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The Nissen fundoplication (NFP) for the management of severe gastroesophageal reflux (GER) in infants and children has become one of the most frequently performed operations in pediatric surgical centers in the United States. Short-term outcome, morbidity, and mortality are consistently favorable in several large series. The long-term success of this procedure is presumed but has not been established objectively. To examine the late results of this operation, 46 infants and children were carefully evaluated more than 5 years after NFP (mean, 6.7 years). Evaluation included parental interview, physical examination, upper gastrointestinal series, and esophageal pH monitoring. The mean age at the time of operation was 4.13 years. Fifty-seven percent of the patients had significant neurologic impairment, and 80% had at least one serious additional medical problem. Twenty-four percent of the children died during the period of follow-up--all but one death related to serious underlying medical problems. Of the 35 survivors, 26 (74.3%) have no symptoms; five (14.3%) have mild symptoms potentially referable to GER that necessitate little if any treatment; four (11.5%) have had symptomatic recurrence of GER necessitating repeat fundoplication. Three of these patients now have no symptoms. Forty-five percent of the patients had at least one postoperative complication. NFP provides efficacious, long-term treatment of GER in infants and children, with acceptable morbidity. Mortality in this group of children is related primarily to associated diseases rather than to GER.

Sepsis is characterized by Adult Respiratory Distress Syndrome (ARDS)-like pulmonary dysfunction largely attributed to alveolar capillary endothelial cell injury which causes increased microvascular permeability and interstitial edema formation. In addition, quantitative and qualitative abnormalities of the pulmonary surfactant system may be important features of some clinical and experimental lung injuries. This study was designed to investigate the relationship of bacteremia and endotoxemia to pulmonary surfactant production in vivo. A technique for estimation of pulmonary surfactant phospholipid synthesis measuring incorporation of a stable isotope precursor [( 2-13C]acetate) into dipalmitoylphosphatidylcholine (DPPC) in alveolar lavage fluid was developed. Male 350 g Sprague-Dawley rats had placement of central venous catheters. After overnight recovery, sublethal bacteremia (Escherichia coli, 1 x 10(8) organisms, iv) and sublethal endotoxemia (Difco; 10 mg/kg, iv) were induced. Both were associated with lung microvascular permeability increases consistent with capillary endothelial injury. Eight-hour infusions of [2-13C]acetate were given. After sacrifice, bronchoalveolar washings and lung tissue were obtained and [2-13C] incorporation into lavage and lung DPPC was measured by gas chromatography mass spectroscopy. Endotoxin-treated animals had a 21.5% reduction in label incorporation into DPPC [1.215 +/- 0.145 APE (%) sham versus 0.954 +/- 0.144 APE (%) experimental, P greater than 0.05] and bacteremic animals had a 56.9% diminution of [2-13C]acetate incorporation [1.215 +/- 0.145 APE (%) sham versus 0.524 +/- 0.56 APE (%) experimental, P less than 0.05]. Bacteremia-induced dysfunction of alveolar type II epithelial cells manifested as diminished alveolar surfactant phospholipid production may be a contributing factor to sepsis-induced respiratory failure.

During a recent prospective nonrandomized comparison of noninvasive imaging techniques in 100 children with suspected major blunt abdominal injury, an interesting subset of patients was defined. Of 95 hemodynamically stable patients, 44 were found to have immediate elevation of hepatic enzymes (SGOT, SGPT greater than 30 IU). Nineteen of these children (43%) were subsequently shown to have significant liver injuries. No child with a liver injury had normal enzymes on admission. The level of enzyme elevation (SGOT chi 890 +/- 142 IU, SGPT chi 536 +/- 105 IU) in those with liver injuries is significantly greater than those without injury (SGOT chi 273 +/- 44 IU, SGPT chi 115 +/- 19 IU) (P less than or equal to 0.0001 SGOT. P less than or equal to 0.0001 SGPT). Our study has allowed definition of a group of children who are at significant risk for liver injury based on immediately available serum determinations of GOT and GPT. We have begun to use this information in our institution to select children for further noninvasive imaging. We recommend that these studies be obtained emergently in all children with suspected upper abdominal trauma.

Cerulein-induced acute pancreatitis in rats is associated with a reversible lung injury that is characterized by alveolar capillary endothelial-cell injury, increased microvascular permeability, interstitial edema formation, and intraalveolar hemorrhage and fibrin deposition. The role of mediators in this injury was analyzed using gravimetric data, microvascular permeability indices, electron microscopy, and a quantitative morphometric analysis. Neutrophil depletion induced by a specific antibody was highly protective against lung injury. Interruption of the complement pathway (using low dose Naja naja cobra venom factor) also protected against lung injury. Catalase and superoxide dismutase were also protective. The iron chelator deferoxamine and the hydroxyl radical scavenger, dimethylsulfoxide, were not protective against acute lung injury. These data suggest that complement, neutrophils, and neutrophil-derived (H2O2-dependent) oxygen products mediate lung injury that occurs secondary to cerulein-induced pancreatitis. In contrast to other models of neutrophil-dependent, oxygen-radical-mediated lung injury, this lung injury does not appear to be an iron-dependent and hydroxyl-radical mediated injury. We postulate that the process of acute pancreatitis leads to complement activation followed by neutrophil recruitment, sequestration, and adherence to alveolar capillary endothelial cells. Ultimately lung injury appears to result from local endothelial-cell injury secondary to neutrophil-generated oxygen products that may be myeloperoxidase dependent.