Primary reversed gastric tube reconstruction in long gap esophageal atresia.

BACKGROUND/PURPOSE: Esophageal reconstruction in long-gap esophageal atresia (EA) poses a technical challenge with several surgical options. The purpose of this study was to review the authors' experience with the reversed gastric tube (RGT) in esophageal reconstruction. METHODS: This series describes 7 babies with pure EA treated at 2 centers between 1989 and 2001. Data, gathered by retrospective chart review, included clinical details of the esophageal and associated malformations, technique and timing of repair, early and late complications, and long-term follow-up. Institutional review board (IRB) approval of this study has been obtained. RESULTS: Seven babies were included. Associated malformations were present in 4: trisomy 21 in 2 and imperforate anus in 2. After gastrostomy tube placement, patients were treated with gastrostomy tube feedings and continuous upper pouch suction. Median gap length was 5.5 vertebral segments (range, 3 to 9). RGT with a posterior mediastinal esophagogastric anastomosis was performed at median age of 62 days (range, 38 to 131). There were no anastomotic leaks. Three patients had strictures, one required resection. Exclusive oral nourishment was achieved in 5 patients by 6 months of age. At last follow-up (mean, 4.5 years), 6 patients were receiving oral nutrition exclusively, and all were maintaining growth curves. CONCLUSIONS: In long gap EA, early esophageal reconstruction using an RGT can be performed with minimal morbidity and promising short-term results.

Surgical implications of urachal remnants: Presentation and management.

BACKGROUND/PURPOSE: The abdominal manifestations of urachal remnants often prompt referral to the pediatric general surgeon. The purpose of this study was to evaluate the authors' management of this anomaly. METHODS: The authors performed a retrospective review of patients presenting to their institution with urachal remnants between 1984 and 2001. Clinical and radiographic details of presentation, management, and outcomes are described. RESULTS: Twenty-six patients presented at a median age of 4 years (range, 2 days to 12 years), 16 were boys, and 18 required inpatient care. Eleven (42%) presented with infection, 7 (27%) with clear drainage, 3 (12%) with umbilical polyps/granulation, 3 (12%) with pain, one (4%) with recurrent urinary tract infections, and one (4%) with an asymptomatic punctum. One had an associated anomaly (hypospadias). Urinalysis and urine cultures did not correlate with infection. Ultrasound scan was diagnostic in greater than 90% of cases. Overall, 20 patients underwent primary cyst excision, and 6 underwent incision and drainage (I&D) with delayed excision. Five patients underwent primary excision while infected, and 2 had postoperative complications (wound infection and urine leak). All 6 patients who underwent 2-stage procedure initially presented with infection, and none had complications. CONCLUSIONS: Persistent urachal remnants can present at any age with a variety of clinical manifestations. Ultrasound scan is a reliable diagnostic tool. Additional diagnostic studies generally are not warranted. Simple excision of noninfected lesions is appropriate. In cases of acute infection, initial I&D with delayed cyst excision may be preferable to avoid unnecessary complications.

Inflammation and platelet-activating factor production during hepatic ischemia/reperfusion.

The role of platelet-activating factor as a potential mediator of hepatic inflammatory injury associated with liver ischemia/reperfusion was investigated using a partial no-flow model in rats in vivo. Platelet-activating factor levels of livers from sham-operated rats and from animals experiencing hepatic reperfusion for less than 6 hr were very low. They were observed to increase significantly after 12 hr of reperfusion and reached peak levels after a 24-hr reperfusion period, a time when maximal hepatic injury and inflammation occurred. Treatment of experimental rats with WEB2170, a platelet-activating factor receptor antagonist, attenuated the hepatic injury and inflammation, as evidenced by decreases in plasma ALT and in hepatocyte necrosis and neutrophil infiltration. Both inactivation of Kupffer cells with gadolinium chloride and inhibition of the formation of reactive oxygen species with allopurinol reduced platelet-activating factor production in the liver, whereas induction of neutropenia had no effect, suggesting that interaction of Kupffer cells with oxygen-derived free radicals may be a plausible mechanism for hepatic platelet-activating factor accumulation. It is concluded that platelet-activating factor contributes to the inflammatory consequences of ischemia/reperfusion underlying late-phase hepatic injury.

Role of platelet-activating factor in pancreatitis-associated acute lung injury in the rat.

Acute necrotizing pancreatitis induced by infusion of bile salt into the pancreatic duct in rats is consistently associated with acute lung injury similar to the adult respiratory distress syndrome. The role of platelet-activating factor (PAF) in this pancreatitis-associated remote organ failure (lung injury) was investigated. Pulmonary tissue levels of PAF were increased gradually and reached a level of 1345 +/- 455 pg/g (6 times the control level) at 12 hours after induction of pancreatitis, whereas pancreatic PAF levels were undetectable and blood PAF remained unchanged. This local pulmonary PAF accumulation occurred at approximately the same time as the progression of lung injury. Pulmonary responses detected (i.e., eicosanoid production, leukocytic infiltration, Evan's blue extravasation, beta-glucuronidase release) were attenuated to varying degrees by treatment of rats in which pancreatitis was initiated with the PAF receptor antagonists (WEB2170 and BN52021). Rat lung lavages were examined after a 12-hour course of pancreatitis and no changes in PAF concentration, surfactant content, and phospholipase A2 (PLA2) activity were noted. Intravenous administration of PLA2 promoted pulmonary PAF production in experimental rats with pancreatitis but not in normal rats. This observation indicates that PLA2, which was determined to be elevated in plasma during pancreatitis, may be responsible for the accumulation of PAF in the lung. In conclusion, pancreatitis-associated lung injury appears to result from an endogenous inflammatory response in which PAF may play an important role.