Endocarditis By Dr. Abdelaty Shawky Assistant professor of pathology

Endocarditis * Types: (1). Non-infective endocarditis A. Rheumatic endocarditis. B. Verrucous (libman sack) endocarditis: with SLE. C. Non-Bacterial thrombotic endocarditis. (2). Infective endocarditis A. Acute Infective endocarditis B. Sub-acute Infective endocarditis 2

Verrucous (Libman-Sacks) endocarditis 3

Less common, non-infective endocarditis attributable to elevated levels of circulating immune complexes may occur in patients with systemic lupus erythematosus 4

Nonbacterial Thrombotic Endocarditis NBTE 5

Characterized by the deposition of small masses of fibrin, platelets, and other blood components on the leaflets of the cardiac valves. There is no infective organism (sterile). Aortic valve is most common site. Clinically: asymptomatic, if large: may embolize. * Pathogenesis/ association: – Subtle endothelial abnormalities. – Hypercoagulability. – Association with malignancy (50%). 6

Infective Endocarditis 7

* Definition: infection of the cardiac valves or mural surface of the endocardium, resulting in the formation septic vegetations (thrombi). * Divided into: a. Acute infective endocarditis. b. Subacute infective endocarditis. 8

Acute infective endocarditis * Etiology: Acute suppurative inflammation that affects healthy valves. Organisms: Highly virulent as staph. aureus, strept. hemolyticus and gonococci. 9

* Lesions: Mitral & aortic valves are most commonly affected. Tricuspid is affected in IV drug abusers. The mural endocardium may be also affected. The affected valve and mural endocardium show acute suppurative inflammation + vegetations. 10

Vegetations are: * N/E: multiple, large, yellowish, friable found anywhere on the cusps. * M/P: the vegetations consist of platelet, fibrin, bacteria, numerous neutrophils & pus cells. Myocardial shows microabscesses. The pericardial sac is filled with pus. 11

* Complications: 1. Embolic complications: Detached septic vegetations leads to systemic pyemia. 2. Toxemic complications: Severe toxemia 12

* Prognosis: Rapidly fatal due to; 1.Severe toxemia (septicemia). 2.Cusp perforation (acute heart failure). 13

Subacute infective endocarditis * Etiology: Subacute inflammation that affects abnormal valves in;  Rheumatic valvulitis  Congenitally abnormal valves.  Prosthetic valves. Caused by Less virulent bacteria as strept.viridans. 14

* Lesions: Mitral & aortic valves are commonly affected. The mural endocardium may be also affected The affected valve and the mural endocardium show; the lesion of the corresponding disease (e.g. rheumatic, congenital) + vegetations. 15

Vegetations are: * N/E: multiple, large, gray, friable found anywhere on the cusps. * M/P: the vegetations consist of platelets, fibrin, bacteria and some inflammatory cells mainly histiocytes. The Myocardium shows degenerative changes. 16

* Complications: 1. Embolic complications: Infarctions: in kidney, spleen and brain, retina, heart. Mycotic aneurysms: mainly in cerebral and mesenteric. Petechial hemorrhage: in skin, mucous membranes and serous membranes. Osler’s nodules: small. tender, intracutaneous nodules in pulps of fingers & toes. 17

2. Toxemic complications: Moderate toxemia: fever, anemia, clubbing of fingers, splenomegaly, petechial hemorrhage and focal glomerulonephritis (flea bitten kidney) 18

* Prognosis: Heal by fibrosis leads to valve lesion either stenosis or incompetence. 19

Endocarditis of the mitral valve (subacute, caused by Streptococcus viridens). vegetations are denoted by arrows. 20

Slide C. Histologic appearance of vegetation of endocarditis with extensive acute inflammatory cells and fibrin. Bacterial organisms were demonstrated by tissue Gram stain. 21

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