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Results for “GASTRIC MUCOSA PROLAPSE”

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At least 217 records · Page 12Linked to original sources
PubMed1990

Mechanical gastritis involving the cardia: the trauma of retching and vomiting.

In two patients, frequent retching and vomiting preceded acute upper gastrointestinal hemorrhage. Congestion and edema were limited to the prolapsed portion of the stomach, the cardia, where discrete erosions and small shallow ulcers were seen. At endoscopy, prolapse of the gastric mucosa into the esophageal lumen was quite evident whenever the patients retched. The endoscopic features and pathogenesis of Mallory-Weiss syndrome were readily differentiated. It seemed probable that repeated retching causing intussusception of the cardia of the stomach can mechanically produce gastritis and should be a recognizable cause of acute upper gastrointestinal bleeding. I take this entity to be an independent superficial mucosal disease of the stomach.

Adult↗
PubMed1977

Progression of Menetrier's disease with postoperative gastrojejunal intussusception.

A unique case of Menetrier's disease of the stomach with long term follow-up is presented to document progression of extent of the disease radiologically and pathologically. This observation provides an insight into the natural history of the condition and suggests that local excision is not necessarily curative. In addition, this case demonstrates the complication of preoperative direct prolapse of involved gastric mucosa through the pylorus, and subsequent postoperative antegrade intussusception of the progressively involved gastric mucosa across a Billroth II gastrojejunostomy.

Adult↗
PubMed1995

The antral nipple sign of pyloric mucosal prolapse: endoscopic correlation of a new sonographic observation in patients with pyloric stenosis.

This study describes the antral nipple sign of pyloric mucosal prolapse, a newly delineated sonographic observation in patients with pyloric stenosis, correlates the endoscopic findings, and examines its prevalence and significance in 31 consecutive patients with pyloric stenosis. Fifty patients who did not have pyloric stenosis served as the control population. The antral nipple sign consists of visualization of prolapsed, hypertrophied pyloric mucosa protruding into the gastric antrum. Using the Wilcoxon scores (rank sums), there was no significant difference among the patients in age, weight, or pyloric muscle dimensions. Although the diagnosis of pyloric stenosis is made on the basis of muscle thickness, we have documented that the pyloric mucosa becomes redundant in infants with pyloric stenosis, permitting a fuller understanding of the anatomic correlate underlying the sonographic images.

Endoscopy, Gastrointestinal↗
PubMed1990

Pyloric deformation from peptic disease. Radiographic evidence for incompetence rather than obstruction.

We have used double-contrast radiographic techniques to clarify what changes in the configuration and movements of the gastroduodenal junction result when peptic lesions involve the distal gastric segment between the proximal (PPL) and the distal pyloric muscle loop (DPL). Among 50 cases of pyloric ulceration diagnosed during a four-year study period, 18 cases fulfilled all study criteria. Ulcers maintained a consistent location with regard to the muscular structures of the pylorus, and by affecting these structures, led to many strange deformations of the gastric outlet including permanent pseudodiverticula and reversal of pyloric angulation. The most common site for peptic lesions in the pyloric segment was the protuberance of the lesser curvature called the pyloric torus; many torus lesions extended into and destroyed the DPL. This led to widening of the gastric outlet and radiographic evidence of increased duodenogastric reflux. Pyloric closure was further impaired in this setting because the mucosa no longer prolapsed into the gastric outlet and did not occlude the pyloric lumen as it normally does. Less common lesions involved the greater curvature and the PPL. In one patient, scarring of the PPL led to an antral web and gastric hyperperistalsis. This was the only patient who required operation for chronic gastric outlet obstruction. One-third of the 18 patients had reflux esophagitis in addition to peptic pyloric disease. In most patients without additional ulcerogenic risk factors, treatment with antisecretory agents led to the healing of ulcer craters. We conclude that the morphologic and functional changes of the gastric outlet caused by peptic lesions depend, in part, on the effect the ulcer has on the underlying pyloric musculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗