Download cardiac infections 2012-13 - University of Yeditepe Faculty of

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.
• 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 (nonbacterial 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%)
Infecting Organisms
• Common bacteria
• S. aureus
• Streptococci
• Enterococci
• Not so common bacteria
• Fungi
• Pseudomonas
• HACEK
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.
Actinobacillus
Cardiobacterium
Eikenella
Kingella
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 specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
Janeway lesion
IE:Janeway Lesions
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
IE: Splinter hemorrhages
Osler’s Nodes
American College of Rheumatology
webrheum.bham.ac.uk/.../ default/pages/3b5.htm
www.meddean.luc.edu/.../
Hand10/Hand10dx.html
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
IE: Osler Nodes
Petechiae
1. Nonspecific
2. Often located on extremities
or mucous membranes
dermatology.about.com/.../
blpetechiaephoto.htm
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
Roth spot
Roth’s spots
Retinal haemorrhages
Also 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 Anatomy
Visceral – 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
• Infectious
Etiology – Acute Pericarditis
– 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.