequences for patients and can contribute to the development of antibiotic-resistant organisms. These risks need to be considered and balanced against the likelihood that treatment will prevent an episode of IE.4,17,19,41 With the lack of well-designed and controlled human studies on the prevention of IE, the current guidelines have been developed based on pertinent literature concerning procedure-related endocarditis, the susceptibility of the usual organisms responsible for IE, results of animal models of IE prophylaxis, and retrospective analysis of prophylaxis in human populations.17,19,25,42 It should be remembered that the rate of IE following procedures that produce bacteremia, even in susceptible individuals, is low and that only about 5% of cases are known to occur following bacteremiacausing procedures in vulnerable individuals.4 In developing prophylaxis regimens, cardiac conditions have been rated as high risk, moderate risk, and negligible risk. The recommendations for which procedures should receive prophylaxis are based on the how likely the procedure is to cause bacteremia with organisms capable of causing IE (Table 6).

CONCLUSION Despite the extensive array of antibiotics that are available today, the incidence of IE has remained relatively stable or even greater than during the preantibiotic era. As individuals live longer with chronic heart disease, they are at greater risk of developing IE either from the chronic heart disease itself or from the implantation of devices or invasive diagnostics used to treat the chronic heart disease. Although not uniformly

fatal as it was in the preantibiotic era, IE still has a high mortality rate of 30% or more. Infective endocarditis has remained a clinical challenge; its presentation causes a wide variety of symptoms that can reasonably be attributed to many other causes. Without a high clinical suspicion for IE, it can easily be missed. Over the past decade or so, S aureus has emerged as the main causative organism responsible for IE. When S aureus is responsible for IE, the disease tends to be a toxic infection characterized by the development of perivalvular abscesses and fistulae. The mainstay of effective treatment for IE is identification of the causative organism and then treatment with appropriate antibiotics for the correct length of time. So important is the accurate identification of the causative organism of IE, that treatment with antibiotics should not be started until blood cultures have been drawn, unless the patient’s situation is critical. Surgery should be considered early in the course of treatment for patients who display acute aortic regurgitation, rupture of an abscess into the pericardial space, valvular obstruction, or severe heart failure that cannot be treated medically, or when antibiotic therapy is not effective. In the last few years, the recommendations for IE prophylaxis have changed considerably. In the past, antibiotic prophylaxis was prescribed liberally for a wide variety of treatments that might cause bacteremia. There is actually little evidence that supports the use of routine antibiotic prophylaxis for IE. Instead, the most recent recommendations for antibiotic prophylaxis tend to be reserved for those patients who have the highest risk for developing IEVpatients who have had a previous episode of IE or who have a prosthetic valve, valvular disease, or septal defects. This represents a significant change for both practitioners and patients, which has been accepted with varying degrees.

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ABOUT THE AUTHOR Linda Josephson, MS, RN, CCRN-CMC, is currently teach as adjunct faculty for local colleges and have worked in critical care for over 30 years. The author has disclosed that she has no significant relationships with, or financial interest in, any commercial companies pertaining to this article. Address correspondence and reprint requests to: Linda Josephson, MS, RN, CCRN-CMC, 153 Uncatena Ave, Worcester MA 01606 ([email protected]).

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Chemoprophylaxis for infective endocarditis.

[Infective endocarditis].

Infective Endocarditis.

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Prevention of infective endocarditis.

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