Infective Endocarditis

Microbial infection of the endocardial surface of the heart, producing vegetations and progressive tissue destruction.

• Affects native or prosthetic valves, the mural endocardium, or intracardiac devices.
• Behaves as a multi-system disease because infected material seeds the bloodstream.

Historically by tempo (acute vs subacute); now by affected tissue/device and likely organism, which better guides management.

Uncommon but highly lethal; the epidemiology has shifted towards S. aureus and healthcare contact.

• S. aureus is now the commonest cause overall.
• In-hospital / 6-month mortality approx 20-30% (verify against 2023 ESC).
• Antibiotics alone cure only about half - around 50% need surgery.

Risk requires both a colonisable surface and bacteraemia.

• Surface/structural: previous IE (highest individual risk), prosthetic valve, rheumatic/degenerative valve disease, bicuspid aortic valve, congenital heart disease, pacemaker/ICD.
• Bacteraemia: IV drug use, indwelling lines/CVCs, haemodialysis, chronic infection, invasive procedures, immunosuppression.

Endothelial injury and turbulent flow create a sterile fibrin-platelet nidus that becomes infected during bacteraemia.

• Turbulence/injury leads to platelet-fibrin deposition (non-bacterial thrombotic endocarditis, NBTE).
• Transient bacteraemia seeds the NBTE; adhesin-bearing organisms (S. aureus, viridans strep, enterococci) adhere and multiply.
• The vegetation becomes a biofilm-protected, high-density, low-turnover focus.

Mostly gram-positive cocci; the differential widens with prosthetic material, IVDU and culture-negative disease.

Classically right-sided (tricuspid), presenting with septic pulmonary emboli rather than systemic emboli.

• Chest pain, dyspnoea, cough, haemoptysis; only about one-third have an audible murmur.
• S. aureus predominates; Pseudomonas and fungal IE are over-represented.

Highly variable; group the features by mechanism to make them memorable.

• Bacteraemia/systemic: fever (~80%), rigors, anorexia, weight loss, night sweats, malaise; raised CRP.
• Valvular: new/changing murmur; heart failure from acute regurgitation.
• Embolic: splenic, renal, cerebral, coronary, pulmonary (right-sided); Janeway lesions, splinter haemorrhages.
• Immune-complex: glomerulonephritis, Osler nodes, Roth spots, arthralgia.

• Heart failure - commonest and most prognostically important (acute valvular regurgitation).
• Perivalvular abscess/fistula - local destruction; may cause conduction block.
• Systemic embolism/stroke - highest in the first 2 weeks, falls on effective antibiotics.
• Mycotic (intracranial) aneurysm; conduction block (root abscess); embolic/immune renal failure.

Suspect it with a new AV/conduction block on ECG, or other high-risk features.

• Aortic-valve IE, S. aureus, prosthetic valve IE.
• Persistent fever or bacteraemia despite appropriate antibiotics.
• ECG is specific but not sensitive - a normal ECG does not exclude abscess.

Blood cultures and echocardiography are the foundation; structure the work-up around what each test is for.

They identify the organism and dictate 2-6 weeks of targeted therapy - take them before antibiotics.

• At least 3 sets from separate venepuncture sites (unless septic shock mandates immediate treatment).
• Multiple sets distinguish contamination from the continuous bacteraemia of IE.
• Tell microbiology you suspect IE (prompts prolonged incubation, serology/PCR for fastidious organisms).

Echo identifies vegetations, abscess and valve destruction; TOE is more sensitive, especially for prosthetics and abscess.

• Both highly specific (~95%); no feature reliably separates infective from non-infective masses. Repeat echo if complications are suspected.

Diagnosis is Definite (pathological, or clinical) or Possible/Rejected; clinical Definite needs 2 major / 1 major + 3 minor / 5 minor.

• Major - microbiological: typical organism from ≥2 cultures; S. aureus now major regardless of acquisition; persistently positive cultures; Coxiella; molecular methods (PCR, sequencing, Bartonella assay).
• Major - imaging: echo, plus cardiac CT and abnormal PET/CT uptake. Major - surgical: direct intra-operative evidence (new 2023).
• Minor: predisposition, fever ≥38C, vascular phenomena, immunologic phenomena, microbiological evidence not meeting a major, and new minor criteria (e.g. new murmur).

Bactericidal, often combination, prolonged, and targeted to organism and MIC.

• Start after cultures unless haemodynamically unstable. NVE ~2-6 weeks; PVE ≥6 weeks.
• Consider OPAT/oral switch in stable streptococcal IE after ≥10 days IV and ≥7 days post-surgery (POET trial).

Three headings (2023 ESC), with surgery undertaken in about half of patients.

• Timing: emergency (<24 h), urgent (3-5 days), non-urgent (same admission).
• 2023 update: do not delay needed surgery after a neurological event - earlier is generally better; more liberal surgery to prevent embolism.

A key exam discriminator - UK (NICE) and European (ESC) guidance diverge.

• NICE CG64 (UK): prophylaxis not recommended routinely for dental/GI/GU/respiratory procedures; treat established infection at the operative site.
• ESC 2023: Class I prophylaxis for high-risk patients (prosthetic valve, previous IE, certain CHD) before high-risk dental procedures; Class IIb for moderate risk.