13.1 Valvular Endocarditis, Vegetations, Abscess, and Complications

Treat endocarditis as a clinical-imaging diagnosis

Infective endocarditis, or IE, cannot be confirmed or excluded by one echocardiogram. Echocardiographic lesions must be integrated with blood cultures, pretest probability, examination, and other imaging. Before scanning, review the affected organism when known, fever and bacteremia course, prior IE, congenital disease, prosthetic valves, intracardiac devices, vascular access, injection exposure, new murmur, heart failure, embolic symptoms, and relevant earlier studies. The sonographer documents findings and limitations; the interpreting and clinical teams apply diagnostic criteria.

TTE is the first-line examination. Acquire complete native and prosthetic valve anatomy in multiple planes rather than stopping after finding one mass. Use parasternal, apical, subcostal, and modified windows; zoom at high frame rate for leaflet motion while retaining wide-field clips that show location. Sweep through each coaptation line, sewing ring, aortic root, mitral-aortic continuity, periannular tissue, and any visible lead. Color Doppler assesses new or worsening regurgitation, paravalvular flow, perforation, and abnormal communications. PW and CW Doppler describe hemodynamic consequences, not infection itself. Compare with prior images because unchanged calcification, sutures, strands, or prosthetic artifacts may mimic new disease.

Describe the lesion rather than naming every mass a vegetation

Vegetation size is measured as maximal length, not color-jet area. Scan orthogonal planes and use the clearest frame without including chordae, reverberation, or adjacent calcium. Report whether mobility is independent of the valve and whether the lesion interferes with closure. Lambl excrescences, redundant chordae, fibroelastoma, thrombus, calcific nodules, sutures, prosthetic material, and side-lobe or reverberation artifacts may resemble infection. A true lesion should remain anatomically coherent through the cardiac cycle and be reproducible in appropriate views. Alter depth, frequency, focus, gain, and insonation angle; a structure that changes position with the beam rather than anatomy is suspect.

Three-dimensional imaging may clarify the attachment, shape, and relation of a mass to prosthetic or native structures, but lower temporal resolution and stitch or dropout artifacts can hide or invent edges. Multiplanar review should confirm the finding in source planes. Absence of a 3-D rendering never overrules a convincing, reproducible 2-D lesion, and a dramatic rendering should not bypass clinical correlation.

Escalate when TTE cannot answer the clinical question

A negative or technically limited TTE does not rule out IE. Small or early vegetations, prosthetic shadowing, device-related infection, obesity, lung interference, and prior valve damage reduce sensitivity. TEE is indicated when suspicion remains high after negative or inconclusive TTE, when a prosthetic valve or intracardiac device is involved, and usually after a positive TTE when local extension or complications must be defined. TEE more clearly evaluates the atrial side of the mitral valve, aortic root and periannular tissue, prosthetic sewing rings, and device leads, but even TEE has blind zones and artifacts.

If the initial study is normal or inconclusive and clinical suspicion remains high, repeat TTE or TEE is generally recommended in about 5–7 days, or sooner if a new murmur, embolus, heart failure, conduction change, or other complication develops. CT can clarify periannular anatomy; metabolic or leukocyte imaging may add evidence in selected prosthetic or device cases. The next test is chosen by the clinical team. The essential echo conclusion states what was visualized, what was not, and whether the examination answers the suspected location.

Search systematically for complications

Valve destruction can cause acute severe MR or AR, pulmonary edema, and low output before chambers enlarge. Periannular infection may form an abscess, pseudoaneurysm, or fistula; new atrioventricular block is an important clinical clue to extension near conduction tissue. Prosthetic infection can produce dehiscence and major paravalvular regurgitation. Left-sided vegetations can embolize to brain, spleen, kidney, or peripheral arteries, whereas right-sided or device-related disease can cause septic pulmonary emboli. Echo may show the cardiac source and consequences but does not exclude extracardiac complications.

Assess ventricular size and function, filling pressure clues, pulmonary pressure, regurgitant severity, pericardial effusion, and shunts or communications. Acute severe regurgitation may have a deceptively brief or lower-velocity signal because pressures equalize rapidly. A large mobile vegetation, new severe regurgitation, suspected abscess, fistula, prosthetic instability, or new ventricular dysfunction requires immediate communication through laboratory policy. Do not delay notification while perfecting optional measurements, and do not prescribe antibiotics or surgery from the scanning room. A defensible endocarditis study combines complete acquisition, explicit uncertainty, timely escalation, and urgent communication.

One negative study does not exclude IE

Escalate to TEE when suspicion remains high, TTE is nondiagnostic, or prosthetic material or a device limits assessment. If suspicion persists after normal or inconclusive imaging, repeat echocardiography in about 5–7 days—or sooner with a new complication—may reveal evolving disease.