Infective Endocarditis

OVERVIEW

  • endocarditis is a disease characterised by inflammation of the endocardium, typically affecting the heart valves and usually caused by infection and can be acute, subacute or chronic
  • most commonly affecting the aortic valve (previously mitral valve)
  • most cases of fulminant endocarditis are caused by S. aureus
  • always suspect endocarditis in S. aureus septicaemia (perform TOE)

CAUSE

Organisms

  • Staphylococcus aureus (MSSA or MRSA)
  • Coagulase negative Staphylococci: S. epidermidis, S. lugdenensis 
  • Streptococcus viridans
  • Streptococcus bovis
  • Enterococcus
  • HACEK organisms

-> Haemophillus aphrophilus, parainfluenzae and paraphrophilus
-> Actinobacillus actinomycetemcomitans
-> Cardiobacterium hominis
-> Eikenella corrodens
-> Kingella kingae

  • Fungi

Culture negative endocarditis

  • Brucella
  • Bartonella
  • Coxiella burnetti (Q fever)
  • Chlamydia
  • Legionella
  • Mycoplasma
  • Whipples disease (Trophyerma whipplei)

RISK FACTORS

Cardiac lesions

  • congenital heart disease
  • rheumatic heart disease
  • mitral valve prolapse
  • valve regurgitation
  • degenerative valve disease
  • prosthetic valve (1-5%) – early (<60 days) or late (>60 days)

Predisposition to infection

  • IV drug use – tricuspid, aortic and mitral valve
  • haemodialysis
  • high risk surgery (e.g. dental, respiratory and infective)
  • long lines
  • bone marrow transplant recipients
  • immunosuppressed (e.g. HIV)

CLINICAL FEATURES

History

  • 50% occur in patients with normal valves!
  • spectrum:
    — asymptomatic
    — malaise, night sweats, anaemia, weight loss
    — crashing cardiogenic shock and sepsis
  • haematuria (glomerulonephritis)
  • embolic complications
    — stroke (esp if PFO), intracranial haemorrhage
    — septic pulmonary emboli
    — splenic infarction, and other end organs, etc
  • presence of risk factors

EXAMINATION

  • Skin rash
  • Splinter haemorrhages and conjunctival haemorrhages
  • Oslers nodes – tender nodules on pulps of fingers and toes
  • Janeway lesions – non-tender haemorrhagic pulps on fingers and toes
  • Roth spots – retinal hemorrhages with a pale centre
  • Splenomegaly
  • New neurological signs
  • New murmur, e.g. aortic regurgitation and associated systemic features
  • Left ventricular failure – basal crackles and effusions
  • Emboli — major arteries, pulmonary, spleen
  • Haematuria

INVESTIGATIONS

Bedside

  • ECG: look for widening PR interval, p mitrale, TWI, dysrhythmia

Laboratory

  • Blood cultures (90% of the time positive)
    — need at least 2 sets drawn 12 hours apart, or
    — minimum of 3 out 4 sets postive with first and last positive set >1 hour apart
  • Serology for causative organisms
  • Rheumatoid factor
  • PCR for microbial 16S ribosomal RNA genes from valve tissue (if culture negative)

ECHO

  • TTE = 60% sensitive, TOE = 90-99% sensitive, specificity of 90%
  • oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation
  • abscess, or
  • new partial dehiscence of prosthetic valve

DIAGNOSIS

Use the Modified Duke Criteria (see MedCalc)

  • Two major criteria, or
  • One major and three minor criteria, or
  • Five minor criteria

Major criteria

  • Positive blood culture for Infective Endocarditis 
    Typical microorganism consistent with IE from 2 separate blood cultures, as noted below:
    — viridans streptococci, Streptococcus bovis, or HACEK group, or
    —community-acquired Staphylococcus aureus or enterococci, in the absence of a primary focus
    or Microorganisms consistent with IE from persistently positive blood cultures defined as:
    — 2 positive cultures of blood samples drawn >12 hours apart, or
    — all of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart)
  • Evidence of endocardial involvement
    Positive echocardiogram for IE defined as :
    — oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or
    — abscess, or
    —new partial dehiscence of prosthetic valve
  • New valvular regurgitation (worsening or changing of preexisting murmur not sufficient)

Minor criteria

  • Predisposition: predisposing heart condition or intravenous drug use
  • Fever: T> 38.0° C (100.4° F)
  • Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
  • Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor
  • Microbiological evidence: positive blood culture but does not meet a major criterion as noted below¹ or serological evidence of active infection with organism consistent with IE
  • Echocardiographic findings: consistent with IE but do not meet a major criterion as noted above

¹ Excludes single positive cultures for coagulase-negative staphylococci, diphtheroids, and organisms that do not commonly cause endocarditis.

MANAGEMENT

Overview

  • resuscitation
  • specific therapy: IV antibiotics +/- surgery
  • supportive care and monitoring
  • treat underlying cause and complications
  • consults: infectious diseases, cardiology, cardiothoracic surgery

IV antibiotics

  • Empiric treatment for community acquired disease with a native valve:
    benzylpenicillin 1.8 g (child: 45 mg/kg up to 1.8 g) IV, 4-hourly
    + flucloxacillin 2 g (child: 50 mg/kg up to 2 g) IV, 4-hourly
    + gentamicin 4 to 6 mg/kg (child <10y: 7.5 mg/kg; 10y+: 6 mg/kg) IV, for 1 dose, then determine dosing interval for a maximum of either 1 or 2 further doses based on renal function)
  • Empiric treatment for hospital acquired disease OR a prosthetic valve OR penicilin hypersensitity OR suspected CA-MRSA:
    vancomycin 1.5 g (child <12y: 30 mg/kg up to 1.5 g) IV, 12-hourly
    + gentamicin 4 to 6 mg/kg (child <10y: 7.5 mg/kg; 10y+: 6 mg/kg) IV, for 1 dose, then determine dosing interval for a maximum of either 1 or 2 further doses based on renal function)
  • duration: usually for at least 1 to 2 weeks (low risk patients may qualify for home-based therapy)
  • gentamicin is is given q24h and is usually stopped after 3 doses unless proven streptococcal or enterococcal endocarditis (give q8h and continue)
  • avoid clindamycin and lincomycin due to high failure rates
  • directed therapy varies according to the underlying causative organism and the valve affected

Surgery (valve replacement)

  • indications

(1) haemodynamic instability
(2) abscess enlargement
(3) abscess (root, paravalvular, intracardiac)
(4) recurrent emboli
(5) organisms: Staphylococcus aureus, Q fever, fungal endocarditis

  • early surgery (<48h) reduces long-term embolic complications, no effect on mortality (Kang et al, NEJM 2012)

PREVENTION

Overview

  • more conservative approach as risks of adverse effects from antibiotics higher than risks of developing IE from dental, GI or GU tract procedure
  • must have high risk patient AND high risk surgery

Risk assessment

  • high risk patients:

1. any prosthetic material in used in valve repair
2. previous infectious endocarditis
3. congenital heart disease (unrepaired cyanotic, partially repaired, or completely repaired <6 months previously)
4. cardiac transplant patients with valvulopathy

  • high risk surgery

1. all dental procedures that involve manipulation of gingival tissue or periapical region of teeth or perforation of oral mucosa
— thus only check ups and simple fillings that don’t involve gingiva don’t need antibiotic prophylaxis
2. respiratory tract surgery
— incision and biopsy, tonsillectomy, adenoidectomy

Antibiotics

  • give a single dose of antibiotic prior to procedure (or within 2 hours of procedure)

1. amoxicillin 50mg/kg PO
2. cephazolin 50mg/kg IV/IM
3. cephalexin 50mg/kg PO (penicillin allergic)
4. clindamycin 20mg/kg PO (penicillin allergic)

  • if currently infected with a bug AND operation is taking place on that area AND the organism is likely to cause infectious endocarditis
    -> consult infectious diseases specialist
    -> give prophylactic treatment perioperatively

COMPLICATIONS

  • embolic (major arteries, brain, limbs, lungs, organs such as spleen)
  • sepsis (local and metastatic abscess formation)
  • valve incompetence and heart failure / cardiogenic shock
  • arrhythmias
  • death

References and Links

LITFL

Journal articles

  • Kang DH, et al. Early surgery versus conventional treatment for infective endocarditis. N Engl J Med. 2012 Jun 28;366(26):2466-73. doi: 10.1056/NEJMoa1112843. PubMed PMID: 22738096. [Review in Crit Care]
  • Prendergast BD, Tornos P. Surgery for infective endocarditis:who and when? Circulation 2010;121:1141-1152 PMID: 20212293
  • Sharma V, Candililo L, Hausenloy DJ. Infective endocarditis: An intensive care perspective. Trends Anaes Crit Care 2010;2 (1) 36-41 [Free Full Text]
  • Sonneville R, Mourvillier B, Bouadma L, Wolff M. Management of neurological complications of infective endocarditis in ICU patients. Ann Intensive Care. 2011 Apr 20;1(1):10. PMC3224466.
  • Thury F, Grisoli D, Collart F, Habib G, Raoult D. Management of infective endocarditis: challenges and perspectives. The Lancet 2012;379:965-975 PMID: 22317840

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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