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PubMed1981

Sonography of hypertrophic pyloric stenosis.

Twenty children with suspected hypertrophic pyloric stenosis were studied by sonography. The thickened pyloric muscle is seen as an anechoic mass 1.5 cm or more in diameter, with strong central echoes. Of the 16 infants with a pyloric mass of 1.5 cm or more, 15 underwent surgery and the diagnosis was confirmed. In four patients with a pylorus less than 1.5 cm, the diagnosis of pyloric stenosis was excluded and all were discharged without surgery. Real-time scanning is useful in localizing the pylorus and in demonstrating lack of passage of gastric content across the narrowed pyloric canal.

Female↗
PubMedDate not supplied

[Ultrasound in the diagnosis of hypertrophic pyloric stenosis].

The paper deals with the advantages of ultrasound diagnosis of hypertrophic pyloric stenosis in newborns. Ultrasound decreases the number of radiological examinations of gastroduodenum and reduces diagnostic exposure of children to X-rays. In the last three years 107 children had manifested clinical signs of hypertrophic pyloric stenosis. The ultrasound studies revealed hypertrophic pyloric stenosis in 55 patients (51.4%). There were 48 boys (87.3%) and 7 girls (12.7%). Patients were aged 17 to 75 days (average about 40 days). The sonogram finding was typical for hypertrophic pylorus, which made the diagnosis easier. There were no false positive or false negative ultrasound findings. All patients with hypertrophic pyloric stenosis were operated on and diagnosis was confirmed. Ultrasound is reliable in diagnosis of hypertrophic pyloric stenosis. Ultrasound examination is technically easy and fast, what is important for urgent surgical therapy. In children with persistent projectile vomiting, suspected of hypertrophic pyloric stenosis, ultrasound is the method of choice and should replace X-ray examinations.

Female↗
PubMed2002

Very early exposure to erythromycin and infantile hypertrophic pyloric stenosis.

OBJECTIVE: To assess the link between very early erythromycin exposure and pyloric stenosis in young infants. DESIGN: Retrospective cohort study. PARTICIPANTS AND METHODS: Medicaid or TennCare (Tennessee's program for Medicaid enrollees and uninsured individuals) births in Tennessee from 1985 to 1997. Cases of infants with a hospital discharge diagnosis of pyloric stenosis and an associated surgical procedure code were used. Erythromycin exposure and other antibiotic exposure between 3 and 90 days of life were identified from prescription files. MAIN OUTCOME MEASURES: Hospital discharge diagnosis of pyloric stenosis, and an associated surgical procedure code. RESULTS: Of 933 239 births in Tennessee during the study period, 314 029 were enrolled in Medicaid. Among these infants, 804 (2.6/1000 infants) met the criteria for pyloric stenosis. Very early exposure to erythromycin (between 3 and 13 days of life) was associated with a nearly 8-fold increased risk of pyloric stenosis (adjusted incident rate ratio, 7.88; 95% confidence interval, 1.97-31.57). No increased risk of pyloric stenosis was seen in infants exposed to erythromycin after 13 days of life or in infants exposed to antibiotics other than erythromycin. CONCLUSIONS: The significant increase in pyloric stenosis in children with very early exposure to erythromycin is consistent with reports of other investigators. The risks and benefits of erythromycin should be weighed carefully prior to initiating such therapy in young infants.

Anti-Bacterial Agents↗
PubMed1981

Tuberculous pyloric stenosis.

A case of pyloric stenosis, caused by abdominal tuberculosis and presenting as an inoperable neoplasm in a member of the indigenous population of the British Isles, is reported. The need for histological confirmation of suspected inoperable malignant tumours is stressed. The pathogenesis and management of the condition are discussed.

Abdomen↗
PubMed1991

Increasing incidence of hypertrophic pyloric stenosis.

The incidence of pyloric stenosis in the Mersey region rose from 1.54/1000 births in 1976-8 to 2.22/1000 births in 1986-8. Reliance on ultrasonography for diagnosis in the 1980s resulted in fewer 'tumours' being felt; diagnostic delay was not shortened overall but serial ultrasonography showed evolving lesions in six patients. Clinical examination and selective use of ultrasonography is advocated.

England↗
PubMed2002

Hypertrophic pyloric stenosis in utero.

Hypertrophic pyloric stenosis (HPS) is the most common surgical condition producing vomiting in infants. It has been reported as early as the 1st week of life. We report an infant with HPS seen on prenatal ultrasound. Although infants with HPS usually present between 3 and 5 weeks of life, HPS must be considered as part of the differential diagnosis of newborns with non-bilious vomiting.

Female↗
PubMedDate not supplied

[Male predominance and birth weight in hypertrophic pyloric stenosis].

BACKGROUND: Infantile hypertrophic pyloric stenosis (IHPS), although fairly frequent, is still an enigmatic disease. Its incidence is increased among relatives of a case and among infants of male sex (M) and of high birthweight. The purpose of this paper is to analyze the pattern of IHPS M predominance according to birthweight (BW). METHODS: 115 consecutive cases charts of IHPS were reviewed and stratified by gender and BW rank (500 g each, beginning at 1,500 g and ending at 3,500 g). Statistical analysis was done by means of chi square and comparation of proportions tests. RESULTS: M predominance was not observed in IHPS patients with a BW of 2,500 g or less (n = 11, 6M). Female infants (F) did not increase their number of cases as the BW rose, but M did, reaching an 8.8 to 1 M to F ratio among those with a BW of 3,500 9 or more (p < 0.005). The proportion of M with a BW of 3,000 g or more was significantly higher than in F (0.826 vs. 0.521, p < 0.005). CONCLUSIONS: In IHPS, the excess of M cases, which is responsible of the M/F disparity, is present only among newborns with a BW of 3,000 g or more. The disease does not show this relation to BW in F.

Birth Weight↗
PubMed2004

Abnormal oral mucosal light reflectance in infantile hypertrophic pyloric stenosis.

OBJECTIVES: Infantile hypertrophic pyloric stenosis (IHPS) is the most common condition requiring surgical intervention during the first weeks of life. The etiology of IHPS is unknown, although both neuronal nitric oxide synthase upregulation and an extracellular matrix abnormality are suspected. Familial predisposition is an important feature. Phenotypical markers of IHPS, such as hypoplasia or agenesis of the inferior labial frenulum, have been described. The authors tested the hypothesis that IHPS is associated with abnormal reflectance of the oral mucosa. METHODS: Twenty-five children with surgically confirmed IHPS and 25 gender- and age-matched control subjects participated in the study. Reflectance of the lower gingival and vestibular oral mucosa in the optical spectrum was measured using an imaging spectrophotometer. RESULTS: Patients with IHPS had significantly higher light reflectance values in the violet, blue, blue-green, green, yellow, and orange sections of the spectrum (all P values < 0.0001), with a maximum distance between group means at the 450-nm wavelength (t-value: 27.66, df = 48). A reflectance cutoff >5.26% at the 450-nm wavelength identified patients with IHPS with 100% sensitivity and 100% specificity. CONCLUSIONS: This study reports a previously unrecognized mucosal reflectance abnormality of the oral mucosa in IHPS, thus offering a new, accurate, and noninvasive phenotypic marker for the condition.

Adult↗
PubMed2001

[Increase of the chondroitin-sulfate proteoglycan, fibronectin and fibroblasts in infantile hypertrophic pyloric stenosis].

INTRODUCTION: Infantile hypertrophic pyloric stenosis (IHPS) consists of hypertrophy of the muscular layer of the pylorus. Its etiology is still unknown. In the last years only few jobs that studied the extracellular matrix (ECM) in the muscular layer in the IHPS have been reported. Our aim was to investigate the expression of two ECM molecules: chondroitin-sulfate proteoglycan (CSPG) and fibronectin (FN), and fibroblasts. MATERIAL AND METHODS: Full-thickness muscle biopsy specimens were obtained from 33 IHPS patients at pyloromyotomy and 12 controls. Indirect immunohistochemistry was performed using CSPG, FN and fibroblasts monoclonal antibodies. The results were showed by a semiquantitative scale as follows: strong (++), moderate (+), weak (+/-), and absent (-). RESULTS: We demonstrated that the CSPG immunoreactivity was localized in the connective tissue septa and the expression of FN molecules in the pericellular space. Both molecules were significantly the increased in the muscle layer of the pylorus with IHPS in relation to control pylorus. We also demonstrated a marked increased expression in the number of fibroblasts in the muscle layer of the pylorus with IHPS. Even-though the most striking increase was localized in the septa, we also observed great number of fibroblasts amongst the smooth muscle cells. CONCLUSIONS: We suggest that IHPS is characterized, not only by the muscle layer hypertrophy, but also by the increase of several ECM molecules, such as CSPG and FN. We also think that the increase of fibroblast could explain the higher expression of both ECM molecules in the muscle layer of pylorus in IHPS.

Chondroitinases and Chondroitin Lyases↗
PubMed1988

Changing patterns in the diagnosis of hypertrophic pyloric stenosis.

The records of 216 infants who had surgical correction of hypertrophic pyloric stenosis between 1980 and 1984 at the Children's Hospital of Alabama were reviewed. A significant increase in the reliance on upper gastrointestinal roentgenographic series and abdominal sonography for confirmation of the diagnosis of hypertrophic pyloric stenosis was noted in our patients when compared to previous reports. Despite the preoperative presence of a palpable pyloric mass in 192 (89%) of the patients, 174 (81%) had a diagnostic imaging procedure. Similar high rates of imaging studies were noted when the records of patients with hypertrophic pyloric stenosis from 1980 and 1984 were reviewed at three other institutions. Palpation of a hypertrophied pylorus is diagnostic of hypertrophic pyloric stenosis. Careful physical examination makes diagnostic imaging unnecessary in the majority of infants with symptoms suggesting hypertrophic pyloric stenosis. Diagnostic imaging for suspected hypertrophic pyloric stenosis should be used only for those infants with persistent vomiting in whom careful and repeated physical examinations fail to detect a palpable pyloric mass.

Diagnostic Imaging↗
PubMed1992

Sonography of hypertrophic pyloric stenosis: frequency and cause of nonuniform echogenicity of the thickened pyloric muscle.

In hypertrophic pyloric stenosis, the muscle is typically described as hypoechoic on sonography. However, we have frequently noted a nonuniform pattern; the pyloric muscle seen in the transverse plane is more echogenic in the near and far fields and less echogenic on the sides. The muscle also appears almost as echogenic as the liver on midline longitudinal sonograms. To establish the frequency of these findings, we reviewed the sonograms of 71 infants with hypertrophic pyloric stenosis. The muscle was imaged directly during surgery in three patients. In an in vitro experiment, muscle arranged to stimulate the pyloric ring was scanned in a water bath. Then, using two sections of muscle, we compared the echogenicity when scanning in a plane perpendicular to the long axis of the muscle fibers with that seen with the beam parallel to the long axis of the muscle fibers. In the transverse plane, nonuniform echogenicity of the pyloric muscle was seen in 59 (98%) of 60 patients. In the midline longitudinal plane, the muscle was equal to or slightly less echogenic than the liver in all patients. Both the in vivo and in vitro studies show that the echogenicity varies with the relationship of the ultrasound beam to the orientation of the circular muscle fibers; this phenomenon is known as the anisotropic effect. Our results show that nonuniform echogenicity of the hypertrophied pyloric muscle is a characteristic sonographic finding caused by the anisotropic effect, which is related to the orientation of the ultrasound beam with respect to the circular fibers of the pyloric muscle.

Humans↗
PubMed1987

Trends in pyloric stenosis incidence, Atlanta, 1968 to 1982.

Four studies reported an increasing incidence of pyloric stenosis during the late 1970s from geographically diverse areas of the United Kingdom. It was suggested that the increased incidence might be related to changes in infant feeding practices. We used data from the Metropolitan Atlanta Congenital Defects Program, a population based birth defects registry, to examine the secular trends and descriptive epidemiology of pyloric stenosis in a North American city. For the period 1968 to 1982, the incidence of pyloric stenosis was 1.33 per 1000 live births; there was no evidence of an increasing trend for either race or sex specific rates of pyloric stenosis. The descriptive epidemiology of the pyloric stenosis cases showed higher rates for males, whites, and infants of higher birth weight. We found no increasing trend in pyloric stenosis incidence in Atlanta, despite well documented changes in US infant feeding practices (an increased prevalence of breast feeding) during the 1970s.

Breast Feeding↗
PubMed1988

The use of ultrasound in the diagnosis of congenital pyloric stenosis.

Thirty-six infants with pyloric stenosis were studied preoperatively by ultrasound and compared with a control group of 24 normal infants aged one month. Measurement of pyloric muscle diameter and muscle wall thickness was significantly different for each measure between groups and they had a nonoverlapping distribution. Ultrasound has a clear place in the diagnosis of pyloric stenosis.

Female↗
PubMed1976

Highly selective vagotomy plus dilatation of the stenosis compared with truncal vagotomy and drainage in the treatment of pyloric stenosis secondary to duodenal ulceration.

Twenty-three consecutive patients with duodenal ulceration complicated by pyloric stenosis who came under the care of one surgeon were treated by highly selective vagotomy (HSV) combined with digital dilatation of the stenosis through a gastrotomy. No form of drainage procedure was used. Thus the antral "mill" and the pyloric sphineter were left intact. Since the stenosis is usually distal to the pylorus rather than truly pyloric such dilatation does not damage the pyloric ring, although it may on occasion lead to perforation of the first part of the duodenum. The subsequent progress of these patients was compared with that of a similar, consecutive series of 23 patients with pyloric stenosis who were treated by truncal vagotomy with a drainage procedure by other surgeons on the same surgical unit. Patients were followed up for between four months and five years. The clinical assessment was carried out in "blind" fashion at a special gastric follow-up clinic. No evidence of recurrent ulceration was found in either group of patients. Two patients from each group subsequently came to reoperation for the relief of gastric stasis. Twenty-two of the 23 patients (96%) who had undergone HSV plus dilatation eventually achieved a good-to-excellent clinical result (Visick grades 1+2), wheras only 17 of the 23 patients (74%) who had undergone truncal vagotomy with drainage achieved such a result. The main clinical difference between the two groups was that side effects such as diarrhoea and abdominal pain or discomfort were more common after vagotomy with drainage than after HSV. These results bear witness to the remarkable propulsive powers of the gastric antrum after HSV, which were evidently sufficient to overcome any tendency to re-stenosis in more than 90% of patients. The 9% incidence of failure due to re-stenosis could perhaps be avoided if a small duodenoplasty were performed instead of simple digital dilatation. The results support the hypothesis that damage to the antral mill and pyloric sphincter can be avoided in the course of operations for "pyloric" stenosis secondary to duodenal ulceration. Avoidance of the drainage procedure is of benefit to the patient, just as it is in patients who have duodenal ulceration without stenosis.

Crohn Disease↗
PubMed2000

Is acid base determination an accurate predictor of pyloric stenosis?

OBJECTIVE: To determine if acid base status predicts which vomiting patients have pyloric stenosis. DESIGN: Retrospective chart review. SETTING: Tertiary paediatric hospital. METHODOLOGY: We compared the clinical and biochemical parameters of 100 patients with a discharge diagnosis of pyloric stenosis and 84 patients of a similar age who presented to the emergency department with vomiting and who had an acid base determination. Patients were included from January 1995 to January 1997. Clinical correlates consisted of age, duration of vomiting, weight loss, gestation, and family history of pyloric stenosis. Biochemical correlates were pH, bicarbonate, base excess (BE), chloride, potassium, and sodium. RESULTS: Independent variables of significance were pH, BE, chloride, bicarbonate, potassium, weight loss (all of which had a P value < 0.0001), and sex (P = 0.006). Each variable was placed in a logistic regression equation with pyloric stenosis being the dominant variable. Variables of significance were pH (P = 0.0001), BE (P = 0.0001), and chloride (P = 0.009). A model for predicting pyloric stenosis using these variables was then created with pH > 7.45, chloride < 98, and BE > +3, with a positive predictive value of 88%. CONCLUSION: Acid base determination is a useful screening tool when considering pyloric stenosis. This model now needs to be validated on a prospective series of patients with vomiting.

Acid-Base Imbalance↗
PubMed1988

G-cell hyperplasia in rats with pyloric stenosis.

Since little is known about the pathophysiology of pyloric stenosis, we created a partial gastric outlet obstruction in 13 Wistar rats by placing a nonabsorbable ligature of defined size around the pylorus. Sham operations were performed in 10 rats. The animals from both groups were killed after four months. G-cell count and gastrin content were determined in 10 parallel strips, which were cut by razor blades mounted on a handle. Gastric size and weight as well as thickness of mucosal and muscular layers and serum gastrin concentration were also determined. Body weight of the animals with pyloric stenosis was lower and gastric weight higher than that of the controls. Furthermore, we found an enlarged G-cell area and G-cell hyperplasia, an increased surface area and thickness of the mucosal and muscular layers of the stomach, and in the majority of rats, elevated serum gastrin levels. Total G-cell count was 583,720 +/- 90,561 in the rats with pyloric stenosis and 385,775 +/- 15,820 (mean +/- SEM) in the control rats (P less than 0.04). We conclude that partial gastric outlet obstruction in rats leads to G-cell hyperplasia and that this experiment may serve as a model for pyloric stenosis in man.

Animals↗