PANCE Blueprint Cardiology (11%)

60 y/o with abdominal pain, vomiting, and altered mental status

Audio: Severe mitral stenosis and regurgitation (rheumatic origin)

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Infective endocarditis is an infection of the inner surface of the heart (endocardium) or heart valves due to an infection in the bloodstream, usually with bacteria (commonly, streptococci or staphylococci) or fungi

It causes fever, heart murmurs, petechiae, anemia, embolic phenomena, and endocardial vegetations

• Acute bacterial endocarditis: Infection of normal valves with a virulent organism (S. aureus)
• Subacute bacterial endocarditis: Indolent infection of abnormal valves with less virulent organisms (S. viridans)
• Endocarditis in intravenous drug users - Staphylococcus aureus
• Prosthetic valve endocarditis - Staphylococcus epidermidis
• Dental procedure, slow onset, damaged valve → Strep viridans (oral flora)

"Always look for the "portal of entry" in the history: Mouth = Viridans; Skin/IVDU = Staph aureus; Genitourinary or gastrointestinal procedures = Enterococcus; Prosthetic valve or intracardiac hardware (biofilm formation)= Staphylococcus epidermidis"

Vegetations may result in valvular incompetence or obstruction, myocardial abscess, or mycotic aneurysm.

• Candida is a slow-growing organism. The most common source is a contaminated line. It typically causes large vegetations in endocarditis.
  • Large vegetation endocarditis in the early post–valve replacement period (2 months post-surgery) is most likely due to fungus, that is, Candida infection. Amphotericin B is recommended, followed by several weeks of antifungals that carry fewer adverse events.
• HACEK organisms tend to grow on native valves
• Staphylococcus aureus causes smaller vegetations; it is more common in injection drug users
• Streptococcus viridans is the most common cause of endocarditis. It typically occurs as a late complication of valve replacement and presents as small vegetations and embolic events.
• Endocarditis can occur at any age. Men are affected about twice as often as women. IV drug abusers and immunocompromised patients are at the highest risk.
• Most patients with a new murmur or change in an existing murmur, signs of heart failure (rales, edema) if valve function is compromised

The peripheral stigmata of infective endocarditis are not always present, and they can be seen in other conditions, such as rheumatic fever and systemic lupus erythematosus. However, they can be a valuable clue to the diagnosis of infective endocarditis, especially if they are present in conjunction with other symptoms of the condition, such as fever, chills, and a heart murmur.

In addition to the four classic peripheral stigmata, there are several other physical signs that can be seen in people with infective endocarditis. These include:

• Petechiae: These are small, flat hemorrhages on the skin. They are caused by bleeding from small blood vessels.
• Purpura: These are larger, raised hemorrhages on the skin. They are also caused by bleeding from small blood vessels.
• Clubbing: This is a thickening of the fingertips and/or toenails. It is caused by a decrease in the amount of oxygen in the blood.
• Splenomegaly: This is an enlargement of the spleen. It is caused by an increased number of white blood cells in the spleen.
• Hepatomegaly: This is an enlargement of the liver. It is caused by inflammation or infection of the liver.
• Hematuria: Due to emboli or glomerulonephritis.
• Neurologic findings consistent with CVA, such as visual loss, motor weakness, and aphasia

Diagnosis requires demonstration of microorganisms in blood and usually echocardiography

• Blood cultures (before antibiotics are started) 3 sets at least 1 hour apart
• EKG at regular intervals
• LABS: CBC, ESR, RF

A transesophageal echocardiogram is the gold standard

Modified Duke Criteria for Diagnosis of Infectious Endocarditis

Definite: 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria

Possible: 1 major and 1 minor criteria, or 3 minor criteria

• Major clinical criteria
  • Positive blood culture: isolation of typical microorganism for IE from 2 separate blood cultures or persistently positive blood culture
  • Single positive blood culture for C. burnetii or antiphase-1 IgG antibody titer >1:800
  • Positive echocardiogram: presence of vegetation, abscess, or new partial dehiscence of a prosthetic valve; must be performed rapidly if IE is suspected
  • New valvular regurgitation (change in preexisting murmur not sufficient)
• Minor criteria
  • Predisposing heart condition or IV drug use
  • Fever ≥38.0°C (100.4°F)
  • Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions
  • Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor (RF). Microbiologic evidence: positive blood culture, but not a major criterion (excluding single positive cultures for coagulase-negative staphylococci and organisms that do not cause endocarditis) or serologic evidence of infection likely to cause IE

Management – treatment consists of prolonged IV antibiotics and sometimes surgery

• IV antibiotics tailored to organism and susceptibility
• Valve debridement, repair, or replacement if indicated
• Start empiric therapy after obtaining 3 sets of blood cultures
  • Empiric therapy includes vancomycin + Ceftriaxone (covers MRSA, MSSA, Strep, Enterococcus)
  • Patients with a prosthetic valve receive IC vancomycin + Cefepime + Rifampin ± Gentamicin
  • IV drug users receive vancomycin (to cover MRSA)
• Use vancomycin in penicillin-allergic patients

Antibiotic prophylaxis (only for high-risk patients)

• Amoxicillin 2 g PO 30–60 minutes before procedure
• Penicillin allergy: Cephalexin 2 g PO, Azithromycin/clarithromycin 500 mg PO or doxycycline 100 mg PO