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Results for “PYLORIC STENOSIS”

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At least 667 records · Page 37Linked to original sources
PubMed1995

Perinatal nitric oxide synthase inhibition retards neonatal growth by inducing hypertrophic pyloric stenosis in rats.

Administration of the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) during pregnancy has been shown to compromise fetal growth. This study was designed to determine whether aminoguanidine, a predominate inhibitor of inducible NOS, affects fetal outcome. In addition, we extended the prenatal administration of L-NAME into the postnatal period (14 d) to determine whether neonatal growth and maturation were also affected. L-NAME, but not aminoguanidine, compromises fetal and placental growth. When compared with control 14-d-old pups, postnatal L-NAME compromised neonatal growth, whether it was given directly (intraperitoneally) (39.7 +/- 1.1 versus 24.1 +/- 1.0 g) or indirectly (38.6 +/- 0.5 versus 22.2 +/- 1.2 g) via maternal breast milk. Neonatal growth retardation was asymmetric, with brain sparing, suggesting a nutritional origin. L-NAME administration resulted in growth retardation that extended into adulthood, without evidence of catch-up growth. Treated neonates displayed the hallmarks of hypertrophic pyloric stenosis. Significant increases in stomach weight/pup weight (9.9 +/- 0.3 versus 8.2 +/- 0.4 x 10(3)) and stomach volume/pup weight (12.0 +/- 0.6 versus 9.4 +/- 0.6 mL/100 g) with a concomitant decrease in small intestine weight/length (2.10 +/- 0.08 versus 3.18 +/- 0.13 g/100 cm) was noted in treated versus control pups (p < 0.05). Muscularis hypertrophy at the pyloric sphincter in the L-NAME-treated pups was noted by histology. Blood pressure was elevated in the L-NAME-treated pups (93 +/- 6 versus 60 +/- 5 mm Hg in control pups, p < 0.05). These findings are consistent with inhibition of neuronal and endothelial NOS activity. We conclude that NO, formed via the constitutive isoforms of NOS, is a critical determinant of fetal and neonatal growth and maturation.

Animals↗
PubMed1986

An immunochemical study with neuron-specific-enolase and substance P of human enteric innervation--the normal developmental pattern and abnormal deviations in Hirschsprung's disease and pyloric stenosis.

Human enteric innervation was studied immunochemically with neuron-specific-enolase (NSE), a specific neurone marker indicative of differentiation, and substance P, a potent member of the family of neuropeptides. By examining various levels of the gut in 28 normal human fetuses of gestational ages 9 to 21 weeks, we showed that enteric neurones as a whole, as well as peptidergic neurones in particular, followed a dual gradient of development proceeding from each end to the middle of the gut. This suggests the need for caution in accepting the hypothesis of the pathogenesis of Hirschsprung's disease based on the concept of a single craniocaudal gradient of enteric neuronal development. In studies of six infants with Hirschsprung's disease, NSE immunostaining was found to be potentially useful for diagnostic purposes. NSE activity suggested that the hypertrophied nerve bundles in aganglionic bowel were metabolically active and functionally mature. Substance P-immunoreactivity was decreased in both aganglionic and distal ganglionic bowel in Hirschsprung's disease, suggesting that substance P-nerves were more extensively affected developmentally than other enteric neurones. In 28 infants with pyloric stenosis (IHPS), the presence of intense NSE activity in the ganglia in the pylorus suggested that these neurones were neither immature nor severely degenerated. A decrease in substance P immunoreactivity in IHPS suggested possible involvement of peptidergic innervation in the pathogenesis of IHPS.

Adolescent↗
PubMed2001

A randomized multicenter study of remifentanil compared with halothane in neonates and infants undergoing pyloromyotomy. II. Perioperative breathing patterns in neonates and infants with pyloric stenosis.

UNLABELLED: Although former preterm birth infants are at risk for postoperative apnea after surgery, it is unclear whether the same is true of full-term birth infants. We evaluated the incidence of apnea in 60 full-term neonates and infants undergoing pyloromyotomy both before and after anesthesia. All subjects were randomized to a remifentanil- or halothane-based anesthetic. Apnea was defined by the presence of prolonged apnea (>15 s) or frequent brief apnea, as observed on the pneumocardiogram. Apnea occurred before surgery in 27% of subjects and after surgery in 16% of subjects, with no significant difference between subjects randomized to remifentanil or halothane anesthesia. This apnea was primarily central in origin, occurred throughout the recording epochs, and was associated with severe desaturation in some instances. Of the subjects with normal preoperative pneumocardiograms, new onset postoperative apnea occurred in 3 (23%) of 13 subjects who received halothane-based anesthetics versus 0 (0%) of 22 subjects who received remifentanil-based anesthetics (P = 0.04). Thus, postoperative apnea can follow anesthesia in otherwise healthy full-term infants after pyloromyotomy and is occasionally severe with desaturation. New-onset postoperative apnea was not seen with a remifentanil-based anesthetic. IMPLICATIONS: Abnormal breathing patterns can follow anesthesia in infants after surgical repair of pyloric stenosis. Occasionally, these patterns can be associated with desaturation. New-onset postoperative apnea was not seen with a remifentanil-based anesthetic.

Anesthetics, Inhalation↗
PubMed2002

Primary hypertrophic pyloric stenosis in the adult: a case report.

A 66-year-old male was admitted with a two-month history of vomiting and weight loss. Endoscopy showed a pyloric obstruction and the patient underwent subtotal gastrectomy with gastro- jejunostomy. The histopathological study of the specimen revealed primary hypertrophic pyloric stenosis without any evidence of duodenal peptic disease. In the adult, this is a rare cause of gastric outlet obstruction of unknown etiology. It is usually recognized by histopathological examination of the specimen after a gastric resection performed to treat gastric outlet obstruction syndrome. However, some endoscopic and radiological signs, such as the cervix sign, or elongation of the pyloric channel, may give clues about the presence of the disease preoperatively. In symptomatic cases, surgery is the preferred treatment modality.

Journal Article↗
PubMed1981

Short segment pyloric narrowing. Pylorospasm or pyloric stenosis?

Short segment narrowing of the pyloric canal is a common finding in infants with chronic vomiting, and most often is due to pylorospasm. In such cases, it is transient, and offers no real problem in diagnosis. On the other hand, when it persists, a question arises as to whether it is due to fixed stenosis. Differentiation of the two conditions is difficult, but important, for while spasm can be treated medically, true stenosis requires surgical intervention. Just how to accomplish this differentiation is the subject of this report, and for the most part, centers around the infant's response to a therapeutic trial of antispasmodics. Patients with pylorospasm respond favorably, while those with fixed stenosis do not. Generally, these latter patients require pyloromyotomy, but in the occasional infant, so little muscle hypertrophy is present that we have found pyloroplasty to be the preferred procedure.

Diagnosis, Differential↗