The incidence of endocarditis in the IVDU has been estimated to be 30 times that of the general population, or approximately 1.4 cases per 10,000 patients per year. Patients with IVDU-related endocarditis usually have no evidence of prior valve damage. Several mechanisms have been proposed by which IVDU contributes to endocardial injury. Talc, a common contaminant of injected material, has been recovered from subendothelial granulations during autopsy of IVDUs. In animal studies, valvular inflammation has been seen after repeated injection with horse serum or dead streptococci, suggesting that frequent antigenic exposure may produce valvular damage. Lastly, IV cocaine use has been associated with increased risk of endocarditis compared with other drugs. A likely basis for this increased risk is the fact that cocaine users inject more frequently, exposing the valves to frequent bacteremia and showers of particulate matter. Cocaine users are less likely to sterilize needles because cocaine does not need to be heated to go into solution. Furthermore, cocaine users are more likely to share needles and be injected by communal needles in "shooting galleries." An alternative explanation is that the vasoconstrictive properties of cocaine may cause interstitial or endothelial damage, predisposing to infection.

The cardinal sign of endocarditis in the IVDU is fever. There may be foci of infection, such as dental abscess, cellulitis, or septic pulmonary emboli. A cardiac murmur is present in over one-half of patients with endocarditis. 27 Right-sided murmurs, which vary with respiration, are usually pathologic and more specific for the diagnosis. Cough, pleuritic chest pain, and hemoptysis are common presenting complaints, particularly in patients with right-sided cardiac infection and septic pulmonary emboli. Pulmonary infiltrates on chest radiographs, associated with moderate hypoxia, have been described in over one-third of patients with IVDU-related endocarditis. Pulmonary findings may falsely lead the clinician to identify the lung as the primary source of infection. Pyuria and hematuria are ascribed to glomerulonephritis, embolic renal infarction, and perinephric abscess.

Blood cultures will be positive in over 98 percent of cases of IVDU-related endocarditis if three to five sets are obtained. True culture-negative endocarditis in the setting of high clinical suspicion and careful laboratory procedure is rare. S. aureus has been isolated from blood cultures in over half of patients. Up to one-third of S. aureus isolates, particularly those reported from large urban areas, are methicillin-resistant. Streptococcus is the second most frequently reported isolate, particularly S. viridens. S. aureus has a predilection for the tricuspid valve, whereas streptococci are more likely to involve left-sided structures.

Other less commonly isolated organisms include enterococci and gram-negative bacteria, particularly P. aeruginosa, Serratia marcescens, and Klebsiella pneumoniae. Other organisms, less frequently identified as causative agents, usually reflect local environmental pathogens or drug-injecting habits. For example, licking the needles prior to injection has been implicated in infections that result from oral pathogens such as Eikinella corrodens, Hemophilus parainfluenzae, Bacterioides spp. and Neisseria spp. Up to 20 percent of IVDU-related endocarditis is polymicrobial in nature. Although rare, fungal endocarditis has been reported increasingly. Most fungal infections are due to Candida spp., in particular C. parapsilosis, which accounts for over half of all isolates.

Although right-sided cardiac structures have been associated with IVDU-related endocarditis, any valve potentially can be involved. The tricuspid valve is infected in 40 to 50 percent, the mitral valve in 30 to 40 percent, the aortic valve in 10 to 20 percent, and multiple locations in 10 to 20 percent. Four types of valvular lesions have been described, vegetations, ring abscesses, cuspal tears or perforations, and ruptured chordae tendineae.

Diagnosis generally requires microbial isolation from a blood culture, which typically takes at least 24 h, and/or the ability to demonstrate typical lesions on echocardiography.16 The classic findings of embolic phenomena, Janeway lesions and Roth spots, are usually not observed until the infection is advanced.

A complete blood count (CBC), chest x-ray, and urinalysis are useful screens, although no single abnormality is specific for endocarditis. Chest radiographs will be abnormal in over 50 percent of patients, and typical findings include infiltrates consistent with septic emboli, pneumonia, or congestive heart failure.

Transthoracic echocardiography (TTE) will reveal diagnostic cardiac lesions up to 80 percent of the time in patients (both IVDU and non-IVDU) in whom the diagnosis is strongly suspected. Transesophageal echocardiography (TEE) is the most sensitive imaging modality for demonstrating vegetations, myocardial and ring abscesses, and tricuspid valve involvement in IVDU-related endocarditis. The timing of echocardiography is debatable. Some echocardiographers advocate early imaging to confirm the diagnosis of endocarditis. Others have suggested that imaging should be performed only on those patients who have positive blood cultures, to assist in determining disease response to therapy and length of treatment.

Attempts to develop criteria that would prospectively identify endocarditis in the IVDU in the ED. with reasonable certainty have failed. «I41, and 16 Generally, patients with suspected endocarditis should be cultured and admitted to the hospital. The need for empirical antibiotic therapy should be determined by the patient's clinical stability and ability to wait 24 h for the initial results of blood cultures. Treatment should be directed to S. aureus and Streptococcus spp., with consideration of local sensitivities and pathogens. Vancomycin or nafcillin and gentamicin are often initial therapy. The addition of an aminoglycoside has been shown to shorten the duration of bacteremia and duration of treatment in patients with S. aureus infections. Although 4 to 6 weeks of antibiotic therapy is standard, excellent cure rates have been achieved with only 2 weeks of treatment for patients with right-sided endocarditis caused by sensitive S. aureus.

Complications of endocarditis range from pump failure secondary to valve insufficiency, dysrhythmias due to myocardial infiltration, and pulmonary and systemic emboli. Mortality is related to the side of the heart involved, vegetation size, response to antibiotics, and compliance with treatment. Left-sided endocarditis is more likely to be complicated by left-sided congestive heart failure, septic cerebral emboli, and the need for surgery. Overall mortality for IVDU-related left-sided endocarditis is 14 to 21 percent, compared with 2 to 7 percent for IVDUs with right-sided endocarditis. Emboli can travel to the extremities, pulmonary bed, spleen, kidney, or brain. With right-sided endocarditis, septic pulmonary emboli occur in 30 to 60 percent of patients. Most complications related to right-sided endocarditis can be managed medically, and the prognosis is excellent. Valve replacement should be considered for those patients with congestive heart failure, failure to respond to antibiotics, myocardial abscess, or recurrent embolization. Early echocardiography can be instrumental in identifying those patients at risk for embolic events by identifying large (>2.0 cm) vegetations on valve leaflets.

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