29  Infective Endocarditis

Author

Dr Samuel Blay Nguah

29.1 Definition

Infective endocarditis (IE) is an infection of the endocardial surface of the heart, typically involving one or more heart valves. It can be caused by bacteria, fungi, or other pathogens, leading to the formation of vegetation on the heart valves or endocardium. A serious condition that can result in significant morbidity and mortality without prompt diagnosis and treatment.

29.2 Incidence/Prevalence

Rare in children, with an estimated incidence of 0.05–0.12 cases per 1,000 pediatric hospital admissions. More common in children with underlying congenital heart disease (CHD), accounting for up to 80% of cases. Increasing prevalence due to improved survival rates of children with CHD and the use of indwelling central venous catheters. Higher incidence in children with prosthetic heart valves or those who have undergone cardiac surgery.

Aetiology

  • Microorganisms:

    • Bacteria: Most common cause, including Streptococcus viridans, Staphylococcus aureus, and Enterococcus species.
    • Fungi: Less common, but Candida and Aspergillus can cause IE, particularly in immunocompromised patients
  • Risk Factors:

    • Congenital heart defects, particularly cyanotic lesions.
    • Prosthetic heart valves.
    • Indwelling devices (e.g., pacemakers, central venous catheters).
    • Rheumatic heart disease (rare in developed countries).
    • Immunosuppression or intravenous drug use (less common in pediatrics).

Pathophysiology

  • Initial endothelial damage due to turbulent blood flow or direct trauma (e.g., from catheters).
  • Formation of sterile thrombotic vegetations at the site of damage.
  • Colonization of vegetations by microorganisms during transient bacteremia.
  • Vegetations grow, consisting of microorganisms, fibrin, and platelets.
  • Can result in local destruction of heart structures, systemic embolization, and immune-mediated complications (e.g., glomerulonephritis).

Signs and Symptoms

  • Non-specific symptoms:

    • Fever (most common presenting symptom).
    • Fatigue, malaise, anorexia, weight loss
  • Cardiac manifestations:

    • New or changing heart murmur.
    • Signs of heart failure (e.g., dyspnea, tachypnea, peripheral edema)
  • Systemic features:

    • Petechiae, splinter hemorrhages.
    • Osler nodes (painful nodules on fingers/toes).
    • Janeway lesions (painless macules on palms/soles).
    • Roth spots (retinal hemorrhages with central clearing).
  • Embolic phenomena:

    • Stroke or other neurologic deficits.
    • Splenic or renal infarction.
    • Pulmonary emboli in right-sided IE.
  • Symptoms may be less pronounced in children, particularly in chronic or subacute presentations.

Investigations

  • Blood cultures:
    • Essential for diagnosis; obtain at least three sets before starting antibiotics.
    • May reveal causative organism in >90% of cases if appropriately timed.
  • Echocardiography:
    • Transthoracic echocardiography (TTE): Initial investigation; non-invasive.
    • Transesophageal echocardiography (TEE): Higher sensitivity, especially for prosthetic valves or difficult-to-image cases
  • Laboratory tests:
    • Full blood count: May show anemia, leukocytosis, or thrombocytopenia.
    • Inflammatory markers: Elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)
    • Renal function and urinalysis: May detect embolic phenomena or immune-mediated injury.
  • Imaging:
    • Chest X-ray: Evaluate for heart failure or pulmonary embolism in right-sided IE
    • CT or MRI: Assess embolic complications (e.g., stroke, abscess).

Treatment

  • Antimicrobial therapy:
    • Empiric treatment with broad-spectrum antibiotics after blood cultures are drawn.
    • Tailor therapy based on culture results and sensitivity testing.
    • Prolonged intravenous antibiotics (typically 4–6 weeks).
  • Surgical intervention:
    • Indicated for severe valvular damage, heart failure, abscess formation, or persistent infection despite antibiotics.
    • Often required for prosthetic valve endocarditis.
  • Supportive care:
    • Management of heart failure or other complications.
    • Anticoagulation generally avoided due to risk of embolization from vegetations

Complications

  • Cardiac complications:
    • Valvular dysfunction (regurgitation or stenosis).
    • Heart failure.
    • Perivalvular abscess.
    • Conduction disturbances (e.g., heart block).
  • Embolic events:
    • Stroke, myocardial infarction, or organ infarctions.
    • Septic emboli causing abscesses.
  • Systemic complications:
    • Immune complex-mediated glomerulonephritis.
    • Disseminated infection or sepsis
  • Prosthetic valve complications:
    • Dehiscence or dysfunction requiring reoperation

Prognosis

  • Depends on the underlying cause, diagnosis timeliness, and treatment appropriateness.
  • Mortality rates in children range from 10% to 25%, higher in fungal infections or prosthetic valve IE.
  • Early surgical intervention improves outcomes in high-risk cases.
  • Long-term follow-up necessary for valve function and detection of late complications.

Differential Diagnosis

  • Non-infective causes of endocarditis-like features:
    • Non-bacterial thrombotic endocarditis (marantic endocarditis).
    • Libman-Sacks endocarditis (associated with systemic lupus erythematosus)
  • Conditions with overlapping symptoms:
    • Rheumatic fever.
    • Systemic vasculitis (e.g., Kawasaki disease, polyarteritis nodosa).
    • Malignancy (e.g., leukemia).
    • Infectious diseases (e.g., osteomyelitis, septic arthritis, tuberculosis)
  • Other cardiac conditions:
    • Myocarditis.
    • Pericarditis.
    • Congenital heart disease exacerbations.

This outline provides a structured approach for understanding infective endocarditis in children and serves as a foundation for deeper study. Let me know if you need any sections expanded or clarified.