Infective endocarditis

Dana DeWitt MD (

Dr. DeWitt, of University of Utah, Salt Lake City has no relevant financial relationships to disclose.

)
John E Greenlee MD (Dr. Greenlee of the University of Utah School of Medicine has no relevant financial relationships to disclose.)
Originalldewitty released October 30, 1995; last updated August 19, 2020; expires August 19, 2023

Overview

An estimated 15,000 to 20,000 new cases of infective endocarditis are diagnosed annually in the United States. Neurologic complications can be the initial or predominant manifestation of the disease and have become a leading cause of disease mortality. Staphylococcus aureus is the leading causative organism, and intravenous drug abuse is disproportionately represented as a risk factor in patients with neurologic complications. Symptomatic cerebral complications occur in up to 55% of patients with infective endocarditis, often before the diagnosis of infective endocarditis is made, and the complications include stroke, intracranial hemorrhage, brain abscess, mycotic aneurysms, and meningoencephalitis. Rapid diagnosis and initiation of antimicrobial therapy remain the most effective means to prevent neurologic complications. Endovascular embolization or coiling of aneurysms or parent arteries can be used to treat selected cases of cerebral mycotic aneurysms. Endovascular thrombectomy is used in select cases of embolic ischemic stroke. Antiplatelet therapy remains controversial for secondary stroke prevention or continuation in patients that were on antiplatelets prior to development of infective endocarditis, but it is considered necessary after stent placement to prevent rethrombosis. Although traditionally postponed, early valve surgery has gained traction in recent years with cumulative evidence of potential mortality benefit in selected cases.

Key points

 

• Gram-positive staphylococci, streptococci, and enterococci account for 80% to 90% of cases of infective endocarditis. Of these, Staphylococcus aureus is the most common organism.

 

• 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.

 

• 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.

 

• Care of the patient with endocarditis may include input from neurologists, infectious disease specialists, radiologists, and cardiothoracic surgeons.

Historical note and terminology

Although infective endocarditis was probably recognized as a specific entity in 1646 by Riviére, its manifestations were not described fully until the 19th century (Major 1945). Virchow, in 1846, was the first to recognize the occurrence of embolic events during infective endocarditis (Major 1945). A little-known English doctor, William Senhouse Kirkes (1822-1864), demonstrated in 1852 that embolic events in infective endocarditis arose from cardiac vegetations (Cameron and Hicks 2000). In 1885, in a series of 3 Gulstonian Lectures at the Royal College of Physicians in London, 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 (Osler 1885a; Osler 1885b; Osler 1885c). 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 of “bacterial” endocarditis, as it became clear that a wide range of pathogens including bacteria, rickettsiae, and fungi could be responsible for the disease (Thayer 1931).

Prior to the advent of antibiotics, although progression to death might take weeks or months, infective endocarditis was invariably fatal. Treatment became possible as penicillin and other subsequent agents became available. Initially, infective endocarditis was heavily associated with rheumatic heart disease and the viridans group of Streptococci were the agents most commonly encountered (Greenlee and Mandell 1973). With the relative conquest of acute rheumatic fever in developed countries, however, Staphylococcus aureus has become the agent most commonly associated with infective endocarditis in most series and the major risk factors have become cardiac valvular disease from causes other than rheumatic carditis, the presence of a prosthetic valve or cardiac device, intravenous drug abuse, the use of indwelling intravenous catheters, immunosuppression, and recent dental or surgical procedures (Murdoch et al 2009; Cahill and Prendergast 2016). Cases of infective endocarditis have also been reported after transcatheter aortic valve replacement or use of Amplatzer devices used to close patent foramina ovale (Stortecky et al 2020; Wang et al 2020). Streptococci still remain important agents of infective endocarditis, in particular in lower income countries (Murdoch et al 2009; Cahill and Prendergast 2016).

Within recent years, 2 therapeutic advances have been of great importance in disease treatment: earlier and more aggressive surgical intervention to repair injured valves and catheter-based techniques for clot extraction or treatment of mycotic aneurysms. Even at present, however, mortality may exceed 25% to 30% (Murdoch et al 2009; Cahill and Prendergast 2016; Holland et al 2016).

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