Congenital diaphragmatic hernia: the impact of embryological studies

In recent years, a substantial research effort within the specialty of pediatric surgery has been devoted to improving our knowledge of the natural history and pathophysiology of congenital diaphragmatic hernias (CDH) and pulmonary hypoplasia (PH). However, the embryological background has remained elusive because certain events of normal diaphragmatic development were still unclear and appropriate animal models were lacking. Most authors assume that delayed or inhibited closure of the diaphragm will result in a diaphragmatic defect that is wide enough to allow herniation of the gut into the fetal thoracic cavity. However, we feel that this assumption is not based on appropriate embryological observations. To clarify whether it was correct, we restudied the morphology of pleuroperitoneal openings in normal rat embryos. Shortly before, a model for CDH and PH had been established in rats using nitrofen (2,4-di-chloro-phenyl-p-nitrophenyl ether) as teratogen. We used this model in an attempt to answer the following questions: (1) When does the diaphragmatic defect appear? (2) Are the pleuroperitoneal canals the precursors of the diaphragmatic defect? (3) Why is the lung hypoplastic in babies and infants with CDH? In our study we made following observations: (1) The typical findings of CDH and PH cannot be explained by inhibited closure of the pleuroperitoneal "canals". In normal development, the pleuroperitoneal openings are always too small to allow herniation of gut into the thoracic cavity. (2) The maldevelopment of the diaphragm starts rather early in the embryonic period (5th week). The lungs of CDH rats are significantly smaller than those of control rats at the end of the embryonic period (8th week). (3) The maldevelopment of the lungs in rats with CDH is "secondary" to the defect of the diaphragm. (4) The defect of the lungs is "structural" rather than "functional". Complete spontaneous correction of these lung defects is unlikely even after fetal intervention. (5) The "fetal lamb model" does not completely mimic the full picture of CDH, because the onset of the defect lies clearly in the fetal period. We believe that our rat model is better. It is especially useful for describing the abnormal embryology of this lesion

Outcome reporting in randomised controlled trials and meta-analyses of appendicitis treatments in children: a systematic review

Background: Acute appendicitis is the most common surgical emergency in children. Despite this, there is no core outcome set (COS) described for randomised controlled trials (RCTs) in children with appendicitis and hence no consensus regarding outcome selection, definition and reporting. We aimed to identify outcomes currently reported in studies of paediatric appendicitis. / Methods: Using a defined, sensitive search strategy, we identified RCTs and systematic reviews (SRs) of treatment interventions in children with appendicitis. Included studies were all in English and investigated the effect of one or more treatment interventions in children with acute appendicitis or undergoing appendicectomy for presumed acute appendicitis. Studies were reviewed and data extracted by two reviewers. Primary (if defined) and all other outcomes were recorded and assigned to the core areas ‘Death’, ‘Pathophysiological Manifestations’, ‘Life Impact’, ‘Resource Use’ and ‘Adverse Events’, using OMERACT Filter 2.0. / Results: A total of 63 studies met the inclusion criteria reporting outcomes from 51 RCTs and nine SRs. Only 25 RCTs and four SRs defined a primary outcome. A total of 115 unique and different outcomes were identified. RCTs reported a median of nine outcomes each (range 1 to 14). The most frequently reported outcomes were wound infection (43 RCTs, nine SRs), intra-peritoneal abscess (41 RCTs, seven SRs) and length of stay (35 RCTs, six SRs) yet all three were reported in just 25 RCTs and five SRs. Common outcomes had multiple different definitions or were frequently not defined. Although outcomes were reported within all core areas, just one RCT and no SR reported outcomes for all core areas. Outcomes assigned to the ‘Death’ and ‘Life Impact’ core areas were reported least frequently (in six and 15 RCTs respectively). / Conclusions: There is a wide heterogeneity in the selection and definition of outcomes in paediatric appendicitis, and little overlap in outcomes used across studies. A paucity of studies report patient relevant outcomes within the ‘Life Impact’ core area. These factors preclude meaningful evidence synthesis, and pose challenges to designing prospective clinical trials and cohort studies. The development of a COS for paediatric appendicitis is warranted

Calculation of delay and rise times for uniformly distributed RLC line

In this theoretical paper, simple explicit delay and rise time expressions for uniformly distributed RLC line are presented. Derivation of these expressions are based on Elmore's definitions. Transfer function for an n-cell RLC ladder network with capacitive load is obtained by using transmission parameter matrix for each cell. In calculation of transfer function, transmission line is modeled by a lumped parameter network. Explicit delay and rise time formulas are computed from transfer function using Elmore's definitions. Examples are included to exhibit the use of the formulations given for delay and rise times. As a special case, proposed expressions are verified with SPICE 5 circuit analysis program for n = 2, 3, 5 -cell ladder networks loaded with capacitor

The role of nitric oxide in an experimental necrotising enterocolitis model

Background: Necrotising enterocolitis (NEC) causes a significant  life-threatening gastrointestinal system (GIS) disease with severe mortality and morbidity, particularly in premature infants. Nitric oxide (NO) has many functions in the GIS. Therefore, in the present study, we evaluated the effects of NO in experimentally induced NEC of newborn 1-dayold rats following hypoxia/reoxygenation (HR).Materials and Methods: Thirty Wistar albino rats (weight, 5¡V8 g) were randomly divided into three groups: group 1 (HR), group 2 (HR + nitroglycerine), and group 3 (control). HR was achieved by placing the ratin carbon dioxide (CO2) for five minutes at 22oC, which was followed by five minutes of 100% oxygen. After HR, nitroglycerine was administered for three days at 50 µg/Kg/day. On day 4, the rats were decapitated and the intestines between the duodenum and sigmoid colon were resected and histopathologically examined.Results: The histopathological fi ndings of groups 1 and 2 were  characteristic of NEC. Intestinal injury in group 1 was signifi cantly more prevalent than that in group 2 (X2 = 21.55, P = 0.000). The intestinal injury score in group 3 was signifi cantly lower than that in the other groups (P < 0.05).Conclusions: NO treatment was effective for treating experimentally induced NEC.Key words: Hypoxia reoxygenation, necrotising enterocolitis, nitric oxide, premature, rat, treatmen

Gastric serosal tear due to congenital pyloric atresia: A rare anomaly, a rare complication

Congenital pyloric atresia (CPA) is a very rare malformation with unknown aetiology. It has has numerous complications including gastric perforation, aspiration pneumonia. Gastric perforations in newborns occur by three mechanisms: trauma, ischaemia, or spontaneous. Here, we report a newborn with CPA presenting with gastric serosal tearing without full-cut gastric perforation. The diagnosis was confi rmed with the help of plain abdominal radiograph, ultrasound, contrast-study, and at operation. Treatment of CPA is surgery irrespective of the type of atresia. We performed serosa repair and then the solid, cordlike atretic pylorus was excised with accompanying gastroduodenostomy. Our patient had an uneventful course and was discharged at the end of the second postoperative week.Key words: Congenital abnormalities, ıntestinal atresi