4. Infective Endocartidis (1) - Copy.ppt
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INFECTIVE ENDOCARDITIS Definition Infective endocarditis - an infection of the endocardium that usually involves the valves and adjacent structures, - is caused by a wide variety of bacteria and fungi. Common site: -heart valve, - septal defect, - chordae tendinae - mural endocardium Infective...
INFECTIVE ENDOCARDITIS Definition Infective endocarditis - an infection of the endocardium that usually involves the valves and adjacent structures, - is caused by a wide variety of bacteria and fungi. Common site: -heart valve, - septal defect, - chordae tendinae - mural endocardium Infective endocarditis Classification Acute bacterial endocarditis- is caused by virulent organisms and runs its course over days to weeks. Subacute bacterial endocarditis- is caused by organisms of low virulence and runs its course over weeks to months IE on prosthesis - early prosthetic - late prosthetic ENDOCARDITIS Characteristic pathological lesion: vegetation, composed of platelets, fibrin, microorganisms and inflammatory cells. The susceptible host -IE can occur at any age, but today is most common in older adults. -median age of onset: 50 years -Male/female ratio: 2:1 -Most patients have a preexisting cardiac condition that affects the valves. -iv drug abusers at high risk for IE (high frequency of tricuspid valve infection caused by Staphylococus aureus.) Prevalence and risk factors The incidence of infective endocarditis in a general population has been estimated at between 2 and 6 cases per 100,000 persons-years, but it is clearly higher in patients with underlying valvular heart diseases and those with intravenous drug abuse (IVDA). Prevalence and risk factors Although historically rheumatic valvulitis was considered a frequent predisposing factor for endocarditis, times have changed. Mitral valve prolapse, aortic sclerosis, and bicuspid aortic valvular heart disease are now more frequent causes. In addition, prosthetic valvular heart disease accounts for about one third of all cases of endocarditis, and occurs in 1% to 3% of patients after valvular heart surgery. Prevalence and risk factors Pacemaker (intracardiac device) endocarditis Early cases are frequently caused by Staphylococcus aureus Late cases are caused by Staphylococcus epidermidis. Prevalence and risk factors Infected surgical wounds. Approximately 25% of vascular catheterassociated bacteremias caused by S. aureus may result in endocarditis. A significant risk factor for endocarditis is IVDA. Patients who use injection drugs tend to be younger and may be coinfected with human immunodeficiency virus (HIV). Pathogenesis and pathology The surface of damaged valves by congenital or rheumatic disease or by previous infective endocarditis is occupied by small aggregates of platelets→ endothelial damage→ fibrin organization leading to formation of vegetations = friable masses that may embolize + attachement of microorganisms that multiply rapidly→ may progress to frank abcesses that extend into the valve structure or into the myocardium. Signs and symptoms Patients with subacute IE often present with nonspecific flu-like symptoms, while patients with acute IE often present with signs of acute sepsis. Cardinal manifestations: Fever and chills (seen in ∼ 90% of patients) night sweats, weight loss Dyspnea, cough, pleuritic chest pain Arthralgias, myalgias Signs and symptoms Cardiac manifestations A new heart murmur or change in a preexisting murmur (seen in ∼ 75% of patients) Almost always, a regurgitant heart murmur is heard, usually in the mitral or aortic valve position Regurgitant murmur in the tricuspid area, in persons who inject drugs, Heart failure (e.g., dyspnea, lower limb edema) due to valve insufficiency Arrhythmias: (e.g., heart block). Signs and symptoms Surprisingly, most patients, especially younger ones, do not seek medical advice until fatigue or fever becomes unbearable or they suffer a major complication, such as an embolic event or heart failure. Patients who have had heart surgery in the recent past usually seek medical advice earlier because of their heightened awareness of postoperative complications. Signs and symptoms Extracardiac manifestations are typically caused by septic microemboli and/or immune complex precipitation. Peripheral embolic and immunologic phenomena: seen in only 5–10% of patients. Emboli to intraabdominal organs Acute renal injury Including hematuria and anuria Due to renal artery occlusion or glomerulonephritis Splenomegaly and possible LUQ pain Due to splenic artery occlusion or splenic abscess Neurological manifestations (e.g., seizures, paresis): due to septic embolic stroke, hemorrhage, meningitis, encephalitis, and/or abscess. Pulmonary manifestations: caused by septic emboli resulting from tricuspid valve involvement Others: Arthritis Skin or mucosal lesions These include subconjunctival and soft palate petechiae, hemorrhages within the nail beds (splinter hemorrhages), painful subcutaneous nodules on the palms or soles (Osler's nodes), and generalized rashes. Patients may also present with painful embolic lesions on the fingers or toes, which may be visible. Criteria that should raise suspicion of IE High clinical suspicion (urgent indication for echocardiographic screening and possibly hospital admission) -new valve lesion/(regurgitant murmur) - embolic event(s) of unknown origin (esp. cerebral and renal infarction) - sepsis of unknown origin - haematuria, glomerulonephritis, and suspected renal infarction - fever together with other risk factors for IE Low clinical suspicion - fever with none of the above DIAGNOSIS IE The diagnosis of IE is based on a clinical suspicion supported by consistent microbiological data and the documentation of IE-related cardiac lesions by imaging techniques. Evidence of involvement of cardiac valves (native or prosthetic) or prosthetic intracardiac material is a major diagnostic criterion of IE. Echocardiography is the first-line diagnostic imaging technique. Other imaging modalities such as CT, nuclear imaging, and magnetic resonance imaging (MRI) are currently part of the diagnostic strategy of suspected IE. MICROBIOLOGICAL DATA Positive blood cultures remain the cornerstone of IE diagnosis and provide live bacteria for both identification and susceptibility testing. At least three sets of blood cultures should be obtained at 30-minute In the absence of previous antimicrobial therapy, this is virtually always sufficient to identify the usual causative microorganisms. The need for culture before antibiotic administration is self-evident. MAJOR CRITERIA IE MINOR CRITERIA DIAGNOSIS-DUKE CRITERIA Diagnosis Further refinements in the diagnosis have occurred with the use of echocardiography. Transesophageal echocardiography is preferred over the transthoracic approach because it usually provides superior imaging for detecting vegetations and abscesses. TEE TREATMENT Successful treatment of IE relies on microbial eradication by antimicrobial drugs. Surgery contributes by removing infected material Bactericidal regimens are more effective than bacteriostatic therapy Drug treatment of PVE should last longer (≥6 weeks) than that of NVE (2–6 weeks) but is otherwise similar TREATMENT TREATMENT EMPIRICAL TREATMENT Antibiotics-Empiric antibiotic therapy The goal is to provide broad-spectrum coverage for potential bacterial causes of IE (including multidrug-resistant organisms) until blood culture results are available. Treatment of IE should be started promptly. Three sets of blood cultures should be drawn at 30-minute intervals before initiation of antibiotics. The initial choice of empirical treatment depends on several considerations: Previous antibiotic therapy. IE in a native valve or a prosthesis (and if so, when surgery was performed [early vs. late PVE]). Native valve endocarditis and late PVE regimens should cover staphylococci, streptococci, and enterococci. Early PVE or healthcareassociated IE regimens should cover methicillin-resistant staphylococci, enterococci and, ideally, non-HACEK Gram-negative pathogens. The place of the infection (community, nosocomial, or non-nosocomial healthcare-associated IE) and knowledge of the local epidemiology. EMPIRICAL TREATMENT Once the pathogen is identified (usually within 24 h), the antibiotic treatment must be adapted to its antimicrobial susceptibility pattern STREPTOCOCCI-cure rate 95% STAPHYLOCOCCUS Staphylococcus aureus is usually responsible for acute and destructive IE, whereas CoNS can induce more protracted valve infections. STAPHYLOCOCCUS Enterococcal IE is primarily caused by E. faecalis (90% of cases) and less often by Enterococcus faecium (5% of cases), or other species. enterococci are highly resistant to antibiotic-induced killing, and eradication requires prolonged administration (up to 6 weeks) The treatment in PVE due to non-HLAR Enterococcus spp is the same as for NVE Enterococcal IE GRAM NEGATIVE Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella, and Kingella (HACEK) Gram-negative bacilli are fastidious organisms that require special investigations when they are the suspected cause of IE . Some HACEK group bacilli produce beta-lactamases, and therefore ampicillin is no longer the first-line option. They are susceptible to ceftriaxone, other thirdgeneration cephalosporins, and fluoroquinolones. The standard treatment is ceftriaxone 2 g/day for 4 weeks in NVE and for 6 weeks in PVE. BLOOD CULTURE NEGATIVE IE FUNGI are most frequently observed in PVE and in IE affecting PWID or immunocompromised patients. Candida and Aspergillus spp. predominate Mortality is very high (>50%), and treatment necessitates combined antifungal administration and with a low threshold for surgery. INDICATIONS FOR SURGERY INDICATIONS FOR SURGERY INDICATIONS FOR SURGERY Outcomes Persistent Fever Persistent fever during the treatment of endocarditis is worrisome. Annular or ring abscesses may cause this and are strong indications for surgery. Other causes of fever include myocarditis, pulmonary and systemic emboli, and intravascular catheter site infections. Drug fevers without other manifestations, such as rash and renal findings, are unusual, but must also be considered. Neurologic Complications Neurologic complications from endocarditis are common and can management dilemmas. Leading causes are stroke, encephalopathy, and retinal emboli. Brain abscesses and mycotic aneurysms are relatively infrequent. As a general rule, anticoagulation should be avoided because of the increased risk of intracranial bleeding ! One may elect to continue anticoagulation in patients with mechanical heart valves, but dosing should be in the low therapeutic range to minimize the risk of bleeding. Survival In the preantibiotic era, survival after infective endocarditis was unlikely. However, despite striking advances in management, mortality remains around 20%. The most frequent cause of death is congestive heart failure, less frequently followed by major embolic events and ruptured mycotic aneurysms. Prophylaxis Guidelines Although the risk of side effects clearly outweighs the benefit in patients at low risk for endocarditis, prophylaxis remains an accepted practice in higher risk patients. Guidelines, now recommend that prophylaxis should only be given to patients who have the highest risk of complications of endocarditis Patients at Highest Risk for Adverse Outcomes from Endocarditis 1. Prosthetic cardiac valve disease , intracardiac devices 2. Previous infective endocarditis 3. Congenital heart disease (CHD) - unrepaired cyanotic CHD; - completely repaired CHD with prosthetic materials - incompletely repaired CHD with residual defects at prosthetic patches or devices 4. Cardiac transplantation with valvular defects Furthermore, the list of procedures for endocarditis prophylaxis has been considerably shortened- for example, only for dental work involving gingival tissue and the periapical regions of the teeth, or for perforations of the oral mucosa . Other invasive procedures that might warrant prophylaxis include diagnostic studies or drainage of infected spaces where streptococci, enterococci. or S. aureus are proven or likely pathogens. Factors associated with an increased rate of relapse Summary Staphylococcus aureus is probably more common now than Streptococcus viridans as the cause of native valve endocarditis. Transesophageal echocardiography is superior to transthoracic imaging for detecting vegetations and abscesses. Antibiotic prophylaxis for invasive dental procedures remains recommended, but only for patients at high risk of complications from endocarditis.
