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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastroparesis after a pylorus-preserving pancreatoduodenectomy has two main aspects, namely early gastric stasis and subsequent postprandial delayed gastric emptying. Early gastric stasis producing an excessive amount of gastric juice during the immediate postoperative period might be caused by the absence of phase III activity of the gastric migrating motor complex (MMC), and such symptoms usually subside within a month or two. Subsequent postprandial delayed gastric emptying leading to belching, fullness of the stomach, nausea, and vomiting after the resumption of oral intake normally continues for up to 6 months before complete recovery. There are many possible mechanisms to explain these phenomena. The early recovery of phase III of the MMC does not necessarily predict an early relief of postprandial delayed gastric emptying, thus suggesting that these two phenomena are caused by various mechanisms. The phenomena, mechanisms, and treatment strategies for gastroparesis after pylorus-preserving pancreatoduodenectomy are described in this review.
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PMID:Gastroparesis after a pylorus-preserving pancreatoduodenectomy. 1586 14

Diabetic gastroparesis is a long term complication of diabetes mellitus which could basically be defined as dysregulated gastric emptying leading to various pathological, biochemical and clinical changes in absence of any structural changes. Symptoms include nausea, vomiting, bloating, epigastric pain, anorexia, weight loss and so on. For symptomatic gastroparesis prokinetic drugs like metoclopramide, domperidone, cisapride, erythromycin and itcopride are used. Itopride is currently emerging as a prokinetic drug of choice. There is also scope of surgery.
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PMID:Management of diabetic gastroparesis. 1617 96

Gastroparesis frequently happens during migraine attacks, postponing the onset of action of orally administered drugs. Furthermore, triptans seem to work better in the earlier phases of the migraine attacks. Therefore, associating a gastrokinetic drug with a triptan may translate into better efficacy and higher consistency of response. Trimebutine is an opioid derivative with exclusive action on receptors of the Meissner and Auerbach plexus throughout the digestive tube. It has no absorption or central penetration. Herein we contrast the combination of rizatriptan plus trimebutine with rizatriptan alone in the acute treatment of migraine. Forty patients with migraine consecutively seen in our clinic were randomized to treat two consecutive moderate or severe attacks with one tablet of 10 mg rizatriptan plus one capsule of 200 mg trimebutine and two attacks with the same triptan and placebo, in counterbalanced order. We collected information on the severity of the attack, as well as presence of nausea and photophobia at the time of drug intake, and after 1, 2 and 4 h. Recurrence and adverse events were also contrasted. Sixty-four attacks were treated with each drug regimen. At 1 h postdose, 30 (46.8%) of 64 attacks treated with the combination resolved completely, vs. eight (12.5%) of the rizatriptan-treated attacks, a difference of 34% (P < 0.01). At 2 h postdose, 47 (73.4%) attacks treated with the combination vs. 20 (31.2%) of those treated with rizatriptan alone resolved completely, a difference of 42% (95% confidence interval 26, 58, P < 0.001). Regarding nausea and photophobia, the combination was also associated with significantly better response. Recurrence was similar among the two drug regimens, as well as adverse events. The combination rizatriptan and trimebutine is more effective than rizatriptan alone. The combination does not increase adverse events or recurrence of pain.
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PMID:Rizatriptan vs. rizatriptan plus trimebutine for the acute treatment of migraine: a double-blind, randomized, cross-over, placebo-controlled study. 1677 4

Gastroparesis, or delayed gastric emptying, is a common cause of chronic nausea and vomiting as seen in a gastroenterology practice. Diabetic, postsurgical, and idiopathic causes remain the three most common forms of gastroparesis. In addition to nausea and vomiting, symptoms of gastroparesis may include early satiety, postprandial fullness, and abdominal pain. Physiologic changes that may explain symptoms in patients with gastroparesis, in addition to delayed gastric emptying, include impaired fundic accommodation, antral hypomotility, gastric dysrhythmias, pylorospasm, and perhaps visceral hypersensitivity. Diagnosis of gastroparesis is best determined using a radioisotope-labeled solid meal with scintigraphic imaging for at least 2 hours, and preferably 4 hours, postprandially. Most commonly, a 99mTc sulfur colloid-labeled egg sandwich with imaging at 0, 1, 2, and 4 hours is used. Extension of the gastric emptying test to 4 hours improves the accuracy of the test, but unfortunately, this is not commonly performed at many centers. Emptying of liquids remains normal until the late stages of gastroparesis and is less useful. The aims of treatment should be to control symptoms and maintain adequate nutrition and hydration. Patients should be advised to eat small meals and to limit their intake of fat and fiber. Additional dietary recommendations may include increasing caloric intake in the form of liquids. For diabetic patients, control of blood glucose levels is important, as symptom exacerbation is frequently associated with poor glycemic control. Specific treatment often begins with metoclopramide, 10 mg, up to four times daily, after a discussion of possible side effects with the patient. An antiemetic agent, such as prochlorperazine, 5 to 10 mg orally or 25 mg by suppository, can be added on an as-needed basis every 4 to 6 hours to control nausea. If these antiemetic medications are not effective, or if side effects develop, orally dissolving ondansetron, 8 mg every 8 to 12 hours, can be tried on an as-needed basis. If this regimen is unsuccessful, then alternative prokinetic agents--erythromycin, 125 mg, or tegaserod, 6 mg, prior to meals--can be tried. For cases refractory to these treatments, referral to a center with US Food and Drug Administration permission to use domperidone should be considered. Alternatively, symptom modulators such as low-dose tricyclic antidepressants can be tried to reduce symptoms, but these do not improve gastric emptying. In patients for whom all medical therapy fails, other options that are tried at experienced centers include the injection of botulinum toxin into the pylorus, placement of a feeding jejunostomy, and/or placement of a gastric electrical stimulator.
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PMID:Delayed gastric emptying: whom to test, how to test, and what to do. 1683 48

Gastroparesis is a condition of abnormal gastric motility characterized by delayed gastric emptying without evidence of mechanical outlet obstruction. The authors describe complete remission of recurrent postprandial discomfort, nausea, and vomiting within 1 week of starting mirtazapine in a gastroparetic patient who had failed to respond, in 7 months, to conventional prokinetics (erythromycin, metoclopramide, domperidone, perphenazine, itopride, bethanechol, and/or tegaserod) and pyloric injection of botulinum toxin. This is the first report to show that mirtazapine may be an effective alternative when gastroparesis is refractory to conventional measures.
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PMID:Mirtazapine for severe gastroparesis unresponsive to conventional prokinetic treatment. 1695 34

Metoclopramide is a dopamine receptor antagonist that is used to treat diabetic gastroparesis, chemotherapy-induced nausea, and migraines. It is known to cause extrapyramidal side effects such as tardive dyskinesia, parkinsonism, dystonia, and akithisia, but not chorea. We describe a patient who presented with choreiform movements shortly after the administration of intravenous metoclopramide. Her work-up for secondary causes of chorea was otherwise negative and her symptoms abated with the administration of oral quetiapine and intravenous diazepam.
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PMID:Acute chorea associated with metoclopramide use. 1712 36

Gastroparesis is a symptomatic disorder of the stomach characterized by slow or delayed gastric emptying. Diabetes and idiopathic factors account for over 60% of gastroparesis cases. Symptoms associated with delayed gastric emptying include nausea, vomiting, abdominal bloating and early satiety. Delayed gastric emptying due to gastroparesis is managed by dietary adjustments, prokinetic medications, avoidance of medications that retard gastric motor activity and optimizing glycemic control in diabetic patients. Electrical stimulation and gastric pacing are an evolving treatment option for patients who do not respond to standard medical therapy. This article provides a review of gastric motility, the etiologies of gastroparesis and therapeutic approaches to this disorder.
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PMID:Gastroparesis. 1739 32

Hemolysis is something that occurs to a small degree with every dialysis treatment. As we monitor our patients and the equipment we use, we hope that we have looked at everything and that our patients will be safe. We were extremely fortunate that we did not have a mortality related to this event. All of the hospitalized patients recovered and HP went on to receive her kidney transplant and is doing well. CG came back to dialyze in our unit after his physician was satisfied that our problem had been solved. In retrospect, we did not realize that we had an instrument in use that picked up the hemolysis long before we did. Our blood volume monitors showed us the increase in blood volume as the cells were lysed and vascular volume increased as the intracellular fluids were released. The concurrent rise in BP with these patients was also indicative of increased vascular volume. The blood volume monitor also showed the drop in hematocrit as red cells were lysed. We are now more experienced in interpreting these parameters and we are grateful to have this monitor on all of our patients and to have a new parameter to watch for to help forestall any further problems. Our patients' symptoms were baffling at the time because there were no overt signs of hemolysis. There was no "cherry pop" or brown colored blood in the lines or dialyzers which are what we have been taught to look for. Patients #1 and #3 essentially had no symptoms till the next day. Patient #2 exhibited nausea and some mild abdominal pain, which was also not new for him with his diabetic gastroparesis. Our nursing staff was very "gun shy" following this episode and some staff members seriously considered a change in profession. Fortunately they did not and opted to stay. It was brought home to all that dialysis, though it may seem to be a routine procedure, is inherently risky. Diligence and careful monitoring of all of our patients during their runs needs to be our utmost priority. Hemolysis to this degree is fortunately rare and we are grateful to have had an education with a positive outcome for all concerned.
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PMID:Hemolysis: a hidden danger. 1748 53

Dopamine antagonists, such as metoclopramide and domperidone, and the motilin receptor agonist erythromycin have been the cornerstones in drug treatment of severe gastroparesis for more than a decade. No new drugs have been approved for treatment of this disorder in this period. Instead, the 5-HT4 agonist cisapride has been withdrawn due to side-effects. The effectiveness of intrapyloric botulinum toxin for gastroparesis remains to be shown. In the last decade, gastric electrical stimulation (GES) with a fully implantable device has evolved as a promising treatment, with significant effects on nausea and vomiting in most patients with severe, drug-refractory diabetic gastroparesis and postsurgical gastroparesis. A proportion of patients with severe idiopathic gastroparesis and patients with idiopathic nausea and vomiting also respond. More research is needed to achieve precise selection of responders/non-responders to GES, and to study the potential benefit of GES in other patient groups suffering from severe nausea or vomiting.
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PMID:Severe gastroparesis: new treatment alternatives. 1764 6

Gastroparesis is a chronic alteration of gastric motility characterized by symptoms suggestive of mechanical obstruction and delayed gastric emptying in the absence of obstruction. Gastroparesis can be idiopathic or attributable to neuropathy or myopathy as in diabetes mellitus and scleroderma or can occur after vagotomy. Diagnosis is based on symptoms (nausea, vomiting, abdominal distension and early satiety), physical examination (capotement) and on complementary investigations, the procedure of choice being isotope gastric emptying tests. Treatment depends on the clinical repercussions. In most patients, gastroparesis can be controlled by prokinetic drugs, dietary measures, exclusion of drugs that alter gastric emptying, and exhaustive control of blood glucose levels. In patients with severe gastroparesis, hospital nutritional measures (intravenous and/or enteral), gastric decompression and intravenous antiemetic and prokinetic agents are required. Aggressive nutritional therapies (parenteral or enteral nasojejunal nutrition), intrapyloric injection of botulinum toxin, implantation of a gastric stimulation device, or gastrectomy should only be used in patients unresponsive to conservative treatment or if there is selective alteration of gastric motility.
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PMID:[Diagnostic and therapeutic approach to patients with gastroparesis]. 1766 20


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