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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of Sandifer syndrome with chronic torticollis and gastroesophageal reflux (GER). The infant exhibited regurgitations and vomiting from birth. Torticollis with a permanent tilt of the head towards the right developed at age six months. At 16 months, persistence of the vomiting and abnormal attitude of the head and neck led to a CT scan that outruled a brain tumor. Esophageal pH recordings disclosed severe gastroesophageal reflux (pH less than 4 for 46% of the time over 24 hours) and endoscopy showed ulcerated peptic esophagitis. Surgical treatment of the GER ensured both resolution of the reflux and disappearance of the torticollis, establishing the causal relationship between the former and latter manifestations.
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PMID:[Torticollis in children: do not forget the Sandifer syndrome]. 231 62

In a group of 12 patients with reflux esophagitis resistant to the medical treatment and normal LES pressure, gastric emptying and bile-gastric (B.G.) reflux (HIDA-CCK test) were determined. All of the patients had delayed gastric emptying associated in seven with high levels of B.G. reflux. Two of the patients had an unsuccessful fundoplication two years ago and five have been cured of duodenal 3 or gastric 2 ulcer with antacids. Although there was an evolution to an ulcer scar in all of these patients the abdominal post-prandial pain persisted and some of them maintained occasional bilious vomiting. Deep gastritis with dysplasia and metaplasia of the gastric mucosa was demonstrated in all of these five patients. The esophagitis was an isolated phenomenon in 3 patients, one had a peptic esophageal stricture above de cardia, and another one a Barrett esophagus. A proximal gastric vagotomy (PGV) and pyloroplasty was performed in patients with delayed gastric emptying without BG reflux. The other 7 patients with concomitant high BG reflux were treated by a duodenal diversion to a Roux-en-Y loop and P.G.V. Esophageal and gastric symptoms disappeared soon after surgery. Esophageal biopsies were normal six months after surgery and the intense gastritis changed to a less serious form of superficial gastritis. It is concluded that delayed gastric emptying associated or not with high values of BG reflux can be the most important pathogenic factor that cause reflux esophagitis in this group of patients. The improvement of gastric emptying and elimination of BG reflux can be the proper method to treat these situations.
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PMID:[Surgical therapy of reflux esophagitis in patients with normal lower esophageal sphincter pressure]. 277 77

Vomiting, hematemesis, and esophagitis resulting from gastroesophageal reflux or hiatal hernia are frequently observed in severely handicapped children. This study was conducted to determine whether the use of a new H2-antagonist, famotidine, could prevent recurrence of reflux esophagitis among such children. Seventeen severely handicapped, bedridden children admitted to a children's medical center between April 1985 and September 1986 were studied. All had vomiting or hematemesis as a main symptom, and the cause of esophagitis was suggested to be gastroesophageal reflux in 13 cases and hiatal hernia in four. Six had been previously treated with cimetidine or other drugs or a combination thereof without relief. Famotidine was administered at about 1 to 2 mg/kg/day, two times daily to patients weighing more than 10 kg and three times daily to those weighing less than 10 kg. In 13 cases, famotidine was administered intravenously for between seven and ten days and then given orally, while the rest were given the drug orally from the outset. The following results were obtained: (1) improvement was seen within seven days after start of famotidine treatment, and reduction of vomiting or hematemesis or both was reached within two weeks in 70% of cases and within three weeks in 94%; (2) famotidine was markedly effective in 29% and moderately effective in 41%; in no case was the drug ineffective; (3) no side effects were observed; five patients had transient, mild elevation of SGOT . SGPT, but this was not attributable to the drug.
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PMID:Effect of a new H2-blocker, famotidine, in reflux esophagitis among severely handicapped children. 288 29

Experimentally, the gastric and the duodenal mucosa can both be damaged by acute exposure to small intestinal juice. Though chronic exposure to bile causes mucosal erythema and hyperplasia, the gastric mucosal barrier is not damaged. Duodenogastric reflux is relevant in the pathogenesis of postoperative bilious vomiting and probably of "alkaline" reflux esophagitis. The exact mechanism of mucosal damage has not been established. Duodenogastric reflux is likely to be irrelevant in the pathogenesis of (microscopic) gastritis, of gastric ulcer, and of reflux esophagitis without previous gastric surgery.
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PMID:[Is a duodenogastric reflux of pathogenic significance?]. 305 2

Exercise-induced gastroesophageal reflux (GER) is described in an athletic child with chronic abdominal pain and vomiting in conjunction with strenuous exercise. Although continuous 24-h pH probe monitoring was negative for GER, simultaneous pH probe and exercise stress testing (treadmill) showed a prolonged, continuous episode of acid reflux throughout exercise and the 30-min recovery phase. The authors are unaware of other cases of exercise-induced GER in children and suggest that simultaneous pH probe and exercise stress testing may be a useful technique to evaluate exercise-induced symptoms in children. Moreover, the presence of acid reflux during stress may warrant exercise restriction during the early management of reflux esophagitis.
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PMID:Exercise-induced gastroesophageal reflux in an athletic child. 368 87

Of 49 patients with achalasia treated surgically between 1975 and 1985, 12 (8 women, 4 men) had undergone transthoracic esophagomyotomy previously. Four had had concomitant upper gastrointestinal surgery. All 12 patients complained of dysphagia; other symptoms included regurgitation, nocturnal aspiration, heartburn, chest pain, vomiting, upper gastrointestinal bleeding and weight loss. The average time from initial operation to onset of symptoms was 9 months. Preoperative investigations and operative findings identified the cause of dysphagia as inadequate or healed esophagomyotomy with persistent or recurrent achalasia (eight patients--two had partially disrupted fundoplications contributing to their dysphagia), hiatus hernia with reflux esophagitis causing esophageal spasm or peptic esophageal stricture (two patients) and incorrect initial diagnosis and treatment (two patients). Treatment, with the aid of intraoperative manometry, included repeat Heller myotomy (five patients), Hill antireflux repair (four patients), takedown of Nissen fundoplication and extension of myotomy (two patients). The average follow-up was 16 months. Eight patients had good results, two required further operation and one underwent multiple dilatations postoperatively. The causes of recurrent dysphagia following surgery for achalasia are diverse and patients require individualized investigation and treatment. Remedial surgery for achalasia can correct postoperative dysphagia but results are less successful than those following an adequate initial operation.
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PMID:Reoperation after failed esophagomyotomy for achalasia. 370 56

Clinical findings, symptoms and predisposing factors were studied in 43 patients with oesophageal candidiasis, 40 patients with peptic oesophagitis and 40 normal controls. Oesophageal candidiasis was confirmed cytologically. 2.4% of patients who had undergone gastroscopy had oesophageal candidiasis; only three of them had simultaneous candidiasis of the oral cavity. Cardiac failure, oesophageal varices, hiatus hernia and gastric ulcer were common associated disorders. 42% of patients with candidal oesophagitis were symptom-free. Most common symptoms were vomiting, retrosternal and epigastric pain. Peptic oesophagitis was more frequently associated with symptoms. Predisposing factors were present in 88% of cases of oesophageal candidiasis: alcoholism, hepatic cirrhosis, diabetes mellitus, malignant tumours and other wasting diseases. 18 patients had had treatment with cimetidine; they included all 13 patients whose candidiasis was first detected at check endoscopy.
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PMID:[Candidiasis of the esophagus. Prospective study of incidence, type of complaints and predisposing factors]. 373 73

Lower esophageal strictures in infants in more than 90% of cases are related to reflux esophagitis, while the remainder are congenital or induced by injuries such as penetrating trauma or corrosion by caustic agents. Among congenital disorders cartilaginous remnants in the esophagus are very rare, but it is a possibility that should always be considered, especially if signs of esophagitis are not seen on esophagoscopy. The first aim, when evaluating the vomiting or regurgitating infant, is to establish whether this is due to an organic disorder. When stricture of the esophagus becomes evident following prolonged vomiting, clinicians tend to attribute this to reflux with peptic injury, and in most of the cases that will be correct (1). Carefully performed investigation will bring forth those rare etiologic factors that can be easily overlooked (2). The investigation has to include radiographic studies, esophagoscopy, pH monitoring, and in selected cases, manometry. Recognition of the correct etiologic factor that caused the stricture will pave the way for adequate management. We report on two patients with congenital stenosis of the lower esophagus due to cartilaginous rings, one of which was diagnosed preoperatively.
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PMID:Congenital stenosis of the esophagus due to tracheobronchial remnants: a missed diagnosis. 379 20

Gastroesophageal reflux is a frequent occurrence in infancy. Most frequently, gastroesophageal reflux (GER) is due to a functional disturbance and lack of coordination of esophageal motility and lower esophageal sphincter incompetence. Vomiting is the sole symptom in the great majority of infants and responds readily to postural and dietary therapy. A malposition and defective fixation of the cardia and abdominal esophagus is the pathophysiologic substrate of hiatus hernia. Although most patients with hiatus hernia have GER, hiatus hernia is only symptomatic with concomitant GER. Differentiation between hiatus hernia and GER should therefore be dispelled. Treatment of hiatus hernia with GER is directed towards placing the patient in an upright position, even 24 h a day if necessary in a patient severe symptoms. The duration of therapy can be weeks to months. Small, frequent feedings are of additional importance, while thickening of formula with cereals were found unnecessary. Over the last few years, we have been able to observe 22 infants under 1 year of age with GER and hiatus hernia. In 19 of these patients-among them also patients with reflux esophagitis-this conservative treatment regimen has been successful. Drugs like antacids or cimetidine to lower gastric were considered unnecessary. Bethanechol was considered contra-indicated due to its discomforting side effects in infants. Three patients have been treated surgically during this period of time. In contrast, hiatus hernia in older children-mainly mentally retarded children-with GER has to be treated surgically; conservative therapy is usually without effect. The rare clinical condition of brachyesophagus is considered a malformation and requires surgical therapy in every instance.
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PMID:Conservative treatment of gastroesophageal reflux and hiatus hernia. 392 34

The etiology, pathogenesis, diagnosis, and treatment of reflux esophagitis are reviewed. Reflux esophagitis is the subjective or objective response to gastroesophageal reflux (GER), which is defined as the entrance of gastroduodenal contents into the esophagus not associated with vomiting or belching. The pathogenesis of reflux esophagitis may involve a number of mechanisms, including changes in lower esophageal sphincter pressure, gastric volume, composition of the refluxate, esophageal acid clearance, and esophageal tissue resistance. The most common symptom of reflux esophagitis is heartburn. Regurgitation of fluid into the mouth, usually after bending or during the night, is an unequivocal symptom of GER. Treatment can be divided into three phases. Phase 1 involves the avoidance of certain foods and habits, elevation of the bed head, antacid, and alginic acid-antacid therapy. Phase 2 involves drug therapy with agents not yet approved by the FDA for this indication: bethanechol chloride, cimetidine, and metoclopramide hydrochloride. Bethanechol chloride 25 mg is generally given four times daily. Cimetidine is given in doses of 300-400 mg after meals and at bedtime. Metoclopramide hydrochloride is administered in doses of 10 mg before meals and at bedtime. Phase 3 is antireflux surgery. Clinical experience has shown that phase 1 therapy is successful for about 75% of all patients. Of the 25% that do not respond to phase 1 therapy, about 90% will respond to phase 2 therapy, leaving only 5-10% of all patients with this disorder who will require phase 3 treatment. Current data favor cimetidine and bethanechol over metoclopramide. The least proof of efficacy and the most frequent adverse side effects are seen with metoclopramide. Cimetidine and bethanechol appear to have similar efficacy and relatively infrequent side effects. Evidence confirming the superiority of cimetidine over bethanechol is lacking. Further research is needed to determine the optimal pharmacologic combinations and treatment regimens.
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PMID:Current concepts in the pathogenesis and treatment of reflux esophagitis. 636 Apr 95


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