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CARDIAC INFECTIONS Assoc Prof Dr. Meral SÖNMEZOĞLU Yeditepe University Hospital.

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Presentation on theme: "CARDIAC INFECTIONS Assoc Prof Dr. Meral SÖNMEZOĞLU Yeditepe University Hospital."— Presentation transcript:

1 CARDIAC INFECTIONS Assoc Prof Dr. Meral SÖNMEZOĞLU Yeditepe University Hospital

2 Learning Objectives Recognize the risk factors, signs, and symptoms of cardiac infections Understand the many approaches to diagnosing endocarditis, myocarditis and pericarditis. Appreciate the necessity of rapid treatment. Anticipate possible complications.

3 Cardiac Infections Endocarditis Myocarditis Pericarditis

4 INFECTIVE ENDOCARDITIS

5 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

6 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)

7 Further Classification 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

8 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.

9 Acute NVE Frequently involves normal valves and usually has an aggressive course. Rapidly progressive illness in persons who are healthy or debilitated Virulent organisms, S aureus and group B streptococci are typically the causative agents

10 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

11 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.

12 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 aureus may now be the most common infecting organism in both early and late PVE

13 Pathophysiology 1.Turbulent blood flow disrupts the endocardium making it “sticky” 2.Bacteremia delivers the organisms to the endocardial surface 3.Adherence of the organisms to the endocardial surface 4.Eventual invasion of the valvular leaflets

14 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 9,10 cfu/gram of tissue)

15 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%

16 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

17 Predisposing factors rheumatic heart disease (25-30%) congenital heart disease (10-20%) mitral valve disease (10-30%) IV drug abuse (15-35%) no predisposition (25-45%)

18 Common bacteria S. aureus Streptococci Enterococci Not so common bacteria Fungi Pseudomonas HACEK Infecting Organisms

19 Overall, S aureus infection 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.

20 Infecting Organisms HACEK - slow growing, fastidious organisms that may need 3 weeks to grow out of culture Haemophilus sp. Actinobacillus Cardiobacterium Eikenella Kingella

21 Native valve endocarditis Viridans streptococci (30-60%) Staphylococcus aureus (30-40%) usually causes acute endocarditis Gram negative bacteria (e..g.Haemophilus) (5-10%) Coagulase negative staphylococci (e.g. S.epidermidis) (5%) Streptococcus pneumoniae (1-3%) Fungi (1-2%)

22 Prosthetic valve endocarditis Coagulase negative staphylococi (10-33%) Streptococci (1-31%,the proportion of cases of endocarditis due to streptococci increases progressively in the first 12 months post valve replacement) S. aureus (20%) Gram negative bacteria (10%) Fungi (1%)

23 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)

24 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).

25 Symptoms 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 The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia

26 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

27 Duke’s Criteria MAJOR Positive blood culture for appropriate organism Evidence of endocardial involvement MINOR Predisposition Fever Vascular phenomena Immunological phenomena Microbiological evidence not meeting major criteria Echo finding not meeting major criteria Raised inflammatory markers DIAGNOSIS Two major One major + Three minor Five minor

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29 Janeway Lesions 1.More specific 2.Erythematous, blanching macules 3.Nonpainful 4.Located on palms and soles

30 Janeway lesion

31 IE:Janeway Lesions

32 Splinter Hemorrhages 1.Nonspecific 2.Nonblanching 3.Linear reddish-brown lesions found under the nail bed 4.Usually do NOT extend the entire length of the nail

33 IE: Splinter hemorrhages

34 Osler’s Nodes 1.More specific 2.Painful and erythematous nodules 3.Located on pulp of fingers and toes 4.More common in subacute IE American College of Rheumatology webrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../ Hand10/Hand10dx.html

35 IE: Osler Nodes

36 Petechiae Photo credit, Josh Fierer, M.D. medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html Harden Library for the Health Sciences www.lib.uiowa.edu/ hardin/ md/cdc/3184.html 1.Nonspecific 2.Often located on extremities or mucous membranes dermatology.about.com/.../ blpetechiaephoto.htm

37 Roth spot Roth’s spots Retinal haemorrhages Also seen in leukaemia, Diabetes, pernicious anaemia

38 Exams and Tests CBC -anemia Chest x-ray Echocardiogram ECG Erythrocyte sedimentation rate (ESR) Repeated blood culture and sensitivity

39 Investigations Blood tests FBC U&E CRP to monitor disease activity LFT Blood cultures are essential, with a minimum of three samples taken 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 for culture negative IE if splenic absceses are suspected

40 Investigations Chest radiograph - this may detect septic lung infarcts (commoner in IE secondary to drug abuse), signs of cardiac failure, and evidence of pulmonary infection Urine dipstick/ MSU to detect haematuria Electrocardiogram to provide a "baseline“ prolongation of the PR interval may mean the development of an aortic root abscess) Abdominal ultrasound or CT Abdomen may be indicated

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42 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

43 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.

44 Treatment If patient stable defer until adequate blood cultures done liaise with microbiology re appropriate antibiotics International guidelines exist Review with culture results Usually six weeks treatment, at least four on iv

45 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

46 Treatment Parenteral antibiotics –High serum concentrations to penetrate vegetations –Prolonged treatment to kill dormant bacteria clustered in vegetations Surgery –Intracardiac complications Surveillance blood cultures

47 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

48 MYOCARDITIS

49 Myocarditis an inflammation of the heart muscle an uncommon disorder that is usually caused by viral infections such as coxsackie virus, adenovirus, and echovirus

50 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

51 Symptoms History of preceding viral illness Fever Chest pain that may resemble a heart attack Joint pain or swelling Abnormal heart beats Fatigue Shortness of breath Leg swelling Inability to lie flat *total absence of symptoms is common

52 Additional symptoms Fainting, often related to arrhythmias Low urine output Other symptoms consistent with a viral infection -- headache, muscle aches, diarrhea, sore throat, rashes

53 Exams and Tests Electrocardiogram (ECG) Chest x-ray Ultrasound of the heart (echocardiogram) -- may show weak heart muscle, an enlarged heart, or fluid surrounding the heart. White blood cell count Red blood cell count Blood cultures for infection Blood tests for antibodies against the heart muscle and the body itself Heart muscle biopsy - rarely performed

54 Treatment Antibiotics reduced level of activity low-salt diet. Steroids and other medications may be used to reduce inflammation. Diuretics

55 Treatment If the heart muscle is very weak, standard medicines to treat heart failure are also used. Abnormal heart rhythm may require the use of additional medications, a pacemaker or even a defibrillator. If a blood clot is present in the heart chamber, blood thinning medicine is given as well.

56 Possible Complications Heart failure Pericarditis Cardiomyopathy

57 Prevention Prompt treatment of causative disorders may reduce the risk of myocarditis.

58 PERICARDITIS

59 Acute Pericarditis Inflamation of the pericardium Idiopatic Viral TB Post-MI Autoimmune disease Uraemia Treat cause//NSAIDs Myocarditis rarer but can co-exist

60 Acute Pericarditis

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64 Pericardium Visceral / serous –Direct contact with epicardium (ST elev) – single layer mesothelial cells Parietal / fibrous – mesothelial and fibrous layer

65 Pericardial Anatomy Visceral – transparent Parietal – translucent Transverse sinus – curved probe

66 Acute Pericarditis Pericarditis –Acute With or without tamponade –Pericardial window –Chronic Constrictive pericarditis –Total pericardioectomy »Cardiopulmonary bypass –Lymphadenitis Cervical (scrofula) Mediastinal –Drainage

67 Etiology – Acute Pericarditis Infectious – Viral : Coxsackie, Echo, EBV, Influenza, HIV – Bacterial: TB, staph, hemophillus, pneumococcal, salmonella – Fungal/other: histo/blasto/coccidio, rickettsia Rheumatologic –SLE, Sarcoid, RA, Dermatomyositis, Ankylosing Spondylitis, Scleroderma, PAN Neoplastic –Primary: angiosarcoma, mesothelioma –Metastatic: breast, lung, lymphoma, melanoma, leukemia Immunologic –Celiac sprue, Inflammatory Bowel Disease Drug –Hydralizine, Procainamide Other –MI, Dressler’s, Post Pericardiotomy, Chest Trauma, Aortic dissection – Uremic, Post Radiation – IDIOPATHIC

68 Acute Pericarditis – Clinical History – preceding viral illness, etc Symptoms –Chest pain Signs – Friction Rub ECG – early: PR / ST changes – late: isoelectric ST/ T inv

69 History Often preceding viral illness 1-2wk prior Chest Pain –Sudden, sharp,pleuritic, constant – worse supine/ L lat decub, relief sitting up – radiation: back, trapezius ridge – symptoms usually resolve by 2 weeks, ECG abnormalities may persist for months

70 Auscultory – Rub(s) Endopericardial (classic) – “triphasic”: atrial sys, ventricular sys, early diastole – may only hear 2 phase (afib or tachycardia) or 1 – loudest LSB, raised extremities/increased venous return Pleuropericardial – “exopericardial”, extension into adjacent structures – marked resp variation, musical quality Conus – dilation of pulm conus in hyperactive heart – PE, thyroid storm, acute beriberi Pneumohydropericardium –air/gas overlying pcard fluid – metallic tinkle (small amt) ; churning/splashing “mill-wheel sound” (lg)

71 ECG PR depression ST elevation – concave up, ST/T V6 >.25, no reciprocal DDx: – Acute MI – Early Repolarization – Myocarditis – Aneurysm – other: Brugada, BBB

72 ECG

73 Acute Pericarditis - Stages Stage I – first few days  2 weeks – ST elev, PR depression – up to 50% of pt with sxs/rub do NOT have/evolve stage I 1 Stage II – last days  weeks – ST returns to baseline, flat T Stage III – after 2-3 weeks, lasts several weeks – T wave inversion Stage IV – lasts up to several months – gradual resolution of T wave changes 1 Spodick DH, Pericardial Disease. Braunwauld 6 th

74 Cardiac Isoenzymes - ? helpful 2 year study, ER based 1 – 14 pt with 2/3 findings (CP typical for PCARD, rub, and ECG changes c/w PCARD) – 71% had elevated TropI (pk 21) with negative CAD workup Not reliable to differentiate MI vs PCARD 1 Brandt RR, et al. Am J Card 2001, June 1

75 Treatment NSAIDS/ASA – ASA 650 q3-4hr – Ibuprofen 300-600 q 6-8 hrs x 1-4days Avoid Indocin, reduces CBF Steroids – if no response after 48hr NSAID – use concurrent NSAID Colchicine –.6 q12 chronic +/- NSAID – useful in recurrent pericarditis – symptom free period 3.1 +/- 3mos vs 43 +/- 35mos (p<.00001) in largest multicenter trial to date 1 –Anecdotal evidence of benefit in Acute PCARD, effusion 1 Adler Y, et al. Circulation, 1998 June 2

76 Complications Pericardial Effusion/Tamponade Constrictive Pericarditis – can be “transient” – 10% may have transient sxs within 1 st month, resolves by 3 months Recurrent Pericarditis (20-25%) –Rx – NSAIDS/Colchicine +/- steroids

77 Gross Pathology “Bread & Butter” appearanceFibrinous stranding

78 Possible Complications Arrhythmias, such as atrial fibrillation Cardiac tamponade

79 Constrictive pericarditis, where inflammation of the pericardial sac results in fibrosis and thickening of the pericardium with adhesions (sticky scars) between the pericardium and the heart. The pericardium creates a rigid "case" around the heart, which can severely limit the ability of the heart to fill with blood. Patients with constrictive pericarditis may develop heart failure, which responds poorly to treatment.

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