Infective Endocarditis

Definition

Infective endocarditis (IE) is an infection of the endocardium of the heart.

Classifications

50% endocarditis occurs in normal valve. It follows acute course -present with heart failure endocarditis occurs in abnormal valve → subacute course

Risk factors

Previous IE with valvular damage Invasive vascular procedures Recreational drug abuse Rheumatic heart disease (fewer than 20% of cases of IE) Elderly patients with calcific aortic stenosis Congenital heart disease accounts for 15% of cases (bicuspid aortic valve being the most common) Prosthetic valve implants

Pathogenesis

All cases have a nonbacterial thrombotic endocarditis (a sterile fibrin-platelet vegetation) as the prerequisite for adhesion and invasion. The site of this thrombus is influenced by the Venturi effect, with deposition of thrombus on the low pressure side. There are differences in the different clinical situations: Acute IE:- The thrombus may be produced either by the invading organism or by valvular trauma (pacing wires, catheters, etc.). Subacute IE: Sufficient inoculum of bacteria required to allow invasion of the thrombus, bacteria clumping with production of agglutinating antibodies. Nonbacterial thrombotic endocarditis:- This can result from, for example, renal failure, neoplasia, systemic lupus erythematosus (SLE) or malnutrition. The valves most commonly affected by infective endocarditis are (in decreasing order of frequency): Mitral valve Aortic valve Combined mitral and aortic valve Tricuspid valve Pulmonary valve - rare

Aetiology

Bacteraemia – dentistry, UTI, urinary catheterization, cystoscopy, resp infection, endoscopy Colon cancer, gall bladder disease, skin disease, IV cannulation, surgery, abortion, fractures. Streps viridans commonest(35-50%), enterococci, staph aureus/ epidermidis, diphteroids, HACEK group, Coxiella burnetti, chlamydia Candida, aspergillus, Histoplasma SLE (libman-Sacks endocarditis), malignancy

Presentations

History

Indolent process	Fatigue; Low-grade fever; Flu-like illness; Polymyalgia-like symptoms; Loss of appetite; Back pain; Pleuritic pain; Abdominal symptoms (may be pain, vomiting and appendicitis-like symptoms); Symptoms akin to rheumatic fever; Weight loss
History of	Invasive procedures Recreational drug use Dental disease Gingivitis - most cases caused by transient bacteraemia from this Symptoms usually arise 2 weeks after invasive procedures but diagnosed after 6 weeks Fewer than half of patients have previously-diagnosed valvular disease
Embolic features	Acute meningitis - signs and symptoms but with sterile CSF Hemiplegia from emboli in the middle cerebral artery (50% of patients may be first manifestation; has high mortality) Renal infarcts causing painless haematuria Splenic infarction causing pain Blindness from retinal artery occlusion Myocardial infarction from emboli in the coronary artery Pulmonary emboli Interstitial nephritis or proliferative glomerulonephritis from deposition of circulating immune complexes Renal failure may result Musculoskeletal symptoms (nearly half of patients) often from immunologically mediated synovitis Immune-mediated vasculitis (causing Osler's nodes and Roth's spots) Palpitations from immune-mediated myocarditis Back pain (15% of patients) may have origin in immune complex deposition in disc spaces

Physical

Fever	elderly, chronically ill patients with subacute IE may not have fever, but the majority do
Heart murmurs	Most patients have a murmur Exception is right-sided IE where one third have murmurs Only 15% have the classic 'changing murmur' Most common murmur is aortic regurgitation
Petechiae	Conjunctivae Hands and feet (dorsum) Chest and abdominal wall Oral mucosae and soft palate
Linear and red	small tender red-to-purple nodules pulp of terminal phalanges fingers and toes
Osler's nodes	small tender red-to-purple nodules pulp of terminal phalanges fingers and toes
Janeway's lesions	irregular painless erythematous macules on the thenar and hypothenar eminence (usually with acute IE and S. aureus)
Clubbing	only 10% of cases and usually in longstanding subacute IE
Roth's spots	retinal haemorrhages with pale centres
Arthritis	With subacute IE usually asymmetric and up to 3 joints affected (fluid sterile) Acute IE can give acute septic monoarticular arthritis
Splenomegaly	most often observed in longstanding subacute disease and often persists after treatment

Diagnosis

Blood cultures	take 3 sets at different time and from different site at peak fever. 85-90% are diagnosed from the first 2 sets. 10% culture negative.
Blood test	normochromic, normocytic anaemia, neutrophil leucocytosis, high ESR/CRP. Also check U&E, Mg, LFT
Urinalysis-	microscopic haematuria
CXR	cardiomegaly
ECG	prolonged P-R interval
Echo TTE	may show vegetation, but only if > 2mm, TOE is more sensitive and better for visualizing mitral lesions and possible development of aortic root abscess.

Duke Criteria

Major Criteria	Minor Criteria
Positive blood culture typical organism in 2 separate cultures or persistently +ve blood cultures, eg 3 >12h apart (or majority if > 4) Endocardium involved +ve echocardiogram (vegetation, abscess, dehiscence of prosthetic valve) new valvular regurgitation (change in murmur nor sufficient)	Predisposition (cardiac lesion, IV drug abuse) Fever > 38C Vascular/immunological signs +ve blood culture that do not meet major criteria +ve echocardiogram that does not meet major criteria

Definite IE: 2 major or 1 major and 3 minor or all 5 minor criteria

Management

Liase early with microbilogist and cardiologist Empirical therapy: benzylpenicilin 1.2g/4h IV + gentamicin eg 1mg/kg/8h IV (serum peak 3-5mg/L & a pre-dose trough of 1mg/L) for 4wks. If acute, add flucloxacilin to cover staphylocicci Enteroccoci: amoxicilin 1g/6h iv + gentamicin as above Streptococci: benzylpenicilin 1.2g/4h IV 2-4wks, then amoxicilin 1g/8h PO for 2wks. Monitor minimum inhibitory concentration (MIC). Add gentamicin Staphilococci : flucloxacilin 2g/6h IV + gentamicin as above IV. Treat for 6-8wks, stop gentamicin after 1wk. If prosthetic valve or MRSA suspected, substitute flucloxacilin with vancomicin + rifampicin Coxiella: doxycilin 100mg/12h PO indefinitely + co-trimoxazole, rifampicin or ciprofloxacilin Fungi: flucytosine 50mg/kg/6h IVI over 30min followed by fluconazole 50mg/24h PO (higher dose may be needed) Amphotericin if flucytosine or Aspergillus. Miconazole if renal fn is poor.z Surgery is needed in approximately 50% of patients who develop infective endocarditis and careful timing is essential to ensure a good outcome

Complications:

Valve dysfunction Myocardial abscesses Embolic phenomena Heart failure Metastatic infection Immunological disease and organ dysfunction Complications even after bacteriological cure Conduction defects (patients with IE should have daily ECGs)

Prognosis

This varies markedly according to a variety of factors. The following outlines the range of prognosis when managed appropriately: Native valve endocarditis: S. viridans 98% cure rate S. aureus 60-90% cure rate with worse results in occurring in those NOT abusing intravenous drugs Fungal infections - cure rate less than 50% PVE: Cure rates at least 10% lower than above for each variety Surgery needed more often