Infective endocarditis

IE is characterized by infection of the endocardial surface of the heart. It may be classified as acute, subacute, or chronic, depending on the time course of the infection. It is now more commonly classified according to the type of valve (native or prosthetic) and the aetiological agent (e.g. staphylococcal, streptococcal, enterococcal, fungal, culture negative, etc.).

Epidemiology

The incidence of IE is estimated to be 0.16– 5.4 cases per 1000 hospital admissions. Most patients are aged 30– 60 years; male > female. The disease is uncommon in children in the absence of a predisposing condition. Risk factors include congenital heart disease, rheumatic heart disease, degenerative heart disease, prosthetic valves, IVCs, IDU, and mitral valve prolapse.

Pathogenesis

The development of IE requires the simultaneous occurrence of a number of events: alteration of the valvular surface, deposition of platelets and fibrin, colonization by bacteria, bacterial multiplication, and development of a vegetation.

Causes

  • Eighty per cent of cases of native valve endocarditis are due to streptococci (viridans group, S. gallolyticus) or staphylococci.
  • S. aureus is the commonest isolate in IDUs and tricuspid valve IE.
  • S. epidermidis is the commonest isolate in early (<2 months) prosthetic valve endocarditis (PVE).
  • Enterococcal endocarditis is usually associated with malignancy or manipulation of the GU or GI tracts.
  • Other organisms, e.g. Corynebacteria, Listeria, Bacillus, Salmonella, E. coli, Enterobacter, Citrobacter, and Pseudomonas spp., are uncommon.
  • HA CEK organisms or fungi are associated with large vegetations.
  • Culture- negative endocarditis (75%) may be caused by C. burnetii, Chlamydia spp., Legionella spp., M. pneumoniae, Bartonella spp., and Brucella spp.
  • Polymicrobial infections occur in 1– 2%.

Clinical features

  • The incubation period may vary from days to weeks
  • Symptoms are protean and include fever, chills, weakness, dyspnoea, sweats, anorexia, weight loss, malaise, cough, skin lesions, stroke, nausea, vomiting, headache, myalgia, arthralgia, oedema, chest pain, abdominal pain, delirium, coma, haemoptysis, and back pain.
  • Physical findings include fever, cardiac murmur, Roth spots, clubbing, splinter haemorrhages, Osler’s nodes, Janeway lesions, petechiae, peripheral emboli, splenomegaly, and septic complications (pneumonia, meningitis, mycotic aneurysms

Laboratory diagnosis

  • BCs are positive in approximately two- thirds of cases. Three BC sets should be obtained in the first 24h and incubated for 3 weeks.
  • Blood tests may show elevated ESR (90– 100%), anaemia (70– 90%), leucocytosis (20– 30%), leucopenia (5– 15%), and thrombocytopenia (5– 15%). Hypergammaglobulinaemia (20– 30%) may result in falsepositive results for rheumatoid factor and VDRL. Renal impairment and hypocomplementaemia occur in 5– 15%.
  • Urinalysis is frequently abnormal with proteinuria (50– 60%), microscopic haematuria (30– 60%), gross haematuria, pyuria, bacteriuria, red cell casts, and white cell casts.
  • Serology is useful for diagnosis of culture- negative endocarditis.
  • Echocardiography— transthoracic echocardiography (TT E) allows visualization of vegetations in 60– 75% of cases, compared with >95% with transoesophageal echocardiography (TOE).
  • ECG— lengthening of the PR interval in aortic valve endocarditis indicates aortic root involvement.

Management

  • Antimicrobial therapy
  • Surgery is indicated in patients with life- threatening CCF or cardiogenic shock due to surgically treatable valvular disease, if the patient has a reasonable prospect of recovery. Surgery is recommended for annular or aortic abscesses, heart block, recurrent emboli on therapy, antibioticresistant infections, and fungal endocarditis

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