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

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Five children with AML were treated with high-doses of Ara-C (2 g/m2) during consolidation. After 17 cycles the toxicity was evaluated. Granulocytopenia (< 0.5 x 10(9)/l) and thrombocytopenia (< 25 x 10(9)/l) were stated after 15/17 and 13/17 cycles respectively. The nadir of bone marrow suppression appeared between day 10 and 14. In one case treatment related death during severe myelosuppression was noted. In individual cases jaundice with elevated activity of aminotransferases, paralytic ileus and pulmonary oedema were observed. All these adverse reactions were reversible. Other toxicities such as nausea/vomiting, stomatitis, diarrhea, infections and drug related fever were transient. No neurologic toxicity was seen. There is a need for developing a new way of the administration of high-dose Ara-C which could substantially reduce toxicity of the drug.
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PMID:[Preliminary evaluation of adverse effects after administration of arabinoside cytosine (Ara-C) in high doses to children with acute myelogenous leukemia]. 820 12

Headache, nausea, vomiting, insomnia and peripheral edema are the most important symptoms of acute mountain sickness (AMS), which occur within 6 to 12 h. after exposure to altitudes of more than 2500 m a. s. l. Usually, these symptoms resolve spontaneously; however, they may progress to life-threatening cerebral edema in some cases. High-altitude pulmonary edema (HAPE) is a noncardiogenic edema, which is often preceded by acute mountain sickness. Frequency and severity of these illnesses depend on the altitude, the rate of ascent and the degree of individual susceptibility. A low hypoxic ventilatory drive, sodium and water retention as well as increased capillary permeability are the most important pathophysiological factors which contribute to hypoxemia and edema formation in AMS. They are also important in the pathophysiology of HAPE. In addition, excessive hypoxic pulmonary artery hypertension is most likely crucial in the pathogenesis of HAPE. Constitutional factors which regulate ventilation and pulmonary artery pressure under hypoxia are considered the most important determinants of susceptibility to AMS and HAPE.
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PMID:[Clinical aspects and pathophysiology of altitude sickness]. 837 71

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56

The use of dobutamine stress echocardiography for the evaluation of coronary artery disease is rapidly expanding. Despite its widespread use, the feasibility and safety of dobutamine stress echocardiography has not been sufficiently documented. Between November 1992 and June 1995, we performed 1000 dobutamine stress echocardiographies. There were 744 men and 256 women with a mean age of 59 +/- 11 years. Anti anginal medication was not routinely withdrawn before the test. The mean maximal dobutamine dose was 41,4 +/- 10 mu g/kg center dot min(-1). Atropine was given additionally in 440 patients, with a mean dose of 0.5 mg. In patients receiving beta-blockers additional atropine was more often necessary as compared to those not receiving beta-blockers (278/457 = 61% versus 162/543 = 30 %, p < 0.0001). Reasons for discontinuing dobutamine infusion were achievement of target heart rate (64 % of cases) and maximal dose (12 % of cases). In 791 (79,1 %) patients no side-effects of dobutamine stress echocardiography were noticed. Termination of the study because of adverse side-effects occurred in 6.6 %. A total of 103 (10,3 %) noncardiac side-effects were observed: dizziness or nausea 6.4 %, headache 1.7 %. In one patient a focal cerebral seizure occurred. 156 cardiac side-effects occurred: blood pressure decrease of more than 20 mm Hg in 25 patients, extreme palpitations in 16 patients and pulmonary edema in one case. Most common cardiac side-effects consisted of arrhythmias (11.4 %): 9.1 % ventricular and 2.3 % supraventricular arrhythmias. Most ventricular arrhythmias were less severe (uniform and multiform premature ventricular beats, ventricular bigeminy or couplets in 71 patients). Nonsustained ventricular tachycardia, with a maximum duration of 20 s, occurred in 18 patients. In one patient sustained ventricular tachycardia developed and progressed towards ventricular fibrillation. This patient could be successfully defibrillated. Supraventricular arrhythmias presented as new atrial fibrillation in 10 patients, supraventricular tachycardia in three patients, junctional rhythm with a short decline in heart rate in nine patients and a second-degree AV block in another case. Dobutamine stress echocardiography has proven to be a safe and feasible method in the diagnosis of coronary heart disease. Minor side-effects are common and sometimes unpleasant for the patient, but do not often require termination of the study. Severe side-effects are seldom (< 1 %), but nevertheless, adequate medical and technical (defibrillator) support should be rapidly available.
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PMID:[Feasibility and safety of dobutamine stress echocardiography: experiences with 1,000 studies]. 871 45

Medical records of 150 patients with high-altitude pulmonary edema seen over a 39-month period in a Colorado Rocky Mountain ski area at 2,928 m (9,600 ft) (mean age 34.4 years; 84% male) were reviewed. The mean time to the onset of symptoms was 3 +/- 1.3 days after arrival. Common symptoms were dyspnea, cough, headache, chest congestion, nausea, fever, and weakness. Orthopnea, hemoptysis, and vomiting were rare, occurring in 7%, 6%, and 16%, respectively. Symptoms of cerebral edema occurred in 14%. A temperature exceeding 100 degrees F occurred in 20%, and 17% had a systolic blood pressure of 150 mm of mercury or higher. Blood pressures were higher in patients older than 50 years (142 mm of mercury). Rales were present in 85%, and a pulmonary infiltrate was present in 88%; both were most commonly bilateral or on the right side. The amount of infiltrate was mild. Men appeared to be more susceptible than women to high-altitude pulmonary edema. Pulse oximetry in 45 patients showed a mean oxygen saturation of 74% (38% to 93%). Treatment methods depended on severity and included a return to quarters for portable nasal oxygen, an overnight stay in the clinic for continuing oxygen, or a descent to Denver for recovery or admission to a hospital. All patients received oxygen for 2 to 4 hours in the clinic. There were no deaths or complications.
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PMID:High-altitude pulmonary edema at a ski resort. 877 33

Hantavirus pulmonary syndrome (HPS) is a viral infection from a new strain of Hantavirus. The Hantavirus was first discovered in North America in 1993 after an outbreak of fatal illness on a Navajo Indian reservation in New Mexico. Since then, 122 cases of HPS (with a high mortality rate of more than 50%) have been reported in 23 states, with the highest prevalence in the Four Corners area. The reservoir for Hantavirus is small rodents, mostly field mice, vole, and chipmunks. It is transmitted through inhalation of airborne virus from dry rodent excreta and saliva. A North American strain of Hantavirus, named ain nombre virus (SNV), primarily affects the lungs, causing rapid accumulation of fluids and leading to noncardiogenic pulmonary edema, pleural effusion, and acute respiratory distress syndrome (ARDS). In the prodromal stage, HPS presents with flu-like symptoms, nausea, vomiting, and gastrointestinal pain and is often mistaken on the first visit for other infectious diseases or gastroenteritis. In the second acute stage, rapid respiratory deterioration begins: HPS is often misdiagnosed for pneumonia, idiopathic ARDS, and pulmonary edema. HPS treatment with an experimental antiviral intravenous drug, ribavirin, is under investigation. Practitioners must possess through clinical knowledge on the diagnoses, pathology, treatment, and course of the disease to reduce the mortality and morbidity rate of this rare but serious infection. A case report based on a recent HPS death in New York State on Long island in April 1995 is presented.
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PMID:Hantavirus pulmonary syndrome: epidemiology, prevention, and case presentation of a new viral strain. 878 77

During the years 1986 to 1990, an increasing number of cases of acute carbon monoxide (CO) poisoning were encountered in the Emergency Department Hacettepe University Hospital in Ankara, Turkey. Between January 1 and March 31, 1991, all the patients presenting with complaints compatible with CO poisoning were evaluated; the diagnosis was confirmed in 55 of the 5795 people who attended the Emergency Department during this period. In all cases the source of CO intoxication was determined. Among these patients, nausea or vomiting and headaches were the most common complaints (occurring in 100% and 85%, respectively). At least transient impairment of alertness was observed in 29% of cases. The carboxyhaemoglobin levels ranged from 3.80 to 48.1% (median 14.2%). Two comatose patients who developed a non-cardiogenic pulmonary oedema required mechanical ventilation. One of them was discharged from the hospital with mild cerebral disability. Another patient developed an acute myocardial infarction. In all the cases in this series, the source of CO poisoning was identified as improper combustion of recently marketed steam coal in inadequately ventilated bucket stoves.
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PMID:Carbon monoxide poisoning related to the use of steam coal in poorly ventilated bucket stoves. 942 89

As more people enjoy the outdoors, high-altitude illness is increasingly becoming a problem that family physicians across the country must treat. High-altitude illness, which usually occurs at altitudes of over 1,500 m (4,921 ft), is caused primarily by hypoxia but is compounded by cold and exposure. It presents as one of three forms: acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE). But high-altitude illness can have many other manifestations. Cardinal symptoms include dyspnea on exertion and at rest, cough, nausea, difficulty sleeping, headache and mental status changes. Treatment requires descent, and gradual acclimatization provides the most effective prevention. Acetazolimide is an effective preventive aid and can be used in certain conditions as treatment.
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PMID:High-altitude medicine. 957 28

A 74 year old patient with diabetes mellitus was hospitalized because of nausea, recurrent vomiting and increasing fatigue. Shortly before admittance the patient had diarrhea. He also reported a recent onset of aversion against meat consumption. Clinical investigation revealed a possible right-sided paraumbilical abdominal tumor, normal bowel sounds, a vascular bruit and a normal white blood count with increased band forms. During hospitalisation the general condition of the patient deteriorated rapidly with fever and increasing numbers of immature granulocytes. The patient finally died under the symptoms of a paralytic ileus with hypotonia and hypoglycemia. Autopsy revealed a fist-sized stenosing tumor in the cecum with the histology of a mainly well differentiated, cylindrocellular adenocarcinoma. As immediate cause of death a bilateral paracentral lung embolism with pulmonary edema was found, the latter probably as immediate consequence of preterminal heart failure.
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PMID:[Intestinal paralysis in long-term diabetes mellitus]. 965 91


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