Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042961 (volvulus)
 4,305 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-seven of 101 Nissen fundoplications during the 4-year period, July 1979 to July 1983, were performed on neurologically impaired children. Mean age at the time of surgery was 5.9 years (range 1 month to 22 years). Indications for operation included: persistent vomiting, 57 patients (100%); failure to thrive, 49 patients (86%); repeated episodes of pneumonia, 49 patients (86%); esophagitis, 18 patients (32%); hiatal hernia, 14 patients (25%); episodes of apnea, 10 patients (18%); and esophageal stricture, six patients (10%). Forty-six of the 57 patients had previously failed a standard trial of nonsurgical management. Gastroesophageal reflux was documented by barium esophagograms in 51/56 patients (91%), chalasia scans in 28/32 patients (88%), esophagitis or stricture at endoscopy in 21/23 patients (91%), and acid reflux on pH monitoring in 13/16 patients (80%). Operative management included gastrostomy in 55 of the 57 patients and this was permanent in 50. Gastrostomies had previously been performed in nine patients but had failed to provide a reliable method of enteral feeding because of chronic reflux and aspiration. The surgical complication rate was 12%. Intraoperative esophageal perforation occurred in two patients, splenic tear in one, hepatic vein laceration in one, and a tight wrap in one. After surgery, bowel obstruction from adhesions developed in one patient and a midgut volvulus in another. Five of the children have died, none from causes related to the surgical procedure. Clinical and radiologic follow-up evaluations of all survivors have been done, with a mean follow-up of 3 years. In four patients the repair was felt to be inadequate. One patient had an esophageal stricture and three had recurring episodes of pneumonia. Three children showed radiologic evidence of persistent reflux, but only two were symptomatic. Two patients required a second antireflux procedure for reflux and are now free of symptoms. Nissen fundoplication appears to be a safe and beneficial procedure in neurological impaired children. Long-term follow-up evaluation of these patients showed satisfactory growth as well as a significant decrease in pulmonary disease associated with aspiration.
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PMID:The effectiveness of Nissen fundoplication in neurologically impaired children with gastroesophageal reflux. 2325 71

A total of 82 patients with gastroesophageal reflux were consecutively treated with stapled, uncut gastroplasty and complete fundoplication over a 12-year period. The conditions treated included symptomatic reflux; esophageal stricture; massive hernia; collagen esophagus; short esophagus; Barrett's esophagus; recurrent, massive bleeding or anemia; small gastric remnant after gastrectomy; and acute volvulus. The transthoracic approach of stapled, uncut gastroplasty gives superb exposure. Outstanding features of the procedure are the safety and versatility resulting from the small amount of fundus required, no need either to ligate short gastric vessels or to suture the esophagus itself, and preservation of anatomical continuity between the wrapping fundus and the wrapped gastric tubular segment. There have been no deaths and no cases of anatomical or symptomatic recurrence in the series. Complications included some nondebilitating and mainly self-limiting symptoms.
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PMID:Stapled, uncut gastroplasty for hiatal hernia: 12-year follow-up. 638 91

Cystic fibrosis (CF), the most common lethal autosomal recessive disease in white populations, is characterized by dysfunctional chloride ion transport across epithelial surfaces. Although recurrent pulmonary infections and pulmonary insufficiency are the principal causes of morbidity and death, gastrointestinal symptoms commonly precede the pulmonary findings and may suggest the diagnosis in infants and young children. The protean gastrointestinal manifestations of CF result primarily from abnormally viscous luminal secretions within hollow viscera and the ducts of solid organs. Bowel obstruction may be present at birth due to meconium ileus or meconium plug syndrome. Complications of meconium ileus include volvulus, small bowel atresia, perforation, and meconium peritonitis with abdominal calcifications. Older children with CF may present with bowel obstruction due to distal intestinal obstruction syndrome or colonic stricture, and tenacious intestinal residue may serve as a lead point for intussusception or cause recurrent rectal prolapse. Radiologic studies often demonstrate thickened intestinal mucosal folds in older children and uncommonly show colonic pneumatosis, peptic esophageal stricture due to gastroesophageal reflux, and duodenal ulcer. Appendicitis due to inspissated secretions is uncommon. Obstruction of ducts and ductules produces exocrine pancreatic insufficiency, pancreatitis, cholestasis, cholelithiasis, and cirrhosis with portal hypertension. On imaging studies, the pancreas is commonly small and largely replaced by fat, sometimes displays calcifications, and is rarely replaced by macrocysts. Radiologic features of hepatobiliary disease include an enlarged radiolucent liver from steatosis, gallstones, a shrunken nodular liver, splenomegaly, and portosystemic collateral vessels. With the improved survival of CF patients, an increased risk for developing gastrointestinal carcinomas has been established, many occurring as early as the 3rd decade.
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PMID:Gastrointestinal manifestations of cystic fibrosis: radiologic-pathologic correlation. 883 77

Acute esophageal necrosis (AEN), commonly referred to as "black esophagus", is a rare clinical entity arising from a combination of ischemic insult seen in hemodynamic compromise and low-flow states, corrosive injury from gastric contents in the setting of esophago-gastroparesis and gastric outlet obstruction, and decreased function of mucosal barrier systems and reparative mechanisms present in malnourished and debilitated physical states. AEN may arise in the setting of multiorgan dysfunction, hypoperfusion, vasculopathy, sepsis, diabetic ketoacidosis, alcohol intoxication, gastric volvulus, traumatic transection of the thoracic aorta, thromboembolic phenomena, and malignancy. Clinical presentation is remarkable for upper gastrointestinal bleeding. Notable symptoms may include epigastric/abdominal pain, vomiting, dysphagia, fever, nausea, and syncope. Associated laboratory findings may reflect anemia and leukocytosis. The hallmark of this syndrome is the development of diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to involve variable length of the organ. Classic "black esophagus" abruptly stops at the gastroesophageal junction. Biopsy is recommended but not required for the diagnosis. Histologically, necrotic debris, absence of viable squamous epithelium, and necrosis of esophageal mucosa, with possible involvement of submucosa and muscularis propria, are present. Classification of the disease spectrum is best described by a staging system. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, nil-per-os restriction, supportive red blood cell transfusion, and intravenous acid suppression with proton pump inhibitors. Complications include perforation with mediastinal infection/abscess, esophageal stricture and stenosis, superinfection, and death. A high mortality of 32% seen in the setting of AEN syndrome is usually related to the underlying medical co-morbidities and diseases.
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PMID:Black esophagus: acute esophageal necrosis syndrome. 2061 76