INFECTIVE ENDOCARDITIS
Infective endocarditis (IE) is an important cause of mortality and morbidity in children with pre-existing heart diseases, defined as the infection of mural or valvular endocardium or endothelium of great vessels adjacent to heart (endarteritis).
Etiology: S. viridans and Staph. aureus are leading causes of IE, though others, e.g. enterococci, gram negative organisms, e.g. Pseudomonas and fungal infections, e.g. C. albicans are emerging as important pathogens in partially-treated, immunocompromised or nosocomial cases.
Etiopathogenesis: IE is extremely rare in normal heart, with almost all cases having pre-existing CHD/RHD or postoperative nidus, e.g. Blalock-Taussig shunt or valvular prosthesis. IE is more common in VSDs, ToF, AS and AR and rare with PS, ASD and PDA.
Source of infection is usually a distant septic focus, e.g. dental, ENT or skin infections or surgical interventions, e.g. cardiac catheterization, genitourinary surgery or dental procedures. Cardiac infection generally begins at the site of damaged endocardium, where high- pressure jet of blood flow is directed. Hence, IE lesions are usually right ventricular in VSD, left ventricular in AR and over aortic endothelium in AS or coarctation of aorta. Localization of infection at affected site initiates inflammatory response with accumulation of fibrin and platelets, leading to formation of vegetations- the pathognomonic of IE. Vegetations in IE are typically small, friable and easily detachable to cause thromboembolic complications.
Clinically, IE presents as acute or subacute illness with:
• Persistent fever with chills and constitutional features, e.g. weight loss, anorexia and night sweats.
• Cardiac signs of endomyocardial injury, e.g.
- New or changing murmurs
- Cardiomegaly and/or refractory CCF
• Peripheral signs of vasculitis, e.g.
- Splenomegaly
- Moderate to severe anemia
- Microscopic or gross hematuria
- Clubbing and splinter hemorrhages over nails
- Petechiae lesions over skin/mucus membranes
- Roth spots-petechiae over retina
- Osler nodes-tender erythematous nodules over finger pulp
- Janeway lesions-non-tender erythematous patches over palm and soles
• Signs of thromboembolic complications, e.g.
- Metastatic systemic abscesses in left-sided IE
- Pulmonary embolism in right-sided IE.
Diagnosis of IE must be considered in any cardiac case with persistent unexplained fever, especially if the triad of clubbing, splenomegaly and marked pallor is present. It is confirmed by:
• Blood cultures: Since bacteremia in IE is low-grade and intermittent, preferably six or at least three samples of minimum 10 ml each, should be collected at frac12; hourly interval for aerobic, anaerobic and fungal cultures. However, cultures are negative in ~50% cases, specially after partial antibiotic therapy and do not exclude IE.
• Echocardiography is extremely valuable to demonstrate vegetations or secondary lesions, e.g. ruptured chordae or perforated cusps, etc. LV lesions are better visualized (90%) than RV lesions (70%). However, small vegetations of lt;2 mm can be easily missed and a negative ECHO does not exclude IE.
• Supportive investigations include hemogram for normocytic, normochromic anemia, thrombocytopenia and raised ESR; as well as urinalysis for microscopic hematuria/albuminuria, which is present in gt;90% cases.
Duke criteria (1994) may be used to assist diagnosis of IE, based on the presence of—(a) any two major or (b) one major and 3 minor criteria or (c) five minor criteria. Diagnosis is considered as quot;possiblequot; if only 1 major and 1 minor criteria or only 3 minor criteria are fulfilled.
• Major criteria include—(a) positive blood culture on at least two separate samples, and (b) echocardiographic evidence of intracardiac mass, abscess, prosthetic valve dehiscence or new valvular regurgitation.
• Minor criteria include—(a) predisposing factor, e.g. heart disease, (b) fever, (c) immunological phenomena, e.g. glomerulonephritis, arthritis, Osler nodes, Roth spots, etc. (d) vascular phenomena, e.g. major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions, etc., and (e) single positive blood culture or serologic evidence of infection.
Treatment: Early and appropriate, essentially intravenous, antimicrobial therapy in high doses for minimum
4-6 weeks is the mainstay of treatment in IE. Important steps in management of IE include:
a. Empirical therapy, before the culture reports or in cases with negative cultures. Currently, drugs of choice for native valve IE is Ampicillin+Sulbactum (300 mg/kg/d Q4-6 hr) with Gentamycin (3 mg/ kg/d q8hr) for 4-6 weeks. Vancomycin (40 mg/kg/d q8 hr) may be used in cases with penicillin allergy or suspected staphylococcal IE, along with Gentamycin and ciprofloxacin (20-30 mg/kg/d q12 hr).
More intensive therapy is required in cases with prosthetic valves of 1 year with Vancomycin plus gentamycin plus cefepime plus Rifampicin.
b. Specific antimicrobial therapy is instituted after culture reports and sensitivity profile (Table 17.29), which should continue for min 4-6 weeks.
c. Supportive therapy includes treatment of CCF, anemia and symptomatic management.
d. Surgical intervention is indicated in cases with ruptured aortic sinus, aneurysms, intractable CCF with severe valvular lesion (AR/MR) and failure of medical treatment.
Prevention: Antimicrobial prophylaxis (Table 17.30) prior to dental or other surgical procedures is essential to prevent IE in cases with heart disease, along with maintenance of good oral hygiene and early diagnosis and treatment of common infections.
IE prophylaxis is not recommended for ostium secundum ASD and mitral valve prolapse without
TABLE 17.30: Antimicrobial prophylaxis for IE
*in penicillin allergic cases
regurgitation. After cardiac surgery or device closure, it is recommended only during first six post-operative months, unless residual lesion is present.
17.9