IM

INFECTIVE ENDOCARDITIS
PERICARDIAL DISEASES
Dr. Allan B. Ruales
072009
Quiz:
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Total absence of pericardium produces obvious

clinical disease - FALSE
Acute pericarditis: radiate to left shoulder and
trapezius - TRUE
Pericardial effusion Ewarts sign positive: TRUE
IE reliant to antibiotics 4weeks TRUE
RHD in IE is autoimmune in nature
MC cause of IE staph aureus TRUE
Non-infectious pericarditis acute MI TRUE
Oslers node nontender - FALSE
Dresslers syndrome in post MI -

Infective Endocarditis
Microbial infection on the endothelial surface of
the heart
Vegetation characteristic lesion
o Mass of platelets and fibrin enmeshed
with abundant microorganisms and
scant inflammatory cells
Treatment: reliance to antibiotic treatment,
prolonged period of time
Classification
Acute
Marked toxicity that progresses days to several
weeks
Usually caused by Staph aureus
Subacute
Toxicity quite modest
More likely caused by viridians
Infection commonly involves the heart valves (direct or
development of NBTE) and divided into:
Native valve endocarditis with the ff
predisposing conditions: RHD, CHD, MVP,
degenerative heart disease, ASH, IV drug use
Prosthetric valve endocarditis
Clinical Features
Symptoms of infection
1. Local destructive effects of intracardiac
infection
2. Embolization of bland or septic fragments
of vegetations to distant sites resulting in
infarction or infection
3. Hematogenous seeding of remote sites
during continuous bacteremia
4. Abnormal response to immune complexes
-

Highly variable and non-specific

Fever MC symptom and sign
o Subacute IE: low grade
Heart murmurs acute IE
Splenomegaly
Petechiae MC but not specific for IE
Splinter or subungual hemorrhages dark red

INFECTIVE ENDOCARDITIS

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Oslers nodes small, tender subcutaneous

nodules in the pulp of the digits
Janeway non-tender lesions

Diagnosis
High index of suspicion
s/s often constitutional
Fever plus one or more of ff:
predisposing cardiac lesion
bacteremia
embolic phenomena
evidence of active endocardial process
o destruction of valves, abscess
IE must be considered in the ff:
significant VHD and persistent unexplained
fever
IV drug abuser with fever (cough and pleuritic
chest pain)
Young with unexpected stroke or SAH
Devt of a new regurgitant murmur
In patients with prosthetic valve, presence of
fever or dysfunction
Diagnosis with certainty
Vegetations obtained at cardiac surgery,
autopsy or artery (embolus) examined
histologically and microbiologically
Highly sensitive and specific diagnostic schema
Duke criteria
Diagnostic criteria
Definitive IE
o Pathological criteria

Microorganism: demo by
culture or histology in a
vegetation or in a vegetation
that has embolized

Pathologic lesion: abscess or

vegetation lesions
Clinical dx: 2 major or one major 3 minor, 5
minor
Possible IE
Rejected IE
o No pathological evidence at surgery or
autopsy
o Sustained resolution of manifestations
Criteria for diagnosis
Major
1. Positive blood culture
4 separate blood cultures extracted at different
sites
*Staph aureus: MC cause of Acute IE
2. Evidence of endocardial involvement
Positive echocardiogram oscillating
intracardiac mass or abscess or new partial
dehiscence of prosthetic valve
New valvular regurgitation
Minor
1.

Predisposition: predisposing heart condition or

IV drug use

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2.
3.
4.
5.
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Fever >/= 38o

Vascular phenomena
Immunological phenomena
Microbiological evidence
Echocardiogram

Echocardiography
Visualize vegetations and intracardiac
complications
Absence of visualized vegetations does not
exclude the possibility of IE
Intracardiac complications
Valve disruption
Perivalvular abscess
Septal abscess
Prosthetic valve dehiscence
Treatment
Major obj: infecting microorganism must be
eradicated
Antimicriobial therapy guidelines
o Bacteriostatic agents
o In endocarditis: bacteria located within
vegetations which phagocytic cells
cannot penetrate so that bactericidal
agents are needed to cure
Treatment should begin promptly but usually
not immediate in patients with subacute IE
(can allow 1-2 day delay)
Prolonged therapy: 4weeks or more due to total
reliance on antimicrobial agents to eradicate
infection and the organisms within vegetations
are less susceptible to the bactericidal action of
antibiotics because they have very high
population densities which results in a state of
reduced metabolic activity
Cardiac surgery
Absolute indications
o Moderate to severe CHF due to valve
dysfunction
o Unstable prosthesis
o Uncontrolled infection
o Relapse after optimal therapy
Relative indication
o Relapse after optimal therapy (native)
o Staph aureus endocarditis
o Very large vegetations
*page 796
Prevention as recommended by the AHA with cardiac
predisposing factors
Dental procedures
Tonsillectomy or adenoidectomy
Surgery involving GI or UR mucosa
Gallbladder surgery
Vaginal hysterectomy
UT surgery including prostate
Relative high risk (p.797)
Prosthetic heart valves
Previous IE

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PDA
VSD
Coarctation of aorta
Surgically repaired intracardial lesion

Antibiotic regimen for IE prophylaxis in Adults at

moderate or high risk
Oral cavity, respiratory tract or esophageal
procedures
o Standard regimen amoxicillin 2gm npo
1hr before procedure
o Inability to take oral meds ampicillin
2gm IV or IM within 30mins of
procedure
For high risk patients administer a half-dose 6hours
after the initial dose
GU and GI ampicillin
PERICARDIAL DISEASES
Pericardium
Congenital absence does not produce an
obvious clinical disease
Normal fluid in the pericardial cavity: 15-20cc
which is an ultrafiltrate of plasma
Function: prevents sudden dilatation of cardiac
chambers
Facilitates atrial filling during ventricular
systole
Pericarditis
MC pathologic process: Acute pericarditis
Clinical
-

classification (p. 1489)

Acute
Subacute
Chronic

Etiologic classification
Infectious viral
Noninfectious pericarditis acute MI, uremia,
neoplasia
Pericaditis presumably related to
hypersensitivity or autoimmunity
o Rheumatic fever
o Drug-induced (hydralazine,
phenytoin..)
o Postcardiac injury

Post myocardial infection

(Dresslers syndrome)

Post pericardiotomy
Acute Pericarditis
Cardinal manifestations
o Pain: severe retrosternal and left
precordial, referred to the back and left
trapezius ridge

Relieved by sitting up and

leaning forward

Intensified by lying supine,

coughing
o Friction rub: 3 components per cycle

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Heard on expiration, high

pitched, scratching and grating
ECG: changes secondary to acute
subepicardial inflammation

Widespread elevation of ST
segment
Effusion: impt when develops within a
relatively short time since it may lead
to cardiac tamponade

Enlarged cardiac silhouette

with faint heart sounds

Positive Ewarts sign

CXR water bottle

configuration
Echocardiography: effective diagnostic
technique

Check if anterior or posterior

Pericardiocentesis: exudates bloody fluid

Cardiac tamponade
Accumulation of fluid in pericardium sufficient
to cause obstruction to the inflow of blood to
the ventricles
3 MC causes: neoplastic, idiopathic pericarditis,
uremia
Principal features:
o Elevated intracardiac pressures
o Limitation of ventricular filling
o Reduction of cardiac output
Amount of fluid: 200cc when fluid develops
rapidly or >2000cc in slowly developing
effusions
Vol of fluid varies directly with the thickness of
ventricular myocardium and inversely with the
thickness of the parietal pericardium
Classic
-

findings
Dec arterial pres
Elevated venous pres
Faint heart sounds

Clinical manifestations
Tamponade developing slowly will present with
the ff: dyspnea, orthopnea
Tamponade is considered in any patient with the ff:
Hypotension, inc jugular venous pressure with
prominent x descent
Paradoxical pulse - HALLMARK
Clear lung fields, enlargement of cardiac
silhouette
Decreased amplitude of QRS, electrical
alternans on ECG
Echocardiography: establish diagnosis
o Collapse RA
Management: pericardiocentesis
o Can be therapeutic/diagnostic
Acute Idiopathic Pericarditis
More frequent in young adults but can occur in
all ages
Associated with effusion and pneumonitis

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Few days to 4weeks

(+) friction rub
Self-limited
Recurrences can occur 25%
Treatment:
o Bed rest and ASA, if needed
indomethacin

Post-Cardiac Injury Syndrome

Acute form of pericarditis after previous injury
to the myocardium with blood in pericardial
cavity
Manifestations:
o Pain
o 1-4weeks after the injury with fever
(40o),
o pericarditis,
o pleuritis,
o pneumonitis
1-2 weeks course
Fibrinous pericardial effusion
Treatment: ASA analgesic
Other Diseases that can present as Acute Pericarditis
Acute fibrious pericarditis associated with AMI
Due to collagen vascular disease
Drugs
Acute rheumatic fever
Chronic Pericardial Effusion
Detected on Xray (enlarged cardiac silhouette)
Pericardiocentesis: diagnostic
Grossly sanguinous fluid neoplasm, TB
Chronic Constrictive Pericarditis
MC cause: TB
Results when healing of acute fibrinous or
serofibrinous pericarditis or a chronic
pericardial effusion followed by obliteration of
pericardial activity
Impediment of ventricular filling in mid to late
diastole (tamponade is throughout diastole)
Y descent is most prominent (X descent in
tamponade)
Presence of square root sign during diastole
(also seen in restrictive cardiomyopathy)
Clinical and lab findings
o Weakness
o Kussmauls sign (inspiratory increase in
systemic venous pressure)
o Pulse pressure is normal or reduced
o Paradoxical pulse in 1/3 of cases
Congestive hepatomegaly with ascites:
abnormal liver enzymes
Apex beat reduced which retracts in systole
(pericardial knock)
CXR: (+) calcification
Doppler echo: transvalvular and pulmonary
venous flow which decrease during inspiration
and increase during expiration
MRI and CT: more accurate than echo

IM

Ddx:
-

Cor pulmonale
o RV enlargement
o Both associated with severe systemic
venous hypertension with little
pulmonary congestion and heart is
usually not enlarged with inspiratory
fall in arterial pressure
o Presence of advanced parenchymal
pulmonary disease is obvious
o Kussmauls sign is negative
TS: with murmur and coexistence with MS,
absence of paradoxical pulse, and no Y descent
Restrictive cardiomyopathy endomyocardial
biopsy

Treatment
Pericardial resection is the only definitive
treatment and should be carried out early in
the course

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