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  • Updated 07.05.2023
  • Released 10.30.1995
  • Expires For CME 07.05.2026

Infective endocarditis



Infective endocarditis is a potentially lethal condition associated with a myriad of neurologic consequences, including stroke, mycotic aneurysms, vasculitis, discitis, meningoencephalitis, myelitis, and mononeuritis. Despite therapeutic advances, the incidence of infective endocarditis is rising on a global scale. Rapid identification and treatment via medical and surgical techniques in a multidisciplinary and collaborative fashion are necessary to achieve good functional outcomes.

Key points

• The neurologic complications of infective endocarditis are due to septic embolism to cerebral arteries. This may result in embolic stroke, infection of vessel walls with mycotic aneurysm or vascular rupture, and extension outside the affected vessel to cause meningitis or brain abscess.

• Although infective endocarditis typically develops on previously damaged cardiac valves, endocarditis in individuals abusing drugs intravenously may develop on valves that are normal. In both cases, infection results in valvular vegetations.

• Diagnosis of infective endocarditis requires a high index of clinical suspicion, careful cardiac and neurologic examination, and identification of the causative agent from blood cultures. Patient evaluation includes echoencephalography and other methods to detect valvular vegetations and injury as well as imaging of the brain and its supplying vessels, electroencephalography if seizures are suspected, and cerebrospinal fluid analysis.

• Rapid diagnosis and early antibiotic intervention remain the mainstays to avoid neurologic complications. Valvular surgery is indicated in many patients.

• Cardiac surgery should be performed as soon as possible (< 48 hours) where indicated. However, if ischemic or hemorrhagic stroke is present, delaying 1 to 2 weeks or 4 weeks, respectively, may be of benefit.

• The use of antithrombotics while being treated for infective endocarditis should be approached with caution.

Historical note and terminology

Although infective endocarditis was probably recognized as a specific entity in 1646 by Riviere, its manifestations were not fully described until the 19th century (75). In 1846, Virchow was the first to recognize the occurrence of embolic events with infective endocarditis (75). In 1852, a little-known English doctor, William Senhouse Kirkes (1822–1864), demonstrated that embolic events in infective endocarditis arose from cardiac vegetations (16). In a series of three Gulstonian lectures at the Royal College of Physicians in London in 1885, Sir William Osler drew on his enormous experience in both medicine and pathology to provide the first truly comprehensive account in the English language of what he termed “malignant endocarditis” (93; 101). In his lectures, Osler pointed out that the disorder resulted in meningeal or other central nervous system complications in 12% of patients. Thayer proposed the term “infective endocarditis” to replace the older term “bacterial endocarditis” as it became clear that a wide range of pathogens, including bacteria, rickettsiae, and fungi, could be responsible for the disease (121; 122).

Prior to the advent of antibiotics, infective endocarditis was invariably fatal. Treatment became possible as penicillin and subsequent agents became available. Initially, infective endocarditis was heavily associated with rheumatic heart disease, and the viridans group of streptococci were the agents most encountered (45). With the relative conquest of acute rheumatic fever in developed countries, however, Staphylococcus aureus has become the agent most associated with infective endocarditis within Western populations (86; 14). However, streptococci remain a significant cause of infective endocarditis in developing countries (86; 14; 96).

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