Infective Endocarditis

IE is an infection of native or prosthetic heart valves, endocardial surface or an indwelling cardiac device (such as a pacer or defibrillator). In recent years, we’re seeing it happen in older and more chronically ill patients. And more MRSA.

The diagnosis is tricky because the presentation can be fairly subtle. You need a high index of suspicion, fever and:

  • unclear infectious source
  • new regurgitant murmur
  • embolic events of unknown source

Get 3 sets of BCx in the ED before antibiotics and possibly a TTE. Patients should receive IV Abx and 1/2 of them require valve replacement or debridement surgery. Indications for surgery are:

  • development of heart failure
  • perivalvular abscess formation
  • uncontrolled infxn
  • Large, Mobile vegetations (that may flick off)

Epidemiology

IE is still pretty rare: 3–10 per 100k per year. Risk factors include:

  • In low income countries: rheumatic heart disease
  • In developed countries: IVDU, valve disease, congenital heart disease, prosthetic valves & devices

The mean age has gone up from 45 (1980) to 70 (2001), with increasing numbers of comorbidities and more males. Half of native valve IE are healthcare associated (such as dialysis).

Microbiology

  • Gram positive cocci
    • most common
    • MRSA in IVDA, HD
    • HC associated = more abscesses, emboli, death
    • coag negative staph (S epidermidis forms a biofilm protecting it from Abx, S lugdunesis, S capitis) = lower virulence but can better stick to prosthetic material
  • Enterococcus
    • community-acquired (in developing countries)
    • Strep mutans, salivarius, anginosus, mitis, sanguinnis = mouth + GI
    • Group D strep = liver dz and colon CA
  • HACEK group (gram neg) slow growing
    • Haemophillus
    • Aggregatibacter
    • Cardiobacterium
    • Eikenella corrodes
    • Kingella kingae

Pathophysiology

Normal epithelium resists infection and thrombus formation, so we need three deviations for a vegetation to form:

  1. Damaged valve
  2. Pathogens to adhere to damaged valve
  3. Pathogens survive there

Damaged endothelium attracts fibrin and platelets to which bacteria can stick. IVDA or dental infections just get bacteremic so often, they don’t even need damaged endothelium or valves.

  1. Infected thrombus forms
  2. Inflamed endothelial cells release cytokines that attract more cells
  3. Infected vegetation forms
  4. Bacteria stick to this causing more inflammation
  5. Bacteria hide under the thrombus or biofilm (S epidermidis)

Valve destruction results in:

  • Aortic valve = high risk of heart failure (most common cause of death in IE)
    • left sided septic emboli cause brain abscesses (that bleed) and infarctions of organs
  • Mitral valve = higher risk of chordae or papillary muscle rupture
    • right sided septic emboli cause septic PE’s
  • Myocardium = heart blocks and abscesses

Clinical Features

Usually pretty subtle which is why it’s often missed or delayed Dx. #1 Sx is fever (90%). #1 sign is new mrumur (50–85%). Look for sequelae:

    CHF (sudden onset)
    conduction blocks (perivalvular abscesses)
    Strokes (usu convert to hemorrhagic)
    Septic PE
    Rare but testable manifestations:

    • Roth spots: retinal hemorrhage with white center due to immune complex deposition (also from leukemia, DM and other diseases)
    • Osler nodes: painful immune complex collections on palms and soles
    • Janeway lesions: µ-abscess of dermis, non-tender on palms and soles
    • Splinter hemorrhages: hemor that look like splinters under the nails

Diagnosis

You need a high index of suspicion to make this diagnosis.

  1. Fever + Risk factors:
    • Cardiac risk factors
      • Prior IE
      • Prosthetic valve or device
      • Valvular or CHD
    • Non-cardiac risk factors
      • IVDA
      • Immunosuppression
      • Indwelling catheter
      • Chronic hemodialysis (HC Associated)
  2. Sepsis w/o origin
  3. New cardiac murmur (listen in a quiet room)

Echocardiogram

Get as soon as possible. TTE (sens = 40–63%) in the ED and a TEE (sens = 90–100%) later. TEE can find paravalvular abscess, valve prolapse, valve perf, psuedoaneurysm, chordae rupture, vegetations on pacer. TTE works better on young skinny IVDA.

Blood cultures

To maximize the yield of blood cultures get 10 mL in each bottle q20m x 3 each from a diff spot, then give Abx (if the patient is stable enough). Coag neg strep = frequent contaminant (so 3 diff spots). That would mean Abx after 1h, but can give at 45 minutes if needed. Cultures take days to grow, so there are faster PCR and DNA assays under trials.

Duke Criteria

This is a research tool, not diagnostic.

Criteria Description
Major 1. +BCx x 2 with typical organism
2. Persistent +BCx 12h apart
3. ONE +BCx = Coxiella burnetii or anti-phase I IgG titles > 1:800
4. Echo = involvement
Minor 1. Heart condition or IVDA
2. Fever > 38
3. Emboli or infarcts
4. Glom-nephritis, Osler nodes, Roth spots, RF
5. +BCx (not meeting major)
6. ↑ESR/CRP, clubbing, splinter hemorrhage, splenometagly, microscopic hematocrit, abnormal but non-Dx Echo

Treatment

  1. Stabilization
  2. Generally should be admitted:
    • D/C if neg BCx, well appearing & reliable to follow-up (so observe for a day while waiting for BCx)
    • Admit all prosthetic valves (too much M&M)
    • IVDA + fever + no source = admit till neg BCx (unrealiable to follow-up)
  3. Consultations:
    • CV surgery: see indications
    • ID: high likelihood or + echo
    • Neuro: neuro embolic
  4. Antibiotics
    • See table below
    • Target S aureus, Strep, Enterococci, GNR = HACEK (ceftriaxone). AG have a synergistic effects with ß-lactams and Vanc. Treat for 4–6w until cultures are negative.
  5. Surgery
    • Indications
      • vegetation > 10 mm
      • severe valvular insufficiency
      • intracardiac abscess
      • pseudoaneurysm
      • valvular perforation or dehiscence
      • decompensated heart failure
    • usually valve replacement, but occ mitral and tricuspid debridement is possible
  6. Stroke
    • No tPA (S aureus becomes ICH)
Category Abx Europe
Native valve Vanc 15mg/kg q8h + Ceftriaxone 2g qD Unasyn and Gent
Prosthetic valve <12m Vanc + Gent 1 mg/kg q8h Vanc, Gent, Rifampin 600 mg q12h PO
Prosthetic valve >12m Vanc + Gent Unasyn + Gent

Prognosis

  1. Initial TEE for Dx and baseline
    • Subsequent if pt gets CHF, block or worse Sx
  2. Increased risk of recurrence (1–3% per patient-year)
    • Repeat TTE and inflam markers @ 1m, 3m, 6m, 12m
    • Good dental hygiene
    • Educate on CHF

Prevention

The goal is to minimize chances of bacteremia. Good oral hygiene and dental care, strict sterile technique in procedures, limit central lines.

UK in 2008 said no Abx needed prior to procedures and there’s been no increase in IE. Except for:

  • Dental procedures that manipulate the gums or perforate oral mucosa (Amox 2g PO or amp 2g IV/IM or keflex 2g PO or clinda 600 mg IM/IV)
  • I&D – jury is out.

Macros

INFECTIVE ENDOCARDITIS

This patient has the following risk factors for infective endocarditis:

- Fever + Risk factors:

- ***Cardiac risk factors: Prior IE, prosthetic valve or device, valvular or congenital HD

- ***Non-cardiac risk factors: IVDA, immunosuppression, indwelling catheter, chronic hemodialysis

- ***Sepsis w/o origin

- ***New cardiac murmur (listen in a quiet room)

Consultation: cardiothoracic surgery

- ***vegetation > 10 mm

- ***severe valvular insufficiency

- ***intracardiac abscess

- ***pseudoaneurysm

- ***valvular perforation or dehiscence

- ***decompensated heart failure

Consultation: Infectious Disease

- ***high likelihood

- ***positive TTE

Category Abx Europe
Native valve Vanc 15mg/kg q8h + Ceftriaxone 2g qD Unasyn and Gent
Prosthetic valve <12m Vanc + Gent 1 mg/kg q8h Vanc, Gent, Rifampin 600 mg q12h PO
Prosthetic valve >12m Vanc + Gent Unasyn + Gent

Reference

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