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

Paraduodenal hernia (PDH) is an unusual condition that is caused by congenital intestinal malrotation. Noncatastrophic presenting symptoms and their responses to surgery have not been well-characterized. Barium upper gastrointestinal (UGI) series and small bowel follow-up x-rays, performed from December 1995 to September 1996, were sequentially reviewed by one radiologist (J.M.) to identify patients with small bowel series compatible with a PDH. Case histories were reviewed for symptomatic presentation, associated evaluation, and treatment. Based on the 294 UGIs and small bowel follow-throughs performed during this 10-month period, 6 cases were suspected to have a PDH. A right PDH was confirmed in the three patients who underwent surgical exploration (prevalence 1%). Preoperative patient symptoms included nausea, bilious vomiting, and right upper quadrant pain. Repair of the hernia defect resulted in complete resolution of chronic symptoms. Preoperative upper endoscopy, performed in three patients, was not helpful in identifying the disorder. Preoperative computerized tomography obtained in two patients was diagnostic for a right PDH. One symptomatic patient with vomiting and gastric stasis did not have surgery because of a terminal illness. The remaining two patients had no symptoms attributable to PDH. Patients with PDH frequently have chronic UGI symptoms. An upper endoscopy cannot be used to exclude this entity. After surgery, UGI symptoms from PDH are likely to resolve.
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PMID:Paraduodenal hernia: a treatable cause of upper gastrointestinal tract symptoms. 1103 2

Hemodialysis patients frequently experience such dyspeptic symptoms as nausea, vomiting, abdominal distension, early satiety, and anorexia. Gastroparesis might be a cause of malnutrition, and parameters of gastric emptying are inversely correlated with serum albumin levels. The aim of the present study is to determine whether delayed gastric emptying is related to dyspeptic symptoms. In 54 hemodialysis patients, a standardized history for dyspeptic symptoms was taken. In addition, gastric emptying for solids was measured in 26 patients, using the (13)C-octanoic acid breath test. There was a high prevalence of dysmotility-like dyspepsia in the hemodialyzed population. A significant difference in gastric emptying between dyspeptic hemodialysis patients and healthy volunteers and between dyspeptic and nondyspeptic hemodialysis patients was shown. There was a significant correlation between gastric emptying and dysmotility-like dyspepsia. Serum albumin level inversely correlated with gastric emptying. In conclusion, there is a high prevalence of dysmotility-like dyspepsia in hemodialysis patients. Dyspeptic patients have significantly delayed gastric emptying compared with both healthy volunteers and nondyspeptic patients.
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PMID:Delayed gastric emptying in dyspeptic chronic hemodialysis patients. 1105 52

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Gastric emptying scintigraphy (GES) is usually performed for up to 2 hr to measure the gastric emptying (GE) of solids. Symptomatic patients, however, may have borderline results at 2 hr, making it difficult to determine whether a gastric motor disorder is present. The aim of this study was to assess whether extending GES to 4 hr is useful in evaluating patients for gastroparesis and to correlate the results of GES with patient symptoms. We studied 129 patients undergoing GES at Temple University Hospital between July 1998 and March 1999. Solid-phase GE was measured at 0, 0.5, 1, 2, 3, and 4 hr after ingestion of a 99mTc sulfur colloid-labeled egg meal. Dyspeptic symptoms of upper abdominal discomfort, early satiety, postprandial abdominal bloating, nausea, vomiting, and anorexia were graded as none, mild, moderate and severe (0, 1, 2 and 3, respectively) with the sum representing a total symptom score. Of 129 patients, 86 had normal GE at 2 hr; 26 of the 86 normal scans at 2 hr were delayed at 3 hr. Six of the 60 scans normal at 2 and 3 hr were delayed at 4 hr. Of 43 patients with delayed GE at 2 hr, 39 were delayed at 3 hr and 35 were delayed at 4 hr. Overall, the percentage of patients with delayed GE increased from 33% at 2 hr only to 58% using the results of the 2-, 3-, and 4-hr scans (P < 0.05). There was a significantly greater symptom score in patients with delayed GE compared to patients with normal GE (8.4 +/- 0.5 vs 7.1 +/- 0.5; P < 0.05). Conclusion, prolonging GES after ingestion of a 99mTc-labeled egg meal from 2 to 4 hr increased the number of symptomatic patients found to have delayed GE. These results suggest that GES should be performed for up to 4 hrs when the 2-hr result is normal.
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PMID:Extending gastric emptying scintigraphy from two to four hours detects more patients with gastroparesis. 1127 Jul 90

This prospective audit aimed to evaluate a guideline for the management of nausea and vomiting in palliative care inpatients. Clinical pictures were used to guide diagnosis and treatment, with potentially reversible causes being addressed where appropriate. Over a 3-month period, 40 patient episodes occurred, all of which were included in the audit. The commonest clinical pictures were gastric stasis/outlet obstruction (35%) and chemical/metabolic (30%). Management according to the guideline was effective. Nausea was abolished in 28 of 34 cases (82%) and vomiting resolved completely in 26 of 31 cases (84%). Symptoms were totally controlled in a mean time of 3.4 days. Nausea and vomiting, although distressing symptoms, can be controlled in the majority of cases. Multi-centre prospective audit, using a standardized tool, may prove useful in allowing larger numbers of patients to be systematically analysed and individual centres to compare outcomes.
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PMID:Use of clinical pictures in the management of nausea and vomiting: a prospective audit. 1140 96

Nutrition support in gastroparesis begins with encouraging smaller volume, low-fat, low-fiber meals and, if necessary, liquid caloric supplements. There should be a low threshold for placing a jejunal feeding tube either by laparoscopy or mini-laparotomy. Parenteral nutrition should be used only briefly during hospitalization and not encouraged or sustained as an outpatient. Metoclopramide is now the prokinetic of choice for patients who can tolerate this agent; subcutaneous administration is an important method that allows for continued guaranteed absorption. Low-dosage erythromycin also has a prokinetic role alone or in combination with metoclopramide. Domperidone, a centrally acting antiemetic and prokinetic, is only be available to US citizens who can access sources in Canada or Mexico. Antiemetics should be used extensively because nausea is a very severe debilitating symptom, which is under-appreciated and under-treated by physicians. We recommend scopolamine patches to gain maximal absorption, in spite of vomiting and unpredictable oral intakes. The 5-hydroxytryptamine-3 (5-HT3) antagonists ondansetron and granisetron are the most powerful agents. Relief bands using the P6 acupuncture point are useful adjunct. Special vigilance should be paid to situations that can undermine medical therapy or result in breakthrough symptoms, such as hyperglycemic events in patients with diabetes, migraine headaches, cyclic nausea and vomiting, menstrual cycles, rumination syndrome (psychogenic vomiting), and elevated herpes simplex titers. Most excitingly, the era of gastric electrical stimulation has arrived for patients not responding to standard medical therapy. The dramatic improvement in nausea and vomiting, as well as a sustained evidence of improved quality of life, gastric emptying, nutritional status, and decreased hospitalizations by this device are documented by long-term follow-up of more than a year for patients in this country and world-wide.
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PMID:Gastric Dysmotility and Gastroparesis. 1146 76

Patients often develop nausea, vomiting and bloating after bone marrow transplantation (BMT). These symptoms may interfere with nutrition and the ability to take oral medications. Gastroparesis is a recognized cause of these symptoms in non-transplant patients but less is known about patients who undergo BMT. Between January 1996 and March 1997, a total of 151 patients underwent BMT. Eighteen patients (12%) developed persistent symptoms suggestive of gastroparesis (persistent nausea, vomiting or bloating). Scintigraphic gastric emptying studies were performed to assess for gastroparesis. Prokinetic agents were administered at the time of study. The records on these patients were compared with those of all other patients undergoing BMT during the same time period without these symptoms. Nine patients who demonstrated delayed gastric emptying were further evaluated with esophagastroduodenoscopy and biopsy. Biopsy samples were reviewed for evidence of graft-versus-host disease (GVHD). Fourteen of 18 patients demonstrated delayed gastric emptying and most responded to prokinetic agents given at the time of study. Age, conditioning regimen, cytomegalovirus antigenemia and acute GVHD did not appear to be associated with the development of gastroparesis. Allogeneic BMT recipients were at higher risk than autologous BMT patients (26% vs 0%, P < 0.0001). of allogeneic bmt recipients, there was a nonsignificant trend of patients receiving tacrolimus to be less likely to experience gastroparesis than those receiving cyclosporine (27% vs 48%, P = 0.08). For the nine patients undergoing upper endoscopy, GVHD on gastric biopsy was an uncommon finding and was mild when present. Gastroparesis appears to be a common cause of nausea, vomiting and bloating following allogeneic BMT. This may occur less often with tacrolimus than cyclosporine because of the former agent's prokinetic properties. Patients usually respond to prokinetic drugs at the time of scintigraphy. GVHD and CMV infection do not appear to be major contributing factors.
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PMID:Gastroparesis following bone marrow transplantation. 1149 45

We observed two patients with diabetes who were suffering from nausea, vomiting and epigastralgia after meals. These symptoms subsided when lying on their left side. Since the 2 patients had autonomic neuropathy, at first, the symptoms seemed to be attributable to diabetic gastroparesis. However, they were diagnosed as having superior mesenteric artery syndrome by hypotonic duodenography. These finding suggest that in diabetic patients who have a history of excessive weight loss superior mesenteric artery syndrome should be ruled out even though they have autonomic neuropathy.
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PMID:Diabetes mellitus associated with superior mesenteric artery syndrome: report of two cases. 1151 13

The objective of this review is to outline gastrointestinal factors that may be relevant to nausea and vomiting of pregnancy. Gastric neuromuscular dysfunctions of the stomach include abnormalities in gastric myoelectrical activity, gastric tone, and contractility, all of which may result in gastroparesis. These abnormalities in gastric neural activity and smooth muscle function are associated with nausea and vomiting in nonpregnant patients. Gastric dysrhythmias are disturbances of gastric pacesetter potential patterns that are present during the nausea of motion sickness, drug-induced nausea, in patients with diabetic gastropathy, and women with nausea of pregnancy. In pregnant women with abdominal pain, nausea, and vomiting, standard gastrointestinal diseases such as gastroesophageal reflux, peptic ulcers, and cholecystitis must be considered. A diagnostic approach and therapeutic options for treating nausea and vomiting of pregnancy based on understanding of gastric neuromuscular dysfunction is outlined.
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PMID:Gastrointestinal factors in nausea and vomiting of pregnancy. 1201 86

This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of nausea and vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias. Antral distension and increased intestinal delivery of lipids may cause slow-wave disruption and development of nausea. This may be mediated by cholinergic and serotonergic pathways. Similarly, progesterone and estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals. Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with motion sickness. This may be mediated by vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of nausea and vomiting, the search has begun for novel antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of prostaglandin synthesis inhibitors, central muscarinic receptor antagonists, and dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically implanted neurostimulator has shown promise in reducing emesis in patients with gastroparesis and gastric dysrhythmias.
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PMID:Physiology and pathophysiology of the interstitial cells of Cajal: from bench to bedside. VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias. 1206 86


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