FRCA Notes

Infective Endocarditis

Endocarditis appears only once in the curriculum, under knowledge of 'antibiotic prophylaxis against surgical infection including subacute bacterial endocarditis'.

A recent BJA Education article on the topic, and updated ESC guidance, may form the basis of a Final FRCA exam question in the not-too-distant future.

Resources

  • Annual incidence 3-10 per 100,000
  • 2x male preponderance
  • Majority of patients >65yrs

  • Most endocarditis is bacterial, with Gram-positive cocci being the major culprits

Gram-positive cocci

  • Streptococci (17 - 31%):
    • Strep. viridans
    • Strep. bovis (which may indicate underlying malignancy)

  • Staphylococcus aureus (28 - 43%)
    • MSSA is more commonly implicated in community-acquired endocarditis
    • MRSA tends to occur from nosocomial endocarditis

  • Coagulase-negative staphylococci (13%)
  • Enterococci e.g. E. faecalis (13%)

Other bacteria and fungi

  • Culture-negative endocarditis (7- 10%)
  • HACEK organisms (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella and Kingella) (2-3%)
  • Fungal (e.g.Candida, Aspergillus) (1-3%)


Cardiac factors Non-cardiac factors
Bicuspid aortic valve IVDU
Mitral valve prolapse Haemodialysis
Rheumatic valve disease Chronic liver disease
Congenital cardiac disease
(excludes isolated ASD, fully repaired VSD/PDA)		 Malignancy
Prior infective endocarditis Advanced age
Implanted cardiac devices Immuno-compromise or -suppression
Valve replacement Poorly controlled DM
Hypertrophic cardiomyopathy Long-term venous access device

Antibiotic prophylaxis

  • Patients with cardiac risk factors listed in the table above are deemed by NICE to be at increased risk of developing infective endocarditis
  • However the same guidance recommends that no routine additional antibiotic prophylaxis is given for those undergoing:
    • Dental procedures
    • Upper or lower GI procedures
    • Urological, gynaecological or obstetric procedures (inc. childbirth)
    • ENT procedures, bronchoscopy or other respiratory tract procedures

  • These perhaps contradictory statements are explained by the fact it is felt:

    • 'The likelihood of preventing IE by using antibiotics is less than the risk of the antibiotics causing serious adverse events'

  • We should instead focus on:
    • Promotion of oral hygiene
    • Giving anti-microbial prophylaxis to at-risk people undergoing an interventional procedure that is considered likely to cause bacteraemia
    • Timely treatment of sepsis

  • Patients having procedures not on the list above aren't covered in the scope of the guidance
  • So too the route of administration and duration of any chosen antibiotic prophylaxis is not mentioned
  • Typically oral amoxicillin or clindamycin are used if prophylactic antibiotics are to be employed

  • Endothelial damage encourages platelet aggregation and clotting cascade activation on the endothelium
  • This leads to formation of a sterile vegetation, which can be colonised if bacteraemia occurs

  • In IVDUs, the pathophysiological mechanism is repeated exposure of the valvular endothelium to micro-organisms from injection
  • As injection is venous, 85% have right-sided endocarditis with the tricuspid valve most commonly implicated

  • Vegetations typically appear on 'upstream' (inner) valve surfaces, and overall the most common valves affected are:
    1. Mitral
    2. Aortic
    3. Mitral and aortic
    4. Tricuspid
    5. Pulmonary

  • Leaflet destruction ± the presence of the vegetation itself causes valvular regurgitation
  • This may lead to heart failure in and of itself, although there are contributions from sepsis, inflammatory myocarditis and coronary embolisation too
  • There may be abscess formation ± intra-cardiac fistula formation

  • A spectrum of disease exists, from acute fulminant disease to sub-acute progression, with a variety of organs affected

Cardiovascular

  • Severe valvular regurgitation
  • Cardiac failure ± pulmonary oedema
  • Aortic root abscess
    • May lead to intracardiac fistulae (most commonly aorta-to-RV or RA-to-LA)
  • Dysrhythmia
  • Septic shock

Neurological

  • Fatigue
  • Septic emboli leading to impaired cognition, altered/fluctuating consciousness and confusion

Renal

  • Glomerulonephritis
  • Acute kidney injury

Gastrointestinal

  • Splenomegaly
  • Acute liver injury
  • Weight loss

Haematological

  • Anaemia (normocytic)
  • Features of embolic phenomenon e.g. Roth spots, Janeway lesions, Osler's nodes, splinter haemorrhages

Infectious/immunological

  • Pyrexia
  • Rigors
  • Night sweats
  • Positive rheumatoid factor

Duke Criteria

  • These classic diagnostic criteria are low sensitivity
  • Mayn't account for cases from culture-negative endocarditis, infected prostheses or right-sided endocarditis
  • In order to diagnose IE, the patient must have both major criteria, five minor criteria, or one major & two minor criteria

  • Major criteria
    • Positive blood cultures
    • Positive echocardiogram findings of:
      • Oscillating intracardiac mass
      • Intracardiac abscess
      • Partial dehiscence of a prosthetic valve

  • Minor criteria
    • Predisposition e.g. IVDU, heart condition
    • Fever
    • Vascular or immunological phenomenon e.g. arterial emboli, septic infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions
    • Other microbiological evidence e.g. PCR, positive serology

Bloods

  • FBC: raised white cell count and normocytic anaemia
  • CRP ± PCT: raised
  • LFTs: may be deranged
  • U&E: acute kidney injury common

Blood cultures

  • Three sets from separate sites over at least 1hr
  • Minimum 30ml total volume from the three sets
  • Positive in 80% of cases of endocarditis
  • May need separate serology sent for Coxiella, Bartonella, Legionella, Chlamydia, Mycoplasma and Brucella

Echocardiography

  • TTE
    • Sensitivity only 55% for native valves, even less so for prosthetic ones
    • If inconclusive and high suspicion, should perform TOE

  • TOE
    • Highly sensitive and specific
    • Required if suspicion of left-sided disease even if TTE clearly demonstrates right-sided disease

Cross-sectional imaging

  • Fluorodeoxyglucose PET
  • Radiolabelled leukocyte single-photon emission CT
  • CT C/A/P to check for visceral embolisation and aortic root abscess
  • CT or MRI of the brain to check for septic emboli

  • Multidisciplinary approach with an 'Endocarditis team' inc. Microbiology, Cardiology and Cardiothoracic surgeons ± other teams' input

Antimicrobials

  • Empirical IV antibiotics according to local policy, which is guided by the patient's risk factors, whether it's a native or prosthetic valve and their risk of MDR organisms
  • Further antibiotic therapy guided by Microbiology and culture results
  • Evidence base for choice/duration of antibiotics is not robust

  • Fungal endocarditis may necessitate long-term (even lifelong) oral azole therapy

Cardiac surgery


Indications for cardiac surgery in endocarditis
Involvement of intracardiac prosthetic material
Severe mitral or aortic regurgitation with vegetations >10mm
Uncontrolled infection
Systemic embolisation with vegetations >10mm
Isolated large vegetations >15mm or more
  • Over 50% of patients meet these criteria for cardiac surgery
  • Evidence base surrounding early surgery is conflicting
  • Cardiac surgery is contraindicated by significant neurological injury e.g. intracranial haemorrhage, coma

  • May need pre-operative coronary angiography is there is concerns regarding coronary embolisation and consequent coronary artery disease
  • Intraoperative TOE is mandatory to assess valve repair/prosthesis, evaluate cardiac function and thus titrate haemodynamic support

Surgical intervention

  • The goal is debridement of infected material ± repair/replacement of damaged structures
  • Mitral valves can often be repaired (80%) which carries fewer complications than replacement
  • Aortic valves often require replacement
  • Necessitates CPB, although patients with endocarditis may have exaggerated systemic inflammatory responses to CPB compared to other patients

Coagulopathy

  • Patients often have coagulopathy/thrombocytopaenia
  • A balance needs to be struck between:
    • Adequate replacement of clotting factors and platelets to manage coagulopathy
    • Caution in an already-hypercoagulable state as part of the disease process
  • Intra-operative coagulation management should be as standard, namely:
    • TXA
    • Anticoagulation for CPB (see separate page)

Cardiovascular

  • Multiple cardiovascular features (see Clinical Features section)
  • Complications of cardiac surgery and cardiopulmonary bypass

Systemic emboli

  • Risk arises linearly between vegetation size, mobility and embolic complications
  • Sites include:
    • Cerebral septic emboli ± mycotic aneurysms
    • Hepatic
    • Splenic (often silent)
    • Lower limbs

AKI

  • Polyfactorial AKI from:
    • Sepsis
    • Hypotension
    • Embolic renal infarction
    • Glomerulonephritis
    • Use of nephrotoxic antibiotics such as gentamicin
    • Contrast agents
    • Effects of cardiopulmonary bypass

Infectious

  • Refractory septic shock
  • Persisting infection (positive blood cultures after 7-10 days appropriate antibiotics)

Mortality

  • Short-term mortality quoted as 10-24%; NICE say it's ~20%
  • Predictors of poor outcome include:
Patient factors Clinical factors Micro factors Echo factors
Advanced age Heart failure S. aureus Severe regurgitation/prosthetic valve dysfunction
Prosthetic valve endocarditis Renal failure Fungal infection Low ejection fraction
Diabetes mellitus Ischaemic or haemorrhagic stroke Non-HACEK Gram-negative bacilli Peri-annular complications
Severe comorbidities Septic shock Large vegetations Pulmonary hypertension