ER Episode

Synopsis of Scene

Patho Foci

"Abby Road"

A 12- 13-year old boy, named Marty is in the ER. He has a low-grade temperature. Examination reveals bruises on his back. When asked, "how did you get them", he replies, "I don’t know". He also has several suspicious looking lesions on his leg. When asked, "what’s this", he replies, "mosquito bites". The nurse replies, with some sarcasm, " in February?" Obviously, something is suspicious, Marty is not being fully honest. The doctor orders a CBC, Chem 20 and "tox" screen. In leaving she says to the nurse, "those are infected track marks" (referring to the lesions on the leg).

In a subsequent scene more information is obtained. In a dramatic confrontation he confesses to injecting himself with human growth hormone (which he has obtained from the Internet). He has used his grandmother’s insulin syringes to inject himself. This explains the marks on his legs. He is giving himself human growth hormone because he is tired of being beaten up in school and feels that if he gets bigger, his problems with being beaten up will resolve.

Additional data from a physical exam is now revealed. He has a heart murmur, and splinter hemorrhages. The diagnosis of bacterial endocarditis is made.

• The patho of infective endocarditis
• Most common symptoms of infective endocarditis
• The diagnosis and treatment of infective endocarditis

Pathophysiology

Endocarditis (inflammation of the endocardium of the heart) occurs when platelets and fibrin becomes deposited on the endothelial (inner) surface of the heart. This is unusual since, ordinarily, the endothelium is non-thrombogenic (i.e. does not easily allow clots or thrombi, to form on its surface). For the thrombotic lesion to begin growing some type of predisposing factor is usually present which stresses the endothelium. For example, there might be acquired or congenital heart disease that results in high jet streams of blood flow that damage the endothelium, or there might be damage done to the endothelium by the placement of intracardiac catheters. The deposition of immune complexes, as might occur in the context of systemic lupus erythematosus (SLE) or rheumatic heart disease, might cause damage to the endothelium. When the endothelium is damaged, platelets can adhere to it. The platelets then degranulate and stimulate the local deposition of fibrin The appearance of thrombotic lesions on the endothelium of the heart is called nonbacterial thrombotic endocarditis.

If the nonbacterial thrombotic lesion becomes infected then infectious endocarditis is now present. For infection to occur there must be the introduction of bacteria or some other infectious microorganism into the blood stream Frequently, microorganisms are introduced by the following routes: genitourinary catheterization, hemodialysis, dental procedures, intravenous drug abuse, skin infections, cardiac surgery.

Microorganisms adhere to the thrombus on the endothelial surfaces and stimulate further deposition of platelets and fibrin. The microorganisms, in a sense, bury themselves within the growing lesion. This proves to be very advantageous to them since it provides them a certain degree of protection against destruction by elements of the immune system. The growing lesion is often referred to as vegetation and most often this vegetation occurs on the endothelial surface of heart valves. As the vegetation grows, so does the risk that emboli will develop, potentially causing damage to a variety of organs in the body.

Bacteria are the leading cause of infective endocarditis. Hence, infective endocarditis can more specifically be called bacterial endocarditis. Bacterial endocarditis, in turn, can be classified as either sub acute bacterial endocarditis (SBE) or acute bacterial endocarditis. In cases of sub acute bacterial endocarditis, infection is often with less virulent organisms, such as Streptococcus viridans. More invasive bacteria such as staphylococci result in a more fulminate, faster developing or acute bacterial endocarditis.