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Coram LLC is a leading national provider of home infusion services, including alternate site of care and specialty pharmacy distribution. 12450 East Arapahoe Road, Suite A, Centennial, CO 80112 • 720.568.3436 For the branch nearest you, visit coramhc.com.

Infective Endocarditis Endocarditis is an infection of the endocardium, the tissue that lines the inside of the heart’s chambers and valves. While rare — there are an estimated 10 cases per 100,000 people each year — endocarditis is a medical emergency.1 It is difficult to treat, with death the outcome in approximately 20% of cases.1 Endocarditis can occur at any age, but is most commonly seen in persons over 50 years of age. The infection can be caused by bacteria or fungi, although fungal endocarditis is even less common than the bacterial kind. The role of viruses as a cause of endocarditis is unclear.

consequences of a stroke. In fact, emboli to the brain, lung, or spleen occur in 30% of patients and are often the presenting sign.2

Infective endocarditis (IE) develops after nosocomial or spontaneous introduction of bacteria into the bloodstream that flows to the surface of the heart valves. This environment, given its lack of dedicated microvasculature, allows bacteria to grow. The organisms adhere to the valves (vegetation) and, if left untreated, may eventually destroy the valves, ultimately resulting in heart failure. If bacterial emboli break off from the vegetation site, they may cause blockage and mimic the

Damage to the native heart valves can be due to disease states such as rheumatic valvular disease, congenital heart disease that affects valvular flow, mitral valve prolapse with an associated murmur, and degenerative heart disease.

C O N T I N U I N G

Risk Factors Risk factors for IE include native heart valve disease, the presence of a prosthetic heart valve, intravenous drug abuse, and a recent history of invasive procedures. Invasive procedures can include placement of a cardiac device or central venous access, surgery, and dental procedures. Patients who are immunocompromised are particularly at risk.

Numbers of valve replacement procedures continue to rise as our population ages. Each type of prosthetic valve has its own risk/benefit profile. Placement of any mechanical device presents a risk of thromboembolism and

E D U C A T I O N

P R O G R A M

requires chronic anticoagulation. A bioprosthesis, such as a porcine valve, will eventually deteriorate and require replacement. Additional host factors also impact the decision regarding which type of valve to use. Early post-valve endocarditis (PVE) is typically due to contamination during valve placement. Late PVE (after 60 days) is more likely to be from hematogenous bacterial spread. Each is distinguished by its own likely pathogens and outcomes.

Signs and Symptoms The clinical picture of IE is variable, depending on factors such as the causative organism, whether a native or prosthetic valve is used, comorbidities including cardiac disease, and other risk factors. Signs and symptoms also vary depending on its classification as acute or subacute IE. An acute IE infection progresses rapidly and patients present with chills, fever, myalgias, and

Table 1: Duke Criteria

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Major Criteria

Minor Criteria

ƒƒ Positive blood cultures

ƒƒ The presence of a predisposing condition

• A positive result from two separate blood cultures for a micro-organism that typically causes infective endocarditis. • Persistently positive blood cultures for 1 of the above organisms from cultures drawn more than 12 hours apart. • Three or more separate blood cultures drawn at least 1 hour apart.

ƒƒ Echocardiographic evidence of endocardial involvement •

Definitive vegetation, myocardial abscess, or new partial dehiscence of a prosthetic valve

ƒƒ Development of a new regurgitant murmur

arthralgias. Subacute infection has an insidious onset, often developing over weeks to months. Patients typically present with vague flulike symptoms. Subacute IE is more common in a patient with an underlying valve or congenital heart defect. The vast majority of patients with IE present with fever and heart murmurs. While less common today, embolic phenomena such as splinter hemorrhages, Roth spots, glomerulonephritis, Osler’s

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ƒƒ Temperature exceeding 100.4°F (38°C) ƒƒ Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions ƒƒ The presence of immunologic phenomena (such as glomerulonephritis, Osler’s nodes, Roth spots, or rheumatoid factor)

nodes, and Janeway lesions may present. Transient petechiae are commonly seen on the soft palate, buccal mucosa, conjunctiva, and skin. Ring abscesses are the pathological hallmark of mechanical valve PVE.

likely show a decreased serum hemoglobin, and microscopic hematuria. While typically present with IE, these findings are common with many infectious episodes and are therefore not specific to endocarditis.

Diagnosis

An echocardiogram is critical, particularly in patients who present with a clinical picture of IE but have nondiagnostic blood cultures. An echocardiogram can also help predict potential complications of IE, especially those that are embolic

Laboratory studies will likely show elevated levels of white cells and C-reactive proteins, as well as an increased erythrocyte sedimentation rate. They will also

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in nature. The echocardiogram can identify and measure bacterial vegetation and determine if the vegetation is mobile or fixed. It is recommended that the echocardiogram be performed as soon as possible — ideally within 24 hours — in all patients with suspected IE.2 Transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) may be the imaging method of choice. Continuous, versus intermittent, bacteremia is a hallmark of IE. The widely used Duke Criteria for diagnosis (see Table 1) recommends repeated blood cultures over a 12-hour period prior to starting antibiotic therapy. However, given the improvement in outcomes when therapy is not delayed, more recent recommendations require two blood cultures at different times within a 1-hour period prior to initiating empiric therapy.2 Positive results from only 1 set of several blood cultures should be interpreted with caution.2 Using the Duke Criteria, a diagnosis of IE can be made if the patient has either pathological evidence of IE (positive microorganisms by culture or histology) or meets the clinical criteria (2 major criteria, 1 major and 3 minor, or 5 minor). See Table 1. According to the Duke criteria, findings that are consistent with IE, yet not definitive, indicate a possible IE infection. The diagnosis of IE is rejected if: a firm alternative diagnosis is made; the IE manifestations resolve within