Clinical Features

The interval between the presumed initiating bacteremia and the onset of symptoms of IE is estimated to be less than two weeks in more than 80 per cent of patients with NVE. Interestingly,in some patients with intraoperative or perioperative infection of prosthetic valves, the incubation period may be prolonged (2 to 5 or more months).

 

Clinical Features of Infective Endocarditis

Osler’s nodes are small, tender subcutaneous nodules that develop in the pulp of the digits or occasionally more proximally in the fingers and persist for hours to several days. These too are not pathognomonic for IE.

Janeway lesions are small erythematous or hemorrhagic macular nontender lesions on the palms and soles and are the consequence of septic embolic events.Roth spots, oval retinal hemorrhages with pale centers, are infrequent findings in patients with IE.

The hallmarks of IE are fever and new murmur (over 85 per cent). However, fever may be absent in the elderly and the uremic or immunosuppressed population. Murmurs may be absent with right sided or mural infections or intracardiac device infection. 

Systemic emboli are among the most common clinical sequelae of IE. Emboli often antedate diagnosis. Although embolic events may occur during or after antimicrobial therapy, the incidence decreases promptly during administration of effective antibiotic therapy. Embolic splenic infarction may cause left upper quadrant abdominal pain and left shoulder pain. Renal emboli may occur asymptomatically or with flank pain and may cause gross or microscopic hematuria. Embolic stroke syndromes, predominantly involving the middle cerebral artery territory, occur in 15 to 20 per cent of patients with NVE and PVE. Coronary artery emboli are common findings at autopsy but rarely result in transmural infarction. Emboli to the extremities may produce pain and overt ischaemia, and those to mesenteric arteries may cause abdominal pain, ileus, and guaiac positive stools.

Neurological symptoms and signs occur in 30 to 40 per cent of patients with IE, are more frequent when IE is caused by S. aureus, and are associated with increased mortality rates.Embolic stroke is the most common and clinically important of the neurological manifestations.Intra-cranial hemorrhage occurs in 5 per cent of patients with IE. Bleeding results from rupture of a mycotic aneurysm, rupture of an artery due to septic arteritis at the site of embolic occlusion, or hemorrhage into an infarct. Mycotic aneurysms, with or without rupture occur in 2 to 10 per cent of patients with IE: approximately half of these involve intracranial arteries. Cerebritis with microabscesses complicates IE caused by invasive, pathogens such as S. Aureus, but large brain abscesses are rare. Purulent meningitis complicates some episodes of IE caused by S. aureus or S.pneumoniae, but more typically the cerebrospinal fluid has an aseptic profile. Other neurological manifestations include severe headache (a potential clue to a mycotic aneurysm), seizure, and encephalopathy.

CHF complicating IE is primarily the result of valve destruction or distortion or rupture of chordae tendinae. Intracardiac fistulas, myocarditis, or coronary artery embolization may occasionally contribute to the genesis of CHF.Renal insufficiency as a result of immune complex-mediated glomerulonephritis occurs in less than 15 per cent of patients with IE. Azotemia as a result of this process may develop or progress during initial therapy. 

Renal dysfunction in patients with IE is most commonly a manifestation of impaired hemodynamics or toxicities associated with antimicrobial therapy (interstitial nephritis or aminoglycoside-induced injury).