Endocarditis - Research Paper Example

? Endocarditis Endocarditis Endocarditis is caused by many bacteria or fungi and is an infection of endocardium that mostly involves the valves or the adjacent structures, hence called infective endocarditis. In rheumatic heart disease, also, the leaflets of the valves become inflamed and edematous leading to endocarditis. Non-bacterial thrombotic endocarditis (NBTE) occurs in normal cardiac valves and is mostly in association with wasting diseases such as cancer. The mechanism is poorly known and does not destroy the valve (Rubin & Resiner 2009). Consequently, infective endocarditis is comparatively the main focus of health clinicians because of its increased incidence and severe outcomes and valve deformities. The incidence of infective endocarditis is estimated to be 5 to 15 cases per 100,000 per year. More than 50% of the people affected with infective endocarditis are above the age of 60 years (Colledge et al 2010). The paper highlights the etiology, signs and symptoms, pathology, clinical diagnosis, investigations and management plan for endocarditis. In a British study rheumatic disease was the underlying cause in 24% cases, congenital heart disease in 19%, other cardiac abnormalities such as calcified aortic valve or floppy mitral valve in 25% and the remainder 32% were thought to have no pre-existing or related cardiac abnormality (Colledge et al 2010). The most common cause for bacterial endocarditis in children is coronary heart disease while 10% of the cases are caused by rheumatic heart disease. Mitral valve prolapse and coronary heart disease are the most frequent causes for bacterial endocarditis in adults. Intravenous drug abuse leading to S. aureus infections, prosthetic valves serving as sites of infection, transient bacteremia from dental procedures, urinary catheterization, gastrointestinal endoscopies or obstetric procedures and elderly population are some of the other important predisposing factors for endocarditis (Rubin & Reisner 2009). Virulent organisms can affect normal valves, however the mechanism is not clearly known. On the other hand, the infection of the damaged valves is caused due to turbulent blood flow leading to affect on the valve’s endothelium. Focal deposition of platelets and fibrin causes the production of small sterile vegetations that are the vulnerable sites for bacterial growth and colonization. Most commonly involved valves are the mitral valve, aortic valve or both of them. Damages valve tissue can also lead to leaflet perforation causing regurgitation. Infected thromboemboli can travel to various systemic sites such as brain, kidneys or spleen causing infarcts or abscess formation (Rubin & Resiner 2009). Endocarditis represents its manifestations in either acute or a “subacute” form. Acute endocarditis is the infection of a cardiac valve by highly virulent suppurative organisms commonly Staphylococcus aureus and S. pyogenes. Subacute bacterial endocarditis is less fulminant and is caused by a comparatively less virulent organism such as Streptococcus viridians or Staphylococcus epidermidis. In sub-acute endocarditis a structurally abnormal valve is affected for instance which has been deformed by rheumatic heart disease (Rubin & Reisner 2009). However, the stages are usually overlapped because of various factors such as previous antibiotic therapy, site of infection or the type of bacteria. Subacute stage is characterized by persistent fever, complains of unusual tiredness, weight loss or night sweats. This should be suspected if any of the above symptoms develop in a congenital or valvular heart disease patient. Other features include purpura and petechial hemorrhage in skin, splinter hemorrhages under finger nails. Osler’s nodes, a product of vasculitis are rare. Digital clubbing is a late sign and frequently the spleen is palpable. Microscopic hematuria is also commonly observed. Acute endocarditis presents as a severe febrile illness with prominent heart murmurs and visible petechiae. Cardiac or renal failure may develop rapidly and embolic events are also common. Post-operative endocarditis manifests in a patient with a recent heart surgery and is characterized by unexplained fever. Morbidity and mortality in this case is high and a redo surgery is required urgently. Clinical diagnosis of endocarditis is made on the basis of the modified Duke’s criteria (Colledge et al 2010). Duke’s criterion is essential for clinical diagnosis. Major criteria includes "(a) positive blood culture with typical organisms form two cultures, persistent positive cultures from 12 hours apart samples or three or more positive blood cultures taken 1 hour part and, (b) endocardial involvement with positive echocardiographic findings of vegetations or valvular regurgitation". Minor criteria includes "(a) predisposing valvular or cardiac abnormality, (b) intravenous drug abuser, (c) pyrexia greater than 38 C, (d) embolic phenomenon (e) vasculitic phenomenon, (f) blood cultures suggestive ,and (g) suggestive echocardiographic findings". Diagnosis of definite endocarditis is established if any of the two major or one major and three minor or five minor criteria are reported. Possible endocarditis is suspected when one major and one minor or three minor criteria are manifested or reported in the investigations (Colledge et al 2010). Echocardiography is one of the key investigations for detection and following the progress of the valve vegetations. It also helps to assess the valve deformity and any kind of abscess formation. Even vegetations of small size of 2-4 mm can be detected through transthoracic echocardiography. Trans-esophageal echocardiography can help visualize the smaller ones ranging from 1-1.5mm which is crucial in identifying abscess formations and previous prosthetic valve patients. Transthoracic echo is 65% sensitive in detecting the vegetations while the trans-esophageal echo has more than 90% sensitivity (Evangelista & Gonzalez-Alujas 2004; Colledge et al 2010). Blood culture is also a crucial investigation because it helps in indentifying the infective organism and planning the antibiotic treatment course. 3 to 6 blood samples should be taken before therapy is started and should not wait for pyrexia to commence (Colledge et al 2010). Management of endocarditis depends on the type of infective organism, whether prosthetic valve is involved, any penicillin allergies and the mode of presentation of the patient. In acute patients, flucoloxacillin and gentamicin are recommended while in subacute cases benzyl penicillin and gentamicin are recommended. In cases of penicillin allergy or prosthetic valve, triple therapy of vancomycin, gentamicin and oral rifampicin should be administered. 2 week treatment course is sufficient for less virulent strains. Benzyl penicillin and gentamicin course of 4 and 2 weeks respectively is considered for S. viridians and S. bovis strains. In cases of entercocci infection, ampicillin and gentamicin are given for four weeks. In Staphylococcus infections, benzyl penicillin is recommended and flucoloxacillin, vancomycin and gentamicin are administered in cases of penicillin resistant strains for four weeks. All antibiotics are administered through intravenous routes. Cardiac surgery is indicated in cases when heart failure is suspected, failure of antibiotic therapy, large vegetations with risk of systemic emboli and abscess formation. Antimicrobial therapy is recommended before commencing with the surgery (Colledge et al 2010). Infective endocarditis is one of the critical heart conditions which lead to valvular deformities if not treated promptly and rapidly. Study has showed that the incidence of infective endocarditis is higher in those cases which have a pre-existing cardiac abnormality or have a history of drug abuse or prosthetic heart valves. Infective endocarditis can be diagnosed on the basis of the clinical manifestations which are characteristic and can be easily observed. Investigations such as blood cultures and echocardiography are key investigations for endocarditis. Treatment plan should only be planned after obtaining bacteria culture reports and the management plan is devised on the basis of the type of organism. Prompt diagnosis and management can prevent complications of endocarditis and also highlight any cases of possible of suspected endocarditis. Fig 1: A figure of Bacterial endocarditis showing destructive vegetations in the mitral valve (Rubin & Reisner 2009). Fig 2: A figure of a patient with characteristic splinter hemorrhages under his finger nails and petechial hemorrhages on his abdomen (Barza 1993). Fig 3: Large vegetations in the mitral valve visible in the echocardiography (Evangelista & Gonzalez-Alujas 2004). Fig 4: A flowchart representing the use of echocardiography in suspected cases of infective endocarditis (IE) ,TTE, transthoracic echocardiography, TEE, trans-esophageal echocardiography (Haldar & O’Gara 2006). References Barza, M. (January 01, 1993). Skin and Nail Lesions in Endocarditis. New England Journal of Medicine, 329, 22, 1626. Colledge, N. R., Walker, B. R., Ralston, S., Davidson, S., & Britton, R. (2010). Davidson's principles & practice of medicine. Edinburgh: Elsevier/Churchill Livingstone. Evangelista, A., & Gonzalez-Alujas, M. T. (January 01, 2004). Echocardiography in infective endocarditis. Heart (british Cardiac Society), 90, 6, 614-7. Haldar, S. M., & O'Gara, P. T. (June 01, 2006). Infective endocarditis: diagnosis and management. Nature Clinical Practice Cardiovascular Medicine, 3, 6, 310-317. Rubin, E., & Reisner, H. M. (2009). Essentials of Rubin's pathology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Read More