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Results for “PYLORIC STENOSIS”

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PubMed1999

Postoperative ad lib feeding for hypertrophic pyloric stenosis.

PURPOSE: The aim of this study was to compare three methods of postoperative feeding after pyloromyotomy for hypertrophic pyloric stenosis (HPS). METHODS: The authors reviewed retrospectively the charts of 308 patients who underwent pyloromyotomy for HPS from 1984 to 1997. Nineteen patients had prolonged hospitalization for other reasons and were excluded from the study, leaving 289 patients for analysis. All procedures were performed by a single group of pediatric surgeons. The individual preferences of these surgeons resulted in three different feeding schedules: R, strictly regimented (>12 hours nothing by mouth, then incremental feeding over > or =24 hours), I, intermediate (>8 hours nothing by mouth, then incremental feeding over <24 hours), or A, ad lib (< or =4 hours nothing by mouth, with or without a single small feeding, then ad lib feedings). RESULTS: Of the 289 patients, 248 (80.5%) were boys. The average age of the patients was 5.64 weeks (range, 1 to 21 weeks). A total of 265 of 289 (92%) were full term. Thirty-nine of 289 (13.5%) had a family history positive for pyloric stenosis. A total of 104 of 289 (36%) were first-born infants, 89 of 289 (31%) were second born. The diagnosis of pyloric stenosis was made by a combination of physical examination findings and diagnostic image for most patients. An "olive" was palpated in 60.6% of the patients. Sixty percent (60.4%) of patients had an upper gastrointestinal series performed, and 42.5% were examined by ultrasonography. Overall, 53% of the patients had postoperative emesis. Only 3.5% had emesis that persisted greater than 48 hours after surgery. Patients fed ad lib after pyloromyotomy had slightly more emesis (2.2 A v. 1.2 R, and 0.7 I episodes, P = .002), but tolerated full feedings sooner than patients fed with a regimented or intermediate schedule. No patient required additional therapy or readmission after tolerating two consecutive full feedings, suggesting that this might be a suitable discharge criterion for most patients with HPS.

Feeding Methods↗

PubMed1998

A comparison of awake versus paralyzed tracheal intubation for infants with pyloric stenosis.

UNLABELLED: This prospective, nonrandomized, observational study of 76 infants with pyloric stenosis was conducted at an academic children's hospital and compared awake versus paralyzed tracheal intubation in terms of successful first attempt rate, intubation time, heart rate (HR) and arterial hemoglobin oxygen saturation (SpO2) changes, and complications. Three groups were determined by intubation method: awake (A) with an oxygen-insufflating laryngoscope, after rapid-sequence induction (R), or after modified rapid-sequence induction (M) including ventilation through cricoid pressure. Successful first attempt intubation rate was 64% for Group A versus 87% for paralyzed Groups R and M (P = 0.028). Median intubation time was 63 s in Group A versus 34 s in Groups R and M (P = 0.004). Transient, mild decreases in mean HR and SpO2 and incidences of significant bradycardia and decreased SpO2 did not vary by group. Complications, including bronchial or esophageal intubation, emesis, and oropharyngeal trauma, were few. Senior anesthesiologists intervened in four tracheal intubations. We advocate anesthetized, paralyzed tracheal intubation because struggling with conscious infants takes longer, often requires multiple attempts, and prevents neither bradycardia nor decreased SpO2. After induction, additional mask ventilation with O2 confers no advantage over immediate tracheal intubation in preserving SpO2. IMPLICATIONS: In our children's hospital, awake tracheal intubation was not superior to anesthetized, paralyzed intubation in maintaining adequate oxygenation and heart rate or in reducing complications, and should be abandoned in favor of the latter technique for routine anesthetic management of otherwise healthy infants with pyloric stenosis.

Anesthesia↗

PubMed2006

Proton pump inhibition is a feasible primary alternative to surgery and balloon dilatation in adult peptic pyloric stenosis (APS): report of six consecutive cases.

INTRODUCTION: Surgery has been the gold standard in the treatment of adult pyloric stenosis (APS). The introduction of proton pump inhibitors (PPIs) in 1989 revolutionised the treatment of peptic ulcer disease and its complications. PATIENTS AND METHODS: We carried out a prospective study to evaluate the effectiveness of PPIs as an alternative to surgery for treatment of APS. Six consecutive patients admitted with a diagnosis of adult peptic pyloric stenosis between November 1999 and August 2002 were studied. The diagnosis was confirmed with endoscopy. All patients were commenced on a twice-daily dose of intravenous PPI. This was changed to oral treatment after 2 days. Main outcome measures evaluated were resolution of symptoms on PPIs and failure of medical therapy. RESULTS: There were five females and one male. Median age at diagnosis was 72 years (range, 30-90 years). Median duration of symptoms was 2 weeks (range, 1-5 weeks). Of the patients, five had a history of peptic ulcer disease. Complete resolution was achieved in 5 patients (83%). Median duration for resolution of symptoms was 9 days (range, 5-14 days). All patients were changed to oral PPIs after 2 days. One patient did not respond to oral therapy and required surgical intervention (pyloroplasty). Median follow-up was 26 months (range, 6-48 months). There was no recurrence of symptoms. All patients were discharged on low-dose PPI. CONCLUSIONS: This study supports the view that proton pump inhibitors are a safe and feasible alternative to surgery in adult pyloric stenosis secondary to peptic ulcer disease.

Adult↗

PubMed2000

Molecular cytogenetic characterisation of partial trisomy 9q in a case with pyloric stenosis and a review.

Partial trisomy 9q represents a rare and heterogeneous group of chromosomal aberrations characterised by various clinical features including pyloric stenosis. Here, we describe the case of a 1 year old female patient with different dysmorphic features including pyloric stenosis and prenatally detected partial trisomy 9q. This partial trisomy 9q has been analysed in detail to determine the size of the duplication and to characterise the chromosomal breakpoints. According to the data gained by different molecular cytogenetic techniques, such as fluorescence in situ hybridisation (FISH) with whole and partial chromosome painting probes, yeast artificial chromosome (YAC) probes, and comparative genomic hybridisation (CGH), the derivative chromosome 9 can be described as dup(9)(pter-->q22. 1::q31.1-->q22.1::q31.1--> q22.1::q31.1-->qter). Four breakpoint spanning YACs have been identified (y806f02, y906g6, y945f5, and y747b3) for the proximal breakpoint. According to this new case and previously published data, the recently postulated putative critical region for pyloric stenosis can be narrowed down to the subbands 9q22.1-q31.1 and is the result of either partial trisomy of gene(s) located in this region or a gene disrupted in 9q31.

Chromosome Banding↗

PubMed1994

A medium term follow-up study of patients with hypertrophic pyloric stenosis.

A structured questionnaire was sent to the parents of 120 children from a cohort 192, who had undergone a pyloromyotomy for pyloric stenosis at Westmead Hospital during the years 1984-91. Information was gained from 85 children in 82 families regarding gastrointestinal complaints and family history of pyloric stenosis. There were few gastrointestinal problems, no reports of recurrent abdominal pain, but two reports of clinically significant vomiting (2.3%) and one of infantile colic. Of the 85 individuals studied, 21 (24.7%) had a positive family history of pyloric stenosis, a higher frequency than previously reported.

Child↗

PubMed1992

[Functional pyloric stenosis in sheep].

The clinical findings, the autopsy and the histology of functional pyloric stenosis in three sheep between four and eight years old are described. A chronic ulcer with structural alterations of the pyloric protuberance was found in the first animal. In the second sheep there were several polyps in the pylorus, and in the third erosions throughout the whole pylorus, and a few hyperplastic areas of epithelium at the junction between pylorus and duodenum. The abomasum was moderately to extremely congested and the contents weighed between 6.7 and 13 kg. In addition to these findings chronic and unspecific abomaso-duodenitis was found in all three sheep. These three cases can be attributed to the distal functional pyloric stenosis (Hoflund syndrome).

Abomasum↗

PubMed1993

Pyloric stenosis: the Christchurch experience.

OBJECT: Evaluation of the performance of a general paediatric unit in diagnosis and treatment of infantile hypertrophic pyloric stenosis, including morbidity and measurable outcomes in relationship to changing management. METHODS: Retrospective case note audit. RESULTS: In the 11 year period 1980-91, 103 infants underwent surgical correction of pyloric stenosis, after correction of metabolic disturbance. There was a predominance of males (82.5%), but the incidence of first born infants affected was no greater than the population birth order. While the clinical diagnosis was firm in the majority of infants, over 75% had at least one radiologic imaging procedure. On objective criteria, 80% of patients were less than 5% dehydrated, despite having electrolyte and acid-base derangement. The relatively high incidence of mucosal perforation (31.1%) did not lead to further morbidity. The incidence of postoperative vomiting (19.4%) was significantly less than in previously reported series. There were no deaths, one patient suffered longterm neurologic deficit following profound hypoglycaemia. A change in preoperative management to aggressive rehydration did not reduce morbidity, and was associated with an increased median postoperative stay. CONCLUSIONS: Pyloric stenosis remains a relatively common surgical problem of infancy. The cornerstone of diagnosis remains a clinical one; however there is a place for radiology. Operative repair is elective, following correction of metabolic derangement. In a general paediatric unit, long term sequelae of initial morbidity are rare.

Body Weight↗

PubMed1994

The ultrasonic diagnosis of infantile hypertrophic pyloric stenosis: technique and accuracy.

The role of ultrasound for the diagnosis of pyloric stenosis has yet to be definitely established. We have carried out 147 ultrasound examinations of 142 infants (99 male and 43 female) with a history of projectile vomiting or the possibility of a pyloric mass. Measurements of the pyloric canal length, transverse pyloric diameter and muscle wall thickness were taken from a longitudinal view of the pylorus and related to previously described control data. The accuracy of the ultrasound examination was related to the finally established diagnosis. The results obtained revealed a sensitivity of 97% and specificity of 99% with positive predictive value of 99%. The three diagnostic errors (1 false positive and 2 false negative) occurred during the 'learning curve' of the radiologists and were the 15th, 29th and 35th cases examined, indicating that almost a 100% accuracy can potentially be achieved. This study confirms that ultrasound examination is the first line of investigation in a child in whom the clinical diagnosis of hypertrophic pyloric stenosis is uncertain and indicates that unnecessary surgery can thereby be prevented.

False Negative Reactions↗

PubMed1995

Two brothers with an unbalanced 8;17 translocation and infantile pyloric stenosis.

Two half-brothers are described who had developmental delay and minor dysmorphic features, both of whom had operative treatment for pyloric stenosis. They had identical unbalanced karyotypes: 46,XY,-17,+der(17)t(8;17) (q24;q25). This was inherited from their mother who had the balanced form of the translocation. She was of normal intelligence and had no history of pyloric stenosis herself or in her extended family. It is suggested that the unbalanced chromosomal rearrangement could have been associated with the development of pyloric stenosis in these two brothers.

Adult↗

PubMed2005

Pyloric stenosis in in vitro fertilized triplets--is it a coincidence?

Infantile hypertrophic pyloric stenosis was previously reported in multiple births, but there were only 3 triplets in the literature and all were naturally conceived. Assisted reproductive technologies, such as in vitro fertilization, are accused for increasing the risk for some anomalies in children. Triplets of in vitro fertilization, all of whom were operated on because of pyloric stenosis, are presented.

Female↗

PubMed2003

Chronic gastric volvulus and hypertrophic pyloric stenosis in an infant.

Chronic secondary mesenteroaxial gastric volvulus associated with hypertrophic pyloric stenosis has rarely been mentioned in the general medical literature. We report the case of a 2-month-old boy whose clinical symptoms, which included distension of the stomach and projectile vomiting, suggested the diagnosis of hypertrophic pyloric stenosis but who was later diagnosed with chronic secondary mesenteroaxial gastric volvulus. Sonographic examination revealed findings consistent with a rotated stomach, and subsequent plain chest radiography demonstrated a left diaphragmatic eventration. An upper gastrointestinal series radiographic examination with barium contrast enhancement confirmed the diagnosis of mesenteroaxial gastric volvulus. Surgery was performed, and the boy recovered well. A follow-up sonographic examination performed 3 months post-operatively revealed no abnormalities. This case demonstrates that primary or secondary gastric volvulus, although rare in children, should be considered in the differential diagnosis of pediatric patients with a history of vomiting.

Chronic Disease↗

PubMed2004

Patient with partial trisomy 9q and learning disability but no pyloric stenosis.

Partial trisomy of the long arm of chromosome 9 represents a very rare and heterogeneous group of chromosomal aberrations. Associated clinical features include learning disability and pyloric stenosis. We present the first patient to be reported with a duplication of the chromosome region 9q22.1-->q33. The patient (female, age 17 years) presented with growth retardation, microcephaly, facial dysmorphia, oesophageal atresia, aortic stenosis, ventricular septal defect, atrial septal defect II, hypothyroidism, and learning disability, but no pyloric stenosis. A review of all cases of partial trisomy 9q reported in the literature demonstrates that learning disability is a characteristic feature of this group of chromosomal aberrations. However, there are cases of duplications of the same chromosome 9 material, with and without pyloric stenosis. This study provides new information for future genetic counselling, especially in cases of prenatal diagnosis of partial trisomy 9q.

Abnormalities, Multiple↗

PubMed2001

Sonography and color Doppler sonography for monitoring conservatively treated infantile hypertrophic pyloric stenosis.

OBJECTIVE: To evaluate the role of sonography in infants with hypertrophic pyloric stenosis undergoing conservative medical treatment. METHODS: Twenty-two infants (17 male and 5 female; age range, 1-12 weeks) were clinically and sonographically considered suitable for conservative treatment and underwent follow-up during the course of the disease. Sonography was performed under a standardized protocol and included color Doppler sonography. RESULTS: Fifteen infants (mean age, 9 weeks) needed surgery. They initially had a mean pyloric length of 18 mm, a diameter of 10.5 mm, and a wall thickness of 4 mm, with visible passage of food into the duodenum. These values deteriorated during follow-up (mean preoperative values: length, 20 mm; diameter, 12 mm; and wall thickness, 4.5 mm); furthermore, passage of food through the pyloric canal ceased. Seven infants (mean age, 3 weeks) were successfully treated conservatively Their initial mean pyloric measurements were slightly smaller (length, 15 mm; diameter, 10 mm; and wall thickness, 3.8 mm) and did not deteriorate during follow-up. In all of them, sonography showed improvement of passage through the pyloric canal within several days, as shown and documented by color Doppler sonography; morphologic changes persisted longer despite clinical improvement. CONCLUSIONS: Sonography, including color Doppler sonography, is a valuable tool for monitoring infants with hypertrophic pyloric stenosis undergoing conservative treatment; however, initial sonograms cannot predict the further course of the disease.

Atropine Derivatives↗

PubMed1996

Early infantile hypertrophic pyloric stenosis: surgery at 26 hours of age.

A newborn baby with hypertrophic pyloric stenosis on the first day of life is presented with a review of the literature regarding this early age of onset. The average age at onset of symptoms is usually 3.5 weeks. Very rarely symptoms start at birth or are sometimes delayed until 3 months of age or more (20). There are several reports (2, 3, 5, 6, 11, 14, 18, 19) of infants with onset of symptoms and eventual operation within the first day or two of life and indeed with vomiting from birth (2, 3, 5, 6, 11, 14, 18, 19). To our knowledge this case report documents the youngest baby ever operated upon for infantile hypertrophic pyloric stenosis at 26 hours of age.

Fatal Outcome↗

PubMed1999

Jaundice with hypertrophic pyloric stenosis as an early manifestation of Gilbert syndrome.

Jaundice associated with hypertrophic pyloric stenosis was recognised in three patients; previous reports have suggested that this is a possible early manifestation of Gilbert syndrome. Most patients with Gilbert syndrome are homozygous for a (TA)(7)TAA polymorphism in the gene promoter coding for bilirubin glucuronosyltransferase. Two of the reported patients were homozygous for the (TA)(7)TAA polymorphism whereas the third was heterozygous for the same polymorphism. Furthermore, no other factors contributing to jaundice in the three patients were found. These results suggest that jaundice associated with hypertrophic pyloric stenosis is due to molecular defects within the gene promoter.

Adult↗

PubMed1994

Abnormal distribution of nerve terminals in infantile hypertrophic pyloric stenosis.

Smooth muscle biopsy specimens obtained from nine infants with infantile hypertrophic pyloric stenosis (IHPS) and from three controls were studied immunohistochemically with respect to the distribution of nerve terminals and neurofilaments. To label nerve terminals and neurofilaments, monoclonal antibodies (MAb) 171B5 and 2F11 were used, respectively. In all specimens of the control group, nerve terminals were numerous in both the myenteric plexus and the muscle layer. There were abundant neurofilaments in the myenteric plexus and a moderate number in the muscle layer. In all specimens of the IHPS group, the density of nerve terminals and neurofilaments was reduced in the muscle layer. In the myenteric plexus, there was no such reduction. The results indicate poor neuronal innervation of the muscle layer in the pylorus of infants with IHPS. This poor innervation may be related to the pathogenesis of pyloric stenosis and hypertrophy.

Antibodies, Monoclonal↗

PubMed1987

Ultrasonography in the diagnosis of pyloric stenosis.

We evaluated 101 children for hypertrophic pyloric stenosis (HPS) at Arkansas Children's Hospital. Diagnosis was based upon a palpable epigastric "olive" characteristic of HPS, or sonographic measurements of the pylorus. In 28 children, the diagnosis was confirmed by physical examination alone; the remaining 73 had ultrasound examination. Pyloric measurements included muscle thickness, transverse diameter, and total length. Pyloric function was also studied during examination. Using a thickness of less than 4 mm, a diameter of less than 13 mm, and a length of less than 17 mm as normal criteria, 31 cases of HPS were correctly diagnosed by ultrasonography. In the remaining 42, no pyloric abnormality could be demonstrated on further evaluation.

Evaluation Studies as Topic↗

PubMed2004

Evidence that intrauterine and postnatal androgens affect the development of pyloric stenosis.

BACKGROUND: It is rather well established that the causal antecedents of pyloric stenosis (PS) contain both genetic and environmental factors. However, in spite of substantial quantities of epidemiological data, no widespread environmental causal agent has yet been established. There have been recent extensions of our knowledge of the endocrine consequences of fetal growth restriction and of the endocrine determinants of sex ratio. It seemed worth reviewing the epidemiological data on PS in the light of these new developments to see whether this would provide a basis for a plausible hypothesis on these suspected environmental causes of PS. METHODS AND RESULTS: The search terms "pyloric stenosis" and ("epidemiology" or "risk factors") were combined on the Ovid Medline data base for the years 1966 onwards. The data from the resulting papers were augmented by notes occasioned by almost daily reading at the Library of the Royal Society of Medicine (London) for the past 25 years. (Electronic data retrieval systems do not access incidentally recorded data such as sib sex ratios). CONCLUSIONS: It is hypothesized that high intrauterine and early postnatal androgen levels constitute an environmental cause of PS.

Androgens↗