Infective endarteritis in a 2-month-old infant associated with silent patent ductus arteriosus / Sessiz patent ductus arteriozus'lu 2 aylik bir cocukta infektif endarterit.
Infective endarteritis (IE), which was a serious complication of clinically apparent patent ductus arteriosus (PDA), has become extremely rare because of early closure of PDA (1-3). However, it is not known if silent PDA, which is not detectable by cardiac auscultation but can be recognized only by colored-flow echocardiography, increases the risk of IE or not (4). Thus, antibiotic prophylaxis or closure of silent PDA against the risk of IE is not recommended (4-6). There are only a few reports of IE associated with silent PDA in medical literature (7, 8). In this article a case of IE in a 2 month-old infant with silent PDA is reported.
A 2-month-old male infant was hospitalized because of fever lasting for three days. His physical examination revealed 37.6 C[degrees] axillary's temperature, mild pharyngeal erythema, 2 cm hepatomegaly below the right lower costal margin, but no pathological heart sound or murmur and no splenomegaly.
Physical examinations of the other systems were normal. The patient was not anemic, the number of thrombocytes was normal and the white blood cell count was 10600/[mm.sup.3] with the dominancy of polymorphonuclear granulocytes. Erythrocyte sedimentation rate was 34 mm/hour. Urine analysis, serum urea, creatinine, aspartate aminotransferase and alanine aminotransferase, immunoglobulin levels were normal. [beta]-hemolytic, group D streptococcus was grown in his blood culture after three days of his admission to the hospital. The 2-dimensional and color Doppler echocardiography was performed to investigate the origin of bacteremia. It revealed 2 vegetations with the diameters of 2.5 and 2.9 mm on the left side of the wall of the main pulmonary artery, and very tiny retrograde turbulent flow into the left side of main pulmonary artery consistent with PDA (Fig. 1, 2a). Continuous flow pattern that was typical for PDA was hardly demonstrated by HPRF Doppler (Fig. 2b). There was no sign of pulmonary hypertension or widening of the left heart chambers as a sign of left ventricular volume overload. Treatment with penicillin G and gentamicin was started according to antibiogram. He became afebrile two days after the treatment, blood culture that was obtained one week later after the beginning of the treatment became sterile. The patient completed six-week course of antibiotics. The size of the vegetation decreased and eventually disappeared. Patency of ductus arteriosus that was not detectable by auscultation persisted after the patient was 6 months old at follow-up. Sweat test, employed because of family history of cystic fibrosis in a brother and asymptomatic high level of sweat chloride in his mother, revealed a chloride level of 68 mEq/L. Later development of frequent lower respiratory tract infections, pseudo-Bartter syndrome that was recognized by alkalosis associated with hypokalemia and positive F508 mutation test confirmed the diagnosis of cystic fibrosis. Transcatheter closure of the PDA was suggested but the family preferred surgical ligation. Thoracotomy without cardiopulmonary bypass revealed presence of small PDA and uneventful ligation of the PDA was performed at age of six months.
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During the pre-antibiotic era, IE was a fatal complication of PDA and the annual risk of IE in these patients was estimated to be 0-45% (1, 2). Especially in the industrialized world, infective endarteritis complicating PDA is very rare nowadays and the risk is very low (3, 5). Fatal cases of IE complicating patent ductus arteriosus were associated with large ductus. It is assumed that a small duct to be less susceptible than a large one to IE (5, 6). On the other hand, in developing countries the incidence of IE complicating patent ductus arteriosus is much closer to the natural history of PDA in pre-antibiotic era (9). Every isolated PDA with an audible and typical continuous murmur should be closed irrespective of the size, because untreated persistent ductus arteriosus is a favorable site of IE (5, 6). Surgical or transcatheter occlusion of PDA eliminates the risk of I E.
The term silent ductus arteriosus was coined to describe the preterm infant with respiratory distress syndrome in whom continuous murmur is not heard (4). Doppler ultrasonography has made possible to detect very small PDA that can not be identified clinically. Houston et al (4) suggested that some patients considered to have IE with a normal heart might have a silent PDA or evidence of such an association would justify ligation or antibiotic cover as prophylactic measures. However, they did not recommend endocarditis prophylaxis for every silent ductus.
There is no currently published evidence that the incidence of IE in patients with hemodynamically trivial, silent PDA have increased. But Balzer et al (7) reported a case of endarteritis associated with a clinically silent PDA. They suggested that all cases of PDAs regardless of its clinical characteristics should be closed. We also report a case of IE associated with silent PDA. We think that cystic fibrosis is a coincidence since it is obvious that the incidence of IE has not been increased in patients with cystic fibrosis. Estimated prevalence of silent PDA's were found as 0.5-1% in normal population, but IE associated with silent PDAs were reported in only few patients before the present case (7, 8). On the other hand residual shunts, which are usually inaudible or associated with nonspecific systolic murmur, are not uncommon in patients who underwent transcatheter closure of PDA. Latson and his associates (10) reported that patients with silent PDA after device occlusion are not at a higher risk for developing endocarditis.
Although the natural history of a small patent arterial duct with a negligible left to right shunt is not known with certainty, this and previous reports may indicate that silent PDA has a risk of developing IE. In cases of unexplained fever and bacteremia, endarteritis with a pre-existing silent PDA should be considered and investigated by 2-dimensional and color Doppler echocardiography. But, it cannot be recommended that antibiotic prophylaxis or closure of every silent PDA routinely unless exact incidence of IE will be cleared out by long-term prospective studies in patients with silent PDA.
(1.) Campbell M. Natural history of persistent ductus arteriosus. Br Heart J 1968; 30: 4-13.
(2.) Johnson DH, Rosenthal A, Nadas AS. A forty-year review of bacterial endocarditis in infancy and childhood. Circulation 1975; 5: 581-8.
(3.) Thilen U, Astrom-Olsson K. Does the risk of infective endarteritis justify routine patent ductus arteriosus closure? Eur Heart J 1997; 18: 503-6.
(4.) Houston AB, Gnanapragasam JP, Lim MK, Doig WB, Coleman EN. Doppler ultrasound and the silent ductus arteriosus. Br Heart J 1991; 65: 97-9.
(5.) Huggon IC, Qureshi SA. Is the prevention of infective endarteritis a valid reason for closure of the patent arterial duct? Eur Heart J 1997;18: 364-6.
(6.) Sullivan ID. Patent arterial duct: when should it be closed? Arch Dis Child 1998; 78: 285-7.
(7.) Balzer DT, Spray TL, McMullin D, Cottingam W, Canter CE. Endarteritis associated with a clinically silent patent ductus arteriosus. Am Heart J 1993; 125: 1192-3.
(8.) Parthenakis F I, Kanakaraki M K, Vardas P E. Silent patent ductus arteriosus endarteritis. Heart 2000; 84: 619.
(9.) Sadiq M, Farhan L, Asif U-R. Analysis of infective endocarditis in patent ductus arteriosus. Am J Cardiol 2004; 93: 513-5.
(10.) Latson LA, McManus BM, Doer C, Kilzer K, Cheatham JP. Endocarditis risk of the USCI PDA umbrella for transcatheter closure of patent ductus arteriosus. Circulation 1994; 90; 2525-8.
Ahmet Celebi, Abdullah Erdem, Haluk Cokugras *, Gulay Ahunbay **
Department of Pediatric Cardiology, Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Center and Research Hospital Departments of * Pediatric Cardiology and ** Pediatric Infectious Disease, Cerrahpasa Medical Faculty University of Istanbul, Istanbul, Turkey
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|Title Annotation:||Case Reports / Olgu Sunumlari|
|Author:||Celebi, Ahmet; Erdem, Abdullah; Cokugras, Haluk; Ahunbay, Gulay|
|Publication:||The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)|
|Article Type:||Case study|
|Date:||Sep 1, 2007|
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