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T F Tracy

Publications and source records attributed to T F Tracy.

At least 37 records · Page 2Linked to original sources
PubMed1998

Cholestatic liver injury increases circulating TNF-alpha and IL-6 and mortality after Escherichia coli endotoxemia.

We employed a bile duct ligation (BDL) model of cholestatic liver injury to test the hypothesis that this form of preexisting hepatic dysfunction alters the kinetics of circulating TNF-alpha and IL-6 after Escherichia coli endotoxemia, thereby augmenting mortality and lung injury by a TNF-alpha:leukotriene (LT) axis of inflammation. Male rats were catheterized 13 d after BDL or sham surgery and studied while awake 18 to 24 h later. Cholestasis after BDL was confirmed by baseline serum bilirubin (BDL = 7.34 +/- 0.72 mg/dl, mean +/- SEM, n = 17 versus Sham = 0.25 +/- 0.07, n = 20; p < 0.005) and histopathology. Sham and BDL animals received E. coli lipopolysaccharide serotype O55:B5 (LPS, 5 mg/kg i.v.) or 0.9% NaCl (NS) ending at t = 0 and were monitored over 24 h for vital signs and hemodynamics. In parallel studies, lipoxygenase inhibition was performed using diethylcarbamazine or the 5-lipoxygenase activating-protein inhibitor MK-886. Blood was collected at baseline and at t = 1.5, 3.5, and 24 h for formed elements and for serum endotoxin, TNF-alpha, IL-6, bilirubin, and alanine aminotransferase (ALT). Organs were evaluated at 24 h for histopathology, including neutrophil (PMN) densities and wet/dry weight (W/D) ratios. Cholestasis reduced survival after otherwise nonlethal endotoxemia, with seven of 11 BDL + LPS rats dying within 24 h versus no deaths in BDL + NS (n = 6), Sham + LPS (n = 14), or Sham + NS (n = 6) animals (p < 0.01). Despite equivalent serum endotoxin between groups, circulating TNF-alpha was 8-fold higher in BDL + LPS than in Sham + LPS rats at 1.5 and 3.5 h (p < 0.001), whereas serum TNF-alpha did not differ between BDL + NS and Sham + NS rats. IL-6 likewise was increased differentially by 1.5 h in BDL + LPS animals (11.98 +/- 2.42 ng/ml) versus Sham + LPS rats (3.05 +/- 0.58 ng/ml, p < 0.05). Hypothermia, bradycardic hypotension, and leukopenia were most severe and prolonged in BDL + LPS rats, which also had significantly higher ALT values, W/D ratios, and organ PMN counts. LT inhibition failed to reduce BDL-related differences in serum cytokines or survival after endotoxemia. Thus, cholestasis augments inflammatory responses to gram-negative endotoxemia, sensitizing the host to enhanced fluid flux in multiple organs and to mortality by a LT-independent mechanism.

Alanine Transaminase↗
PubMed1998

Gadolinium chloride suppresses hepatic oval cell proliferation in rats with biliary obstruction.

Liver injury due to bile duct ligation (BDL) is histologically characterized by cholestasis, bile ductular proliferation, hepatocellular damage, portal fibrosis, and ultimately biliary cirrhosis. Stem cells within the liver may act as progenitor cells for small epithelial cells termed oval cells that can differentiate into bile duct cells or hepatocytes, whereas myofibroblasts are the principal source of collagen production in fibrosis. The aims of this study were to determine 1) whether BDL induces oval cell proliferation and 2) whether blockade of Kupffer cells affects oval cell proliferation, bile duct proliferation, and myofibroblast transformation in experimental biliary obstruction. Male Sprague-Dawley rats were divided into two groups to receive either a single dose of gadolinium chloride (a selective Kupffer cell blocking agent) or vehicle. One day later, the gadolinium- and vehicle-treated groups were further subdivided to receive either BDL or sham operation. The rats were sacrificed on day 7 postoperatively. Serum was collected for measurement of aspartate aminotransferase, gamma-glutamyl transpeptidase, and bilirubin levels. Liver tissue was taken for evaluation of fibrosis, bile ductular cells, oval cells, and myofibroblasts. BDL resulted in elevated aspartate aminotransferase, gamma-glutamyl transpeptidase, and bilirubin in serum, and gadolinium pretreatment did not modify these effects. BDL induced marked oval cell proliferation, which was completely prevented by gadolinium pretreatment. Gadolinium did not affect the induction of bile duct expansion or myofibroblasts after BDL. We conclude that experimental biliary obstruction induces oval cell proliferation, which can be prevented by gadolinium pretreatment. This suggests that bile ductular proliferation and myofibroblast transformation are not mediated by Kupffer cells and that ductular proliferation can proceed in the absence of oval cells. Alternatively, gadolinium may directly affect oval cell proliferation after BDL.

Animals↗
PubMed1997

Blunt intestinal injury in children. Diagnostic and therapeutic considerations.

OBJECTIVES: To identify computed tomographic (CT) findings in children who have experienced blunt trauma and who have known intestinal injuries and to correlate these findings with the findings of the initial physical examination. DESIGN: A retrospective review of children (aged < 18 years) known to have an intestinal injury as a consequence of blunt trauma. SETTING: A university-affiliated children's hospital with a level 1 pediatric trauma center. PATIENTS: Children younger than 18 years who were admitted for examination of injuries or for management of complications related to intestinal injuries. INTERVENTIONS: Clinical and radiographic evaluation and laparotomy for intestinal injuries other than duodenal hematoma. MAIN OUTCOME MEASURES: The identification and correlation of relevant findings during the physical examination, on the CT scan, and during surgery. The assessment of intervals from injury to diagnosis and intervention and the description of associated injuries. RESULTS: Twenty-two patients sustained intestinal injuries as a result of blunt trauma. Most (15) of the patients were passengers injured in motor vehicle crashes; 14 of these patients were wearing seat belts. Focal blows to the abdomen from bicycle handlebars, hockey sticks, or falls onto blunt objects were implicated in the remaining patients. For 19 of the 22 patients, the initial physical examination was conducted at Cardinal Glennon Children's Hospital, St Louis, Mo, and 18 of the 19 patients underwent a concurrent CT evaluation. Peritonitis was found in 5 of these 18 patients. Tenderness on physical examination was noted in 9 of the 18 patients (tenderness was not noted in 3 patients, and 1 patient had unreliable examination findings due to a cervical spinal cord injury). Computed tomographic findings of pneumoperitoneum and extravasation of enteral contrast material were uncommon but diagnostic (in 5 patients). Free fluid in the pelvis in the absence of a solid organ injury, bowel wall thickening, and fluid-filled loops of bowel were more frequently useful signs of possible intestinal injury (in 9 of the 18 patients) and led to earlier exploration when used in conjunction with physical examination as an indication for surgery. Most injuries were treated with segmental resection or suture repair, but enterostomies were required in 2 patients. Complications (i.e., the need for enterostomy and fascial dehiscence) were seen as a result of late or missed diagnosis, which could occur as late as 4 to 6 weeks after injury as intestinal obstruction due to stricture. CONCLUSIONS: The initial physical examination findings and CT evaluation can independently identify the presence of intestinal injury in approximately 25% of cases. In the remainder of cases, the awareness of the more subtle findings of bowel injury on a CT scan can complement the physical examination findings and potentially lead to a more timely intervention for bowel injury.

Adolescent↗
PubMed1997

NF-kappaB activation and modulation in hepatic macrophages during cholestatic injury.

Cholestatic liver injury induces an inflammatory response that follows the activation of hepatic macrophages. Constitutive activation of the transcription factor, NF-kappaB, was found in these macrophages over the course of hepatic injury. Since NF-kappaB activation has been shown to have a key role in the inflammatory process, the modulatory effects of the antioxidant, alpha-tocopherol succinate, and the glucocorticoid, dexamethasone, on NF-kappaB activation were examined in this study. Male Sprague Dawley rats underwent 2-7 days of common bile duct division and ligation (CBDL) or sham laparotomy. Hepatic macrophages were isolated by collagenase Pronase perfusion and purified by centrifugal elutriation. Activation was determined by electrophoretic mobility shift assay and ELISA. We determined that NF-kappaB activation in injured hepatic macrophages could only be inhibited by dexamethasone. Dexamethasone-mediated inhibition of NF-kappaB activation required the synthesis of a regulatory protein since cycloheximide-treated cells were resistant to its effects. Furthermore, dexamethasone-treated hepatic macrophages showed elevated steady-state levels of IkappaB-alpha mRNA, suggesting the role of IkappaB-alpha as a potential regulatory mediator. Consistent with constitutive transcriptional activation we showed constitutive secretion of TNF-alpha from injured hepatic macrophages which could be inhibited by dexamethasone. These data show for the first time, in a biologically significant model of hepatic injury, constitutive activation of the key inflammatory transcription factor NF-kappaB and cytokine TNF-alpha. These results support an approach focused on the NF-kappaB/IkappaB-alpha pathway as a critical target for therapeutic intervention during hepatic injury, and the consideration of possible steroid-based therapies.

Analysis of Variance↗
PubMed1996

Cholestatic liver injury down-regulates hepatic glutathione synthesis.

Hepatocellular injury caused by cholestasis may be caused in part by oxidant stress. The purpose of this study was to establish how acute cholestasis might alter hepatic glutathione homeostasis and to determine whether injured hepatocytes are capable of reverting to normal glutathione homeostatic mechanisms. Acute cholestasis was achieved by surgical ligation of the common bile duct in rats. Bile duct ligation induced a 3.7-fold increase in hepatic glutathione content over 4 days. This increase was not due to increased hepatic activity of gamma-glutamylcysteine synthetase (GCS); on the contrary, whole-liver GCS activity was substantially diminished in the bile duct-ligated liver to 34 and 11% of normal after 4 and 7 days, respectively. To determine if hepatocytes removed from the cholestatic environment maintained these changes in glutathione homeostasis, hepatocytes were isolated from bile ductligated livers and established in primary culture. In cells isolated after 4 days of bile duct ligation, the elevated hepatocyte glutathione content decreased and the low GCS activity increased over 2 days in culture. More importantly, the ability of postcholestatic hepatocytes to substantially increase their glutathione synthetic capacity by increasing GCS activity in response to stress was preserved. This compensatory increase was due primarily to new protein synthesis. Together, these observations suggest that acute cholestasis impairs the ability of the liver to synthesize glutathione by down-regulating the key regulatory enzyme for its synthesis in response to acutely elevated glutathione levels and that the impaired glutathione synthetic capacity is corrected after cells are removed from the cholestatic environment.

Animals↗
PubMed1996

Critical analysis of the operative treatment of Hirschsprung's disease.

OBJECTIVE: To critically analyze complications and long-term results of the operative treatment of Hirschsprung's disease. DESIGN: Medical records of patients with Hirschsprung's disease were reviewed retrospectively. Follow-up was obtained using a standardized telephone questionnaire. SETTING: Major pediatric referral center. PATIENTS: Eighty-two infants and children (68 boys, 14 girls) were treated for Hirschsprung's disease during a 20-year period (1975 to 1994). The age at diagnosis was younger than 30 days in 47 neonates (57%), 30 days to 1 year in 22 infants (27%), and older than 1 year in 13 children (16%). Aganglionosis was limited to the rectosigmoid region in 66 patients (81%). Fifty-five Soave (endorectal) and 27 Duhamel (retrorectal) primary pull-through operations were performed. MAIN OUTCOME MEASURES: Postoperative complications, reoperations, hospitalization, and current bowel habits. RESULTS: Eighteen children (67%) undergoing the Duhamel operation recovered uneventfully compared with 33 children (60%) undergoing the Soave operation. The complications following the Duhamel operation included enterocolitis in five cases (19%), rectal achalasia in four cases (15%), and persistent rectal septum in two cases (7%). Additional operations, which included myomectomy, rectal septum division, diverting enterostomy, and sphincterotomy, were required in seven patients (26%). Only one patient required more than one reoperation. In contrast, complications following the Soave operation included enterocolitis in 15 cases (27%), rectal stenosis in 12 (22%), anastomotic leak in four (7%), late perirectal fistula in three (5%), rectal prolapse in one (2%), and recurrent severe constipation in one (2%). Sixteen patients (29%) required additional operations, including diverting enterostomy, myomectomy, redo pull-through, sphincterotomy, fistulectomy, and revision of rectal prolapse. In this group nearly two reoperative procedures per patient were required. Telephone follow-up (mean, 89.3 months) after pull-through operations in 61 patients (74%) showed a mean of 2.8 stools per day, with 13 patients (21%) requiring daily medications. CONCLUSIONS: The most common operations (Soave and Duhamel) for Hirschsprung's disease result in an uneventful recovery in only 60% to 67% of patients. Although both Soave and Duhamel pull-through operations have nearly identical reoperation rates (26% vs 29%), complications after Soave pull-through operations often require multiple, more extensive procedures. Short-term total continence rates for both procedures are less than 50%, however, 100% became continent by 15 years after the pull-through procedure. Further refinement in operative technique and close follow-up are warranted.

Anastomosis, Surgical↗
PubMed1996

The inflammatory response in pediatric biliary disease: macrophage phenotype and distribution.

PURPOSE: Extrahepatic biliary obstruction in infants and children leads to ductal hyperplasia and portal fibrosis. Inflammatory mediators responsible for increased cellular proliferation and matrix deposition are hypothesized to result from the intrahepatic recruitment and activation of lymphocytes and macrophages (M phi). The authors previously showed components of this mechanism in studies that demonstrated increased adhesion molecule expression in biliary atresia, as well as evidence of altered hepatic M phi function during the course of experimental cholestatic liver injury. Therefore they sought determine the expression of macrophage receptor markers CD68 and CD14 in pediatric biliary disease. METHODS: Sixteen liver specimens were snap-frozen and cryosectioned onto polylysine-coated slides. Sections were stained with murine monoclonal antibodies to CD68 (resident M phi) and CD14 (monocyte-M phi lipopolysaccharide [LPS] receptor) glycoproteins. The sections were analyzed using a semiquantitative scale of proliferation and were position-graded from 0 to 3 (maximal). RESULTS: Blinded analysis showed that marked proliferation of CD68-positive cells occurred in five of the six patients with biliary atresia (BA) and in one patient who had severe cholestasis. Normal perisinusoidal liver M phi were found in specimens from patients with hepatitis (2), choledochal cyst (1), and congenital hepatic fibrosis (1). Similarly, expression of CD14 periportal M phi was found only in patients with BA or cholestasis (1.9 +/- 0.3 [mean +/- SEM]) and was absent in other diseases. Strong sinusoidal expression of CD14 was evident in all patients who had extrahepatic biliary obstruction. An early biopsy specimen from a premature infant with BA did not show cholestasis, fibrosis, CD68 Mø proliferation, or CD14 expression; however, another biopsy specimen, obtained further in the course of jaundice showed the progressive development of all features. CONCLUSION: These findings suggest proliferation of resident M phi in association with cholestasis. The presence of the LPS receptor on periportal cells during cholestatic liver injury points to a potential source of cytokines responsible for the inflammatory reaction of biliary atresia.

Antigens, CD↗
PubMed1996

Delayed rupture of the abdominal aorta in a child after a suspected handlebar injury.

Blunt abdominal trauma resulting in a laceration of the abdominal aorta is extremely rare. Only one previous example of this injury has been reported in a child. We present the clinical course and surgical management of blunt disruption of the infrarenal aorta in a 13-year-old boy with a subsequent delayed rupture of a third aortic laceration. This is the youngest patient to die from this type of injury after blunt abdominal trauma.

Abdominal Injuries↗
PubMed1996

Alterations in tumor necrosis factor-alpha expression by hepatic macrophages following acute cholestatic liver injury.

The liver is unique for its large resident macrophage (HM phi) population as a potential source of immunoregulatory cytokines. The present study was designed to determine HM phi function in a rat model of cholestasis (CBDL). Northern blot analysis of TNF-alpha mRNA showed a profound difference in the dose response to bacterial lipopolysaccharide (LPS) between sham and CBDL HM phi. Sham HM phi demonstrated an 8-fold difference in induction of TNF-alpha mRNA versus CBDL HM phi. TNF-alpha secretion, determined by enzyme-linked immunosorbent assay, was significantly higher from LPS-activated sham HM phi versus the same cells activated with Gram-positive bacterial peptidoglycan while CBDL HM phi were more responsive to peptidoglycan than to LPS. These results demonstrate stimulus- and response-specific functional alterations in the HM phi population during acute cholestatic injury. We speculate that these functional alterations are phenotypically induced in acute liver injury resulting in responses that are not characteristic of normal HM phi.

Acute Disease↗
PubMed1996

Lipopolysaccharide and tumor necrosis factor-alpha synergy potentiate serum-dependent responses of rat macrophages.

Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) are major mediators of sepsis and multiple organ failure. Serum-mediated macrophage activation requires lipopolysaccharide (LPS) and its serum binding protein, lipopolysaccharide binding protein as a ligand for the receptor CD14. This study was designed to determine whether cytokines participate in regulation of serum-mediated LPS activation. Rat macrophages were stimulated with LPS with and-without TNF-alpha or IL-1 beta and activation was determined by detection of TNF-alpha by specific enzyme-linked immunosorbent assay or TNF-alpha mRNA by Northern blot analysis. The addition of TNF-alpha but not IL-1 beta, in the presence of serum, leads to potentiation of macrophage activation after LPS stimulation. This effect could be specifically inhibited by neutralization of LPS with polymyxin B or an antibody against TNF-alpha. This study shows that LPS and TNF-alpha synergize to potentiate serum-mediated macrophage activation. These results demonstrate another element of the control mechanism of cytokine secretion following macrophage activation in sepsis.

Animals↗
PubMed1996

Molecular and cellular control points in pediatric liver injury and repair.

Several exciting areas of cellular and molecular biology of the liver have led to a better understanding of the mechanisms of pediatric liver injury and repair. Soon these advances will lead to treatment options for specialized areas of pediatric hepatology. Most of the current goals of surgical therapy lead to either successful hepatic resection for tumors or biliary decompression for atresia. We have come to accept the unfortunate fact that ongoing chronic liver disease ultimately leads to replacement by transplantation. The purpose of this article is to demonstrate areas of recent basic science advancement, directly related to pediatric liver disease, that may provide opportunities and new strategies to obviate the progression from early injury to end-stage liver disease or to augment repair of the injured liver.

Biliary Atresia↗
PubMed1995

Enterostomy and its closure in newborns.

OBJECTIVES: To examine the morbidity and mortality in 109 newborns who required enterostomy for intestinal necrosis, perforation, or obstruction and to analyze the complications associated with enterostomy closure. DESIGN: Data were collected retrospectively from hospital and office charts. Follow-up was 1 to 6 years. SETTING: Tertiary care, newborn intensive care unit at a children's hospital. PATIENTS: A referred sample of 109 newborns (aged 0 to 28 days) with bowel necrosis, obstruction, or perforation, who underwent enterostomy as part of their therapy. INTERVENTIONS: Operative formation of any enterostomy during laparotomy for bowel necrosis, obstruction, or perforation and subsequent closure. MAIN OUTCOME MEASURES: Morbidity and mortality associated with newborn enterostomy and its closure. RESULTS: Patients underwent jejunostomy (n = 31), ileostomy (n = 62), or colostomy (n = 16) for necrotizing enterocolitis (n = 79), atresia (n = 15), idiopathic perforation (n = 8), volvulus (n = 4), or meconium ileus (n = 3). Seventeen (16%) died postoperatively of sepsis, respiratory distress, further necrotizing enterocolitis, or intraventricular hemorrhage. Complications developed in 10 (34%) of the remaining 29 patients who underwent jejunostomy, whereas in 13 (26%) of 50 patients who underwent ileostomy and three (23%) of 13 patients who underwent colostomy, complications requiring revision developed. Ninety-two patients underwent enterostomy closure 14 to 65 days after enterostomy. Four later died of continuing respiratory distress and liver failure. Fifteen (56%) of 27 jejunostomies, 28 (57%) of 49 ileostomies, and nine (75%) of 12 colostomies were closed uneventfully, whereas two jejunostomy and eight ileostomy closures dehisced, requiring repeated enterostomy and secondary closure. All 10 children with anastomotic dehiscence had necrotizing enterocolitis originally, showed poor weight gain (< 30% per month), and had low serum albumin levels (22 +/- 3 g/L) compared with children with successful primary closure (> 30% weight gain per month; serum albumin level, 37 +/- 6 g/L; both Ps < .05). CONCLUSION: These data show that enterostomy is a potentially morbid condition in the newborn and is prone to complications but should be closed only when the child is in satisfactory nutritional condition.

Enterostomy↗
PubMed1995

CD14-lipopolysaccharide receptor activity in hepatic macrophages after cholestatic liver injury.

BACKGROUND: Increased septic complications and altered cytokine responses to bacterial endotoxins are lethal consequences of chronic liver disease. Kupffer cells (HM phi) control the clearance of lipopolysaccharide (LPS) and subsequent cytokine responses. The purpose of this study is to determine the phenotype and function of HM phi after cholestatic liver injury. METHODS: Male Sprague-Dawley rats underwent 4 days of common bile duct division and ligation or sham laparotomy. HM phi were isolated by collagenase-pronase perfusion and purified by centrifugal elutriation. RESULTS: Indirect immunofluorescence and Western blot analysis with monoclonal antibodies OX42 and ED9 showed that HM phi from cholestatic rats expressed MAC-1 (CD11b) and the LPS receptor CD14, respectively. HM phi from sham animals were negative for CD14 and CD11b by use of immunofluorescence; however, Western blot detected low levels of CD14 in controls. Functional analysis for tumor necrosis factor-alpha release after LPS stimulation showed that HM phi isolated from cholestatic livers exhibited serum (normal rat serum) dependent stimulation (1 ng/ml LPS + 1% normal rat serum; n = 12; p < 0.05 at 8 hours, t test) consistent with the presence of CD14 on their cell surface. CONCLUSIONS: This study shows that HM phi isolated after common bile duct division and ligation are phenotypically and functionally different from normal HM phi. The appearance of serum-dependent LPS responses within the injured liver may play an important role in the immunologic alterations associated with hepatic disease.

Animals↗
PubMed1994

The expression of regenerative growth factors in chronic liver injury and repair.

Acute hepatic injury initiates known cellular and molecular events for regeneration. In contrast, the molecular mechanisms of repair following chronic liver injuries have not been defined. Transforming growth factor alpha (TGF alpha) and hepatocyte growth factor (HGF) are hepatocyte mitogens whose in vivo expression in liver is central to the regulation of regeneration. To study the role of TGF alpha and HGF in liver injury and repair, we used a model of reversible biliary obstruction without a bilioenteric anastomosis. In rats, the common bile duct was obstructed either by a vessel loop suspended from the abdominal wall (LOOP) or by ligation and division (DLD). After 7 days of obstruction, animals were autopsied or were decompressed by subcutaneous release of the loop and then autopsied at 1, 2, 4, 7, or 10 days of postdecompression. Serum bilirubin (mg/dl) increased to 14.8 +/- 2.9 (DLD) and 10.3 +/- 3.0 (LOOP) (+/- SEM, NS, ANOVA) at 7 days of obstruction. Liver sections demonstrated equal ductal hyperplasia and collagen deposition after LOOP and DLD. Biliary decompression reversed bile duct proliferation and normalized bilirubin. Analysis of injured and repairing liver mRNA by ribonuclease protection assay showed that TGF alpha mRNA levels were not significantly altered by injury or during repair. HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression, peaking at 2 days of repair. This evidence of modulation of HGF during liver repair following chronic cholestatic injury suggests that HGF may have a role in cellular proliferation during repair or act as a compensatory growth factor during injury.

Animals↗
PubMed1994

Predictive capabilities of preoperative and postoperative pulmonary function tests in delayed repair of congenital diaphragmatic hernia.

To improve the survival of newborns with congenital diaphragmatic hernia (CHD), preoperative stabilization with conventional ventilatory therapy and extracorporeal membrane oxygenation (ECMO) have been used. Measurements that quantify pulmonary function may allow an accurate assessment of lethal pulmonary hypoplasia and predict outcome. Pulmonary function tests (PFTs) were obtained in 20 infants preoperatively and postoperatively; these included measurements of compliance, dynamic compliance, and tidal volume. Overall survival was 75%. Six surviving infants were initially managed with ventilator therapy alone, followed by repair (group 1). The remaining 14 patients, who were moribund at presentation or whose initial ventilator therapy failed, were placed on ECMO and received repair during bypass; nine survived (group 2), and five died (group 3). Compliance, dynamic compliance, and tidal volume obtained at initial presentation and immediately preoperatively were significantly higher for group 1 as compared with groups 2 and 3. Infants whose initial compliance was greater than 0.25 mL/cm H2O/kg and initial tidal volume was greater than 3.5 mL/kg did not require ECMO. Ultimate improvement in compliance was noted in 5 of 6 patients in group 1, 8 of 8 patients in group 2, and 5 of 5 in group 3. This improvement followed an initial decline in compliance in 9 of 14 survivors, from 15% to 76%. All six patients in group 1 had tidal volumes of more than 4 mL/kg, as did 7 of 9 patients in group 2. Only one patient among the ECMO nonsurvivors (group 3) had a postoperative tidal volume of this magnitude. These data suggest that initial PFTs may predict which infants will require ECMO.(ABSTRACT TRUNCATED AT 250 WORDS)

Extracorporeal Membrane Oxygenation↗
PubMed1993

Congenital duodenal obstruction: a 32-year review.

Although survival in infants with congenital intestinal obstruction has improved, duodenal obstruction continues to present unique challenges. One hundred thirty-eight newborns and infants (aged 0 to 30 days) were treated for congenital duodenal obstruction. Sixty-five were boys and 73 were girls. Sixty-one (45%) were premature. Forty-six had an intrinsic defect (atresia, web, stenosis, or duplication), 64 had an extrinsic defect (annular pancreas or malrotation with congenital bands), while 28 had various combinations of these. Presenting signs included vomiting (90%, bilious in 66%), abdominal distention (25%), dehydration (24%), and weight loss (17%). Although plain film abdominal x-ray was diagnostic in 58%, upper and/or lower gastrointestinal contrast studies were obtained in 71% of infants to confirm diagnosis. Thirty-eight percent of patients had associated anomalies, including Down's syndrome (11%), cardiac defects, other atresia, other trisomy syndrome, imperforate anus, and central nervous system anomalies. Fourteen patients (10%) had 3 or more other anomalies, many of which required additional surgical therapy. The operative repair of the various defects included Ladd's procedure for malrotation (31%), duodenoduodenostomy (14%), duodenojejunostomy (22%), gastrojejunostomy or gastroduodenostomy (4%), excision of the web and duodenoplasty (3%), or combination of the above (22%). Gastrostomy was placed in 61%. One hundred twenty-eight patients survived (93%). The causes of death were combinations of sepsis, pneumonia, brain hemorrhage, short bowel, and cardiac anomaly. Eight of 10 (80%) who died had other serious anomalies. Twenty patients (14%) required reoperation 5 days to 4 years postoperatively for obstructing lesions (5), wound dehiscence (3), anastomotic leak or dysfunction (6), other atresias (2), choledochal cyst (1), pyloric stenosis (1), and gastroesophageal reflux (2).(ABSTRACT TRUNCATED AT 250 WORDS)

Duodenal Obstruction↗
PubMed1993

The right lower quadrant "revisited".

Appendicitis remains a common and morbid illness in children. The history, epidemiology, pathophysiology, clinical presentation, diagnostic evaluation, and management of acute appendicitis are discussed in this article.

Acute Disease↗