Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A polyp-fold complex at the gastroesophageal junction is a rare finding. We made this diagnosis in a 51-year-old man who presented with abdominal discomfort after an episode of protracted vomiting. The esophagogastric polyp-fold complex is not always associated with reflux esophagitis, as was originally proposed.
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PMID:The esophagogastric polyp-fold complex. 650 17

Eight patients with nonmalignant intrathoracic esophageal perforations recognized more than 48 hours (48 hours to 14 days) after rupture were treated at Toronto General Hospital between 1973 and 1978. Perforation was due to postemetic rupture in 7 patients and to instrumentation in 1. The patients were seen with pain (8), vomiting (7), fever (7), shock (4), respiratory insufficiency (5), pleural effusion (7), pulmonary infiltrates (7), and leukocytosis (6). All patients were managed with thoracotomy. Direct suture closure of the perforation was carried out in 4 patients with midesophageal perforations. Postoperative localized leaks developed in 2 of these patients but healed with conservative management. Cervical esophagostomy and esophageal diversion were used in 1 patient in whom a severe empyema developed in the postoperative period. Direct suture closure, reinforced with a gastric patch, was used to close three lower esophageal perforations. None of these patients had a postoperative leak but all developed subsequent reflux esophagitis. All 8 patients survived. In patients with delayed recognition of a nonmalignant intrathoracic esophageal perforation, elimination of continued chemical and bacterial contamination can be achieved by a clear definition and closure of the esophageal mucosal margins. The obliteration of potential pleural spaces by good tube drainage, lung decortication, and the elective use of mechanical ventilation with positive end-expiratory pressure decreases the incidence of uncontrolled intrapleural sepsis.
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PMID:The management of nonmalignant intrathoracic esophageal perforations. 678 26

Current methods to evaluate patients with esophageal disease include barium swallow with fluoroscopy, which is useful in demonstrating structural defects. Disordered motility is better evaluated with a cine-esophagram. Recent application of radioisotopes has been useful in evaluation of esophageal reflux and the post-treatment of achalasia. Esophageal motility studies may evaluate lower esophageal sphincter and upper esophageal sphincter pressures and the response of the body of the esophagus to series of swallows. Since there is no "gold standard" for the evaluation of reflux esophagitis, some of the tests designed to evaluate reflux and the patient's reaction to acid in the esophagus include the acid infusion test, the standard acid reflux test, the acid clearance test, and 24-hour pH monitoring. Endoscopy with either the flexible or the rigid instrument is important for the diagnosis of obstruction or esophagitis and allows direct visualization of the esophagus. The treatment of reflux esophagitis is discussed. The differential diagnosis of dysphagia may include achalasia, diffuse esophageal spasm, and mechanical obstruction of the esophagus due to rings, webs, strictures, and benign or malignant tumors. The evaluation of dysphagia should include radiologic as well as endoscopic evaluation. Treatment of obstruction varies according to the nature of the lesion. The Mallory-Weiss syndrome or bleeding from the mucosal tears of the gastroesophageal junction and Boerhaave's syndrome, spontaneous esophageal perforation, are two disorders associated with vomiting. The Mallory-Weiss syndrome usually resolves without specific therapy, but a high index of suspicion is required for patients with chest pain after vomiting, as spontaneous perforation necessitates immediate surgery. Most diverticula need no treatment, but the Zenker diverticulum, if symptomatic, should probably be surgically repaired.
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PMID:Evaluation and management of diseases of the esophagus. 703 70

Pathologic gastroesophageal reflux encountered during the neonatal period can be associated with projectile vomiting often of bile stained gastric content. Between 1960 and 1979, symptomatic gastroesophageal reflux was diagnosed in 36 neonates. Duodenogastroesophageal reflux was present in 16 or 44.4% of this group. This abnormal phenomenon is classically encountered in our experience during the neonatal period. The in-series incompetence of the pyloric and lower esophageal sphincteric mechanisms gives rise to a variant of the so called phreno-pyloric syndrome. The seriousness of this association is emphasized in our series by the high incidence of complications encountered in the patients with this syndrome, i.e., gastroesophageal bleeding in 44% esophagitis with stricture of formation in 12.5%. Conservative management of the cases encountered with this syndrome was successful except in two cases where reflux esophagitis was complicated by severe stricture formation. It is postulated that the pathogenesis of this form of phreno-pyloric syndrome is most probably based upon a motility disturbance of the upper gastrointestinal tract, involving the hormone motilin.
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PMID:The phreno-pyloric syndrome in symptomatic gastroesophageal reflux. 707 96

A patient with persistent vomiting in pregnancy due to oesophageal stricture secondary to reflux oesophagitis is reported. Reflux oesophagitis is common during pregnancy but usually responds to small frequent meals, the avoidance of certain positions and simple antacid therapy. Where symptoms are persistent and become worse in late pregnancy we suggest that more energetic therapy in the form of cimetidine or alginate antacid mixture (Gaviscon) should be considered to prevent oesophageal stricture formation.
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PMID:Oesophageal stricture due to reflux oesophagitis in pregnancy. Case report. 730 80

A 3-mo-old female presented with growth retardation, vomiting, reflux esophagitis, recurrent aspiration pneumonias, and was found to have megaesophagus and microgastria. After the failure of conservative therapy a double-lumen jejunal (Hunt-Lawrence) pouch with distal Roux-en-Y anastomosis was anastomosed to the stomach to increase the gastric reservoir. One year later, there has been progressive weight gain, the megaesophagus and gastroesophageal reflux have lessened significantly, pneumonia has not recurred, and the tracheobronchitis and esophagitis have resolved. This suggests that the gastroesophageal reflux and megaesophagus were due to an inadequate reservoir with a secondary gastric overflow as the esophagus dilated to enlarge the reservoir capacity of the upper gastrointestinal tract. Utilization of a jejunal pouch increased the size of the gastric reservoir, allowed resolution of the secondary esophageal changes, and permitted normal growth to proceed.
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PMID:Management of congenital microgastria with a jejunal reservoir pouch. 746 90

Gastroesophageal reflux (GER) is the movement of gastric contents retrograde into the esophagus. Sometimes the refluxate is seen as emesis, but often reflux is "silent," meaning that there are no discrete symptoms during an episode. In adults, the most common symptom of GER is heartburn, whereas in infancy excessive crying and malaise are symptoms that prompt investigation for GER, with or without esophagitis. Symptoms of esophagitis in infancy may include arching (hyperextension) of the torso and refusal of feedings. Tube feedings may be required to treat infants with failure to thrive who refuse oral feedings. Paradoxically, tube feedings increase the number of GER episodes. A hypothetical explanation for refusal of food in infancy is that pain with swallowing (odynophagia) or heartburn are consequences of peptic esophagitis. As a result, infants will learn to refuse food if it hurts or if they fear that it will hurt to eat. Another possible mechanism is visceral hyperalgesia, a neuropathic condition in which prior experience changes sensory nerves so that previously innocuous stimuli are perceived as painful. Some infants may have especially sensitive sensory nerves in the upper gastrointestinal tract, which predisposes visceral hyperalgesia to develop. Thus pain occurs from luminal distension or acid reflux in the absence of tissue damage. The evaluation of babies who won't eat includes a careful history and physical examination to exclude the possibility of chronic systemic illness. Refusal to feed is an unusual manifestation of a common condition: GER disease. The initial tests for GER usually include a barium swallow study to assess the upper gastrointestinal anatomy, endoscopy and esophageal biopsy to assess esophagitis, and an intraesophageal pH study, which is useful in "silent" reflux to quantitate the duration of esophageal acid exposure and to correlate discrete symptom episodes with periods of reflux. The treatment of infants and toddlers who refuse to eat because of pain resulting from visceral hyperalgesia or reflux esophagitis involves removing the pain associated with eating and making eating a pleasurable experience. Treatment for esophagitis may include maintaining an upright posture after meals and thickened feeds, medication to improve gastrointestinal motility or to decrease acid secretion, or fundoplication.
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PMID:Gastroesophageal reflux: one reason why baby won't eat. 798 64

Omeprazole has been marketed in France since 1989, for the healing of peptic ulcers, erosive reflux esophagitis and the Zollinger Ellison syndrome. It is a proton pump inhibitor which inhibits the acid secretion in the stomach. In the majority of the clinical trials, omeprazole has been found to be well tolerated: headache, dizziness, skin rash, constipation have just been noted. Since September 1989, 143 adverse reactions have been reported to pharmacovigilance centres and Astra France: 37 neurological and psychiatric side effects, especially confusion in patients with hepatic diseases and/or advanced age; 35 cutaneous reactions, generally rash and urticaria; 22 hematological effects: leucopenia and agranulocytosis have been reported but the relation with omeprazole is very uncertain; 10 gastrointestinal effects, generally diarrhoea, nausea, vomiting and abdominal pain; 8 hepatic disorders, especially moderate elevation of aminotransferases. This study confirms the safety of this drug, during short treatment; the frequency of notified adverse effects is about 1/12 200 treatments of 4 weeks. The ministry of health, has decided, in november 1991, to inform the prescribers of this potential toxicity of omeprazole, particularly, of the risk of confusion, hepatotoxicity and leucopenia.
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PMID:[Evaluation of unexpected and toxic effects of omeprazole (Mopral) reported to the regional centers of pharmacovigilance during the first 22 postmarketing months]. 814 27

Esophageal hiatal hernia was diagnosed in 11 young Chinese Shar-Pei dogs between October 1985 and July 1991. The dogs ranged in age from 2 to 11 months and included 3 females and 8 males. The most common clinical signs were regurgitation, vomiting, and hypersalivation. Physical examination was normal in 6 dogs; abnormal physical examination findings in the other 5 dogs included fever, dehydration, hypersalivation, and pulmonary wheezes and crackles. Laboratory evaluation was significant only for neutrophilia in 5 dogs. A diagnosis of hiatal hernia was made on the basis of survey thoracic radiographic and/or barium esophagram findings of displacement of the esophagogastric junction and stomach into the thoracic cavity; the diagnosis was confirmed by surgery in 9 dogs and at necropsy in 2 dogs. Megaesophagus (n = 7), gastroesophageal reflux (n = 4), and esophageal hypomotility (n = 1) were additional findings in some dogs. Aspiration pneumonia was diagnosed in 7 of the dogs. Medical therapies formulated for the therapy of presumed reflux esophagitis generally failed to resolve the clinical signs associated with the hiatal hernia. Hiatal herniae were surgically repaired in 9 of the Shar-Peis by various combinations of diaphragmatic crural apposition, fixation of the esophagus to the diaphragmatic crus (esophagopexy), and left fundic tube gastropexy. Eight of the animals survived surgery, six of which have been asymptomatic since surgery (19 to 36 months). The megaesophagus, esophageal hypomotility, and bronchopneumonia resolved in all of these dogs.
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PMID:Congenital esophageal hiatal hernia in the Chinese shar-pei dog. 824 9

An 82-year-old man suffered from recurrent melena due to reflux esophagitis and aspiration pneumonia, which were caused by severe gastroesophageal reflux. We constructed a gastric stoma by percutaneous endoscopic gastrostomy (PEG) and fixed a transgastrostomal jejunal tube (TGJ tube) in the jejunum through the stoma. Direct administration of fluid into the jejunum was followed by a significant reduction in gastro-esophageal reflux. The reflux esophagitis and aspiration pneumonia did not recur. There was no vomiting, self-extubation, or restlessness that might have been caused by dementia, and the patient was could discharged cared for at into home.
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PMID:[Gastro-esophageal reflux successfully treated with transgastrostomal jejunal tube feeding]. 907 7


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