The clinical presentation of endocarditis depends upon the rapidity of onset, the virulence of the underlying organism, and the coexistence of underlying cardiac disease. More aggressive organisms in the setting of preexisting valvular disease will result in an accelerated course, with rapid diagnosis and early surgical intervention. Less virulent organisms may cause less destruction of cardiac structures, resulting in an elusive clinical course and prolonged illness.
Patients with acute endocarditis usually present early in the infection with substantial illness. Findings include high fevers, chills, rigors, and malaise, with progression to sepsis and circulatory collapse if untreated. Complications are common (see following) due to the aggressive nature of the infection, particularly embolic phenomena. Valvular disease may be extensive with resultant congestive heart failure in otherwise healthy individuals.
The initial presentation in the subacute setting commonly occurs between 2 and 4 weeks after infection. The symptoms are milder and more subtle, with lower fevers and generalized malaise. Other symptoms include weight loss, myalgias, and fatigue, which can mimic malignancy or other chronic illness. If there has not been significant cardiac destruction, most symptoms will resolve on appropriate antibiotic therapy.
Many patients with subacute endocarditis will be diagnosed after a complication has arisen, such as an embolic neurologic event. Other complications of embolism include arterial insufficiency, abdominal pain (bowel or splenic infarction), visual changes (retinal artery occlusion), myocardial infarction (coronary artery occlusion), and hematuria (renal infarction). Multiple septic emboli to the lungs can present as recurrent pneumonia or chest pain from pulmonary infarction.
Two potentially lethal complications of subacute endocarditis are heart failure and intracranial hemorrhage. Although the infection may be successfully treated with antibiotics, the residual structural damage to the heart may progress to heart failure. Thus, a patient with “healed” endocarditis should not be considered cured unless the valvular and ventricular function is stable over a period of time. Mycotic aneurysms from septic emboli to the brain are usually asymptomatic, but can rupture and result in devastating intracranial hemorrhage.
Prosthetic Valve Endocarditis
As with acute and subacute endocarditis, prosthetic valve endocarditis is classified according to time frame from surgery. Early prosthetic valve endocarditis is defined as infection occurring within 60 days of operation, and is usually due to either intraoperative contamination or infection in the early postoperative period. Common organisms are skin colonizers and respiratory tract pathogens. The presentation is similar to acute endocarditis and is associated with complications after surgery. Late prosthetic valve endocarditis is defined as infection occurring after 60 days from operation and presents similar to subacute endocarditis. The offending organisms are the same as those with native subacute infections.
Complications of Infective Endocarditis
The majority of patients with endocarditis will have developed complications, either as the initial presentation or during the course of the disease. The most common complications include congestive heart failure, abscess formation, and embolism. Other less common complications include pseudoaneurysm, mycotic aneurysm, fistula, and conduction disturbances.
Congestive heart failure is the most common cause of death and typically is caused by valvular destruction and insufficiency. Less common causes of congestive heart failure from endocarditis are coronary artery embolization with subsequent myocardial infarction, acute papillary muscle rupture, and valvular stenosis from very large vegetations. Patients with aortic valve disease are particularly prone to develop congestive heart failure.
Extension of the endocarditis process into surrounding myocardium results in abscess formation. This most commonly occurs with aortic valve involvement, forming a root abscess (Fig. 38-2). Mitral valve involvement can result in interventricular or interatrial abscess. Suspicion of abscess should be raised in patients with conduction abnormalities, pericarditis, congestive heart failure, and prosthetic valves. Transesophageal echocardiography (TEE) has the highest sensitivity for the detection of perivalvular abscess.14 Echocardiographic criteria for abscess include aortic root thickness greater than 9 mm, perivalvular density greater than 14 mm in the septum, sinus of Valsalva aneurysm or fistula, and instability (“rocking”) of a prosthetic valve.15
Aortic root abscess. There is extension of the infection beyond the aortic annulus into the anterior leaflet of the mitral valve.
Embolism of the vegetation has the potential for significant morbidity and mortality, and is more common in younger patients.16,17 Stroke occurs most commonly from native mitral valve endocarditis, as these lesions are usually larger than aortic valve vegetations.18 In patients with prosthetic valve endocarditis, there is no difference in stroke rate between aortic and mitral valve involvement.18 Predictors of stroke include left-sided endocarditis, mitral valve involvement, and size greater than 7 mm.18
Pseudoaneurysm occurs when the infective process liquefies and forms a cavity. Pulsatile pressure weakens the cavity and eventually blood enters the space, forming the pseudoaneurysm. The incidence of pseudoaneurysm ranges from 2 to 10 percent, and can occur in the setting of root abscess as well as along previous suture lines.19 Rupture of pseudoaneurysm from IE is likely and requires prompt surgical attention.
Persistent bacteremia or embolization of infected vegetative material from the active endocarditis can result in metastatic abscess. Mycotic aneurysm occurs when a distant abscess forms in an arterial branch. Intracranial mycotic aneurysms typically form in the middle cerebral artery and can produce intracranial hemorrhage. Metastasis of infected material to other organs can result in splenic abscess, septic arthritis, and septic pulmonary embolism.
Fistula formation occurs when an abscess or pseudoaneurysm ruptures into a surrounding structure. Rupture into a cardiac chamber forms an intracardiac shunt, whereas rupture into the pericardium will produce tamponade. Although fistulas are rare, mortality exceeds 50 percent.20
Conduction abnormalities are the result of infective destruction of conduction tissue. First-degree atrioventricular block is most commonly observed.21 Any new change in the electrocardiogram should raise the suspicion of abscess. Mortality can be increased in the presence of a conduction abnormality.21