The last fifty years of neonatal surgical management.

Neonatal surgical mortality has steadily fallen over the last five decades. Improved survival does not appear to be related to the introduction of new operative procedures. Most of the basic procedures were developed by 1960. Eight developments appear to be responsible: (1) The growth of pediatric surgery resulted in widespread availability of neonatal surgeons and dissemination of knowledge about newborn surgical emergencies. (2) The parallel growth of pediatric anesthesia, beginning in 1946, provided specialized intraoperative management of the neonate. (3) Understanding neonatal physiology is the key to successful management; major advances occurred between 1950 and 1970. (4) New inventions revolutionized patient care; the transistor (1947) made it possible for medical devices to sense, amplify and control physiologic responses and opened the communication and computer age. (5) Neonatal mechanical ventilation had a prohibitive mortality and was seldom utilized; the development of CPAP and a continuous flow ventilator in the 1970s allowed safe ventilatory support. (6) Total parenteral nutrition (1968) prevented starvation that frequently affected infants with major anomalies. (7) The effective treatment of infection began with the clinical use of penicillin (1941); antibiotics have reduced mortality but infants suffering from the septic syndrome have a prohibitive mortality; cytokine, proinflammatory agent research, and the development of anti-inflammatory and blocking agents in the 1980s have not affected mortality. (8) The establishment of newborn intensive care units (1960) provided an environment, equipment, and staff for effective physiologic management.

Immunoglobulin A supplementation abrogates bacterial translocation and preserves the architecture of the intestinal epithelium.

BACKGROUND: Breast milk has been shown to prevent gut-origin infections in neonates through undefined mechanisms. Putative protective factors in breast milk include immunoglobulin (Ig)A, IgG, and lactoferrin. We examined their role in bacterial translocation in neonatal rabbits. METHODS: IgA, IgG, and lactoferrin were isolated from rabbit breast milk through gel filtration and ion-exchange chromatography. Neonates were randomized to receive breast milk, formula alone, or formula supplemented with IgA, IgG, or lactoferrin. Quantitative cultures were performed on day 7 for bacterial translocation. Hematoxylin-eosin-stained sections of distal ileum were examined by light microscopy. Transmucosal bacterial passage was determined in vitro, and the ileal mucosal membranes were examined by confocal microscopy. RESULTS: IgA supplementation abrogated bacterial translocation. IgG and lactoferrin had no significant effect. Neonates that received IgA or breast milk gained more weight than those in the other groups. IgA reduced transmucosal bacterial passage in vitro. In contrast to the normal-appearing distal ileum of neonates fed breast milk, intestinal epithelium from neonates that received formula or formula with IgG or IgA demonstrated prominent vacuoles by light microscopy. Those fed formula alone or formula with lactoferrin had slightly shortened villi. CONCLUSIONS: IgA supplementation prevents bacterial translocation by enhancing gut mucosal barrier function.

Pure endotoxin does not pass across the intestinal epithelium in vitro.

Numerous reports suggest that endotoxin (LPS) may play a central role in triggering the inflammatory cascade that leads to the systemic inflammatory response syndrome. Although conditions that promote bacterial translocation in vivo may also facilitate direct translocation of LPS, the exact mechanisms by which LPS crosses the intestinal barrier to reach the systemic circulation are unknown. This study was designed to determine whether pure endotoxin could pass across injured rat ileal mucosa in the Ussing chamber. Sprague-Dawley rats were subjected to mild or severe hemorrhagic shock following carotid artery cannulation, and then resuscitated. Control animals underwent carotid artery cannulation only (sham-shock). Bacterial translocation to the mesenteric lymph nodes, liver, or spleen was measured after 24 h. Transmucosal passage of fluorescein isothiocyanate (FITC)-labeled E. coli C-25, or FITC-conjugated LPS was measured in the Ussing chamber. Intestinal membranes were examined by light and confocal laser microscopy. Severe hemorrhagic shock resulted in a 60% mortality rate and a 100% incidence of bacterial translocation in surviving animals. Sham-shock rats had a 100% survival rate and a 33% incidence of bacterial translocation. Transmucosal passage of FITC-E. coli C-25 was similar in both groups; however, passage of FITC-LPS was never detected. Histologic analysis confirmed mucosal injury to the intestinal epithelium of rats subjected to severe hemorrhagic shock, and confocal laser microscopy demonstrated passage of FITC-E. coil C-25, but not of FITC-LPS across the ileal membranes. Disruption of the intestinal epithelium with a potent mucolytic agent did not result in significant increase in transmucosal passage of FITC-LPS. We conclude that pure LPS does not pass across the intestinal mucosa in vitro. Transmucosal passage of LPS in vivo may be due, at least in part, to the release of bacterial cell wall fragments containing LPS from killed bacteria that had previously translocated.

Transmucosal passage of bacteria across rat intestinal epithelium in the Ussing chamber: effect of nutritional factors and bacterial virulence.

Transmucosal passage of bacteria across the intestine, the essential and prerequisite step for bacterial translocation, cannot be effectively studied using in vivo models of translocation. We have adapted the Ussing chamber into a fresh, sterile organ culture system that can facilitate the study of bacterial-epithelial interactions. Intestinal membranes were mounted in the Ussing chamber and perfused with a solution rich in putative mucosal micronutrients. The transmembrane potential difference was constantly monitored as a marker of intestinal integrity. Transmucosal passage of various bacteria across the normal intestinal epithelium was quantitated, and the mucosal membrane was examined by light and transmission electron microscopy. The addition of potassium cyanide to the mucosal perfusate resulted in an irreversible loss of potential difference. Oxygen deprivation also led to a precipitous drop in potential difference, but it was reversible with prompt reoxygenation. In contrast, intestinal membranes perfused with a solution consisting of Dulbecco's modified Eagle's medium + 20 mM glutamine maintained their potential difference for a sustained period (>180 min). Both the viability and structural integrity of the ileal intestinal membrane were maintained in culture ex vivo using this perfusate. Qualitative differences were observed in the mechanism of transmucosal passage of mild to moderately virulent bacteria such as Escherichia coli C-25 and Proteus mirabilis M-13, which pass through the intestinal epithelium without causing overt damage to the mucosa, and more virulent organisms such as Salmonella typhimurium, which cause extensive mucosal damage by light and transmission electron microscopy. The Ussing system should provide a useful model of intact organ culture for the study of the mechanisms of bacterial translocation and the pathogenesis of enteric infections.

Cardiac arrest before repair or extracorporeal membrane oxygenation cannulation does not increase the mortality rate associated with congenital diaphragmatic hernia.

Despite recent advances in the management of high-risk congenital diaphragmatic hernia (CDH), mortality remains high. Deaths occur later because infants with inadequate pulmonary parenchyma are treated aggressively but eventually succumb to respiratory failure. In an attempt to identify absolute predictors of mortality the authors examined retrospectively their experience with CDH to determine if cardiac arrest before repair or initiation of extracorporeal membrane oxygenation (ECMO) invariably increased mortality. The authors reviewed the charts of 119 infants who had high-risk CDH treated between 1981 and 1994. They were divided into two groups: those that suffered cardiopulmonary arrest (CA, n = 21) before CDH repair or ECMO cannulation; and those that did not (NCA, N = 98). The authors compared mortality rate, ventilatory parameters, duration of, and complications on ECMO, as well as length of hospitalization between groups. Twenty-one infants suffered CA before initiation of ECMO support or CDH repair. Three infants (14%) suffered CA before arrival at our institution; seven (33%) after, and 11 (53%) both before and after arrival. There was no difference between the CA and NCA groups in terms of birth weight, gestational age, race and gender mix, or pregnancy and delivery complications. Five-minute Apgar scores were significantly lower in the CA group compared with the NCA group (4.6 v 5.7, P = .04). The CA group also had significantly worse "best postductal" blood gas and ventilatory parameters. There was no significant difference in length of hospitalization, time from admission to ECMO cannulation or CDH repair, or incidence of complications while on ECMO between the two groups. CA cases were more likely to require ECMO support (76% v 48%, P = .02) and to stay on ECMO for a more prolonged period than NCA cases (5.8 v 3.8 days, P = NS). However, there was no significant difference in overall survival between CA and NCA cases (43% v 51%, P = NS). Cardiopulmonary arrest before repair of CDH or ECMO cannulation is not a univariate independent predictor of mortality and therefore should not preclude these high-risk infants from maximum intensive care therapy, including ECMO cannulation.

An analysis of the operative experience of North American pediatric surgical training programs and residents.

There has been a rapid increase in the number of pediatric surgical training programs. To meet the goals of quality patient care and surgical education, training and practice activities must be objectively monitored. The aim of this study was to collect and analyze the experience of American and Canadian Pediatric Surgical training centers and residents. The authors collected the 1-year operative experience of 31 American and six Canadian training programs and the 2-year operative experience of the 25 most recently graduated residents. Categories analyzed included total cases, defined categories (neonatal, important, and tumor cases), routine cases, thoracic, cardiac, urologic reconstructive, head and neck, endoscopy, vascular, plastics and burn procedures. From these data six assumptions about the training in pediatric surgery were addressed. (1) The operative activity of the United States and Canadian training programs and residents are comparable. The results show that there are few major differences in operative experience. (2) There should be variability in operative experience between programs but little variability between residents. The North American operative experience for both residents and institutions are marked by high variability and leftward shift in the frequency distributions. (3) A resident's training should consist of a significant portion of "index cases" and fewer routine cases. The residents perform 28% of their total cases in the three defined categories (index cases) and 26% as routine cases. (4) Pediatric surgeons are the true general surgeons, performing operations in areas such as cardiac, reconstructive genitourinary, plastic, and burn surgery. Examination of the data shows that most programs and residents perform few cases in these four areas. (5) Certain procedures such as thoracic, genitourinary, vascular, head and neck, and endoscopy remain within the domain of pediatric surgery. The results show that this assumption is true for thoracic, vascular, head and neck, and endoscopy but not for genitourinary, and there is wide variability between institutions and between residents. (6) "Core" pediatric surgical conditions such as esophageal atresia, biliary atresia, and intersex are still available in significant numbers to train residents. The data show that a surprising number of programs and residents perform few or none of the core operations. This analysis is the first step toward monitoring of pediatric surgical resident education. A future study is underway to evaluate the current experience of practicing pediatric surgeons who have taken the recertification examination.

Inhibition of nitric oxide with aminoguanidine reduces bacterial translocation after endotoxin challenge in vivo.

BACKGROUND: Administration of lipopolysaccharide (LPS) has been shown to increase bacterial translocation (BT) in vivo and in vitro. In addition, LPS upregulates inducible nitric oxide synthase expression in the intestinal epithelium-a phenomenon that can either enhance microbial killing, or alternatively, promote BT by impairing the gut barrier. OBJECTIVE: To determine the effect, if any, of an inhibitor of nitric oxide synthase, namely, aminoguanidine (AG), on BT after LPS challenge. DESIGN: Sprague-Dawley rats were randomized to receive either AG or normal saline solution via subcutaneously placed osmotic pumps (Alzet), followed 18 hours later by LPS injection (5 mg/kg or 20 mg/kg intraperitoneally). Quantitative cultures of the cecum, mesenteric lymph nodes, liver, and spleen were obtained, and plasma nitrite and nitrate levels were measured at 24 hours. Transmembrane potential difference and mucosal permeability to fluorescein isothiocyanate-labeled dextran and fluorescein isothiocyanate-labeled Escherichia coli C25 were measured in the Using chamber. The intestinal membrane was examined by light, transmission electron, and confocal laser microscopy. RESULTS: Rats that were given high-dose LPS had elevated levels of nitrite and nitrate and a 100% incidence of BT. In contrast, AG infusion significantly reduced both BT (22%) and nitrite and nitrate levels. Animals that received LPS and normal saline solution had a significantly lower transmembrane potential difference than those that received LPS and AG. High-dose LPS resulted in sloughing of the apical enterocytes at the villus tips where bacterial entry seemed to occur, as seen with confocal laser microscopy. CONCLUSIONS: Inhibition of nitric oxide production with AG decreases BT after high-dose LPS challenge. The mechanism may involve increased cellular viability and decreased damage to the gut mucosal barrier in rats that receive AG.

The microenvironment influences the pattern of bacterial translocation in formula-fed neonates.

The authors previously demonstrated that neonatal rabbits fed conventional formula have a significantly greater incident of bacterial translocation than do neonatal rabbits fed breast milk. They hypothesized that exogenous bacteria in the formula and/or the microenvironment of the neonatal rabbit may contribute to the higher incidence of bacterial translocation. In the present study, the authors examined the incidence of bacterial translocation in neonatal rabbits fed pasteurized formula, unsterile formula, or breast milk while being housed in a clean or unsterile environment. The rabbits were divided into five groups. Groups I and II were fed pasteurized formula; groups III and IV were fed unsterile formula. In addition, groups I and III were housed in a clean environment, and groups II and IV were kept in an unsterile environment. The neonates in group V were fed breast milk and were kept in an unsterile environment. On the seventh day, the animals were killed, and the mesenteric lymph nodes, liver, and spleen were cultured for the presence of bacteria. Bacterial translocation occurred in 100% of group IV neonates. A clean environment (groups I and III) eliminated gram-negative bacterial translocation. A reduction (50%) in the overall incidence of bacterial translocation was obtained by pasteurizing the formula (group I v group III). Group II had significantly less gram-negative bacterial translocation than did group IV. None of the neonates in group V had translocation. The data show that a clean environment abrogates gram-negative bacterial translocation. Pasteurizing the formula significantly reduces the incidence of gram-negative bacterial translocation, and further reduces overall bacterial translocation in a clean environment. The authors hypothesize that control of the microenvironment can significantly influence the pattern of bacterial translocation in formula-fed neonates, and thus potentially reduce the incidence of gut-origin sepsis. Factors present in breast milk inhibit bacterial translocation, regardless of the microenvironment.

Is computed tomography a useful adjunct to the clinical examination for the diagnosis of pediatric gastrointestinal perforation from blunt abdominal trauma in children?

Perforations of the gastrointestinal (GI) tract, compared to solid organ injuries, are a relatively infrequent sequela of blunt abdominal trauma in children. The purpose of this study is to review retrospectively the diagnostic modalities used in 30 children with proven traumatic intestinal perforations treated at one institution. Since computed tomography with intravenous and oral GI contrast is commonly used in the diagnosis of suspected solid organ injury from blunt abdominal trauma, we evaluated retrospectively the computed tomographic (CT) scan findings in these children in an attempt to accurately predict or suggest GI perforation. Between January 1987 and December 1993, 5,795 children were admitted. Three hundred fifty suffered blunt abdominal trauma of which 30 patients (8.5%) required surgery for a GI perforation and formed the basis for this study. Data collected were mechanisms of injury, results of admission and serial clinical examinations, results of radiologic imaging, associated injuries, operative findings, and outcome. Follow-up was obtained on all patients and averaged 2.5 years. Blows to the abdomen (handlebars, cars, kicks) were the most common cause of perforation, followed by seatbelt injuries. Eleven patients underwent immediate laparotomy an average of 0.75 hours after admission. The indication for surgery was shock (three), clinically apparent peritonitis (five), and free air on plain abdominal radiograph (three). Nineteen patients underwent "later" laparotomy, an average of 3.4 hours after admission, all because of the eventual development of peritonitis. Retrospective review of these CT scans revealed free air anterior to the liver in three, and the remaining 16 had CT findings suggestive of GI injury such as free fluid, focal fluid-filled thick-walled bowel loops, and mesenteric infiltration. There were five (26%) false negative CT scans performed an average of 5.0 hours after injury. We believe serial physical examinations are the gold standard for diagnosing pediatric GI perforation from blunt abdominal trauma. The CT scan may be a useful adjunct to the diagnosis of an intestinal perforation in patients who have no immediate indication for surgery. Presently, the only CT finding that is an absolute indication for laparotomy is free air (in the absence of pulmonary/mediastinal injury or barotrauma). The other CT "findings" need to be validated prospectively.

Necrotizing enterocolitis.

Advances in neonatal care have resulted in an enlarging population of vulnerable premature newborns at risk for necrotizing enterocolitis (NEC). This article presents data supporting a unifying hypothesis for the initiation of NEC based on bacteria as the inciting agent(s), and the preterm baby as the vulnerable host. Facts and controversies concerning the pathology, microbiology, clinical presentation, management and outcome of infants afflicted with NEC are presented.

Postoperative selective bowel decontamination prevents gram-negative bacterial translocation in small-bowel graft recipients.

Gram-negative septic episodes are a potential risk of small-bowel transplantation; bacterial translocation through the graft is considered the mechanism. As a measure to prevent this complication, we evaluated postoperative selective bowel decontamination (SBD) in the rat model of orthotopic small-bowel transplantation [Lewis (LEW) and Brown-Norway (BN) rats as donors and recipients]. For 4 days after transplantation we gave FK 506, 2 mg/kg, which prevents rejection and results in indefinite recipient survival. For SBD, 24 mg/kg/day polymyxin E and 20 mg/kg/day tobramycin were administered via orogastric gavage to allograft recipients, both with and without FK 506 therapy. On Day 9, all rats were sacrificed, the peritoneal cavity was swabbed, and mesenteric lymph nodes (MLN), spleen, liver, and ileum were harvested for microbial qualitative and quantitative analysis. Animals with positive peritoneal swab cultures were excluded. SBD resulted in a significant reduction of the quantitative gram-negative bacterial flora in the ileum and cecum and of bacterial translocation to the MLN [0% versus 50% (no FK 506 therapy) and 8% versus 50% (FK 506 treated)]. In the allograft groups not treated with FK 506, SBD failed to significantly prolong survival, suggesting that acute rejection is not hastened by infection (bacterial translocation). We conclude that SBD in small-bowel-graft recipients prevents bacterial translocation by reducing intestinal gram-negative bacterial flora; this may reduce local and systemic infections by gut-derived organisms.

The effect of endotoxin on intestinal mucosal permeability to bacteria in vitro.

OBJECTIVE: To examine the role of the intestinal mucosa in bacterial translocation, in vitro bacterial passage across ileal mucosal segments mounted in Ussing chambers were studied in control and endotoxin (lipopolysaccharide)-treated rats. DESIGN: Experimental study. MATERIALS AND METHODS: Three groups of rats were studied. The experimental group received an intraperitoneal injection of lipopolysaccharide, while controls received an equivalent volume of saline solution; a third group received no treatment. Twenty-four hours later, all groups underwent laparotomy and organ culture to assess bacterial translocation. At the same time, a segment of mucosa from the terminal ileum of each animal was mounted in a Ussing chamber, and the transmucosal passage of labeled Escherichia coli from the luminal to serosal surface was assessed by results of serial cultures. RESULTS: In vivo bacterial translocation occurred in 100% of the lipopolysaccharide-treated animals, significantly higher than the incidence seen in controls (25%; P < .05). In vitro passage of labeled E coli across ileal mucosa in the Ussing chamber occurred in 78% of lipopolysaccharide-treated animals, while in controls transmucosal passage was seen in only 14% (P < .05). Histologic examination of mucosa from both groups using light and transmission electron microscopy demonstrated no structural differences between groups. CONCLUSIONS: Increased permeability to bacteria at the mucosal level contributes to the bacterial translocation seen in endotoxemia.

Effect of secretory IgA on transepithelial passage of bacteria across the intact ileum in vitro.

BACKGROUND: Bacterial translocation is a process believed to result in nosocomial infections. Secretory IgA (sIgA) may have a role in the prevention of translocation by its ability to bind and aggregate bacteria, a function termed "immune exclusion." The present study was done to determine the effect of specific binding of sIgA to bacteria on the movement of these organisms across the intact epithelial membrane. STUDY DESIGN: Bacterial translocation across intact intestinal segments of rats were assessed in vitro using the Ussing model. Secretory IgA (0.25 mg per mL) from pooled human colostrum was added to the perfused segments of ileum in the Ussing system. Subsequently, the membranes were exposed to 5 x 10(9) cfu per mL Escherichia coli on their mucosal side. A second experiment tested the effect of human IgG when perfused with E. coli using the same preparation. All experiments had paired matched rats in a control group without immunoglobulin. The ability of sIgA and IgG to bind to E. coli was studied by an in vitro assay, as well as by transmission electron microscopy and immunofluorescence of random IgA/E. coli experiments. Measurements obtained in all experimental and control groups were the incidence and amount of bacterial passage and the potential difference generated by the intestinal segments (an index of viability). RESULTS: There were no differences in potential difference between control and experimental groups in either of the two experiments. Secretory IgA bound E. coli and completely prevented passage of E. coli as compared with rats in the control group. IgG bound E. coli; however, the incidence of passage was equal to that of rats in the control group. However, the presence of IgG resulted in a significantly reduced number of bacteria that passed when compared with controls (p < 0.05). Electron microscopic studies revealed intact surface morphology and immunofluorescence revealed aggregates of IgA and E. coli on the mucosal, but not submucosal, surface of the ileal membranes. CONCLUSIONS: This study provides direct evidence of immune exclusion by sIgA. When bound to bacteria, it prevents passage across a morphologically intact segment of viable intestinal tissue.

Quantitative and morphologic analysis of bacterial translocation in neonates.

OBJECTIVE: To elucidate the mechanisms of bacterial translocation in animals fed a conventional formula by correlating transmucosal bacterial passage in vitro with the structural characteristics of the neonatal intestinal mucosa. DESIGN: Newborn rabbits were randomized to receive a conventional formula or breast milk. Bacterial translocation to the mesenteric lymph nodes, liver, and spleen was quantitated after 7 days, and transmucosal passage of bacteria was measured in vitro using the Ussing chamber. The mucosal membranes were examined by light, transmission electron, and confocal laser scanning microscopy. RESULTS: Bacterial passage was rarely seen in the breast milk-fed animals in contrast to the formula-fed animals. Unlike the normal-appearing membranes from breast milk-fed animals, the epithelial cells of formula-fed animals were vacuolated but healthy, with normal polarization and microvillus border by confocal laser scanning microscopy. Villi of formula-fed animals were less densely packed than those of the breast milk-fed animals. Bacterial adhesion, internalization, and transmucosal passage were seen only in membranes from formula-fed animals. Transmission electron microscopy demonstrated bacteria incorporating into the epithelial surface through an active phagocytic process, with rearrangement of the actin cytoskeleton. Once internalized, these bacteria were seen within the cytoplasmic vacuoles and subsequently in the submucosa. No bacteria passed between epithelial cells. CONCLUSION: Morphological changes in the intestinal mucosa of formula-fed newborn rabbits may increase permeability to bacteria.

Breast milk protects the neonate from bacterial translocation.

Clinical and experimental evidence suggests that breast milk enhances the neonatal gut barrier. Using bacterial translocation (BT) as a measure of gut barrier function, a series of experiments was designed to explore the relationship between the neonatal gut barrier and breast milk as well as the factors associated with the feeding of breast milk. Full-term newborn rabbits were assigned to one of four groups: formula-fed (group I), fed with colostrum plus formula (group II), breast-fed with breast milk (group III), and fed with colostrum plus stored breast milk (group IV). At 7 days of age, body weights were obtained, the rabbits were killed, and the mesenteric lymph nodes (MLN), liver, and spleen were quantitatively cultured for translocating bacteria. The cecum was cultured for aerobic and anaerobic enteric organisms. Distal ileal tissues were examined by light and transmission electron microscopy and compared among groups. The viability of cells in the stored, frozen breast milk was assessed by Trypan blue staining. Group I rabbits had significantly lower mean body weights compared with the other groups. The animals breast-fed breast milk had no BT to the MLN or liver and had a 9% incidence of BT to the spleen. There was no difference between BT in groups III and IV. The stored breast milk contained no viable cells. The incidence of BT to all three areas was significantly lower than in groups I and II. The animals fed with formula alone had the highest incidence of BT to the MLN (88%), liver (60%), and spleen (32%). BT in this group was significantly higher compared with groups III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia blocks nonshivering thermogenesis in the neonatal rabbit.

Nonshivering thermogenesis (NST) is a normal physiological response of the neonate to cold exposure, characterized by increased blood flow to metabolically active brown fat stores. It is standard practice during neonatal surgery to warm the ambient environment in order to avoid consuming vital energy stores. While NST has been well-studied in the neonate, the response during anesthesia and paralysis has not been fully characterized. Rabbit pups (aged 1 to 7 days) were randomized into several groups. The experimental groups consisted of animals mechanically ventilated and administered either metocurine, pancuronium, curare, fentanyl, nitrous oxide (N2O), or halothane. The controls were spontaneously breathing animals. Oxygen consumption (VO2), an index of metabolic activity, was measured at thermoneutrality (39 degrees C) and after cold exposure (25 degrees C). Control and metocurine animals had a significant increase in VO2 in response to cold exposure. The increase in VO2 was not noted in animals that received curare, pancuronium, fentanyl, N2O, or halothane. To test the effect of anesthetic withdrawal during cold exposure on VO2, additional series of animals were studied. One group received continuous halothane throughout the period of cold exposure; the other had cessation of the halothane during cold exposure. Both groups were rewarmed subsequently. The animals that had withdrawal of halothane during cold exposure had a marked and significant increase in VO2 compared with the control group (continuous halothane). VO2 returned to near-baseline levels upon rewarming. The authors conclude that many commonly used anesthetic and paralyzing agents inhibit the thermogenic response to cold exposure. However, cessation of anesthesia (halothane) in a cold environment results in a marked increase in metabolic activity.

Necrotizing enterocolitis in the extremely low birth weight infant.

Improved neonatal management has resulted in an enlarging population of extremely low birth weight (ELBW) infants. These infants have a high incidence of necrotizing enterocolitis (NEC) and a high mortality rate. The authors compared two groups of NEC patients: ELBW infants (< 1,000 g and/or < or = 28 weeks' gestation) and "standard" premature infants (29 to 36 weeks' gestation). NEC was classified according to the extent of bowel involvement: (1) focal, (2) diffuse, or (3) pan involvement (pan necrosis). Clinical laboratory, radiological, pathological, and bacteriologic findings, management, and mortality were analyzed. There were no significant differences between the groups with respect to gender, race, delivery mode, or incidence of prenatal or perinatal problems. The most common presenting signs in both groups were abdominal distension, vomiting, and feeding intolerance. The onset of signs and the time of first feedings were significantly later in the ELBW group. Pneumatosis was the most frequent initial radiological finding (60% of the ELBW group, 75% of the premature group). Portal vein air (PVA) was present in 29% of the ELBW and premature infants. Seventy-one percent of ELBW infants with PVA had pan involvement, versus 40% of premature infants (P < .05). There were significant differences in the peritoneal cultures between the groups. The premature group had significantly more Escherichia coli (54% v 23%). The ELBW group had a wider variety of microorganisms (eg, Clostridium sp, Pseudomonas sp, and yeast). Survival was significantly higher for the premature group (84% v 55%). The mortality rate was 93% when pan involvement was present in the ELBW group.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of intestinal mucus in transepithelial passage of bacteria across the intact ileum in vitro.

BACKGROUND: Although gastrointestinal mucus is one of a number of putative host defense mechanisms that protect the gut barrier against microbial translocation, little experimental data are available to show its role in this process. The present study sought to determine the role of mucus depletion on the transepithelial passage of bacteria across viable segments of rat ileum mounted in Ussing chambers in vitro. METHODS: Intestinal mucus was depleted in 12 rats after injection with pilocarpine (160 mg/kg intraperitoneally) 45 minutes before intestinal harvest. The mucosal surfaces of the perfused gut segments mounted in the Ussing chamber were exposed to 5 x 10(9) CFU/ml Escherichia coli C-25. Viability was monitored by continuous measurements of the potential difference generated by the membranes. The electrical characteristics were unaltered by pilocarpine pretreatment or exposure to bacteria. RESULTS: Bacterial passage occurred in 100% of pilocarpine membranes as compared with 33.3% in controls (p < 0.05). Pilocarpine-treated membranes resulted in 19.9 +/- 7.5 mg of retrievable mucus as compared with 28.8 +/- 7.2 mg in controls (p < 0.05). Light and transmission electron microscopy revealed an intact epithelial surface in all membranes. There was a marked decrease in mucus on the surface of pilocarpine-treated membranes. CONCLUSIONS: Intestinal mucus secretion is a critical factor in the barrier function of the gut, and its depletion results in a dramatic increase in bacterial passage across the intact rat ileum.

Improved sternal fixation in the correction of pediatric pectus excavatum.

Pectus excavatum is the most common congenital chest wall deformity; it is manifest by abnormal costal cartilage segments causing sternal depression and rotation. The most popular repair involves resection of the abnormal costal cartilage segments, followed by sternal osteotomy and fixation to the adjacent chest wall. Methods of sternal fixation have included metal bars and struts, K-wires, pins, sutures, synthetic mesh, vascularized rib struts, and large AO plates, but they have not included more recent rigid fixation technology. Current rigid fixation techniques allow incorporation of malleable, low-profile reconstruction plates that can be contoured to correct the three-dimensional aspect of these defects. Three pediatric patients are presented in whom plate fixation was utilized for sternal fixation. Current reconstruction plate technology provides an improved fixation alternative for the correction of congenital chest wall anomalies, as well as offering similar potential advantages for traumatic, oncologic, and reconstructive surgery of the thorax.