CARDIAC INFECTIONS
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Transcript of CARDIAC INFECTIONS
CARDIAC INFECTIONS
Assoc Prof Dr. Meral SÖNMEZOĞLUYeditepe University Hospital
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.
Cardiac Infections
• Endocarditis• Myocarditis• Pericarditis
INFECTIVE ENDOCARDITIS
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)
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
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.
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
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 aureus may now
be the most common infecting organism in both early and late PVE
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
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)
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
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%)
• Common bacteria• S. aureus• Streptococci • Enterococci
• Not so common bacteria• Fungi• Pseudomonas• HACEK
Infecting Organisms
Infecting Organisms• 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.
Infecting Organisms
HACEK - slow growing, fastidious organisms that may need 3 weeks to grow out of culture
Haemophilus sp.ActinobacillusCardiobacteriumEikenellaKingella
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%)
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%)
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).
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
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’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
Janeway Lesions
1. More specific2. Erythematous, blanching macules 3. Nonpainful4. Located on palms and soles
Janeway lesion
IE:Janeway Lesions
Splinter Hemorrhages
1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail
IE: Splinter hemorrhages
Osler’s Nodes
1. More specific2. Painful and erythematous nodules3. Located on pulp of fingers and toes4. More common in subacute IE
American College of Rheumatologywebrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../
Hand10/Hand10dx.html
IE: Osler Nodes
Petechiae
Photo credit, Josh Fierer, M.D. medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html
Harden Library for the Health Scienceswww.lib.uiowa.edu/ hardin/md/cdc/3184.html
1.Nonspecific2.Often located on extremities
or mucous membranesdermatology.about.com/.../ blpetechiaephoto.htm
Roth spot
Roth’s spotsRetinal haemorrhagesAlso seen in leukaemia,Diabetes, pernicious anaemia
Exams and Tests
• CBC -anemia• Chest x-ray • Echocardiogram• ECG • Erythrocyte sedimentation rate (ESR) • Repeated blood culture and sensitivity
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
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
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
• 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
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
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
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
Additional symptoms • Fainting, often related to arrhythmias • Low urine output • Other symptoms consistent with a viral
infection -- headache, muscle aches, diarrhea, sore throat, rashes
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
Treatment
• Antibiotics• reduced level of activity• low-salt diet. • Steroids and other medications may be
used to reduce inflammation. • Diuretics
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.
Possible Complications
• Heart failure• Pericarditis • Cardiomyopathy
Prevention
• Prompt treatment of causative disorders may reduce the risk of myocarditis.
PERICARDITIS
Acute Pericarditis
Inflamation of the pericardium• Idiopatic• Viral• TB• Post-MI• Autoimmune disease• Uraemia• Treat cause//NSAIDs• Myocarditis rarer but can co-exist
Acute Pericarditis
Pericardium
• Visceral / serous – Direct contact with epicardium (ST elev)– single layer mesothelial cells
• Parietal / fibrous– mesothelial and fibrous layer
Pericardial AnatomyVisceral – transparent
Parietal – translucent
Transverse sinus – curved probe
Acute Pericarditis
• Pericarditis– Acute
• With or without tamponade– Pericardial window
– Chronic• Constrictive pericarditis
– Total pericardioectomy» Cardiopulmonary bypass
– Lymphadenitis• Cervical (scrofula)• Mediastinal
– Drainage
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
Acute Pericarditis – Clinical
• History– preceding viral illness, etc
• Symptoms– Chest pain
• Signs– Friction Rub
• ECG– early: PR / ST changes– late: isoelectric ST/ T inv
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
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)
ECG
• PR depression• ST elevation
– concave up, ST/T V6 >.25, no reciprocal• DDx:
– Acute MI– Early Repolarization– Myocarditis– Aneurysm– other: Brugada, BBB
ECG
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 I1
• 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 6th
Cardiac Isoenzymes - ? helpful
• 2 year study, ER based1
– 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
1Brandt RR, et al. Am J Card 2001, June 1
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 date1
– Anecdotal evidence of benefit in Acute PCARD, effusion
1Adler Y, et al. Circulation, 1998 June 2
Complications
• Pericardial Effusion/Tamponade• Constrictive Pericarditis
– can be “transient” – 10% may have transient sxs within 1st month, resolves by 3 months
• Recurrent Pericarditis (20-25%)– Rx – NSAIDS/Colchicine +/- steroids
Gross Pathology
“Bread & Butter” appearance Fibrinous stranding
Possible Complications • Arrhythmias, such as atrial fibrillation
• Cardiac tamponade
• 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.