Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or the surfaces of intracardiac devices. Endocarditis is characterized by lesions, known as vegetations, which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inï¬ammatory cells.In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify. There are several ways to classify endocarditis. The simplest classification is based on cause: either infective or non-infective, depending on whether a microorganism is the source of the inflammation or not. Regardless, the diagnosis of endocarditis is based on clinical features, investigations such as an echocardiogram, and blood cultures demonstrating the presence of endocarditis-causing microorganisms. Signs and symptoms include: fever, chills, sweating, malaise, weakness, anorexia, weight loss, splenomegaly, flu like feeling, cardiac murmur, heart failure, petechia of anterior trunk, Janeway's lesions, etc. Endocarditis is an infection of the inner lining of your heart (endocardium). Endocarditis generally occurs when bacteria or other germs from another part of your body, such as your mouth, spread through your bloodstream and attach to damaged areas in your heart. Left untreated, endocarditis can damage or destroy your heart valves and can lead to life-threatening complications. Treatments for endocarditis include antibiotics and, in certain cases, surgery. Endocarditis is uncommon in people with healthy hearts. People at greatest risk of endocarditis have damaged heart valves, artificial heart valves or other heart defects.
The initial symptoms of endocarditis are similar to the flu and include: a high fever (101.4oF), chills, headache, joint and muscle pain. Endocarditis may develop slowly or suddenly depends on the cause of the infection and whether you have any underlying heart problems. Endocarditis signs and symptoms vary, but may include: Fever and chills, A new heart sound made by blood rushing through your heart, Fatigue, Aching joints and muscles, Night sweats, Shortness of breath, Paleness, Persistent cough, Swelling in your feet, legs or abdomen, Unexplained weight loss, Blood in your urine (either visible or found in a doctor's viewing of your urine under a microscope), Tenderness in your spleen is an infection-fighting abdominal organ on your left side, just below your rib cage, Osler's nodes are red and tender spots under the skin of your fingers, Petechiae is a tiny purple or red spots on the skin, whites of your eyes or inside your mouth. In the United States, the 2009 incidence of IE was approximately 12.7 cases per 100,000 persons per year. The age-adjusted hospital admission rate has increased 2.4% annually from 1998-2009. This rate has risen significantly from that of the previous 50 years (2-4 cases per 100,000 persons per year). The incidence of IE in other countries is similar to that in the United States. From 1998-2009, the proportion of patients with intracardiac devices increased from 13.3% to 18.9%, while the proportion of cases with a background of HIV infection or HIV drug abuse fell. Between 1998 and 2009, the mean age of patients has risen from 58.6 to 60.8 years. Currently, more than 50% of patients are older than 50 years. Mendiratta et al, in their retrospective study of hospital discharges from 1993-2003 of patients aged 65 years and older with a primary or secondary diagnosis of IE, found that hospitalizations for IE increased 26%, from 3.19 per 10,000 elderly patients in 1993 to 3.95 per 10,000 in 2003. This increase in age has continued, with the mean age of patients in 2009 at 60.8 years. In Rio de Janeiro University Hospitals, S. aureus (30 %) was the predominant cause of IE, 32.5 % was from HAIE and 16.1 % from CAIE. Streptococcus spp. (45.1 %) was the main etiology of CAIE (p=0.001).
There were 3-5 % with CAIE due to coagulase-negative Staphylococci. S. aureus (38.2 %) and Enterococcus spp. (27.5 %) were the most frequent cause of HAIE; the prevalence of methicillin-resistant S. aureusin this cohort was 5-5.5 %. In our analysis of risk factors related to in-hospital mortality in IE patients were: their age being over 45-years-old and chronic renal insufficiency. Studies of IE have been scant in Brazil, especially the past decade described 20 cases of IE with, neurological thromboembolic manifestations, formation of aneurysms and subarachnoid hemorrhages. Tiossi and collaborators 10 analyzed 20 IE patients who died. Mansur et al. 11 analyzed 300 cases in the city of São Paulo. The present study had as its objective the study of patients affected by IE, in order to increase awareness of the present situation of the disease as it currently exists. To achieve this aim, epidemiological factors, risk factors, clinical presentation, etiology, complicating factors, diagnostic methods, treatment and evolution of cases diagnosed as IE at the Clinics Hospital of the Medical School of Ribeirão Preto of the University of São Paulo (HCFMRP-USP) between 1992 and 1997 were analyzed. The major goals of therapy for infective endocarditis (IE) are to eradicate the infectious agent from the thrombus and to address the complications of valvular infection. The latter includes both the intracardiac and extracardiac consequences of IE. Some of the effects of IE require surgical intervention. Emergent care should focus on making the correct diagnosis and stabilizing the patient with acute disease and cardiovascular instability. General measures include the following: • Treatment of congestive heart failure • Oxygen • Hemodialysis. The treatment is of types: Antibiotic therapy, Anticoagulation Therapy, Surgery, Vancomycin may also be used if tests reveal that your infection is caused by bacteria that have developed a resistance to penicillin and gentamicin, such as the meticillin-resistant staphylococcus aureus (MRSA) strain of bacteria. In the setting of acute IE, institute antibiotic therapy as soon as possible to minimize valvular damage. Three to 5 sets of blood cultures are obtained within 60-90 minutes, followed by the infusion of the appropriate antibiotic regimen. The initial antibiotic choice is empiric in nature, determined by clinical history and physical examination findings. Empiric antibiotic therapy is chosen based on the most likely infecting organisms. Native valve endocarditis (NVE) has often been treated with penicillin G and gentamicin for synergistic coverage of streptococci. Patients with a history of intravenous (IV) drug use have been treated with nafcillin and gentamicin to cover for methicillin-sensitive staphylococci. The emergence of methicillin-resistant S aureus (MRSA) and penicillin-resistant streptococci has led to a change in empiric treatment with liberal substitution of vancomycin in lieu of a penicillin antibiotic. Prosthetic valve endocarditis (PVE) may be caused by MRSA or coagulase-negative staphylococci (CoNS), thus, vancomycin and gentamicin may be used for treatment, despite the risk of renal insufficiency. Rifampin is necessary in treating individuals with infection of prosthetic valves or other foreign bodies because it can penetrate the biofilm of most of the pathogens that infect these devices. However, it should be administered with vancomycin or gentamicin. These latter 2 agents serve to prevent the development of resistance to rifampicin. Linezolid substitution is done for vancomycin in patients with unstable renal function because of the difficulty of achieving therapeutic trough levels in this situation. Linezolid or daptomycin are options for patients with intolerance to vancomycin or resistant organisms. Organisms with a minimum inhibitory concentration (MIC) to vancomycin of equal to or greater than 2 mcg/mL should be treated with alternative agents. Appropriate regimens should be devised in consultation with a specialist in infectious disease.