Discuss the aetiology, pathogenesis, clinical features, investigations and management of infective endocarditis.

Definition

Infective endocarditis (IE) is microbial infection of the endocardial surface of the heart, most often involving the valves, characterised by the vegetation — a mass of platelets, fibrin, micro-organisms and inflammatory cells. Despite modern therapy it carries a mortality of 15–30%.

Pathogenesis

1. Endothelial injury — from turbulent flow across an abnormal valve, a jet lesion, a catheter or intravenous drug use — exposes subendothelial collagen.

2. Sterile platelet-fibrin thrombus forms (non-bacterial thrombotic endocarditis).

3. Transient bacteraemia — from dental procedures, chewing, tooth-brushing, skin or gut sources — seeds the thrombus.

4. Adherent organisms proliferate within the vegetation, protected from phagocytes and from antibiotic penetration by the fibrin matrix — which is why prolonged, high-dose, bactericidal, parenteral therapy is required.

Predisposing Cardiac Conditions

• Rheumatic heart disease — still the commonest predisposing lesion in India, particularly mitral regurgitation and aortic valve disease
• Congenital heart disease — bicuspid aortic valve, VSD, patent ductus arteriosus, tetralogy of Fallot
• Prosthetic valves — early (< 1 year, usually staphylococcal, acquired perioperatively) and late
• Mitral valve prolapse with regurgitation; degenerative calcific valve disease in the elderly
• Previous endocarditis — the strongest single risk factor
• Intravenous drug use — characteristically causing right-sided (tricuspid) endocarditis
• Intracardiac devices; haemodialysis; immunosuppression

Microbiology

Clinical Features

Constitutional: fever with chills and sweats (present in over 90%), malaise, anorexia, weight loss, arthralgia — an illness that may be indolent over weeks (subacute) or fulminant over days (acute).

Cardiac:

• New or changing murmur — a regurgitant murmur; the change matters more than the murmur itself
• Heart failure — from acute valve destruction, and the commonest indication for surgery
• Conduction abnormalities from a root abscess (a lengthening PR interval is a warning sign)

Peripheral stigmata (immune complex and embolic — classical, though now less often seen):

Embolic and immune complications:

• Systemic emboli — stroke (the commonest and most feared), splenic and renal infarcts, mesenteric and limb ischaemia; mycotic aneurysm with risk of rupture
• Right-sided endocarditis — septic pulmonary emboli with multiple cavitating lung lesions; murmurs are often absent, so a normal cardiac examination in an intravenous drug user must not reassure
• Renal — immune complex glomerulonephritis (with low complement), renal infarction, drug-induced interstitial nephritis

Investigations

1. BLOOD CULTURES — the single most important investigation

• At least THREE SETS from separate venepuncture sites, at intervals, BEFORE antibiotics, with adequate volume in each bottle.
• Do not wait for a fever spike — the bacteraemia in endocarditis is continuous.
• If the patient has already received antibiotics and is stable, stopping them and reculturing after a few days may be justified.
• For culture-negative cases: serology for *Coxiella*, *Bartonella* and *Brucella*, and PCR on valve tissue.

Echocardiography

• Transthoracic (TTE) first — sensitivity around 60–70% for native valves.
• Transoesophageal (TOE) — far more sensitive (> 90%), and mandatory for prosthetic valves, suspected abscess, and when TTE is negative but suspicion remains high.
• Findings: vegetation, abscess, new dehiscence of a prosthetic valve, new valvular regurgitation.

3. Supporting: CBC (normocytic anaemia, leucocytosis), raised ESR and CRP, urinalysis (microscopic haematuria and proteinuria — an important and easily obtained clue), renal function, rheumatoid factor (positive in subacute disease), complement, ECG (a new conduction defect suggests root abscess), chest X-ray, and CT/MRI brain and abdomen for emboli and mycotic aneurysms. PET-CT is increasingly used for prosthetic valve and device infection.

Diagnosis — Modified Duke Criteria

Definite endocarditis: 2 major, or 1 major + 3 minor, or 5 minor criteria.

Management

1. Antimicrobial therapy

• Prolonged high-dose intravenous BACTERICIDAL antibiotics, typically for 4–6 weeks (longer for prosthetic valves), guided by the organism and its minimum inhibitory concentration.
• Empirical therapy while awaiting cultures is directed by the clinical setting — native versus prosthetic valve, community versus healthcare-associated, and local resistance patterns; it must cover staphylococci, streptococci and enterococci.
• Combination therapy with an aminoglycoside is used in defined situations (enterococcal disease, some prosthetic valve infections), with monitoring of levels and renal function.
• Involve microbiology and cardiology early — endocarditis is best managed by a multidisciplinary "endocarditis team".

2. Surgery — indications (and roughly half of patients require it)

• HEART FAILURE from valve destruction — the commonest and most urgent indication
• Uncontrolled infection — persistent fever and positive cultures despite appropriate antibiotics; perivalvular abscess, fistula or new conduction block
• Prevention of embolism — large vegetation (> 10 mm) with a previous embolic event, or very large vegetation (> 15 mm)
• Prosthetic valve endocarditis, especially early; fungal endocarditis (which almost always requires surgery)
• Do not delay surgery for a fixed duration of antibiotics where an indication exists — early surgery improves outcome.

3. Supportive and complication management

Heart failure treatment, anticoagulation decisions (generally continue in prosthetic valves but withhold with cerebral haemorrhage or large infarct), management of embolic complications, treatment of the source (dental review and treatment is essential), and colonoscopy for *S. gallolyticus*.

4. Prophylaxis — much narrower than it once was

Antibiotic prophylaxis is now recommended only for the HIGHEST-RISK patients (previous infective endocarditis, prosthetic valve or prosthetic material used in valve repair, and specified congenital heart disease), and only for dental procedures involving manipulation of gingival tissue or the periapical region or perforation of the oral mucosa. Excellent oral and dental hygiene for all at-risk patients matters more than procedural prophylaxis, since cumulative day-to-day bacteraemia from chewing and brushing far exceeds that from occasional dental visits.