PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PYLORIC STENOSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources
PubMed1973

Congenital hypertrophic pyloric stenosis.

In a large metropolitan general hospital, a high incidence of congenital hypertrophic pyloric stenosis was noted in non-Caucasian groups. Bile-free emesis was consistently reported, and admission was frequently delayed. A prompt diagnosis following admission was not always possible. Unequivocal palpation of a right upper quadrant mass was successful in less than half of the patients in this series, and radiographic studies were helpful in establishing the proper diagnosis in the remainder. Liver fracture can occur with improper abdominal palpation techniques. Despite a surprisingly high complication rate, the ultimate result of operative therapy is uniformly excellent. Three patients not operated upon who were followed for more than two years still have evidence of gastric dysfunction. Postoperative emesis following adequate operation is not unusual, occurring approximately one-third of the time. When postoperative emesis is protracted, incomplete pyloromyotomy should be considered.

Female↗
PubMed2006

Linkage of monogenic infantile hypertrophic pyloric stenosis to chromosome 16p12-p13 and evidence for genetic heterogeneity.

Infantile hypertrophic pyloric stenosis (IHPS) is the most common form of bowel obstruction in infancy. The disease affects males four times more often than females and is considered a paradigm for the sex-modified model of multifactorial inheritance. However, pedigrees consistent with autosomal dominant inheritance have also been documented. We analyzed a 3-generation family with IHPS including 10 affected individuals (5 males and 5 females) and mapped the underlying disease locus to chromosome 16p12-p13 (LOD score 3.23) by using a single-nucleotide polymorphism-based genomewide scan. The analysis of 10 additional multiplex pedigrees yielded negative or nonsignificant LOD scores, indicating the presence of locus heterogeneity. Sequence analysis of candidate genes from the chromosome 16 disease interval excluded the presence of pathogenic mutations in the GRIN2A and MYH11 genes.

Chromosome Mapping↗
PubMed1983

The spectrum of serum electrolytes in hypertrophic pyloric stenosis.

Metabolic alkalosis is regarded as the "classical" electrolyte abnormality occurring with hypertrophic pyloric stenosis (HPS) but recent experience suggests that atypical electrolyte findings frequently occur and delay establishing the correct diagnosis. The records of 65 infants with HPS treated by pyloromyotomy during the past 4 years were reviewed to determine the serum electrolytes at the initial presentation. The four study groups formed included 8 (12.3%) patients in group A with serum bicarbonate (HCO3) below 18 mEq/L (mean 15.7 +/- 0.5 mEq/L); 19 (29%) in group B with HCO3 between 18 and 25 (22.9 +/- 0.3); 22 (33.8%) in group C with HCO3 between 25 and 30 (27.0 +/- 0.3) and 16 (24.6%) in group D with HCO3 over 30 (34.0 +/- 0.9). Established values for normal HCO3 in neonates is 20.1 +/- 2.5 (mean +/- SD). The mean values in group D for HCO3, potassium (4.0 +/- 0.18 mEq/L), and chloride (88.75 +/- 2.15 mEq/L) were each significantly different (p less than 0.001) from determinations of similar electrolytes in other groups. The duration of vomiting in group D of 10.5 +/- 1.3 days is almost double the time (p less than 0.001) in group A, and was associated with more severe dehydration, predominantly acid urine (pH less than 6), and ketonuria as compared to other groups. No significant difference in other demographic characteristics including the age at presentation, the gestational age, sex distribution, or types of formula used was observed. The results of the study emphasize that serum electrolytes in early HPS may be normal, that HCO3 is significantly lower than established normals for older children, and that the effects of hydrogen-ion loss elevating the serum HCO3 precedes alterations in other serum electrolytes.

Alkalosis↗
PubMed1998

Sensitivity and cost minimization analysis of radiology versus olive palpation for the diagnosis of hypertrophic pyloric stenosis.

BACKGROUND/PURPOSE: Two strategies are commonly used for the initial diagnosis of hypertrophic pyloric stenosis (HPS): (1) physical examination and (2) radiologic evaluation using upper gastrointestinal series (UGI) or sonography. The authors wished to determine the sensitivity and relative cost of each strategy. METHODS: The charts of 234 patients presenting over 3 years with a history suggestive of HPS were reviewed retrospectively. Cost, expressed as mean diagnostic charges (MDC) and mean total charges (MTC), was calculated according to two theoretical models. In model A, all patients first are examined by a surgeon. If an olive is palpable, they proceed to surgery. If not, they are sent to radiology. In model B, all patients have radiologic investigation first, and then surgical evaluation if the study result is positive. RESULTS: Of the 234 patients, 150 had HPS (64%). Olives were appreciated in 111 of these (palpation sensitivity of 74%). There was one false-positive olive (0.7%) and no false-negatives. Sonography and UGI were equally accurate (sensitivity of 100%, 0.5% false-positive). Equations were generated to estimate MDC and MTC for our patient population under each model. In model A, MDC = $507 - ($221 x palpation sensitivity) and MTC = $2,543 ($240 x palpation sensitivity). In model B, MDC = $449 and MTC = $2,454, and costs were independent of ability to feel an olive. When cost was plotted against palpation sensitivity, model A yielded a lower MDC than model B if palpation sensitivity was at least 26%, and a lower MTC if palpation sensitivity was at least 37%. Because our palpation sensitivity was 74%, approximately $100 per patient would be saved by sending all infants suspected of having HPS to a surgeon for examination as an initial step. CONCLUSIONS: Although highly sensitive, imaging is superfluous if an olive is palpable. Children suspected of having HPS should have a surgical consultation before a radiology study as long as the surgeon's palpation sensitivity for an olive is at least 37%. Improved palpation skills will result in maximum financial savings.

Costs and Cost Analysis↗
PubMed2006

Pyloric stenosis as a presenting symptom of Crohn's disease.

We report a rare case of pyloric stenosis as a presenting symptom of Crohn's disease. Clinical improvement and long-term relief of pyloric obstruction were obtained following a short course treatment of corticostroids and total parenteral nutrition. In contrast to most of the cases described previously in the literature, surgical treatment was not required.

Adrenal Cortex Hormones↗
PubMed1981

[Pathophysiology of hypertrophic pyloric stenosis in infants (author's transl)].

A review of the publications on mediators of pyloric contraction, together with experimental lesions in animals, suggest that the lesions characteristic of hypertrophic pyloric stenosis in infants (hypertrophy of Torgersen's circular muscle and degenerative changes in Auerbach's myenteric plexus) are probably functional in nature. The hypothesis of a double mechanism is discussed. The primary defect would be an excess of pyloric contraction agonists, such as duodenal hormones and acetylcholine. This would be followed by self-maintenance of the lesions, where pyloric spasm and subsequent distension of the antrum would induce gastrin release with secondary stimulation of duodenal hormone release by oxyntic secretion and acidification of the duodenum.

Gastrins↗
PubMed1979

Serum cholecystokinin, basal acid secretion, and infantile pyloric stenosis.

The fasting serum cholecystokinin-like activity was measured in 21 infants with pyloric stenosis and in 13 normal controls. No significant difference was found between the two groups. The basal acid secretion was measured by continuously aspirating the previously emptied stomach for one hour. The basal gastric volume and the total and the free acidity were all greater in the pyloric group.

Cholecystokinin↗
PubMed1997

The enigma of pyloric stenosis. Some thoughts on the aetiology.

A theory is advanced about the cause of pyloric stenosis of infancy (PS). Developmental changes will conspire to produce pathogenetic gastric hyperacidity within the first 4 weeks of life in babies who develop PS. The prime cause will be an increased gastric acidity due to a genetically determined supernormal parietal cell mass. This theory satisfactorily explains many known clinical features.

Age Factors↗
PubMed1985

Infantile hypertrophic pyloric stenosis: a Dunedin review.

Patients who had undergone a Ramstedt pyloromyotomy for infantile hypertrophic pyloric stenosis in Dunedin over a 10 year period to June 1984 were reviewed. Forty-two cases were recorded. More congenital anomalies than expected, a declining rate of wound complications and a high rate of a positive family history were found. The history is reviewed, the data presented and the results discussed.

Female↗
PubMed1978

[Hypertrophic pyloric stenosis. Review of 314 cases (author's transl)].

Three hundred fourteen patients with hypertrophic pyloric stenosis have been operated from 1969 to 1976. The different etiologies are discussed. Clinical and analytical data are evaluated. Radiology is employed in 99 per 100 of the cases with no complications. Medical treatment used is exposed clearly as well as the surgical procedure (Monereo's modification of the classical Fredet-Ramstedt technique). Postoperative results and complications such as vomiting, wound infection (4.4 per 100), eventration (0.6 per 100) and fatal outcome (0.6 per 100) are thouroughly detailed as well as the associated pathology.

Child↗