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During the 15 year period between 1958 and 1973 the authors operated on 21 cases of pyloric stenosis caused by biliary calculi, occuring in 12 percent of their patients suffering from pyloric stenosis. They call attention to the fact that cholecystectomy made in good time can prevent pyloric stenosis being a complication of neglected cases.
Two infants with recurrent episodes of vomiting had upper gastrointestinal barium studies that did not show radiographic features of pyloric stenosis. However, follow-up abdominal sonograms done 1-2 weeks later documented hypertrophic pyloric stenosis, which led to surgery. This entity is not congenital, but an evolving acquired lesion. Therefore, ultrasound is an excellent modality to evaluate and monitor patients clinically suspected of developing hypertrophic pyloric stenosis despite their initially negative imaging studies.
Although the etiologies of Hirschsprung's disease and infantile hypertrophic pyloric stenosis remain unclear, it is certain that in Hirschsprung's disease, there is an absence of myenteric ganglia. In pyloric stenosis, there is a decreased number of ganglia, but this may be secondary phenomenon. The occurrence of both Hirschsprung's disease and pyloric stenosis in any single patient is uncommon, disputing a common etiology on statistical grounds. The authors have recently seen two infants with both diseases, and have reviewed the histology and pathophysiology analyzing the possibility of a single cause.
BACKGROUND: The pathogenesis of infantile hypertrophic pyloric stenosis (IHPS) is not fully understood. Hypertrophy of the pyloric muscle is probably regulated by growth factors. Recent studies reported an increase in the local synthesis of insulin-like growth factor-1 (IGF-1). There are no reports concerning platelet-derived endothelial cell growth factor (PDEGF) playing an important role in the pathological angiogenesis. The aim of this study was to analyze the expressions of IGF-1 and PDEGF by immunohistochemistry (IHC) in the muscularis propria of the pyloric muscle in children with IHPS. MATERIAL/METHODS: Twenty-two muscle biopsies were obtained at the time of pyloromyotomy. The control group consisted of seven children. Specimens were evaluated by routine histopathological methods and by immunohistochemistry using monoclonal mouse anti-PDEGF or -IGF-1 antibodies. Cells showing positive reaction were counted in five random 200x high-power fields. Values were expressed as the mean +/-SD of the real expression area of the analyzed marker to the total analyzed area. RESULTS: In children with IHPS the average area of PDEGF expression was 62+/-52.5, whereas in the control group it was 15+/-12.1. The average area of IGF-1 expression was 1037+/-491.9) in study group and 259+/-221.44 in the controls. Statistically significant differences were found. CONCLUSIONS: These results show a local increase in the expressions of IGF-1 and PDEGF in the muscularis propria of the pyloric muscle in children with IHPS, which may have implications to the pathogenesis of the disease.
INTRODUCTION: In spite of the clinical experience about infantil Hypertrophic Pyloric Stenosis (IHPS), its etiopathology remains unknown. Recent studies have been focussed in immunohistochemistry techniques for valuing the neuronal development in the pyloric muscle. MATERIAL AND METHODS: We took biopsy from 10 babies diagnosed of IHPS and 10 babies with similar age, died because of other causes. Immunohistochemical study was performed using monoclonal antibodies: S100 protein, GFAP, enolasa and neurofilaments NF. The results were showed semi-quantitativement as strong (++), moderate (+) and absent (-). Immunotinction of the myenteric plexus (ganglion cells and satellite) and nervous fibers of the muscle layer, were done. RESULTS: We observed a poor immunoreactivity in the muscle layer (longitudinal and circular) in the 60-70% of specimens of pyloric muscle in babies with IHPS. GFAP were absent in the 80% in the myenteric plexus. This poor innervation may be related to the etiopathogenesis of pyloric stenosis and hypertrophy.
This article reports a full-term infant with Hirschsprung disease (HD) who was diagnosed to have hypertrophic pyloric stenosis (HPS) and agenesis of corpus callosum (ACC). Pyloric stenosis is known to be associated with HD. To our knowledge, the combination of Hirschsprung disease, hypertrophic pyloric stenosis and agenesis of corpus callosum has not been reported previously. We believe these three conditions are due to an underlying pathophysiologic mechanism.
The authors report on a male infant aged 4(1/2) weeks who underwent a pyloromyotomy for hypertrophic pyloric stenosis. After an uncomplicated postoperative course with normal feeding and weight gain, projectile vomiting reoccurred. The boy underwent a repyloromyotomy for recurrent hypertrophic pyloric stenosis. The underlying cause of a recurrent hypertrophic pyloric stenosis after a successful pyloromyotomy may be explained by the natural history of the disease.
In the past 3 years, three children (ages 2, 4, and 8 years) suffering from peptic pyloric stenosis and repeated vomiting were treated in our department with balloon dilatation followed by H2-receptor antagonist therapy. After the dilatation, all three patients could take solid food without vomiting. There were no complications as a result of the procedures. During a mean follow-up of 17 months (range, 5-30) there was no recurrence of symptoms. The method of dilatation is described, and we recommend it as an option for the initial nonoperative treatment of pediatric peptic pyloric stenosis. The long-term results of balloon dilatation of peptic pyloric stenosis will, however, require further evaluation.
In order to evaluate the potential role of gastrin in the etiology of pyloric stenosis, serum gastrin levels were measured in cord blood of affected infants, matched controls, and mothers of both. No differences were identified when values from infants with pyloric stenosis were compared with those from control infants. Mean cord serum gastrin levels of the infants were significantly greater than the mean maternal gastrin levels. The data effectively dismiss the possibility that elevated serum gastrin concentration in mother or infant at the time of delivery can be implicated as a cause of pyloric stenosis.
We report a hypertrophic pyloric stenosis case with an unusual initial presentation of seizures and Bartter's syndrome like symptoms. This case suffered from vomiting, diarrhea and poor appetite for several days, and seizures developed after these symptoms. From laboratory tests, hypochloremic and hypokalemic metabolic alkalosis associated with hyperreninemia, hyperaldosteronism and normal blood pressure were noted. Pseudo-Bartter's syndrome was diagnosed through these clinical and laboratory tests. Although the first abdominal echo was negative, we still speculated about the peculiar symptoms of vomiting and it's relationship to pseudo-Bartter's syndrome. After all, we found the hypertrophic pyloric stenosis through an upper gastrointestinal series. From these experiences, we postulated that it's very important to put the hypertrophic pyloric stenosis into the differential diagnosis of pseudo-Batter's syndrome.
Genitourinary anomalies were looked for in patients with congenital hypertrophic pyloric stenosis. In a prospective series of 64 patients investigated by intravenous pyelography, 13 were abnormal (20.6%). In a retrospective series of 232 patients, 6 had anomalies of the upper urinary tract (2.7%). In this latter series the incidence of inguinal hernia (3.4%), undescended testes (3.0%), and hypospadias (0.9%) was determined. In another 10 patients urinary tract anomalies (5), urinary infection (2), and a significant family history (3) were found associated with congenital pyloric stenosis. As the incidence of these anomalies is greater than expected, which suggests an interrelationship, a hypothesis has been proposed linking genetic factors and the metabolism of gastrin with the etiology of congenital hypertrophic pyloric stenosis.
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As part of a long-term follow-up of structural disorders present at birth or shortly thereafter in infants born at Group Health Cooperative of Puget Sound, all infants with a diagnosis of pyloric stenosis born between July 1, 1977 and June 30, 1982, were identified. Automated pharmacy profiles were examined to determine whether an association between maternal Bendectin use in the first trimester and infantile hypertrophic pyloric stenosis existed. Among the 3,835 women exposed to Bendectin while pregnant, in this group of 13,346 births, 13 had infants who developed pyloric stenosis, and among the 9,511 women not exposed, 13 had infants who developed pyloric stenosis, resulting in a risk ratio estimate of 2.5 (95% confidence interval (CI) 1.2-5.2). When mothers were divided according to the number of prescriptions for Bendectin filled, the relative risk estimate increased from 1.2 (95% CI 0.4-4.4) in women who filled only one prescription to 7.6 (95% CI 4.9-11.6) in women who filled five or more prescriptions for Bendectin during their pregnancy.
Two cases of infantile hypertrophic pyloric stenosis in infants who were exclusively breastfed are reported. In both cases dietetic management succeeded in avoiding surgery. In one case human milk was substituted with casein hydrolysate formula, while in the other cow's milk was excluded from the diet of the mother. A possible casual relationship between cow's milk intolerance and infantile hypertrophic pyloric stenosis is discussed.
The sonographic findings of 22 infants suspected of suffering from hypertrophic pyloric stenosis are reported. The central importance of the "cockade-sign" for the sonographic diagnosis of hypertrophic pyloric stenosis is stressed. Because of its accuracy sonography can replace radiological examination of the stomach in most cases.
BACKGROUND: Surgery and balloon dilatation are perceived by many as the principal treatments for peptic pyloric stenosis. We questioned whether, with the availability of modern acid suppressant treatment, this was still appropriate or whether patients could be managed with medical treatment alone. METHODS: Seventeen consecutive patients with peptic pyloric stenosis were treated with endoscopic gastric drainage, followed by oral omeprazole in 15 or cimetidine in two. Gastric emptying half times for solids and liquids were assessed in 11 of the 17 patients when they had become asymptomatic. RESULTS: Endoscopic drainage and medical treatment successfully relieved symptoms in all 17 patients, although the gastric emptying studies in 11 patients still showed prolongation in eight. Symptoms resolved completely after a mean of 28 days. Five patients relapsed when changed from omeprazole to cimetidine treatment, but all responded to re-starting omeprazole. Four patients remain well on cimetidine alone. CONCLUSIONS: Medical treatment preceded by endoscopic gastric drainage was effective in all patients in this series and may be the preferred choice of treatment in patients with pyloric stenosis.
The gastrointestinal tract harbors several populations of peptide containing nerve fibers. Among the gut neuropeptides are vasoactive intestinal peptide (VIP), substance P, enkephalin, and gastrin releasing peptide (GRP). We have examined specimens from five patients with pyloric stenosis and from five controls immunocytochemically with respect to the density of nerve fibers containing VIP, substance P, enkephalin, or GRP. In the control specimens VIP and enkephalin fibers were fairly numerous, whereas substance P and GRP fibers were few. In the pyloric stenosis patients the density of VIP fibers and enkephalin fibers was reduced in the smooth muscle. In the myenteric ganglia there was no such reduction. Substance P and GRP fibers were rare as in controls. The results indicate a reduction of VIP and enkephalin fibers in smooth muscle in pyloric stenosis patients and may be interpreted to support the view that an impaired neuronal function is involved in the pathophysiology of pyloric stenosis.
PURPOSE: For diagnosis of infantile hypertrophic pyloric stenosis (HPS), ultrasonography (US) is a useful and objective diagnostic method. In the current study, pyloric diameter, muscular thickness, and pyloric length were measured in normal infants (n = 26) and infants which is an adequate (n = 57). Each score was assigned to relevant measurements, and diagnostic criteria obtained with a scoring system were prepared using statistical skills by the probit analysis. METHODS: For scoring, points were given to relevant measurements in conformity with the probit analysis. Zero points were given to patients with no possibility of HPS, 1 point to those with less than 25% probability, 2 points to those with 25% or more but less than 50% probability, and 3 points to patients with 50% or more probability. Points were totaled, and analysis was performed. RESULTS: The composite score was evaluated by probit analysis, and cases with a composite score of 2 or less were all included in the normal group, whereas those with a composite score of 3 or more were all in the HPS group. Both groups could thereby be 100% identified. CONCLUSION: US was able to diagnose cases with overall score of 2 or less as normal and those with overall score of 3 or higher as having HPS. In addition, after the current diagnostic criteria were prepared, preoperative diagnoses were performed prospectively using them for vomiting neonates and infants, and all cases were correctly discriminated and diagnosed. These findings indicate our ultrasonographic diagnosis criteria are useful for diagnosing HPS.