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CARDIAC INFECTIONS. Assoc Prof Dr . Meral SÖNMEZOĞLU Yeditepe University Hospital. Learning Objectives. Recognize the risk factors, signs, and symptoms of cardiac infections Understand the many approaches to diagnosing endocarditis , myocarditis and pericarditis .
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CARDIAC INFECTIONS Assoc Prof Dr.Meral SÖNMEZOĞLU Yeditepe UniversityHospital
LearningObjectives • Recognize the risk factors, signs, and symptoms of cardiacinfections • Understand the many approaches to diagnosing endocarditis, myocarditisandpericarditis. • Appreciate the necessity of rapid treatment. • Anticipate possible complications.
CardiacInfections • Endocarditis • Myocarditis • Pericarditis
Definition • Infectious Endocarditis (IE): an infection of the heart’s endocardial surface • Classified into four groups: • Native Valve IE • Prosthetic Valve IE • Intravenous drug abuse (IVDA) IE • Nosocomial IE
Sites of lesions • Mitral Valve: 85% (Left atrium/ventricle) • Common site for Strep viridans group • Aortic valve: 55% (Left ventricle) • Emboli would effect systemic organs brain, kidneys, spleen • Tricuspid valve: 20% (Right atrium/ventricle) • Common site for IV drug users (Staph. spp) • Emboli to lung • Pulmonary valve: 1% (Right ventricle)
Acute Affects normal heart valves Rapidly destructive Metastatic foci Commonly Staph. If not treated, usually fatal within 6 weeks Subacute Often affects damaged heart valves Indolent nature If not treated, usually fatal by one year Further Classification
Acute Rapid progression of symptoms Less than 6 weeks duration Significant systemic signs/symptoms Fever Elevated systemic WBC/ left shift Subacute Slower, more chronic progression of symptoms Low grade fevers Vague clinical signs/symptoms weakness, anorexia, malaise,etc. Further Classification
Acute NVE • Frequently involves normal valves and usually has an aggressive course. • Rapidly progressive illness in persons who are healthy or debilitated • Virulentorganisms, S aureus and group B streptococciare typically the causative agents
Subacute NVE • Typically affects only abnormal valves. • Its course, even in untreated patients, is usually more indolent than that of the acute form and may extend over many months. • Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease
Early PVE • Early PVE occurs within 60 days of valve implantation. • Traditionally, • coagulase-negative staphylococci, • gram-negative bacilli, and • Candida species have been the common infecting organisms.
Late PVE • Late PVE occurs 60 days or more after valve implantation. • Staphylococci, • alpha-hemolytic streptococci, and • enterococci are the common causative organisms. • Recent data suggest that S aureusmay now be the most common infecting organism in both early and late PVE
Pathophysiology • Turbulent blood flow disrupts the endocardium making it “sticky” • Bacteremia delivers the organisms to the endocardial surface • Adherence of the organisms to the endocardial surface • Eventual invasion of the valvular leaflets
Pathogenesis • Multiple independent pathophysiological processes • “Trauma” of the heart surfaces • Platelet/fibrin deposition over traumatized tissue (non-bacterial thrombotic endocarditis) • “Bacteremia” subsequent infection of the platelet/fibrin deposition (Bacterial endocarditis) • Bacterial multiplication (10 9,10cfu/gram of tissue)
Epidemiology • Incidence difficult to ascertain and varies according to location • Much more common in males than in females • May occur in persons of any age and increasingly common in elderly • Mortality ranges from 20-30%
Risk Factors • Intravenous drug abuse • Artificial heart valves and pacemakers • Acquired heart defects • Calcific aortic stenosis • Mitral valve prolapse with regurgitation • Congenital heart defects • Intravascular catheters • Permanent central venous access lines • Prior valve surgery • Recent dental surgery • Weakened valves
Predisposingfactors • rheumaticheartdisease (25-30%) • congenitalheartdisease (10-20%) • mitral valvedisease (10-30%) • IV drugabuse (15-35%) • no predisposition (25-45%)
Infecting Organisms • Common bacteria • S. aureus • Streptococci • Enterococci • Not so common bacteria • Fungi • Pseudomonas • HACEK
Infecting Organisms • Overall, S aureusinfection is the most common cause of IE, including PVE, acute IE, and IVDA IE. • Approximately 35-60.5% of staphylococcal bacteremias are complicated by IE. • More than half the cases are not associated with underlying valvular disease.
Infecting Organisms • HACEK - slow growing, fastidious organisms that may need 3 weeks to grow out of culture • Haemophilus sp. • Actinobacillus • Cardiobacterium • Eikenella • Kingella
Nativevalveendocarditis • Viridansstreptococci (30-60%) • Staphylococcusaureus (30-40%) usuallycausesacuteendocarditis • Gram negativebacteria (e..g.Haemophilus) (5-10%) • Coagulasenegativestaphylococci (e.g. S.epidermidis) (5%) • Streptococcuspneumoniae (1-3%)Fungi (1-2%)
Prostheticvalveendocarditis • Coagulasenegativestaphylococi (10-33%) • Streptococci (1-31%,theproportion of cases of endocarditisduetostreptococciincreases progressively in the first 12months post valvereplacement) • S. aureus (20%) • Gram negativebacteria (10%) • Fungi (1%)
Symptoms • Chills • Fatigue • Fever • Heart murmur • Joint pain • Muscle aches and pains • Night sweats • Nail abnormalities (splinter hemorrhages under the nails) • Paleness • Red, painless skin spots on the palms and soles (Janeway lesions)
Symptoms • Red, painful nodes in the pads of the fingers and toes (Osler's nodes) • Shortness of breath with activity • Swelling of feet, legs, abdomen • Weakness • Weight loss Note:Endocarditis symptoms can develop slowly (subacute) or suddenly (acute).
Acute High grade fever and chills SOB Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain Nausea/Vomiting Symptoms The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia
Signs • Fever • Heart murmur • Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes • More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots
Duke’sCriteria • MAJOR • Positive blood culture for appropriate organism • Evidence of endocardialinvolvement • MINOR • Predisposition • Fever • Vascularphenomena • Immunologicalphenomena • Microbiological evidence not meeting major criteria • Echo finding not meeting major criteria • Raisedinflammatorymarkers • DIAGNOSIS • Twomajor • Onemajor + Threeminor • Fiveminor
Janeway Lesions • More specific • Erythematous, blanching macules • Nonpainful • Located on palms and soles
Splinter Hemorrhages • Nonspecific • Nonblanching • Linear reddish-brown lesions found under the nail bed • Usually do NOT extend the entire length of the nail
Osler’s Nodes American College of Rheumatology webrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../ Hand10/Hand10dx.html • More specific • Painful and erythematous nodules • Located on pulp of fingers and toes • More common in subacute IE
Petechiae • Nonspecific • Often located on extremities • or mucous membranes dermatology.about.com/.../ blpetechiaephoto.htm Harden Library for the Health Sciences www.lib.uiowa.edu/ hardin/ md/cdc/3184.html Photo credit, Josh Fierer, M.D. medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html
Roth spot Roth’sspots Retinalhaemorrhages Alsoseen in leukaemia, Diabetes, perniciousanaemia
Exams and Tests • CBC -anemia • Chest x-ray • Echocardiogram • ECG • Erythrocyte sedimentation rate (ESR) • Repeated blood cultureand sensitivity
Investigations • Bloodtests • FBC • U&E • CRP to monitor disease activity • LFT • Blood cultures are essential, with a minimum of three samplestaken from different sites at least an hour apart (preferably more)sent for analysis, before initiation of antibiotics. • Serological tests for exotic organisms are usually done forculturenegative IE if splenicabsceses are suspected
Investigations • Chestradiograph - thismaydetectsepticlunginfarcts(commoner in IE secondary to drug abuse), signs ofcardiac failure, and evidence of pulmonary infection • Urinedipstick/ MSU todetecthaematuria • Electrocardiogramtoprovide a "baseline“ prolongationof the PR interval may mean the development of anaorticrootabscess) • Abdominal ultrasound or CT Abdomen may beindicated
Possible Complications • Arrhythmias, such as atrial fibrillation • Blood clots or an infected clot from the endocarditis that travels to the brain, kidneys, lungs, or abdomen, causing severe damage to, and infection of, these organs • Brain abscess • Brain or nervous system changes • Congestive heart failure • Glomerulonephritis • Jaundice • Severe heart valve damage • Stroke
Prevention • People with certain heart conditions often take preventive antibiotics before dental procedures or surgeries involving the respiratory, urinary, or intestinal tract. • Those with a history of endocarditis should have continued medical follow-up.
Treatment • Ifpatientstabledeferuntiladequatebloodcultures done • liaisewithmicrobiology re appropriateantibiotics • Internationalguidelinesexist • Reviewwithcultureresults • Usually six weeks treatment, at least four on iv
Treatment • Long-term antibiotic therapy is needed to get the bacteria out of the heart chambers and valves. • usually have therapy for 6 weeks • must be specific for the organism • blood culture and the sensitivity tests
Treatment • Parenteral antibiotics • High serum concentrations to penetrate vegetations • Prolonged treatment to kill dormant bacteria clustered in vegetations • Surgery • Intracardiac complications • Surveillance blood cultures
Complications requiring surgery • Infected prosthetic material: less than 1 year out from original heart surgery • Refractory congestive heart failure (Leading cause of death) • Unresponsive infection/ continued infection despite appropriate antibiotics • Pt. experiences more than 1 major emboli
Myocarditis • an inflammation of the heart muscle • an uncommon disorder that is usually caused by viral infections such as coxsackie virus, adenovirus, and echovirus
Myocarditis • may also occur during or after various viral, bacterial, or parasitic infections (such as polio, influenza, or rubella). • exposure to chemicals or allergic reactions to certain medications • associated with autoimmune diseases. • muscle becomes inflamed and weakened