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

Neutropenic enterocolitis is a symptom complex of fever, abdominal pain, distention, nausea, vomiting, diarrhea, and bloody stools occurring in a patient with a low neutrophil count and is most often seen in patients with acute leukemia after a course of chemotherapy. In most cases, neutropenic enterocolitis is a self-limited condition, but complications of transmural intestinal necrosis and bowel perforation may occur in a small number of patients. Surgical management should be reserved for those patients with bowel wall necrosis or perforation; however, early identification of these patients is difficult. We report our experience with the use of diagnostic peritoneal lavage in three patients with the symptoms and signs of neutropenic enterocolitis. In each case, Gram's stain of lavage fluid revealed no evidence of polymicrobial contamination of the peritoneal cavity. All three patients were managed medically, with resolution of their abdominal symptoms. Peritoneal lavage is helpful in excluding bowel perforation and avoiding unnecessary surgical intervention in patients with neutropenic enterocolitis.
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PMID:Selective management of patients with neutropenic enterocolitis using peritoneal lavage. 238 Dec 15

The currently accepted premise that the diagnosis of hypertrophic pyloric stenosis (HPS) should be made on clinical grounds, with ultrasound (US) and upper gastrointestinal series (UGIS) reserved for those with a negative clinical examination, was tested. Variable clinical skills of initial examiners, including pediatric surgeons, made abdominal palpation no more sensitive or specific than US or UGIS. For those with a negative clinical examination, proceeding directly to a UGIS will result in monetary savings, especially if good clinical performance decreases the probability of HPS among those without palpable pyloric "tumors." The benefits of a "US first" approach (no radiation, better patient and parent acceptance, no contrast medium) are less apparent but no less important and increase as clinical experience declines and performance of US improves. Criteria for the clinical or sonographic diagnosis of HPS should be kept strict to avoid false-positive results; false-negatives and other causes of vomiting should be identified by UGIS.
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PMID:A rational approach to the diagnosis of hypertrophic pyloric stenosis: do the results match the claims? 240 9

Dramatic advances in recent years in the diagnosis and treatment of inborn errors of metabolism (IEM) make it imperative for the physician to be both aware of their occurrence and acquainted with their clinical presentations. Many may present with symptoms and signs common to sick infants, such as refusal to feed, vomiting and convulsions. Failure to include IEM in the differential diagnosis may have grave consequences, because only prompt recognition and appropriate treatment of a metabolic crisis can help prevent irreversible brain damage or death. We describe a 3-week-old female infant, eventually diagnosed as having an IEM (3-hydroxy-3-methyl-glutaric aciduria), who was admitted to various hospitals and died during her last admission. We focused on the clinical and laboratory findings of each of the first 2 admissions which might have provided clues to the true nature of the illness had the clinicians been aware of the possibility of IEM. Patients with IEM are generally managed in specialized centers; however, the responsibility for initial recognition and immediate treatment of a metabolic emergency lies with the primary physician. The purpose of our case presentation and the discussion of the lessons derived from it, is to prompt the clinician to an awareness and understanding of a subject that used to be considered reserved for specialists. In fact, all that is needed is clinical alertness and the performance of certain well-focused, simple laboratory tests for IEM.
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PMID:[Inborn errors of metabolism: lessons from a clinical case]. 257 20

The pathophysiology of nausea and vomiting caused by antineoplastic therapy is described, and the literature on selected recent pharmacologic approaches to antiemetic therapy is reviewed. Nausea and vomiting associated with antineoplastic therapy remain serious deterrents to continued, potentially curative therapy for many patients. Although much research has been conducted in the area of antiemetic therapy over the past decade, the mechanisms by which antineoplastic agents cause nausea and vomiting are still not well defined. The most effective antiemetic agents to date are those that antagonize dopamine receptors. Metoclopramide is a dopamine antagonist that has been widely studied for the prevention of antineoplastic-agent-induced nausea and vomiting. Recent studies with this agent focus on routes of administration other than the traditional high-dose intermittent bolus intravenous injections. Continuous intravenous infusions of the drug and high-dose oral administration have been studied in an attempt to decrease the adverse effects associated with the traditional regimen and to allow administration on an outpatient basis. Prochlorperazine, a phenothiazine derivative, has been a mainstay of antiemetic therapy for many years. Although it is generally reserved for use with regimens that cause mild to moderate emesis, recent data suggest that higher-than-traditional doses given intravenously impart greater antiemetic protection. Perhaps the most promising antiemetic research has been conducted with a new group of agents, the serotonin antagonists. Preliminary trials suggest that these agents are comparable in efficacy to high doses of metoclopramide but devoid of many of the adverse effects commonly associated with metoclopramide. Further research in the area of neuropharmacology is necessary to direct the development of the most effective antiemetic agents.
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PMID:Recent advances in the management of nausea and vomiting caused by antineoplastic agents. 265 Sep 57

Acute diarrhea is a common problem in children. Understanding the different pathologic processes that cause diarrhea, and the agents that are associated with those processes, can aid the clinician in predicting the etiology of the diarrhea in an individual patient. Small bowel involvement, most commonly caused by Rotavirus, produces a high incidence of vomiting, often before the onset of diarrhea, and large, watery, and relatively infrequent stools. Large bowel involvement, usually due to Campylobacter, Salmonella, or Shigella produces frequent, often bloody stools containing leukocytes. Treatment of diarrhea should be focused on correcting dehydration, principally with oral rehydration solutions containing appropriate concentrations of electrolytes and carbohydrates. Early refeeding, avoiding foods containing lactose, should be considered for most pediatric patients with acute diarrhea. Antimicrobial therapy should be reserved primarily for parasitic infectious, pseudomembranous enterocolitis, and the early stages of a Campylobacter dysentery. The etiology of acute pediatric diarrhea can be predicted in most patients and early, appropriate treatment can be instituted.
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PMID:Acute diarrhea in children. 266 48

Symptoms of severe nausea, vomiting, abdominal pain, and frequent bezoars, as well as objective gastric retention, can occur following Roux-Y biliary diversion for alkaline reflux gastritis. Medical therapy and prokinetic drugs have proven ineffective. This review evaluates 37 patients who underwent further gastric resection from 1979 to 1987 to improve gastric emptying and resolve symptoms. Fifteen patients underwent perioperative radionuclide solid-food gastric emptying studies. Seventy-three per cent (27 of 37 patients) of the patients who underwent further gastric resection (70% to 95%) had a satisfactory postoperative response. Twenty patients were graded Visick 1 or 2 and 7 Visick-3 patients, although much improved, still had some symptoms of gastroparesis. Twenty-seven per cent (10 of 37 patients) failed to improve and underwent completion total gastrectomy. Overall, 70% of this group had almost complete resolution of their symptoms. Three of 10 patients were considered "failures" due to postprandial pain in 1 and early vasomotor dumping in 2. Of the 10 patients who failed initial revisional surgery, 7 underwent a 70% to 80% subtotal gastric resection (STG) and 3 patients underwent 85% to 95% extensive resection (EXT.G.). Of the 15 patients who underwent perioperative radionuclide evaluation, a mean two-hour gastric retention of 61.4% +/- 4% (SEM) decreased to 25% +/- 4% following further gastric resection. Eight patients were in the STG group and seven patients were in the EXT.G group. Following STG, mean two-hour gastric retention of 58.2% +/- 3.5% decreased to 38% +/- 3% (p less than 0.05). In seven patients who underwent EXT.G, mean two-hour retention of 65% +/- 4% decreased to 10% +/- 2.5% (p less than 0.005). EXT.G resulted in normal gastric emptying and few late failures. In post-Roux-Y patients with symptoms of gastroparesis and documented gastric retention, EXT.G normalizes gastric emptying and restores a better quality of life. Total gastrectomy should be reserved for those patients who are failed by more extensive resection.
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PMID:The surgical treatment of chronic gastric atony following Roux-Y diversion for alkaline reflux gastritis. 273 Jan 85

The safety and efficacy of antiemetic drugs used in the treatment of nausea and vomiting during pregnancy are reviewed. Confirmation of the teratogenicity of drugs in humans is difficult; the risk can be estimated from results of cohort studies and case-control studies. The possible teratogenicity of Bendectin (doxylamine succinate and pyridoxine hydrochloride) was studied thoroughly; although the risk was minimal, the drug was withdrawn from the U.S. market. Whether phenothiazines are teratogenic has still not been conclusively determined. A large number of epidemiological studies have not shown meclizine to be teratogenic in humans. More information about metoclopramide is necessary before it can be safely recommended for use during pregnancy. The risks of using dimenhydrinate and diphenhydramine appear to be low. Pyridoxine is considered safe for use during pregnancy, but its efficacy in treating nausea and vomiting has not been determined. The relative efficacy of these agents has not been determined. The available data suggest that meclizine and dimenhydrinate are the antiemetics that present the lowest risk of teratogenicity; meclizine is the drug of first choice. Phenothiazines should be reserved for treating persistent vomiting that threatens the maternal nutritional status.
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PMID:Safety and efficacy of antiemetics used to treat nausea and vomiting in pregnancy. 287 10

Six premature infants (birth weights 920-1320 g) developed marked abdominal distension after birth, and contrast enema examination showed a microcolon. Four of the six were born to mothers with toxemia who received magnesium sulfate. Bilious emesis was absent in all six, despite marked distension and failure to pass meconium. None of the patients had aganglionosis or cystic fibrosis; five of six were followed without surgery and recovered spontaneously. The sixth had perforation 8 hr after contrast enema and required bowel diversion; this infant also survived. This appears to be an equivalent form in small premature infants of the "small-left-colon syndrome" seen in term infants. Surgery should be reserved for complications; it is not necessarily indicated by the finding of a microcolon in such patients.
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PMID:Microcolon of prematurity: a form of functional obstruction. 348 69

When vomiting is not related to preventing the entry of physically or chemically unsuitable substances into the absorbing gut, it may be regarded as pathologic. The commonest causes of chronic vomiting are structural lesions affecting the mucosa of the upper gastrointestinal tract (often with luminal obstruction) and psychogenic disorders. Diseases affecting extrinsic and intrinsic neural control of gut motility and visceral smooth muscle may also cause unexplained vomiting. A stratified management approach to patients with vomiting is suggested. The first assessment is aimed at exclusion of mucosal lesions of the upper gut and systemic or psychiatric disease that may affect it. Second is a therapeutic trial, usually with a prokinetic agent. The final phase, reserved for recalcitrant undiagnosed patients, is evaluation at special centers with gastric emptying studies, gastrointestinal manometry, other electrophysiologic studies, and, in a few patients, laparotomy with examination of full-thickness biopsy specimens of the small intestine.
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PMID:Unexplained vomiting: a diagnostic challenge. 637 6

In the emergency department, any patient who is suspected of having sustained a caustic ingestion must be handled in a serious manner. All patients should be initially stabilized with regard to airway and circulatory status. Initial questioning concerning the type and quantity of agent ingested will be most helpful. Signs and symptoms of shock, impending perforation, or airway distress take precedence over any further work-up. Patients who have a known history of ingestion require admission to the hospital. Complete physical examination should be carried out, bearing in mind that the lack of oropharyngeal involvement or other symptoms does not rule out the possibility of esophageal burns. One should avoid emesis and should begin early dilutional therapy. Water may be used initially to dislodge adherent solid particles, as well as to dilute the caustic ingestion. It is important not to be excessively aggressive with dilution, as this may cause nausea, vomiting, and possible aspiration. Early otolaryngologic evaluation will be most helpful. The role of early esophagoscopy has been demonstrated to aid greatly in determining the further management. This diagnostic procedure should be carried out within 48 hours after ingestion. Based on the information obtained with esophagoscopy, patients who have had moderate esophageal burns should receive 20 mg methylprednisone intravenously every eight hours if under the age of two and 40 mg intravenously every eight hours if over the age of two. When oral preparations can be used, 2 mg per kg of prednisone should be continued for three to four weeks. Antibiotic coverage should be reserved until the first sign of infection occurs.
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PMID:The emergency management of caustic ingestions. 651 23


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