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 4,305 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neonatal intussusception is an uncommon disease. We report a case of neonatal ileoileocolic intussusception led by an ileal polyp in a female neonate. The patient presented with irritable crying, bilious vomiting and frank bloody stool on the 26th day of life. On physical examination, a mobile abdominal mass was palpated. Abdominal sonography demonstrated a long segment intussusception; associated with a low echogenic mass. At laparotomy, ileoileocolic intussusception led by an ileal polyp was found. Pathology confirmed the diagnosis of polyp. Because intestinal obstruction is the primary manifestation, neonatal intussusception is initially indistinguishable from obstructions due to other reasons like intestinal atresia, congenital bands, necrotizing enterocolitis or midgut volvulus. Our experience showed that although uncommon, intussusception should be considered in the differential diagnosis of intestinal obstruction during the newborn period.
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PMID:Neonatal ileoileocolic intussusception associated with ileal polyp: report of one case. 968 29

We analyzed clinical, biochemical, and histo- logic parameters of ten infants with parenteral nutrition-induced hepatobiliary dysfunction. The data were compared with the results of a rabbit model. All infants were born prematurely with low birth weight. Their clinical diagnoses were necrotizing enterocolitis (6), gastroschisis (1), intrauterine volvulus (1), and lung hypoplasia (2). All required total (TPN) or partial parenteral nutrition for at least 8 weeks. All had repeated episodes of infections or sepsis. A rise in bilirubin and aminotransferase levels occurred after a minimum of 5 weeks; peak bilirubin levels ranged from 4 to 14 mg% and aminotransferases from 40 to 140 IU/l. One child later developed gallstones. Liver biopsies after 1 to 24 months showed fibrosis, bile-duct proliferation, cholestasis, and hydropic degeneration. All of the above-mentioned clinical factors have been accused of causing the observed biochemical and histologic changes. In our rabbit model we were able to produce almost identical symptoms by TPN alone: gallbladder distension, sludge, and stones developed after 1-4 weeks of TPN as well as uncharacteristic changes in aminotransferases and bilirubin after 4 weeks. Liver histology revealed severe hydropic degeneration of zone 3 as early as 1 week after beginning TPN. A rise of fibrosis and bile-duct proliferation after 1 to 4 weeks of infusion was statistically significant. Cholestasis, as was observed in the infants, could not be detected. In our model, all alterations observed could be attributed exclusively to TPN. We therefore assume that TPN was the true cause of the dysfunction. In a second experimental series infusions were reduced to 80% PN and free access to lab chow. These animals produced normal feces, indicating physiologic enteral stimulation. They developed the same degenerative and proliferative histologic changes, whereas gallbladder distension, sludge, and stones were not noted. We conclude that: (1) The TPN solution itself is responsible for the histologic changes in the liver, which is supported by the fact that hydropic degeneration of zone 3 is typical of a direct toxic effect; and (2) Complete enteral starvation with an absence of enteral stimulation causes disease of the lower biliary tract.
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PMID:Parenteral nutrition-induced hepatobiliary dysfunction in infants and prepubertal rabbits. 1052 3

Short-bowel syndrome (SBS) either in adults or in children is considered as an indication to small-bowel transplantation (SBTx), particularly in its most severe form with a residual bowel length below 20 cm. Among factors likely to worsen the prognosis, more recent reports also indicate the number of surgical interventions, early onset sepsis and early development of liver disease. We report six cases of ultra-short-bowel syndrome followed from birth to verify the importance of various prognostic factors. In our case series, the male sex is predominating (5:1). Intestinal resection was indicated in 3 patients for multiple intestinal atresias, in 2 for volvulus and in 1 for necrotizing enterocolitis. The length of intestine remaining was invariably less than 20 cm and 2 patients had a preserved ileocecal valve. In most cases, more than 50% of the colon remained. The number of abdominal operations ranged from 1 to 4. In almost all cases (5 of 6), sepsis and hepatopathy developed early. Our experience suggests that rather than depending on the length of intestine remaining or the presence of the ileocecal valve, the prognosis of patients with the extreme-short-bowel syndrome depends on recurrent neonatal onset sepsis and early onset liver impairment. In addition, our case review shows that the extreme-short-bowel syndrome is not necessarily an indication for bowel transplantation.
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PMID:Ultra-short-bowel syndrome is not an absolute indication to small-bowel transplantation in childhood. 1053 74

Among 36 neonates with intestinal perforations (IP) between 1975 and 1996, 5 had necrotizing enterocolitis (NEC IP) and 10 had focal IPs (FIP). A histologic review of the bowel near the perforations was made to see if there was any difference between cases of NEC IP and FIP. In 1 case of NEC IP, a defect in the musculature was found in addition to disappearance of the mucosal villi and dilated vessels or hemorrhage in the submucosa. Thinning or absence of the intestinal musculature and short villi in the mucosa was observed in 3 cases of FIP, but the acute ischemic changes in FIP were much less than in NEC IP. Hypothesizing that the defective musculature in FIP may be acquired by a vascular accident either before or after birth, we examined the histology of the latest consecutive infants diagnosed as having meconium peritonitis (MP) due to in-utero volvulus and perforation. In the tissue near the perforation, there was an identical focus of thinning and interruption of the musculature while the acute ischemic changes were minimal. We speculate that thinning or absence of the intestinal musculature in FIP may be a result of a transient ischemic event occurring in-utero and that FIP may develop in the damaged intestine after birth when it is fully dilated.
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PMID:The mechanism of focal intestinal perforations in neonates with low birth weight. 1063 31

A case history of a fatal neonatal infection caused by Salmonella enteritidis group D is reported. The baby deteriorated rapidly at 24 hours after birth with clinical signs and symptoms of an acute abdomen. Bloody diarrhea led to a tentative diagnosis of midgut volvulus or necrotizing enterocolitis. Autopsy and bacteriologic investigation revealed sepsis by S. enteritidis group D. The same organism was found in cultures taken from stool and vaginal swabs from the mother. This clearly confirmed transmission of the infection during delivery.
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PMID:Fatal neonatal Salmonella enteritidis sepsis. 1069 1

Bilious vomiting in newborns is an urgent condition that requires the immediate involvement of a team of pediatric surgeons and neonatologists for perioperative management. However, initial detection, evaluation and treatment are often performed by nurses, family physicians and general pediatricians. Bilious vomiting, with or without abdominal distention, is an initial sign of intestinal obstruction in newborns. A naso- or orogastric tube should be placed immediately to decompress the stomach. Physical examination should be followed by plain abdominal films. Dilated bowel loops and air-fluid levels suggest surgical obstruction. Contrast radiography may be required. Duodenal atresia, midgut malrotation and volvulus, jejunoileal atresia, meconium ileus and necrotizing enterocolitis are the most common causes of neonatal intestinal obstruction.
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PMID:Bilious vomiting in the newborn: rapid diagnosis of intestinal obstruction. 1082 Nov 58

The loss of small intestinal mucosal surface area is a relatively common clinical situation seen in both the pediatric and adult population. The most frequent causes include mesenteric ischemia, trauma, inflammatory bowel disease, necrotizing enterocolitis, and volvulus. Following surgical resection, the remnant intestine compensates or adapts to the loss of native bowel by increasing its absorptive surface area and functional capacity. Unfortunately, many patients fail to adapt adequately, and are relegated to lifelong intravenous nutrition. Research into intestinal adaptation following small bowel resection (SBR) has evolved only recently from the gross and microscopic level to the biochemical and genetic level. As understanding of this process has increased, numerous therapeutic strategies to augment adaptation have been proposed. Epidermal growth factor (EGF) is an endogenous peptide that is secreted into the gastrointestinal tract and able to influence gut ontogeny, as well as mucosal healing. Early studies have demonstrated its ability to augment the adaptive process. Focusing on a murine model of massive intestinal loss, the morphological, structural, biochemical, and genetic changes that occur during the intestinal adaptive process will be reviewed. The role of EGF and its receptor as critical mediators of the adaptive process will be discussed. Additionally, the ability of EGF to augment intestinal proliferation and diminish programmed cell death (apoptosis) following SBR will be examined. Enhancing adaptation in a controlled manner may allow patients to transition off parenteral nutrition to enteral feeding and, thereby, normalize their lifestyle.
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PMID:Epidermal growth factor is critical for intestinal adaptation following small bowel resection. 1105 64

Short bowel syndrome is a spectrum of malnutrition resulting from inadequate bowel length. In infant and pediatric patients, the most common causes are necrotizing enterocolitis, abdominal wall defects, jejunal ileal atresia, and mid gut volvulus. There appear to be regional variations in etiology. Since the publication of Wilmore's classic monograph in 1972, there have been significant improvements in monitoring and nutritional support. In the modern era, survival rate ranges from 80% to 94%, and the presence or absence the ileal cecal valve appears to not impact on mortality rate, but does significantly affect the length of time on total parenteral nutrition TPN. The most common morbidities remain sepsis, both central line related and bacterial overgrowth, and TPN cholestasis. Long-term recovery of these children often is remarkably normal, but there is a 10% to 15% incidence of neurologic and developmental defects. The clinical and ethical considerations around the care of infants with 20 to 40 cm of residual bowel remains controversial, as does the place of intestinal transplantation, especially in patients developing gut failure in infancy. Perioperative surgical decision making plays a critical role in the long-term outcome of these patients. This chapter presents an overview of the current status of care and outcome in this difficult population; these topics are further expanded in subsequent chapters.
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PMID:Short bowel syndrome in infants and children: an overview. 1132 5

Intestinal failure requiring total parenteral nutrition (TPN) is associated with significant morbidity and mortality. Intestinal transplantation can be a lifesaving option for patients with intestinal failure who develop serious TPN-related complications. The aim of this study was to evaluate survival, surgical technique, and patient care in patients treated with intestinal transplantation. We reviewed data collected from 95 consecutive intestinal transplants performed between December 1994 and November 2000 at the University of Miami. Fifty-four of the patients undergoing intestinal transplantation were children and 41 were adults. The series includes 49 male and 46 female patients. The causes of intestinal failure included mesenteric venous thrombosis (n = 12), necrotizing enterocolitis (n = 11), gastroschisis (n = 11), midgut volvulus (n = 9), desmoid tumor (n = 8), intestinal atresia (n = 6), trauma (n = 5), Hirschsprung's disease (n = 5), Crohn's disease (n = 5), intestinal pseudoobstruction (n = 4), and others (n = 19). The procedures performed included 27 isolated intestine transplants, 28 combined liver and intestine transplants, and 40 multivisceral transplants. Since 1998, we have been using daclizumab (Zenepax) for induction of immunosuppression and zoom videoendoscopy for graft surveillance. We began to use intense cytomegalovirus prophylaxis and systemic drainage of the portal vein. The 1-year patient survival rates for isolated intestinal, liver and intestinal, and multivisceral transplantations were 75%, 40%, and 48%, respectively. Since 1998, the 1-year patient and graft survival rates for isolated intestinal transplants have been 84% and 72%, respectively. The causes of death were as follows: sepsis after rejection (n = 14), respiratory failure (n = 8), sepsis (n = 6), multiple organ failure (n = 4), arterial graft infection (n = 3), aspergillosis (n = 2), post-transplantation lymphoproliferative disease (n = 2), intracranial hemorrhage (n = 2), and fungemia, chronic rejection, graft vs. host disease, necrotizing enterocolitis, pancreatitis, pulmonary embolism, and viral encephalitis (n = 1 case of each). Intestinal transplantation can be a lifesaving alternative for patients with intestinal failure. The prognosis after intestinal transplantation is better when it is performed before the onset of liver failure. Rejection monitoring with zoom videoendoscopy and new immunosuppressive therapy with sirolimus, daclizumab, and campath-1H have contributed to the improvement in patient survival.
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PMID:Ninety-five cases of intestinal transplantation at the University of Miami. 1199 9

In a current publications, it has been suggested that hypoxia-triggered "good angiogenesis" involving hypoxic up-regulation of vascular endothelial growth factor (VEGF) molecules, genes, and receptors is likely responsible in a major way for the remarkable gut and patient salvage experience associated with use of the "patch, drain, and wait" (PD&W) surgical approach to perforated necrotizing enterocolitis and midgut volvulus (MGV) with extensive ischemia/necrosis. We report a case in which extensive ischemia/necrosis in a newborn with gastroschisis (likely MGV-induced) was managed successfully by PD&W with an associated marked (24-fold) elevation of VEGF in drainage fluid at 7 days post-initiation of PD&W.
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PMID:Marked (24-fold) elevation of peritoneal cavity drainage fluid vascular endothelial growth factor after successful "patch, drain, and wait" approach for extensive midgut necrosis in a newborn. 1241 65


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