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)

Esophageal stricture is a rare complication of paediatric cancer treatment that usually occurs after esophageal exposure to radiotherapy. We describe 4 cases of esophageal stricture during chemotherapy for acute lymphoblastic leukemia. All patients presented with refractory vomiting and were diagnosed with radiologic contrast studies. None of the patients had received radiotherapy. Esophageal candidiasis was seen in 2 patients but the remaining 2 patients had earlier systemic candidiasis. High-dose dexamethasone may predispose these children to both esophageal candidiasis and peptic esophagitis. The etiology of esophageal strictures during treatment for acute leukemia is likely to be multifactorial but systemic candidiasis may play a significant role.
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PMID:Esophageal strictures during treatment for acute lymphoblastic leukemia. 2016 44

We report a rare case of diffuse esophageal intramural pseudodiverticulosis in a 35-year-old man complaining of severe dysphagia and vomiting for several months. The advanced morphological change in the esophagus caused irregular track formation, mimicking an ulcerative lesion on esophagogram. Endoscopic examination revealed an esophageal stricture with intact mucosa. Endoscopic ultrasonography and chest computed tomography showed multiple hyperechoic lesions of unknown nature and multiple air collection sites in the esophageal wall, respectively, making diagnosis difficult. The patient finally received a subtotal esophagectomy because of severe symptoms. The lesion was pathologically proven to be intramural pseudodiverticulosis with marked submucosal fibrosis. Our experience suggests that awareness of this rare pathology and the related image changes will be helpful for early diagnosis and treatment in the future.
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PMID:Esophageal intramural pseudodiverticulosis complicated with stricture. 2043 33

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

Self-expanding metallic stents (SEMS) are the treatment of choice for incurable obstructive malignant esophageal strictures. Although the placement of SEMS is usually performed with fluoroscopic control (FC), recently several authors have shown the feasibility of placing SEMS under endoscopic control alone (EC). However, studies comparing the two techniques are lacking. The objective of this study was to compare the feasibility and safety of SEMS insertion under fluoroscopic control and endoscopic control. The study was performed through the retrospective analysis of patients who underwent SEMS insertion for malignant dysphagia between January 2005 and January 2010. Data concerning early and late complications and survival were retrieved. Early complications were defined as pain, vomiting, bleeding, malposition/migration, perforation, and/or dysphagia occurring until 30 days of SEMS insertion; and late complications as tumor ingrowth and overgrowth, migration, hemorrhage, fistulae, food impaction, and/or esophagitis occurring after 30 days. We placed 126 SEMS of which 87% for esophageal stricture, 8% for esophagus-respiratory fistula, and 5% for extrinsic compression. The mean age of the patients was 62 years, and 93 were male. SEMS insertion was performed with FC in 66 patients and EC in 60. Early complications occurred in 34 patients (52%) in the FC group and 28 (47%) in the EC group (P=0.71), including: pain in 22 patients of the FC group and 15 of the EC group (P=0.31); vomiting in 15 of the FC group and nine of the EC group (P=0.27); malposition/migration in three of the FC group and four of the EC group (P=0.60); hemorrhage in one of the FC group and two of the EC group (P=0.27); and dysphagia in two of the FC group and three of the EC group (P=0.57). Late complications occurred in 20 patients (30%) in the FC group and 22 (37%) in the EC group (P=0.44), including: tumor in/overgrowth in 13 patients of the FC group and 10 of the EC group (P=0.66); prostheses migration in five of the FC group and eight of the EC group (P=0.28); hemorrhage in two of the FC group and two of the EC group (P=0.54); appearance of esophageal fistulae in seven of the FC group and four of the EC group (P=0.43); food impaction in nine of the FC group and eight of the EC group (P=0.96); esophagitis in 12 of the FC group and 15 of the EC group (P=0.35). Median survival was 107 days (95% confidence interval [CI]=6-369 days) with no difference between the two groups. There were no statistical significant differences in the incidence of complications and in survival between patients undergoing SEMS placement under fluoroscopic control or endoscopic control.
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PMID:A comparative study between fluoroscopic and endoscopic guidance in palliative esophageal stent placement. 2215 81

In children, caustic ingestion is due to accidents at home and inadequate storage of caustic agents. In emergency, it is useful to remove the soiled clothes, rinse the affected area, and prevent vomiting and feeding. Caustic ingestion (pH<2 or>12) induces burns of the upper gastrointestinal tract requiring esophagogastro-duodenoscopy between H12 and H24. Strong alkalis cause necrosis with liquefaction of the esophagus, penetrating deeply with a high-risk of perforation. Management of these children requires a specialized care center with an intensive care unit, endoscopic equipment, and a surgical team. Esophageal stricture is the main complication; no prophylactic treatment (steroids) is effective. Strictures occur after the 3rd week, and barium swallow should be performed by the end of the 1st month. Stricture are often multiple, long, and tortuous; endoscopic dilatation is difficult with a high-rate of perforation and a low-rate of success. In situ application of mitomycin C or injection of triamcinolone could reduce the recurrence rate of stricture. In recalcitrant or recurrent strictures, it is recommended to perform an esophageal replacement using a colonic interposition or a gastric tube. Endoscopy should also be performed 15-20years after caustic ingestion to screen for early neoplastic lesions. Prevention is very important for avoiding caustic ingestions. Information and education should be given specifically to the parents of toddlers; caustic products should be stored out of reach of children and they should not be kept with food.
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PMID:[Management of caustic esophagitis in children]. 2314 64

We herein report our technique for laparoscopic esophageal myotomy combined with Collis gastroplasty and Nissen fundoplication for severe esophageal stenosis. Our patient had experienced vomiting since childhood, and his dysphagia had gradually worsened. He was referred to our department for surgery because of resistance to pneumatic dilation. He was diagnosed with a short esophagus based on the findings of a preoperative upper gastrointestinal series and GI endoscopy. After exposing the abdominal esophagus, esophageal myotomy around the esophago-gastric junction (EGJ) was undertaken to introduce an esophageal bougie into the stomach. Then, stapled wedge gastroplasty was performed, and a short and loose Nissen fundoplication was performed. In addition, the bulging mucosa after myotomy was patched using the Dor method. The patient's postoperative course was uneventful. Most patients with esophageal stricture require subtotal esophagectomy. Laparoscopic surgery for patients with benign esophageal stricture refractory to repeated pneumatic dilation is challenging. However, our current procedure might abrogate the need for invasive esophagectomy for the surgical management of severe esophageal stenosis.
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PMID:A novel laparoscopic approach for severe esophageal stenosis due to reflux esophagitis: how to do it. 2464 33

In the present report, we describe a case of long-term follow-up esophageal stricture occurring in a patient with nasogastric tube use. A 63-year-old man who had experienced dislocation of the 6th and 7th cervical vertebrae as the result of an external injury received treatment at another hospital and was admitted to the rehabilitation department of our hospital. After he exhibited normal swallowing in a videofluoroscopic swallowing test, the nasogastric tube was removed and oral feeding with a dysphagia diet was initiated. However, during oral feeding, the patient complained of swallowing difficulties in his lower throat. An esophagogastroduodenoscopy was performed to examine the lesions below the pharynx and a 2-mm stricture was observed. A balloon dilatation was performed for a total of 9 times to extend the stricture. After the procedure, the patient was able to easily swallow a normal diet through the esophagus and the vomiting symptoms disappeared. An esophagography showed that the diameter of the esophageal stricture was 11 mm.
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PMID:Balloon dilatation for an esophageal stricture by long-term use of a nasogastric tube: a case report. 2522 40

Development of infantile hypertrophic pyloric stenosis during postoperative period in EA with TEF is rare. Postoperative vomiting or feeding intolerance in EA is more common which is due to esophageal stricture, gastroesophageal reflux and esophageal dysmotility. A typical case of IHPS also presents with non-bilious projectile vomiting at around 3-4 weeks of life. The diagnosis of infantile hypertrophic pyloric stenosis in this subset is usually delayed because of its rarity. We report a case of IHPS in postoperative EA and emphasize on high index of suspicion to avoid any delay in diagnosis with its metabolic consequences.
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PMID:Infantile Hypertrophic Pyloric Stenosis in Postoperative Esophageal Atresia with Tracheoesophageal Fistula. 2629 Aug 14

Esophageal stenosis is a relatively uncommon condition in pediatrics and requires an accurate diagnostic approach. Here we report the case of a 9-month old female infant who presented intermittent vomiting, dysphagia and refusal of solid foods starting after weaning. She was treated for gastroesophageal reflux. At first, radiological investigation suggested achalasia, while esophagoscopy revelaed a severe congenital esophageal stenosis at the distal third of the esophagus. She underwent four endoscopic balloon dilatations that then allowed her to swallow solid food with intermittent mild dysphagia. After 17 months of esomeprazole treatment off therapy impedance-pH monitoring was normal. At 29 months of follow-up the child is asymptomatic and eats without problems.Infants with dysphagia and refusal of solid foods may have undiagnosed medical conditions that need treatment. Many disorders can cause esophageal luminal stricture; in the pediatric age the most common are peptic or congenital. Careful assessment with endoscopy is needed to diagnose these conditions early and referral to a pediatric gastroenterologic unit may be necessary.
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PMID:Congenital esophageal stenosis diagnosed in an infant at 9 month of age. 2644 66

Eosinophilic esophagitis (EoE) is a chronic allergen-mediated inflammatory disease of the esophagus. This inflammation leads to feeding difficulties, failure to thrive and vomiting in young children, and causes food impaction and esophageal stricture in adolescents and adults. In the 20 years since EoE was first described, we have gained a great deal of knowledge regarding the genetic predisposition of disease, the inflammatory milieu associated with EoE and the long-term complications of chronic inflammation. Herein, we summarize the important breakthroughs in the field including both in vitro and in vivo analysis. We discuss insights that we have gained from large-scale unbiased genetic analysis, a multitude of genetically and chemically altered mouse models of EoE and most importantly, the results of clinical trials of various pharmacologic agents. Understanding these successes and failures may be the key to developing more effective therapeutic strategies.
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PMID:Recent advances in the pathological understanding of eosinophilic esophagitis. 2647 Jun 2


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