phys final-- endocarditis .pdf

Endocarditis Disease summary ○ Definitions Infective endocarditis (IE):Is a life-threatening infection of the endocardial or inner lining of the heart (including cardiac valves).. ○ IE is characterized by the colonization of microbes (most frequently bacteria), l...

Endocarditis Disease summary ○ Definitions Infective endocarditis (IE):Is a life-threatening infection of the endocardial or inner lining of the heart (including cardiac valves).. ○ IE is characterized by the colonization of microbes (most frequently bacteria), leading to the formation of vegetations (i.e., blood clots filled with microorganisms and inflammatory cells) and the destruction of underlying cardiac tissues. ○ The mitral and aortic valves are the most common sites of infection, and Staphylococcus aureus is the most common cause of IE today. ○ IE not only affects the heart, but also can produce a wide variety of systemic clinical manifestations through multiple pathophysiologic mechanisms. Prevalence ○ The prevalence of IE in the United States is approximately 1–4 cases per 100,000 persons. ○ The incidence has not changed significantly during the past 50 years. ○ IE is 2–3 times more common in males. ○ Although IE can occur at any age, more than half of patients are older than 50 years. ○ The majority of people who develop IE (approximately 2 of 3 cases) have a structural heart problem that places them at risk. Causes and risk factors ○ Although a wide variety of microbial agents may cause IE and include viruses, fungi, rickettsiae, and parasites, bacteria are the most frequent etiologic agents (i.e., bacterial endocarditis). ○ The most rapidly progressive and destructive form of IE (i.e., acute IE) is caused by Staphylococcus aureus, which also is the most common etiologic pathogen of IE. ○ Acute IE primarily affects people with previously normal hearts and is also caused by Streptococcus pneumoniae, Streptococcus pyogenes, and Neisseria species. ○ A less serious form of the disease (i.e., subacute IE) is seen most frequently in people with a pre-existing heart condition. ○ Subacute IE is caused by less virulent microbes, such as Streptococcus viridans (more than half of all cases of subacute IE), enterococci, and other varieties of gram-negative and gram-positive bacilli, yeasts, and fungi. ○ Two independent risk factors are often required for IE to develop: a damaged endocardial lining (which exposes underlying collagen that attracts platelets and initiates the formation of a blood clot) a portal of entry by which organisms access the circulation. ○ Although anyone can contract IE, the infection most frequently develops in people with preexisting heart disease. ○ Transient bacteremia may emerge in the course of a high-grade gingivitis or an upper respiratory, gastrointestinal, or genitourinary infection. ○ Bacteremia may also develop from an infectious skin lesion, a surgical procedure, or dental intervention (e.g., extraction, root canal therapy, placement of orthodontic bands, or prophylactic cleaning of teeth).  ○ In hospitalized patients, so-called nosocomial (i.e., hospital-acquired) IE may develop from infected intravascular or urinary tract catheters. Pathophysiology ○ The pathophysiology of IE involves the formation of intracardiac vegetations that have both local and systemic effects. ○ Impingement of jet streams from highly turbulent blood flow (due to abnormal valves or congenital heart defects) provides a susceptible site for infection during episodes of bacteremia. ○ Vegetations consist of a collection of infectious microbial organisms and cellular debris enmeshed in fibrin strands of clotted blood (i.e., thrombus). ○ Research studies suggest that circulating bacteria are able to synthesize polysaccharides (e.g., dextran) that promote their adhesion to endocardial surfaces. ○ Microorganisms that most commonly cause IE (i.e., S. aureus, S. viridans, group A, C, and G streptococci, and enterococci) resist the bactericidal action of serum complement proteins and possess fibronectin receptors for the surface of the thrombus. ○ Within 6 hours after infection, microbial replication occurs and bacterial colonies form within aggregates of fibrin and platelets. ○ Colonies subsequently become deeply embedded within vegetations and inaccessible to host defenses. ○ Furthermore, microbes deep within the vegetation tend to hibernate (because of the lack of available nutrients) and, therefore, are less susceptible to bactericidal antimicrobials that interfere with bacterial cell wall synthesis. Diagnosis: Clinical Manifestations and Laboratory Tests: ○ Medical history is critical and the patient should always be questioned about recent invasive medical and dental procedures and recreational drug use that may have led to the illness. ○ The majority of patients present with a fever that has lasted several days to 2 weeks. ○ With acute IE, fever develops rapidly, is usually high-grade, and accompanied by chills. ○ With subacute IE, fever is usually low-grade and frequently accompanied by other systemic signs of inflammation (e.g., malaise, anorexia, and lethargy). ○ Characteristic peripheral lesions occur in 25% of affected persons and include: petechiae on the palate, conjunctiva, or beneath the fingernails Osler nodes (painful, raised lesions of the fingers or toes) splinter hemorrhages (which present as dark red streaks) under fingernails and toenails Janeway lesions (painless, red lesions of the palms or soles) Roth spots (lesions containing pus within the retina) Pallor Splenomegaly Minor criteria include: ○ 1. the presence of a predisposing influence (e.g., valvular disease or IV drug use) ○ 2. Fever ○ 3. immune complex-mediated complications (e.g., glomerulonephritis, Osler nodes, or Roth spots)  ○ 4. vascular lesions (i.e., petechiae, splinter hemorrhages, or Janeway lesions) ○ 5. positive blood cultures not meeting major criteria described above ○ 6. positive echocardiogram not meeting major criteria If two major criteria, one major criterion and three minor criteria, or five minor criteria are present, a definitive diagnosis can be made with 80% accuracy. If fewer criteria are established, a differential diagnosis is established, or the patient’s fever resolves within 4 days, IE is unlikely. Serious Complications and Prognosis: ○ When IE is not promptly diagnosed and adequately treated, a host of life-threatening complications can occur: damage to heart valves, leading to heart failure Dysrhythmias Infective Endocarditis embolization of vegetations causing infarcts (e.g., stroke), new infections at extracardiac sites, or unilateral blindness when obstruction occurs in a retinal artery vasculitis and aneurysm formation ○ However, most cases of IE can be effectively treated with antibiotics. ○ If infection is caused by S. viridans, enterococci or coagulase-negative staphylococci, symptoms often remit with therapy in 4 days; with S. aureus, symptoms may persist for 12 days Appropriate therapy: ○ Antimicrobial agents are generally given for 4–6 weeks, beginning with IV administration and ending with oral treatment. ○ In some cases, multiple antibiotics are given simultaneously to more effectively eliminate the offending microorganism and prevent drug resistance.