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Spontaneous intestinal perforation and lack of efficacy: case report An 8-day-old male neonate developed spontaneous intestinal perforation following treatment with indometacin, dobutamine and dopamine. He also exhibited lack of efficacy during treatment with indometacin. The male neonate was born at 26 weeks and 5 days of gestational age, with a birth weight of 1100g from a CMV-seropositive mother. His Apgar score was 1 at 1 minute and 5 minute, respectively. Initially, he received unspecified treatment for dyspepsia, respiratory distress syndrome and symptomatic patent ductus arteriosus (PDA). On day 1 of his life, he was initiated with indometacin [indomethacin] and inotropic support including dopamine and dobutamine [dosages and routes not stated]. However, treatment with indometacin was ineffective. On day 3 of life, he was transferred to the hospital for PDA surgery. Subsequent examination was unremarkable for microcephaly, hepatosplenomegaly, rash, jaundice and any neurologic signs. No abnormal findings were noted on blood test. Blood coagulation test was also normal. On the same day, he underwent ligation of the PDA and he was stabilised haemodynamically. On day 4 of life, he started receiving formulated milk feeding, to which unpasteurised breast milk was added on day 7 of his life. However, the dyspepsia was persisting and he developed abdominal distention, therefore, enteral feeding was stopped on day 7 of his life. He was fasted and treated with hyperosmolar enemas; however, he had limited effect. On day 8 of life, abdominal X-ray showed pneumoperitoneum. Subsequent laparotomy showed a perforation of the terminal ileum on the mesenteric side, which was opposite to predilection site of necrotising enterocolitis (NEC). Therefore, the neonate underwent a resection of the perforated site with ileostomy construction. He received packed RBCs during the operation on day 8 of life. The resected ileum examination revealed non-specific inflammatory changes which were consistent with enterocolitis. Cytomegalovirus (CMV) inclusion bodies were not identified. The dyspepsia was still persisting. On day 14 of his life, he exhibited elevated hepatic transaminases. On day 17 of his life, he exhibited abdominal distension again. Abdominal X-ray showed recurrence of pneumoperitoneum. The laparotomy was performed and a perforation was noted at proximal side to the ileostomy. On day 28 of life, serum anti-CMV IgG and IgM were found to be positive. Subsequent pathological examination of the second operation demonstrated CMV intranuclear inclusion bodies in the endothelium of lamia propria. Immunostaining for CMV of the intestinal specimen at first surgery showed small amount of CMV positive cells. Both urine and blood test showed presence of CMV-DNA. The CMV-DNA were also detected in the dried umbilical cord obtained within a week of his life, which suggested that he had a prenatal transmission of CMV from his mother. He was subsequently initiated with off-label IV ganciclovir 12 mg/kg/day for 6 weeks for CMV infection.