1DDX: LECTURE 21 – NOVEMBER 29th, 2006

ENDOCARDITIS

Diseases of the Cardio-vascular system: 6th note package

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• Infective endocarditis is the result of bacterial infection.
• There are similar signs and symptoms for acute and subacute endocarditis.
• Most common cause of acute endocarditis is staph aureus infection.
• “Native valve endocarditis”: valves have never been damaged before.

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ACUTE ENDOCARDITIS:
• Staphylococcus aureus is the most common cause. Can be pneumococcus, gonococcus.
• Rapidly destructive
• Metastasizes
• If untreated, fatal in less than 6 weeks (undiagnosed).

SUBACUTE ENDOCARDITIS
• S. viridens
• Similar signs and symptoms
• Occurs on damaged valves
• Does not produce metastatic foci
• If untreated, undiagnosed, it is fatal but more than 6 weeks.

A. Native Valve Endocarditis:

• Most common >50 years of age
• Strep  normal inhabitant of oral cavity  bacteria in blood  damage to heart
• S. viridens: correlated with dental procedures
• Fungi: poor prognosis: poor availability of anti-fungal agents.
• Fragile vegetations lead to large emboli in lower extremities
• Strep: 55% of cases
• Enterococcus: ~6% nomarl inhabitants of GIT, anterior urethra and sometimes mouth. Most
common in men (age 60), women (<40).
• History of genito-urinary tract infection (?), manipulation, trauma, disease, cystoscopy.
• Staph: known to produce abcess at multiple sites, KI, LU, brain.

b) Cardiac predisposing factors

Patent ductus arteriosus: can be associated with maternal rubella in early pregnancy

B. Endocarditis in intravenous drug abusers:

Frequently young people
Occurs on anatomically normal valves
Infection through skin: most common source of micro-organism
Staph aureus is micro-organism in 50% of cases. Could also be enterococcus, fungus.
Acute onset
Tricuspid valve is most commonly affected (more that 50% of cases)
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Right side of the heart is most commonly affected because the infection enters the venous system
(intra-venous drugs) and goes to the right side of the heart first: tricuspid valve.
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C. Prosthetic valve endocarditis:
• Pacemakers may be foci of infection
• Aortic valve m/c than mitral valve.
• Can begin during operation, cardiac surgery. Infection is usually on the suture line.
• Inflammatory process: vegetations. Contain fibrin, inflammatory cells, bacteria. Fragile
vegetations. Will cause valvular destruction. Reduce the normal orifice of valves, destroy the
normal architecture of endothelial structures.
• Turbulent blood flow occurs: murmurs, hemodynamic changes.

Clinical Symptoms and Signs:

Will depend on damage, what valve is involved.
Final result is congestive heart failure.
S+S start within 2 weeks of precipitating events.
• Fever: How high fever is depends on virulence of microorganism. Low pathogenicity? Slower
onset, mild fever.
• Murmurs: (very important!) Especially significant if a murmur was not heard in the patient before
infection. Murmurs are almost always present. Change in intensity of murmur is important. If it is
getting louder, more pronounced: bad sign!
• Splenomegaly
• Petechia (see locations in notes)
• Clubbing fingers: not pathoneumonic, etiology unknown

Source of pathogens:
• Dental infection: If patients are going for dental surgery, they may be put on antibiotics first.
• Genitourinary infections, pulmonary, cutaneous infections: these may all be precursors.

Embolic effects:
Roth Spots: retinal hemorrhages: seen in up to 5% of patients
Osler’s Nodes: Small painful erythematous subcutaneous nodules, usually on the fingers or toe
pads. May occur in 10-15% of cases
Janeway Lesions: PAINLESS lesions: often go unnoticed by the patient.

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Complications: Splinter hemorrhage on fingernails

Cardiac complications:
• Progressive valvular regurgitation
• Progressive heart failure (any valve failure will impact hemodynamics)
• Pericarditis: infection can spread to pericardium
• Conductive abnormalities (endocardium is involved)

Non-Cardiac:
Renal failure
Systemic embolism
Intracranial hemorrhages
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Meningoencephalitis

Diagnosis:
2 major, 1 major/2 minor, 5 minor (see notes)

Persistently positive blood cultures. Bacteremia is continuous. If you repeat the blood culture in 12
hours, you will have a second positive result. This is a DDx feature of bacterial endocarditis from
other pathologies

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ECG will show destruction of valve, orifice, thickening of wall, because of vegetation. Will support
diagnosis of endocarditis.

Minor criteria:
• Predisposing HT condition, IV drug abuse: PATIENT HISTORY: ask about these things with
persistent fever. Any recent dental work, medical procedures? Cystoscopy, abortion,
Caesarean. This is important.
In acute disease, can’t delay therapy for more than 2-3 hours. Take blood test, but it takes hours to
get result. If you suspect bacterial endocarditis, you can’t wait because it develops rapidly. Get 3
sets of blood cultures within 1 hour. Begin antibiotic treatment according to test and sensitivity.

Suspect if patient presents with unexplained fever, murmur, fatigue.

Renal failure d/t continuous bacteremia. Very susceptible to infection.

Patients usually die from rapidly developing cardiac failure. CHF usually cause of death.

Treatment: vegetations will not disappear, but will stop progression by eradicating micro-organisms.

Diseases of the Cardio-vascular system: 7th note package

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Diseases of the pericardium

Understand the normal functions before looking at pathologies

Diseased pericardium is thickened and fibrosed: reduced ability to stretch. This will cause pericardial
constriction.

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ACUTE PERICARDITIS:
May be sign of:
• Myocardial infarction (Dressler’s syndrome)
• Viral infection
• LUPUS
• Tuberculosis
• Strep/staph infection
• Secondary to malignancy. Pulmonary and breast carciniomas are most common primary sites.
• (See others in notes)
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Clinical Picture:
Chest pain: first symptom
How do you describe chest pain?
• Alleviated by sitting up, leaning forward. Reduces pressure on pericardium.
• Pain is worse in supine position: this increases pressure on pericardium.
• In contrast to angina, pain is NOT relieved by rest or nitroglycerin. No obvious precipitating
factors (exercise, cold weather, heavy meal will bring on angina).
• Pain is sharp, may be stabbing, may radiate to back or left shoulder, mimicking MI or angina.
• Retrosternal, may radiate down left arm and into the neck.
• Pain can also be described as heavy or squeezing.
• In some patient, pain increased by deep inspiration (increases pressure on pericardium)

Pathoneumonic sign: pericardial rub. Occurs during both diastole and systole. Confirms the
diagnosis of pericarditis. Best heard in a patient who has exhaled and leaned forward.
• Accumulation of fluid in pericardium causes cardiac tamponade

Dx:
• Physical Examination will find evidence of pericardial friction rub
• ECG:
o Shows depression of PR and elevation of ST. (you will also see elevation of ST in MI,
but the PR depression does not occur in acute MI. This is a DDx feature between MI
and pericarditis).
o ECG will occur in all leads (diffusely) in pericarditis. In MI, changes will occur in leads
that overly infarcted area only.
o There is no necrotic damage in pericarditis: Q wave will be unchanged.
• Cardiac markers (enzymes and proteins-troponins): will be normal in pericarditis, but will be
elevated in MI.
Echocardiography: will demonstrate pericardial effusion. Direct therapy towards cause: Dressler’s
syndrome, viral infection, treat accordingly.

PERICARDIAL EFFUSION
Accumulation of fluid. Pericardium expands to accommodate.

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When the fluid accumulates rapidly, the pericardium cannot accommodate. Cardiac tamponade
results.

May mimic pericarditis.

Clinical Features:
• Precordium becomes quiet. During pericarditis, you get friction rub, but if fluid accumulates, it
muffles the pericardial friction rub. If symptoms worsen and rub disappears, they have pericardial
effusion.
• Palpation of apical impulse difficult
• Heart sounds soft (due to accumulation of fluid)

DX:
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• Echocardiography: diagnostic, will show accumulation of fluid.
• CXR will show “water bottle appearance” of heart.
• Periocardiocentesis: remove fluid from pericardium and assess. Cell count, bacterial fungal
culture, tumour cells: may be able to determine cause from examination of fluid.
CARDIAC TAMPONADE
• Cardiac tamponade: life-threatening disorder. Very rapid accumulation of effusion, or it is so large
that is compresses the heart, decreases cardiac output (dyspnea, fatigue, tachycardia, orthopnea,
hypotension, leg edema
• Pathoneumonic: pulsus paradoxus: Palpable decrease in pulse amplitude in quiet inspiration.
Systolic BP decreases by more than 10mmHg during inspiration
• Jugular venous distension: will be increased with inspiration: Kussmaul’s sign

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• Narrow pulse pressure: Decreased during cardiac tamponade.
• Shock: cardiac output is very low

Therapy: removal of fluid from pericardial sac (emergency)

CHRONIC CONSTRICTIVE PERICARDITIS

Diffuse thickening of pericardium

Physical signs:
• Liver is involved: chronic pathology

Clinical signs: Dyspnea on exertion, orthopnea, ascites, edema (lower leg), jaundice

Physical examination: see notes

Pulsus paradoxus (physical signs)

Dx:
See notes

Pericarditis may develop in CHF

Case:
SW is a 28-year-old intravenous drug user who is seen in the emergency room with fever and
myalgias. She has been using intravenous drugs (both cocaine and heroin), intermittently for 12
years, and she supports her drug dependency by prostitution. Over the past 6 years she has had
Hepatits B and 4 episodes of sexually transmitted diseases. She reports that she had an HIV
antibody test 6 months ago and she says that the result was negative.
Her physical examination is remarkable: her temperature is 102F (38.8C) orally, her blood pressure
110/60, pulse is 110 beats per minute, respiratory rate is 18 breaths per minute. Skin “tracks” but no
Osler or Janeway lesions. HEENT: fundi are normal without Roth spots. Chest: normal breath
sounds. Cardiac: no Jugular venous distensions. Dynamic PMI (point of maximal impulse), normal
S1, S2, 2/5 systolic murmur at the base. Abdomen: no tenderness or organomegaly, pelvic exam
findings normal. Neurologic findings normal.

Who is the patient? female, 28, drug user

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Complaints: Fever and myalgia (what other complaints could cause this? The flu, other infections that
are not affecting the heart, Hepatitis B, reproductive/urinary tract infection, exacerbation of STD)

She has a fever: could be chronic or acute infection

Pulse is 110: this is high, but this could be sign of cardiac involvment, or could be the result of the
fever.
Osler and Janeway lesions are characteristic of infective endocarditis (these are not presenting, but
they are not pathoneumonic: can’t rule out endocarditis based on the absence of these symptoms)
Chest sounds are normal, therefore she probably doesn’t have a chest infection.
Cardiac exam showed no jugular venous distension, therefore the chambers of heart not involved.
Systolic murmur at the base.
2/6 systolic murmur: this is a mild murmur: 2 out of 6 on scale of intensity.
Most likely infective endocarditis from drug use: has murmur and she is a drug user. More info is
needed to confirm.

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