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

In recent years it has been demonstrated that a group of viruses, Rotavirus for the children and Norwalk agent for adults, are a highly significant cause of acute gastroenteritis during the months of winter ("winter vomiting disease"). The Rotavirus was identified by Bishop et al. as a double-stranded RNA virus that can be isolate from faeces of children with acute gastroenteritis. Viral gastroenteritis is an autolimitate disease, although under certain conditions it may even lead to severe disease and death by profound dehydration and electrolyte imbalance; it is characterized by nausea, vomiting, diarrhea and others minor symptoms. This entity only affects children between 3 months and 6 years of age, with a little prevalence for the males. Breast-fed babies are commonly thought to be less likely than artificial-fed babies to suffer from infective diarrhea. Rotavirus infection is also known to occur in parents of infected children, but in this situation the symptoms are generally mild or absent and they needn't medical attention. The Rotavirus invade mainly the epithelium of the proximal intestine where they make a cytopatic and physiologic alteration (deficience in Na and K-ATPsa activity) that determines a disturbances of water and electrolyte transport across the epithelium thus contribute to the diarrhea. The best methods for detecting this type of viral gastroenteritis are electron microscopy and, specialy, the complement fixation test. In this moment we have not specific therapy for this new disease but because its epidemiological importance it must be in all clinical minds.
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PMID:[Viruses and gastroenteritis (author's transl)]. 624 84

Encouraging results of the combination of upper hemibody irradiation (UHBI) and local chest irradiation (LCI) combined withh standard-dose chemotherapy in patients with extensive small cell bronchogenic carcinoma led us to a second pilot study utilizing the same radiation program combined wit high-dose induction chemotherapy. Fourteen patients with small cell bronchogenic carcinoma, five with extensive disease and nine with localized disease, were treated with cyclophosphamide (1.5 g/m2 iv, Days 1 and 22), lomustine (70 mg/m2 orally, Day 1), and methotrexate (15 mg/m2 twice weekly during Weeks 2, 3, 5, and 6). UHBI (600 rads) was given during Week 6 in a single dose and LCI was given during Week 7 (2000 rads/five fractions) to the tumor and mediastinum. Maintenance chemotherapy began in Week 12 with cyclophosphamide (700 mg/m2 iv every 3 weeks) and lomustine (70 mg/m2 orally every 6 weeks). Twelve patients were evaluable for response and toxicity (eight with limited disease). There were three complete response and seven partial responses after induction chemotherapy. After completion of the consolidation radiation therapy, all 12 patients had a response: six complete responses and six partial responses. Acute toxic effects included nausea and vomiting in eight patients, fever in five, and hypotension and angina in one. Subacute toxic effects included nausea, vomiting, and dehydration in two patients who required hospitalization, prolonged aplasia in one, reversible radiation esophagitis in three. Three patients had radiation pneumonitis including one with bilateral diffuse disease that led to death from respiratory failure. Only two of 12 patients received their maintenance therapy on schedule. Treatment failures occurred within the LCI field in seven patients and in distant metastatic sites in six. The median time to first relapse was 7 months and the median survival was 9 months. Because of toxicity, treatment delays, and poor survival in this group of patients, we cannot recommend this combined modality approach.
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PMID:Upper hemibody and local chest irradiation as consolidation following response to high-dose induction chemotherapy for small cell bronchogenic carcinoma--a pilot study. 628 19

Supravesical urinary diversion using a jejunal conduit may be associated with hyponatremia, hypochloremic-acidosis, hyperkalemia, azotemia, and a clinical picture of nausea, vomiting, dehydration, muscular weakness, elevated temperature, and lethargy. This syndrome is secondary to the loss of sodium chloride into the urine passing through the conduit and absorption of potassium and urea from it. Treatment and prevention of this syndrome consist of adequate supplements of sodium chloride and hydration. Intravenous hyperalimentation as the precipitating factor of a severe form of this syndrome and its successful management are described. The pathophysiology of the jejunal conduit syndrome is also discussed. Great selectivity and extreme caution are recommended with respect to the use of intravenous hyperalimentation in patients with jejunal conduits.
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PMID:The pathophysiology of the jejunal conduit syndrome and its exacerbation by parenteral hyperalimentation. 642 49

A case of central pontine myelinolysis (CPM) following rapid correction of hyponatremia was reported and literatures were reviewed. The case was 61-year-old nonalcoholic female who had taken an operation of craniopharyngioma 23 years ago. Fifteen years later, she received re-operation for the recurrent tumor, followed by replacement therapy of corticosteroid and clofibrate. She was otherwise well until two weeks before entry, when she noticed abrupt onset of high grade fever, nausea, vomiting and general malaise. She was admitted to an emergency hospital because of weakness, disorientation and a slight impairment of consciousness, but she was able to speak and to take some food per os. Laboratory studies disclosed urinary tract infection and showed a serum sodium level of 117 mEq/l, potassium 2.9 mEq/l, a serum osmolarity 232 mO sm/l and urine osmolarity 141 mEq/l. She was diagnosed to have an exacerbation of adrenal insufficiency with hyponatremia and hypotonic dehydration triggered by urinary tract infection. Intravenous administration of vitamin B complex, electrolytes including KCL, 5% glucose solution and physiological saline with a large amount of corticosteroid was performed aggressively. Serum sodium concentration was raised to 161 mEq/l in two days, and the increased level had been maintained more than five days, resulting in coma and flaccid quadriplegia. During this period, there was no episode of hypotension, hypoglycemia, hypoxia nor hepatic failure which could have caused brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine and extrapontine myelinolysis following rapid correction of hyponatremia--report of an autopsy case]. 646 6

The benefits, equipment used, commercially available sources, and the indications and techniques for administration of enteral nutrients are reviewed. In many malabsorption states, enteral feeding is preferable and parenteral nutrients are seldom indicated. Transitional enteral nutrient support usually is indicated after parenteral nutrient therapy. Enteral tube-feeding formulas should be matched to the patient's needs; formulas using blenderized natural foods or intact isolated nutrients are appropriate for patients with intact gastrointestinal tracts. Patients should be monitored for glucosuria and hyperglycemia, bloating, nausea, dehydration, and renal, hepatic and hematologic status. Formula dilution, and a reduced flow rate or use of continuous-drip feeding, will reduce the incidence of osmotic diarrhea. The effectiveness, low cost and low potential for serious complications make enteral feeding preferable to parenteral nutrient therapy for many patients.
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PMID:Enteral feedings. 676 98

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

50% of hospitalized medical emergency cases are cardiological and respiratory emergencies. Myocardial infarction, cardiogenic shock, ventricular arrhythmias and left ventricular failure often cause sudden death occurring within 1 or 2 hours. Therefore immediate management is necessary already in the prehospital phase of cardiovascular events. This does also apply for acute respiratory failure due to obstructive ventilatory disorders. Acute exacerbations of chronic obstructive pulmonary disease frequently are masked and may be misinterpreted as encephalopathy or alcohol withdrawal syndrome. Sedation may be dangerous. Also neuroglucopenic syndrome and hyperosmolar coma are occasionally interpreted wrongly. Thyrotoxic crisis, adrenal crisis and hypercalcemia are characterized by lethargy, mental disturbance and weakness, by dehydration, myopathy, nausea, constipation, diarrhea or tenesms or arrhythmias. In this situation of varied symptoms the most important action is to think of endocrine emergency, which may have multiple etiologies.
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PMID:[Cardiovascular emergencies--endocrine and metabolic crises. Practical hints for the physician in emergency service]. 711 36

Hyperparathyroid crisis is a rare disease but should be suspected in acutely ill patients complaining of weakness, lethargy, nausea, vomiting, confusion and abdominal pain. Despite the variety of clinical manifestations, the syndrome forms a distinctive pattern which, in the presence of a serum calcium level greater than 16 mg/100 ml, should be recognized. The most difficult problem in diagnosis is the differentiation of hyperparathyroid crisis from ectopic parathyroid hormone-producing tumors. The disease is an endocrine emergency which requires prompt surgery after rapid correction of dehydration and hypercalcemia. The best results are achieved by removing offending parathyroid tissue within 72 hours after the onset of symptoms.
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PMID:Primary hyperparathyroidism: hyperparathyroid crisis. 730 6

A cross-sectional survey of inpatient palliative care subjects (n = 52) was performed to determine the severity and distribution of symptoms thought to be associated with dehydration in terminally ill cancer patients and to clarify the association between the severity of these symptoms and commonly used objective measures of dehydration. Each patient rated the severity of seven symptoms using 100-mm visual analogue scales. The symptoms considered were thirst, dry mouth, bad taste, nausea, pleasure in drinking, fatigue, and pain. Associations were sought between these symptoms and predictor variables (fluid intake, plasma osmolality, sodium, and urea) and confounding variables (age, medications, oral disease, and mouth-care regimen). Mean symptom ratings were thirst 53.8 mm, dry mouth 60.0 mm, bad taste 46.6 mm, nausea 24.0 mm, pleasure in drinking 61.6 mm, fatigue 61.8 mm, and pain 33.5 mm. Using multiple-linear regression, no association could be demonstrated between thirst (the principal outcome of interest) and the predictor or confounding variables. Estimates of the study power performed after completion revealed a 76% chance of detecting a 20-mm difference between high and low fluid intake groups. This study provides the first quantitative estimate of the experience of dehydration symptoms in those with advanced cancer. The symptoms appear to be rated moderately severe, but there is no demonstrable association between severity and fluid intake. Further studies with greater statistical power and more accurate hydration assessment would strengthen our understanding of this association.
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PMID:Dehydration symptoms of palliative care cancer patients. 752 78

Gastroparesis is a chronic gastric motility disorder in which there is delayed gastric emptying of solids plus or minus liquids. Symptoms of gastroparesis may range from early satiety and nausea in mild cases to chronic vomiting, dehydration, and nutritional compromise in severe cases. Diagnosis of gastroparesis is based on demonstration of delayed gastric emptying of a radiolabeled solid meal in the absence of mechanical obstruction. A number of gastrointestinal and systemic disorders may impair gastric motility with resultant gastroparesis. Approximately one third of patients with gastroparesis have no identifiable underlying cause (so called idiopathic gastroparesis). Management of gastroparesis involves four areas: (1) nutritional support, (2) antiemetic drugs, (3) prokinetic drugs, and (4) surgical therapy (in a very small subset of patients). Gastroparesis is often a chronic, relapsing condition; 80% of patients require maintenance antiemetic and prokinetic therapy and 20% require long-term nutritional supplementation. In the near future, the most promising advances in the treatment of patients with gastroparesis will most likely come from the area of combination pharmacological therapy. In the long term, developments in the area of intestinal pacing and intestinal transplantation may offer further treatment options in this difficult disorder.
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PMID:Gastroparesis and the current use of prokinetic drugs. 804 84


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