Infectious masses

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Introduction

Infective Endocarditis is an inflammatory condition affecting the inner tissue of the heart as well as intra-cardiac prosthesis, including heart valves and devices. Despite availability of echocardiography and clear guidelines for antibiotic treatment, unfortunately this condition is still associated with an annual mortality of 20-25%.[1][2] Eighty percent (80%) of cases are caused by Staphylococcus, Streptococcus and Enterococcus infections and in the recent years there has been an increasing association of the condition with prosthetic heart valves and hospital acquired infections.[2] Diagnosis is made using the Duke’s criteria, however clinical suspicion is not straightforward, because infective endocarditis manifests similarly to several other conditions and hence the high rate of delayed referrals for echocardiography, the main diagnostic tool for this condition.[2]

Signs and symptoms

  1. Fever (38ͦC)
  2. Systemic embolus
  3. Splinter haemorrhage in nail beds
  4. Osler nodes in the pulps of fingers (painful)
  5. Janeway lesions in palms and soles of feet (painless)
  6. Roth spots (retina)
  7. New murmur on auscultation
  8. Glomerulonephritis
  9. Splenomegaly

A febrile illness of uncertain origin, which is associated with a new regurgitant murmur on auscultation of the precordium, should always be diagnosed as IE until proven otherwise.[2]

Pathogenesis

  • Intact intra-cardiac endothelium is resistant to infection by circulating bacteria.
  • Mechanical disruption of endothelium, especially valve endothelium with local clot formation, can become a medium for microbial adherence and growth, subsequently leading to establishment of infection.
  • Causes of endothelial disruption:
Rheumatic heart disease
Degenerative valve lesion (in >60% of asymptomatic patients above the age of 60)
Prosthetic heart valves
Devices and their leads
Catheters
Structural congenital heart disease including bicuspid aortic valve, septal defects and patent ductus arteriosus (PDA)
IV drug use (affecting right heart in majority of cases)
  • Causative microbes:

Staphylococcus aureus and Streptococcus viridans are by far the commonest organisms, followed by culture negative microbes. Other species of Staphylococcus and Streptococcus, Coxiella burnetti and Haemophilus influenza are less frequent, but not rare.[3]

  • The size of vegetetions is associated with frequency of complications following IE. Moderate size lesions (6-19mm) are the cause of majority of complications, including valvar incompetence, congestive heart failure, embolism and need for surgery.[3]


Classification


1. According to localisation of infection and presence of intra-cardiac material:

  • Left-sided native valve IE.
  • Left-sided prosthetic valve IE(PVE)
Early PVE (< 1year post-procedure)
Late PVE (> 1 year post-procedure)
  • Right-sided native valve IE.
Device related IE (pacemaker/ defibrillator)


2. According to the mode of acquisition:

  • Health care associated IE
Nosocomial (Infection developing in patient hospitalised for >48h prior to onset of signs/ symptoms of IE).
Non- nosocomial (IE developing in < 48h after hospital admission in a patient with previous health-care contact)
Home IV therapy, haemodialysis, IV chemotherapy in < 30 days before onset of IE.
Hospitalisation in an acute care facility in <90 days before onset of IE.
Resident of nursing home or long term care facility.
Community acquired IE :Signs/ symptoms of IE developing in <48h following hospital admission (not fulfilling criteria for health care related infection).
IV drug use associated IE: Infection in an active drug user in the absence of other source of infection.


3. Active IE:

  • IE with positive blood cultures and persistent fever.
  • Active inflammation found at surgery.
  • Patient still on antibiotic therapy.
  • Histopathological evidence of IE.


4. Recurrence:

  • Relapse (Repeated episodes of IE < 6 months after initial episode).
  • Reinfection (Infection by different microorganism or repeated episode of IE >6 months after initial infection).[4]

Diagnosis

  • Diagnosis is made by using Modified Duke’s Criteria:[3]
  • Use of TTE/TOE is essential.
  • TTE is indicated on clinical suspicion of IE.
  • TOE is performed if the following occur:
  1. Presence of prosthetic valve or intra-cardiac device.
  2. Ambiguous TTE images.
  3. Positive result with TTE.
  4. Negative result with TTE, but clinical suspicion of IE remaining.
  5. Following negative TOE (7-10 days) with strong suspicion of IE.
  • Echocardiography can be challenging when dealing with potentially infected devices, very small vegetations (<2mm), presence of pre-existing lesions and in IE without vegetations.
  • Differentials for infected vegetations are:
  • Degenerative valve disease, myxomatous valve disease, systemic lupus, rheumatoid disease, primary antiphospholipid syndrome, thrombus, marantic endocarditis(malignancy), small tumours and chordal rupture.
  • Small abscess can be difficult to identify with ECHO if:
  1. Early disease
  2. Early post-operative period
  3. Presence of device[5]


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  • Images
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Management

  • Treatment with appropriate antibiotic regime +/- surgery according to each hospital’s drug policy.
  • Prolonged antibiotic treatment to ensure high concentration in the bloodstream and penetration into vegetations.
  1. Prosthetic valve endocarditis (PVE) (at least 6 weeks)
  2. Non-vegetation endocarditis (NVE) (2-6 weeks)
  3. Vegetation endocarditis (4-6 weeks)
  • Failure to respond to antibiotics due to the following:
  1. Inadequate antibiotic treatment.
  2. Antibiotic resistance.
  3. Need for surgical removal.
  • Surgery is necessary for the following:
  1. Heart failure as a consequence of infected valve regurgitation.
  2. Prevent systemic embolisation.
  3. Infection extending to peri-valvar area, associated with bradyarrhythmias.

Early surgery is associated with good outcomes.

  • Fungal IE in immunocompromised patients, IV drug users and PVE. Treatment with anti-fungals and valve replacement.[3][6]

References

  1. Prendergast BD. Diagnosis of infective endocarditis. BMJ (Clinical research ed.) 2002 Oct;325(7369):845-6.
  2. 2.0 2.1 2.2 2.3 Connaughton M, Rivett JG. Easily missed? Infective endocarditis. BMJ (Clinical research ed.) 2010 Jan;341:c6596.
  3. 3.0 3.1 3.2 3.3 Habib G, Hoen B, Tornos P, Thuny F, Prendergast B, Vilacosta I, Moreillon P, de Jesus Antunes M, Thilen U, Lekakis J, Lengyel M, Müller L, Naber CK, Nihoyannopoulos P, Moritz A, Zamorano JL. Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European. European heart journal 2009 Oct;30(19):2369-413.
  4. Bayliss R, Clarke C, Oakley CM, Somerville W, Whitfield AG, Young SE. The microbiology and pathogenesis of infective endocarditis. British heart journal 1983 Dec;50(6):513-9.
  5. Stafford WJ, Petch J, Radford DJ. Vegetations in infective endocarditis. Clinical relevance and diagnosis by cross sectional echocardiography. British heart journal 1985 Mar;53(3):310-3.
  6. Que Y-A, Moreillon P. Infective endocarditis. Nature reviews. Cardiology 2011 Jun;8(6):322-36.
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