Complications begin in first few weeks of onset and are divided into cardiac and extra cardiac
Cardiac complications
Valvular stenosis or insufficiency
Perforation, rupture and aneurysm of valve leaflets
Abscess in the valve ring
Myocardial abscesses
Suppurative pericarditis
Cardiac failure from one or more of the foregoing complications
Extra cardiac complications
Extra cardiac manifestations are due to friable vagetations which get dislodged into the blood stream forming emboli
Emboli from left side of the heart – Enters the systemic circulation and affect organs like spleen, brain, kidneys producing infarcts, abscesses and mycotic aneurysms
Kidneys – petechial hemorrhages (Flea bitten). Focal glomerulonephritis and infarction may develop
Spleen – Splenic enlargement and infarction with pain
Brain – infarction with neurological dysfunction
Emboli from right side of the heart – enters the pulmonary circulation and produces pulmonary abscesses
Petechiae may be seen in skin and conjunctiva due to emboli or toxic damage to capillaries
In SABE, Oslers nodes, Roth spots and in ABE , Janeway lesions may appear due to toxic or allergic inflammation of the vessel wall
Oslers nodes – Painful small swelling (1cm) appearing at the tip of fingers or toes caused by deposition of immune complex and hypersensitivity vasculitis
Janeway lesions –
Small erythematous or hemorrhagic, macular non-tender lesions on palms and soles
These are microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis
They are caused by septic emboli which deposit bacteria, forming microabscesses
Roth spots –
Caused by immune complex mediated vasculitis
Retinal hemorrhages with pale center composed of coagulated fibrin
Flame shaped hemorrhages
Focal necrotizing glomerulonephritis due to circulating immune complexes
Reference
Vinay kumar, Abul K.Abbas, Nelson Fausto, Jon C. Aster. Robbins and Cotran Pathologic basis of disease. 8th edition
