[Gastro-jejunal mucosa prolapse].
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BACKGROUND/AIMS: Prolapse gastropathy is a clinical syndrome involving the invagination of a part of the gastric mucosa into the lower esophagus resulting in well demarcated hemorrhagic mucosa and sometimes bleeding. The importance of this syndrome is that it has been reported as a cause of hematemesis. As this syndrome is considered to be seen in patients with retching and vomiting and to be one of the causes of upper gastrointestinal bleeding, this study was undertaken to evaluate its frequency and importance in our patients. METHODS: The study groups comprised of 941 patients with hematemesis and 54 with recurrent retching and vomiting. Biopsies were obtained from the prolapsing mucosa when detected. Hematoxylin and eosin stained specimens were reviewed by an experienced histopathologist. RESULTS: Prolapse gastropathy was detected in 20 patients (2%), of whom six (0.6%) were in the hematemesis group and 14 (25.9%) in the retching and vomiting group. The location of the lesion was the greater curvature in 10 patients (50%), lesser curvature in seven patients (35%) and anterior wall in three patients (15%). In all six cases from the hematemesis group, bleeding was not related to prolapse gastropathy because other causative lesions were identified. Histologic evaluation of the biopsies revealed acute inflammation, chronic inflammation and submucosal hemorrhage. CONCLUSIONS: According to the results of this study, prolapse gastropathy is not a cause of hematemesis. Other causes should be identified when prolapse gastropathy is detected in a patient with hematemesis.
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Gastric mucosal prolapse occurs when a portion of the mucosa of the stomach herniates into the esophagus, resulting in massive hemorrhage. A 19-year-old man presented on two occasions with an upper gastrointestinal hemorrhage as a result of this syndrome. He was definitively treated with a laparoscopic Nissen fundoplication. This case report outlines his presentation, defines and details gastric mucosal prolapse, and discusses the treatment of this syndrome with laparoscopic Nissen fundoplication.
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We studied the nonspecific nature of the histologic findings in the gastric antral vascular ectasia (GAVE) syndrome by using a morphometric comparison with common gastric lesions including hyperplastic polyps and gastritis. Five clinicopathologically confirmed cases of GAVE syndrome and 41 cases of gastric hyperplastic polyps were diagnosed during a 5-year interval at Summa Health Systems (Akron, Ohio). These cases, as well as 16 randomly selected cases of nonspecific gastritis and 9 normal gastric antral biopsy specimens, were evaluated. A semiquantitative comparison of the light microscopic findings believed to be essential in diagnosis of GAVE syndrome, including vascular hyperplasia, mucosal vascular ectasia, intravascular fibrin thrombi, and fibromuscular hyperplasia, was performed. Image analysis morphometric measures of the area ratio (vascular area/total biopsy area), mean vascular area, and number of ectatic vessels per square millimeter of tissue were performed on the CAS 200 Image Analyzer (Becton Dickinson, San Jose, Calif). By morphometric and statistical parametric analysis, several histopathologic variables, including area ratio, mean vascular area, mucosal vascular ectasia, and fibromuscular hyperplasia, did not confidently differentiate the histologic features of gastric hyperplastic polyp from those of GAVE syndrome, but did apparently differentiate GAVE syndrome from gastritis and normal gastric mucosa. The propensity of gastric hyperplastic polyps to undergo prolapse changes and prolapse as one proposed mechanism for development of the GAVE syndrome lesion probably accounts for this morphologic similarity. Specific diagnostic histopathologic changes probably do not exist for the GAVE syndrome.
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Patent omphalomesenteric duct (umbilical enteric fistula) was diagnosed in a 7-day-old infant. The duct closed spontaneously, but at the age of 4 months the infant was readmitted for a resection of the duct. A review of the literature disclosed that 65 cases of patent omphalomesenteric duct have been reported in Japan. The male/female ratio was 2.8:1. Ten out of 36 infants (27.8%) were premature. Surgery was performed in as many patients as possible--55 out of 59 cases (93.2%). The ducts averaged 3.8 cm in length and 1.1 cm in diameter. Errant gastric mucosa was found in 3 out of 30 cases (10.0%). Prolapse of the ileum was present in 28 out of 53 patients (52.8%)--a relatively high incidence. Ten out of 55 patients died (18.2%); 8 of these had a prolapse of the ileum. In view of the high mortality rate of patients with a prolapse of the ileum and the strong possibility of intestinal obstruction, patent omphalomesenteric ducts should be resected surgically.
Of the three methods employed, endoscopy seems to be the most accurate since it permits identification of both anatomical structures and serves as a basis for interpretation of radiology and manometry. Cardial incisura was the easiest and most constantly identifiable structure by the three methods. It must be considered as the union between esophagus and stomach. In small sliding hiatal hernia, the cardial incisura remains below the diaphragm and the gastric mucosa slides up into the chest, resulting in a partial prolapse (hiatal hernia of sliding mucosa). This concept would clarify the difference in interpretation of the most commonly used procedures in diagnosis of sliding hiatal hernia.
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