Endocarditis is an infection of the endocardium—the endothelial membrane that lines the heart chambers and valves. This membranous tissue regulates the chemical environment of underlying muscular tissue by controlling the influx of electrolytes and regulatory proteins; think of it as a type of blood-heart barrier that protects the myocardium.
Infection occurs when microbes invade endocardial tissue, particularly the valve leaflets (see Picturing endocarditis). The microbe is typically bacterial, but fungal and viral organisms are possible sources. Endocarditis may evolve slowly due to infection by less virulent pathogens (subacute) or it may appear as an acute, fulminant disease with a septic presentation; both conditions are referred to as infective endocarditis (IE).
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Decades ago in the preantibiotic era, IE was associated with rheumatic heart disease. Today, there are 10,000 to 20,000 cases annually, and IE is twice as common among men. It occurs primarily in people with congenital heart defects and in older individuals who develop valvular stenosis or regurgitation of the aortic and mitral valves. Injection drug use increases the risk of IE, and the infection often involves the tricuspid valve because it's the first heart structure bathed by contaminated venous blood as it returns to the heart via the vena cava.
Prosthetic heart valves, both mechanical and bioprosthetic, also place an individual at risk. IE occurs two to three times more frequently following prosthetic valve replacement than with other types of heart surgery. Microbes can reach the valve prosthesis directly during surgery and tend to adhere to the valve ring or sutures. Risk of mechanical valve infection is highest during the first postoperative year. However, unlike mechanical prostheses, tissue valve leaflets undergo age-related structural changes; infection of porcine valves can occur up to 18 months postinsertion.
Invasive procedures of the gastrointestinal (GI) and genitourinary (GU) tract; pulmonary, cardiac, and dental procedures; and the presence of an intravascular device place the patient at risk for IE because microbial flora may be diverted into the bloodstream, initiating a bloodborne infection called bacteremia.
Although a wide variety of organisms cause IE, including fungi, viruses, and parasites, bacteria are the most common agents. Staphylococcus aureus, the most common pathogen of acute IE, causes a rapidly progressive and destructive form of the disease. A less virulent organism, Streptococcus viridans, accounts for more than half of subacute IE cases and is seen most frequently in people with preexisting heart conditions. Neisseria species, enterococci, bacilli, yeast, and fungi are also implicated in IE. Accounting for 5% of all cases is a group of organisms known as HACEK (an acronym for Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella), so named because their slow and fastidious growth makes them difficult to be cultured.
Blood cultures identify the causative organism and should be obtained before initiating antibiotic therapy. Typically, two to three cultures from different sites should be obtained within 1 hour. Be aware when reviewing lab reports that a negative blood culture being worked up for IE may reveal another classification of the disease: culture-negative endocarditis. Culture-negative IE can have noninfectious causes, such as vasculitis and systemic lupus erythematosus, or may result from the HACEK group of organisms or fungi. False-negative cultures may also occur with previous antibiotic use.
How do microbes gain entry to the blood and why are they attracted to cardiac structures? You recognize that most of the bacterial organisms that initiate IE are part of the normal flora of the oral cavity, respiratory tract, skin, and GI tract. Other causative microbes, such as yeast and fungi, are present in the soil and environment. The person who develops IE typically has a structural heart problem; is older than age 60; and may have comorbidities that weaken the immune system, such as diabetes, cancer, alcoholism, HIV, or injection drug use. Microbes can gain entry into the blood (bacteremia) when protective skin barriers are disrupted by I.V. devices, diagnostic endoscopes and catheters, self-injection of drugs, and dental manipulation.
There are standards of practice to adhere to when catheters are inserted and specific precautions for maintenance. If care practices are breached, the patient may be at risk for a bloodborne infection. The oropharynx is a reservoir teeming with organisms that can move into the bloodstream, especially when a patient has periodontal disease. Use of a dental root pick, wooden toothpicks, or a high-pressure water irrigator can dislodge microbes into the circulation. Mouth care is vital in preventing disease; good oral hygiene requires a minimum of twice daily brushing using soft bristles, regular gentle flossing of teeth, and twice yearly dental cleaning.
Certain bacteria have the tendency to lodge and adhere to tissue and medical devices such as a prosthetic heart valve. Both S. viridans and staphylococci possess surface proteins that enable them to attach to inflamed endothelial tissue. Some microbes are able to produce a biofilm that protects them from immune defenses. After microbes adhere to damaged heart valves, they multiply rapidly and form dense vegetation—collections of infectious microbes and cellular debris entangled in fibrin stands of clotted blood (thrombus). Microbes that are deeply embedded within the vegetation become dormant due to lack of available nutrients and are less susceptible to bactericidal antimicrobials, presenting a challenge to host defenses (see Bacterial endocarditis).
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Vegetations exist from one to several centimeters in length and fragments may break loose from the valve leaflet, traveling in the bloodstream as emboli and causing infarcts in the heart, lungs, spleen, and kidneys. Attached to the margins of the heart valve, they cause structural damage, resulting in altered blood flow as heard in murmurs and potentially causing heart failure. And because the endocardium is adjacent to the myocardium, inflammation and infection can extend into the muscular layer, leading to conduction disturbances and dysrhythmias. Persistent bacteremia from microbial growth triggers the deposition of immune complexes in tissues, which cause skin manifestations, arthritis, and glomerulonephritis.
Ace patient assessment
A thorough physical assessment serves as a baseline and is useful in detecting changes when they occur. Begin by evaluating orientation and mental status and assess the visual field for deficits that may arise from embolization of blood vessels. Neurologic complications occur in a third of cases, most commonly the result of a piece of vegetation from the left side of the heart that travels to an area of the brain, causing paralysis, blindness, aphasia, and sensory loss.
It's necessary to monitor vital signs frequently because the majority of patients will have a fever with spikes over 102°F when there's significant bacteremia. Recall that the temperature regulating mechanism may not be functional in older patients and they're less likely to have a febrile response. The febrile patient may be tachycardic; note the heart rate and rhythm, the closure and opening of the valves, and the presence of murmurs and extra heart sounds. Auscultate the heart in a Z pattern, starting at the base of the heart at the aortic area, across to the pulmonic area, diagonally to the tricuspid area, and then down to the mitral area at the apex of the heart.
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Assess the skin thoroughly for evidence of peripheral embolization seen as petechiae, the most common skin manifestation. Petechiae are pinpoint, nonraised, round, purplish-red spots caused by minute hemorrhages and are detected on the skin of the hands and feet or on the mucous membranes of the conjunctiva and palate. Splinter hemorrhages are recognized as nonblanching, linear, red-brown lesions found under the nail bed. Other skin lesions may include painless, erythematous lesions on the palms and soles (Janeway lesions) or painful, violet, raised nodules found in the pulp of the fingers and toes (Osler nodes).
Assessing for renal complications is essential because glomerulonephritis may occur secondary to the immune complexes in the renal basement membrane. You'll perform frequent intake and output measurements, determine if there's costovertebral angle tenderness, and monitor blood urea nitrogen and creatinine levels. After antibiotic therapy has begun, you'll continue to assess the renal system, especially if nephrotoxicity is a risk of antimicrobial therapy.
Blood cultures are vital in identifying the organism, and the sensitivity report will guide antimicrobial selection. The Duke Criteria, a set of guidelines for diagnosing IE, states that one positive blood culture with S. aureus, or two positive cultures more than 12 hours apart, or three positive cultures more than 1 hour apart is conclusive for bacteremia. Both anaerobic and aerobic cultures are obtained from different sites using sterile technique.
In acute IE, expect to see an elevated white blood cell (WBC) count and raised erythrocyte sedimentation rate, which reflects systemic inflammation. In endocarditis that evolves slowly due to less virulent organisms, the WBC count may be normal. However, your patient will likely have lower hemoglobin and hematocrit levels, signaling anemia of chronic disease.
If the urinalysis reveals proteinuria and hematuria, these signs point to kidney involvement, possibly due to embolization from vegetation fragments or immune complexes damaging glomeruli. A rheumatoid factor titer should be obtained to exclude rheumatic fever as a cause.
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Echocardiography is crucial in identifying IE. There are two options for echocardiography, a transthoracic echocardiogram (TTE) or a transesophageal echocardiogram (TEE), and both approaches may be ordered. A two-dimensional TTE is the classic echo that you're familiar with. It's less sensitive but provides superior images of the ventricular surfaces of prostheses in the mitral, tricuspid, and aortic positions.
A TEE has a much greater sensitivity of 82% to 92% and is a minimally invasive procedure requiring sedation. It involves endoscopic placement of a transducer in the esophagus, which is directly behind the heart. By rotating and moving the tip of the transducer, the healthcare provider can examine the heart from several different angles and visualize atrial surfaces of the mitral and tricuspid valves and the aortic surface and outflow track. Cardiac abscesses, fistulae, vegetations, and leaky valves are better visualized using a TEE.
Preparation requires explaining to the patient what to expect. To avoid aspiration, the patient must be N.P.O. for 6 to 8 hours before the test. Post procedure it's essential that the cough and gag reflexes are present before resuming food or drink. The throat may be sore, and throat lozenges provide relief. Bleeding and pain aren't expected outcomes and must be reported to the healthcare provider because they may indicate an esophageal tear.
Antibiotic therapy is the mainstay of treatment, which involves placement of a peripherally inserted central catheter to deliver medication for 4 to 6 weeks. The I.V. route is preferred because more consistent therapeutic levels are achieved. The choice of antibiotic depends on the pathogen that was isolated from blood cultures and the patient's history of allergies. Agents that are effective against staphylococci, streptococci, and enterococci are most commonly prescribed because these microbes account for the majority of IE cases. Expect to give penicillin, ampicillin, nafcillin, vancomycin, rifampin, gentamicin, or cefazolin, either alone or in combination, depending on your patient's underlying pathology.
If the infection is caused by S. viridans or enterococci, epidermis symptoms often decrease in 4 days; however, if the virulent S. aureus is the source of infection, expect symptoms to persist beyond a week. It's recommended that blood cultures be obtained following 3 to 4 days of therapy to evaluate if bacteremia is resolving. If negative culture persists in the presence of symptoms, the organisms may belong to the HACEK group of bacteria, and ceftriaxone is the agent of choice. Antibiotics have a high cure rate, particularly among those who have their own heart valves, but patients who develop heart failure despite appropriate therapy may require heart valve replacement surgery. Those who develop large vegetations or who produce multiple emboli may also be surgical candidates. If left untreated, IE has a high mortality rate, especially among those with infected prosthetic valves.
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Misconceptions exist about who should receive antibiotic prophylaxis when undergoing certain procedures. To lessen the risk of developing IE, the American Heart Association (AHA) developed guidelines in 2007 that shift the emphasis away from antibiotic prophylaxis for dental care to improving oral health and access to dental care. Presently, only patients at high risk for adverse outcomes should receive an oral antibiotic, preferably amoxicillin, 30 to 60 minutes before a dental procedure. This group includes individuals with a prosthetic heart valve, a history of bacterial endocarditis, hypertrophic cardiomyopathy, complex congenital heart disease, and complicated mitral valve problems. Antibiotic prophylaxis is also recommended in respiratory, cardiac, integumentary, and musculoskeletal procedures in patients with adverse outcomes from IE.
Prophylactic antibiotics are no longer recommended for patients who undergo GI or GU tract procedures. To assist your patients in managing their health, the American Dental Association partnered with the AHA to develop instructions that summarize the current guidelines for the prevention of IE. You should advise your patients to carry this wallet card and to present it to healthcare providers when treatment is anticipated.
This way for positive outcomes
Nurses, as key members of the healthcare team, can greatly influence the outcome of care. Identifying who's at risk—combined with knowledge of the disease process, microbiology, and the nature of vegetative lesions; physical assessment clues; and how to implement preventive guidelines—is essential to delivering comprehensive nursing care to the patient who develops IE.
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© 2012 Lippincott Williams & Wilkins, Inc.