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Pyloric Stenosis (pyloric + stenosis)

Distribution by Scientific Domains

Medical Sciences	80%
Life Sciences	19%

Kinds of Pyloric Stenosis

hypertrophic pyloric stenosis

infantile hypertrophic pyloric stenosis

Selected Abstracts

A Quantitative Study of the Neural Changes Underlying Pyloric Stenosis in Dogs

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2002
R. M. Abel
Summary This study aimed to quantify the neural changes in congenital pyloric stenosis in dogs and to study the comparative anatomy between this condition in dogs and that in infantile hypertrophic pyloric stenosis. Eight specimens from the pylorus of dogs with pyloric stenosis and six control specimens were examined using conventional histology and immunohistochemistry for a range of neural antigens. The changes in the proportion of nerves immunoreactive for each antigen were quantified and analysed statistically. The morphology of the nerves in the diseased dogs was similar to that in controls. Only vasoactive intestinal peptide was reduced in expression in dogs (median proportion in control dogs 0.57, in diseased dogs 0.17; P = 0.065). This study demonstrates both morphological similarities and significant differences between closely related conditions in dogs, humans and other species. [source]

Pyloric stenosis with reflux oesophagitis in a Thoroughbred filly

EQUINE VETERINARY EDUCATION, Issue 4 2004
P. Heidmann
First page of article [source]

Pyloric stenosis: a rare disease with a typical anamnesis

EQUINE VETERINARY EDUCATION, Issue 4 2004
M. Venner
No abstract is available for this article. [source]

The true cause of pyloric stenosis is hyperacidity

ACTA PAEDIATRICA, Issue 2 2006
Ian Munro Rogers
Abstract Pyloric stenosis (PS) has no known cause. A testable theory of cause is proposed, based on the inheritance of a parietal cell mass (PCM) at the upper end of the normal range. It is proposed that, until 3,4 wk of age, the obligatory high fasting gastrins are at maximal levels and not able to be diminished by increasing antral acidity. Hence, rising acidity is not reduced by a lowered gastrin during this time, and very high acidity occurs. Conclusion: Persisting duodenal hyperacidity is created by an inherited high PCM and loss of gastrin control. These two factors produce pyloric stenosis through work hypertrophy from repeated pyloric contraction in response to hyperacidity. [source]

A controlled rapid-sequence induction technique for infants may reduce unsafe actions and stress

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2009
C. EICH
Background: Classic rapid-sequence induction of anaesthesia (RSI-classic) in infants and small children presents a time-critical procedure, regularly associated with hypoxia. This results in high stress levels for the provider and may trigger unsafe actions. Hence, a controlled induction technique (RSI-controlled) that involves gentle mask ventilation until full non-depolarizing muscular blockade has become increasingly popular. Clinical observation suggests that RSI-controlled may reduce the adverse effects noted above. We aimed to evaluate both techniques with respect to unsafe actions and stress. Methods: In this controlled, randomized simulator-based study, 30 male trainees and specialists in anaesthesiology performed a simulated anaesthesia induction in a 4-week-old infant with pyloric stenosis. Two different RSI techniques, classic and controlled, were applied to 15 candidates each. We recorded the incidence of hypoxaemia, forced mask ventilation, and intubation difficulties. In addition, we measured individual stress levels by ergospirometry, salivary cortisol, and ,-amylase, as well as a post-trial questionnaire. Results: Hypoxaemia always occurred in RSI-classic but not in RSI-controlled, repeatedly resulting in unsafe actions. Subjective stress perception and some objective stress levels were lower in the volunteers performing RSI-controlled. Conclusions: Our data suggest that RSI-controlled, as compared with RSI-classic, leads to fewer unsafe actions and may reduce individual stress levels. [source]

Intrathoracic gastric volvulus mimicking pyloric stenosis

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 2 2003
JJ Munoz
Abstract: A 5-week-old-infant presented to hospital following the acute onset of non-bilious vomiting with clinical and acid,base features suggestive of pyloric stenosis. A chest radiograph obtained because of intercurrent infection unexpectedly revealed a left-sided congenital diaphragmatic hernia. A barium meal demonstrated the presence of an intrathoracic gastric volvulus, requiring urgent surgical management. We discuss the presentation and management of this rare surgical cause of non-bilious vomiting in infancy. [source]

Junctional epidermolysis bullosa with pyloric stenosis

PEDIATRIC DERMATOLOGY, Issue 6 2001
Dean S. Morrell MD
No abstract is available for this article. [source]

Cystic fibrosis and infantile hypertrophic pyloric stenosis: Is there an association?

PEDIATRIC PULMONOLOGY, Issue 5 2002
Khalid S. Kakish MD
Abstract Cystic fibrosis (CF) is the most common lethal genetic disease among Caucasian populations. The generally accepted incidence of CF in the United States is 1 in 3,200 in the Caucasian population. Intestinal obstructions and atresias have been described among patients with CF. An association of CF with infantile hypertrophic pyloric stenosis (IHPS) has not been previously documented. A review in our clinic of 72 patients with CF revealed IHPS in two. The incidence of 2.7% is greater than the 0.3% incidence expected in the general population. This ninefold increase in IHPS in patients with CF suggests an association between the two and warrants further investigation. Pediatr Pulmonol. 2002; 33:404,405. © 2002 Wiley-Liss, Inc. [source]

Hypertrophic pyloric stenosis in mono-ovular extremely preterm twins after use of erythromycin

PEDIATRICS INTERNATIONAL, Issue 5 2008
Hiromichi Shoji
No abstract is available for this article. [source]

Effects of Rikkunshi-to on infantile hypertrophic pyloric stenosis, refractory to atropine

PEDIATRICS INTERNATIONAL, Issue 4 2008
Noboru Oyachi
No abstract is available for this article. [source]

A Quantitative Study of the Neural Changes Underlying Pyloric Stenosis in Dogs

HP10 LAPAROSCOPIC RESECTION OF SUBMUCOSAL GASTRIC LESIONS , THE WHANGAREI EXPERIENCE

ANZ JOURNAL OF SURGERY, Issue 2007
J. Y. Yang
Purpose To evaluate safety of laparoscopic resection of submucosal gastric lesions performed in Whangarei Based Hospital. Methodology From November 2002 to December 2006, 8 consecutive patients underwent the above mention surgery. (M : F = 5 : 3; Average age 63 [range, 43,83]). All patients underwent pre-operative gastroscopy. Wedge resections were performed for anterior wall lesions. (n = 3). Posterior wall lesions were resected via transgastric approach. (n = 4). Retroperitoneal resection was performed for the foregut duplication cyst. (n = 1). All except one lesion were resected using endoscopic GIA stapler. The medical records of the patients were reviewed retrospectively. Results All patients were successfully treated laparoscopically. No conversion to open surgery. Pathology included: Gastrointestinal-stromal tumor (GIST) (n = 5), Malignant leiomyosarcoma (n = 1), Ectopic pancreas (n = 1), and Foregut duplication cysts (n = 1). All achieved adequate negative surgical margin. Average operation time was 106.14 minutes. [Range, 75,150]. Average length of hospital stay was 3.42 days [range, 1,5]. Complication included one wound infection, and one pyloric stenosis. Average length of follow up was 10.96 months [range, 0.46,31.73]. No recurrence detected and all are still alive till date. Conclusion Laparoscopic resection of submucosal gastric lesions is a safe and appropriate alternative to open surgery. Its main advantage over open technique includes shorter length of hospital stay, lower recurrence rate and lower mortality rates. Surgical technique depends very much on tumor size and location. Outcome of the patients described from our centre is comparable to the others published till date. [source]

Risks of selected congenital malformations among offspring of mixed race-ethnicity

BIRTH DEFECTS RESEARCH, Issue 10 2004
Juan Yang
Abstract BACKGROUND Little is known about the occurrence of specific congenital malformations among offspring of mixed race-ethnicity. METHODS Using data from a population-based registry, we explored the occurrence of selected malformation phenotypes in offspring to parents who were of different race-ethnicity. Data were derived from the California Birth Defects Monitoring Program, a population-based active surveillance system for collecting information on infants and fetuses with congenital malformations using multiple source ascertainment. Approximately 2.6 million live births and stillbirths occurred during 1989,2000. Information on parental race-ethnicity (non-Hispanic white, Hispanic, black, and Asian) was obtained from birth certificates and fetal death files. Malformation phenotypes studied were spina bifida, anencephaly, cleft lip, cleft palate, tetralogy of Fallot, d-transposition of great arteries, hypospadias, small intestinal atresia, preaxial polydactyly, microtia, and hypertrophic pyloric stenosis. RESULTS A total of 11.2% of births were to parents of mixed race-ethnicity. Compared to births of parents who were both white, moderately increased risks (risk ratio , 1.7) of anencephaly, polydactyly, and microtia, and decreased risks (risk ratio , 0.6) of hypospadias and hypertrophic pyloric stenosis were observed among births of several mixed race-ethnicity groups. For anencephaly, polydactyly, and microtia, but not other phenotypes, the risks were different depending on whether maternal versus paternal race-ethnicity was considered. Risks observed between births of a nonwhite parent and a white parent and births of parents who were both nonwhite were similar for most malformation phenotypes. CONCLUSIONS Some malformation phenotypes appear to vary in their risk based on mixed racial-ethnic groupings. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source]

Hypertrophic pyloric stenosis and pulmonary hypertension in a neonate.

ACTA PAEDIATRICA, Issue 6 2009
A common mechanism?
Abstract Nitric oxide (NO) is an important mediator of biological functions. Absence or shortage of NO plays a role in the pathogenesis of both hypertrophic pyloric stenosis and persistent pulmonary hypertension. We present a neonate diagnosed with pulmonary hypertension after birth caused by meconiumaspiration syndrome eventually treated with extracorporal membrane oxygenation followed by hypertrophic pyloric stenosis for which a pyloromyotomy was performed. In conclusion, the association of pulmonary hypertension and pyloric stenosis has not been described before and may be explained by a lowered plasma concentration of arginine leading to deficient NO synthesis in the affected organ systems. [source]