Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case report is presented of toxic shock syndrome associated with the use of a contraceptive diaphragm and recent removal of an IUD. A 23 year old woman was admitted to St. Paul's Hospital in Vancouver, British Columbia because of frequent watery diarrhea and vomiting that had begun suddenly 2 days earlier, as well as generalized abdominal and muscular pain, fever and sweating of 1 day's duration. The patient's last menstrual period had ended 3 weeks earlier. Oral contraceptive (OC) therapy had been stopped 9 months earlier, and 2 weeks before admission an IUD had been removed because of dyspareunia. A diaphragm had been inserted 24 hours before the onset of symptoms and was in place at the time of admission. Removal of the diaphragm revealed about 10 ml of greenish yellow pus. Laboratory tests showed multiorgan involvement. The blood urea nitrogen level was 35 mg/dl and the serum creatinine level 2.9 mg/dl. The serum amylase level was 125 IU/l at the time of admission but rose to 1021 IU/l by day 6. The prothrombin time was 16 seconds. Arterial blood gas studies while the patient was breathing room air showed the following: pH 7.36, carbon dioxide tension 20 mm Hg and oxygen tension 84 mm Hg. Urinalysis showed pus and a small amount of glucose. Treatment consisted of blood volume expansion and electrolyte replacement. The patient showed improvement within 48 hours. 6 days after admission an exfoliative desquamating rash developed on the volar surfaces of the fingers and feet, and a slight scaling rash was noted on the face. These cleared spontaneously, without residual scarring. 6 criteria for the diagnosis of toxic shock syndrome have been defined: an increased body temperature; skin manifestations; shock, frequently with orthostatic hypotension and syncope; involvement of multiple organs; diarrhea; and myalgia. Clinicians need to appreciate that tampons are not the only cause of toxic shock syndrome and that the syndrome can occur at times other than during menstruation. Diaphragms may only rarely be associated, but their relation to toxic shock syndrome must be recognized. Counseling on the use of diaphragms should stress the avoidance of prolonged use.
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PMID:Toxic shock syndrome associated with a contraceptive diaphragm. 712 32

Sevoflurane, a new volatile anesthetic agent, is of great potential interest in pediatric anesthesia. Its use for ENT surgery in children was compared with halothane in this study. Altogether 40 children participated in the investigation. In 18 (median age 4.2 years), halothane was used. The remainder (median age 4.0 years) were anesthetized with sevoflurane. After rectal premedication with midazolam and atropine, anesthesia was induced by mask (the agent in O2/N2O, 40/60) using a Mapleson D system. The trachea was intubated without the use of muscle relaxants and the children were then allowed to breathe spontaneously at fresh gas flows set high enough to avoid rebreathing. Hemoglobine oxygen saturation (SpO2), inspired and expired gas concentrations, respiratory rate (RR), heart rate (HR), ECG and blood pressure were followed. Equianesthetic concentrations of the agents were used and induction characteristics were comparable between the two agents. RR and end-tidal CO2 tensions were similar in the two groups. HR and systolic blood pressures were, however, higher with sevoflurane. Cardiac arrhythmias were seen more frequently with halothane (61%) than with sevoflurane (5%). During emergence, postoperative nausea/vomiting was more frequent after halothane anesthesia. Initially, postoperative excitement occurred more often after sevoflurane, when paracetamol was given during anesthesia, which was reduced (P < 0.01) when paracetamol was given at the time for premedication. It is concluded that sevoflurane is an excellent induction agent, and maintains heart rate and systolic blood pressure better than when halothane is used. The incidence of cardiac arrhythmia is lower with sevoflurane than with halothane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sevoflurane for ENT-surgery in children. A comparison with halothane. 767 95

Contradictory results have been reported regarding the participation of bulbospinal inspiratory (BSI) neurons in vomiting contractions of the diaphragm in dogs and cats maintained at low and high end-tidal CO2 levels, respectively. To resolve this discrepancy, effects of CO2 levels on vomiting activities were observed in 159 BSI-neurons of paralyzed decerebrate dogs. About half of the BSI-neurons exhibited a vigorous burst with each fictive retch regardless of the CO2 level and 28 of 51 BSI-neurons produced a burst during the early phase of expulsion. These BSI-neurons were not concentrated in any particular area. While these results do not resolve the above contradiction, they do suggest that some BSI-neurons participate in the vomiting contraction of the diaphragm.
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PMID:Bulbospinal augmenting inspiratory neurons may participate in contractions of the diaphragm during vomiting in decerebrate dogs. 770 May 90

The main clinical features, pathophysiology and underlying mechanisms of drug-induced parkinsonism are reviewed. The clinical manifestations of drug-induced parkinsonism are often indistinguishable from idiopathic Parkinson's disease. However, some subtle differences may exist: for example drug-induced parkinsonism is often associated with tardive dyskinesias, bilateral symptoms and the absence of resting tremor, etc. Besides toxins (eg manganese, carbon monoxide or MPTP), many drugs are known to produce parkinsonism: dopamine blocking drugs (true neuroleptics used as antipsychotics: phenothiazines, butyrophenones, thioxanthenes but also sulpiride, "hidden" neuroleptics prescribed as anti-nausea or anti-vomiting drugs (such as metoclopramide and other benzamide derivatives), dopamine depleting drugs (reserpine, tetrabenazine), alpha-methyldopa, calcium channel blockers (flunarizine, cinnarizine, etc). The putative role of other drugs (eg fluoxetine, lithium, amiodarone) as well as the therapeutic management of this side effect are reviewed.
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PMID:Drug-induced parkinsonism: a review. 785 36

This study was designed to determine the threshold dose for toxicity, the potential for serious medical complications, and the medical care required after unintentional albuterol ingestion in children. This study was prospective and descriptive. Data were obtained on pediatric albuterol ingestions evaluated emergently as reported to three regional poison control centers. Data elements included dose ingested, physical findings, medical treatment, and outcome. During 18 months, 78 patients who ingested albuterol and who received urgent medical evaluation were identified. Mean age was 2.8 years. The amount ingested ranged from 0.2 to 8.8 mg/kg. The most commonly reported signs of toxicity were tachycardia (57%, 44/78), widened pulse pressure (50%, 27/54), hyperglycemia (50%, 12/24), agitation (45%, 35/78), low serum carbon dioxide (42%, 10/24), vomiting (26%, 20/78), and hypokalemia (26%, 9/35). We found a threshold dose o 1 mg/kg for three or more signs of toxicity (P < 0.01). No patient required any specific treatment for toxicity. Seventy-two percent of patients were discharged from medical care within six hours of ingestion. Albuterol overdose in children causes a variety of cardiovascular, neuromuscular, and metabolic effects that are usually benign. The threshold dose for the development of three or more signs of toxicity is 1 mg/kg or three to 10 times the recommended daily dose. Toxicity is short-lived and does not require specific therapy or hospital admission in most cases.
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PMID:Unintentional albuterol ingestion in children. 793 93

Sevoflurane is a "new" volatile inhaled anaesthetic that is currently undergoing phase III clinical trial in Europe and the United States. Owing to the low blood solubility, rapid induction of anaesthesia and emergence from anaesthesia would be expected. In this study, we compared emergence times and haemodynamics in patients receiving either sevoflurane or isoflurane. Furthermore, all adverse effects were recorded and the relationship to the drug administered was rated. METHODS. Fifty ASA physical status I and II patients were studied in an open, prospective, randomised clinical trial. Anaesthesia was induced with fentanyl, thiopentone, and vecuronium for facilitating endotracheal intubation and maintained with sevoflurane or isoflurane, 60% nitrous oxide (N2O) in oxygen (O2), and additional doses of fentanyl (1-2 micrograms/kg.h). The electrocardiogram, blood pressure (non-invasive), O2 saturation, temperature, and end-tidal concentrations of sevoflurane or isoflurane, N2O, and carbon dioxide were monitored continuously. At the end of surgery, administration of sevoflurane or isoflurane and N2O was discontinued without tapering and emergence times were recorded. All adverse events that occurred until the 3rd postoperative day were recorded and the relationship to the inhaled anaesthetic was rated as "none", "unlikely", "possible", "probable", or "highly probable". RESULTS. With the exception of gender, the two patient groups were comparable (Tables 1 and 2). Due to the higher MAC value, mean end-tidal concentrations were higher for sevoflurane (0.82% vs. 0.59% for isoflurane). The duration of anaesthetic exposure was 1.3 MAC h (calculation with FIO2 = 1.0 MAC value) and 3.1 MAC h (calculation with FIO2 = 0.4 in N2O MAC value), respectively, for both inhaled anaesthetics. Pulmonary elimination was faster (Fig. 1) and emergence time shorter (7 min vs. 11.5 min, Table 3) with sevoflurane. There was no difference in the time courses of heart rate and mean arterial blood pressure (Figs. 2 and 3). No adverse effects with a "probable" or "highly probable" relationship to the inhaled anaesthetic were observed. Table 4 shows the adverse events with a possible relationship to the drug administered. Further evaluations of nausea, vomiting, and dizziness are shown in Table 5. DISCUSSION. Emergence time after inhalation anaesthesia depends on pulmonary elimination and MACawake, that is, the end-tidal concentration that would allow opening of the eyes on verbal command. Pulmonary elimination depends on dose applied (MAC h), alveolar ventilation, and blood-gas solubility coefficient. Due to the lower blood-gas solubility coefficient (0.6-0.7 for sevoflurane vs. 1.3-1.4 for isoflurane) and in accordance with the investigations of Frink et al. [4] and Smith et al. [16], emergence time was significantly shorter with sevoflurane. Gender, the only difference between the two patient groups, does not influence pulmonary elimination and MACawake [8]. Supplementing inhalation anaesthesia with fentanyl, there was no difference in the time courses of heart rate and mean arterial blood pressure between sevoflurane and isoflurane. Adverse events with a possible relationship to the inhaled anaesthetic occurred in both groups.
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PMID:[Emergence times, hemodynamics and adverse effects of sevoflurane and isoflurane: an open, randomized, comparative phase iii study]. 797 85

Postoperative intestinal atonia is a complication which is likely to occur in patients predisposed for constipation and in patients after intra-abdominal operations. The postoperative delay of bowel movement, however, is often also related to the type of anaesthesia being used. In order to evaluate the magnitude of an anaesthetic-induced postoperative delay of bowel movement, two types of intravenous-based anaesthesia using fentanyl/midazolam (1 mg/25 mg; dosage 0.1 ml/kg/h), and ketamine/midazolam (250 mg/25 mg; dosage 0.1 ml/kg/h) respectively were compared with a volatile anaesthetic technique (enflurane; mean concentration 1.5 vol%). METHODS. In three groups of patients (each n = 15) undergoing elective surgery of the lower extremities, induction of anaesthesia was accomplished with methohexital (1-1.5 mg/kg) to facilitate intubation. For the maintenance of muscle relaxation vecuronium bromide was used. All patients were given droperidol to prevent postoperative emesis, and they were artificially ventilated with N2O/O2 (60:40) to normal end-expiratory CO2 concentrations. No anticholinergic agents were used at the end of operation since they are known to interfere with bowel motility. In order to determine gastro-intestinal motility, the H2 exhalation test was used. For this purpose 40 g lactulose in 100 ml of water was given to all patients via a gastral tube shortly before extubation. Lactulose is broken down by bacteria once it enters the colon, and H2 is released, taken up by the vascular system and exhaled. Postoperatively, patients were asked to exhale into a 20-ml syringe every 10 min. The content was analysed for hydrogen (ppm), using an electrochemical sensor (GMI exhaled hydrogen monitor). From the time of lactulose instillation to a threefold increase in end-expiratory hydrogen concentration (compared to the preoperative value), gastro-coecal transit time was computed. RESULTS. All three groups of patients were comparable in age, height and body weight. Also, the duration of operation was comparable in all three groups. Mean gastro-coecal transit time was 204 (+/- 19.6, SD) min following enflurane, 302 (+/- 32.8 SD) min following fentanyl/-midazolam and 210 (+/- 28.8 SD) min following ketamine/midazolam anaesthesia. The gastro-intestinal inhibition after the opioid-based anaesthetic technique was significantly prolonged (p < 0.001, Kruskal-Wallis test). There was no significance between patients after ketamine-based anaesthesia and those who had the volatile anaesthetic. DISCUSSION AND CONCLUSION. When using intravenous anaesthesia with an opioid, gastro-intestinal inhibition, especially in patients prone to have constipation, is likely to develop postoperatively. In classical neuroleptanaesthesia and in analgosedation in the ICU, the simultaneous use of the butyrophenone droperidol seems to counteract the inhibition of opioid-related gastrointestinal motility. In cases of opioid-related gastrointestinal atonia a gastrokinetic compound may be necessary to overcome this effect on intestinal motility.
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PMID:[No inhibition of intestinal motility following ketamine-midazolam anesthesia. A comparison of anesthesia with enflurane and fentanyl/midazolam]. 814 42

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

The roles of arterial and central chemoreceptors in the transition from retching to expulsion during vomiting were studied. In spontaneously breathing decerebrate dogs, actual vomiting induced by activation of abdominal vagal afferents always consisted of retching and subsequent expulsion phases. Pulmonary ventilation almost stopped during the retching phase. Arterial blood CO2 tension gradually increased and reached a maximum near the time of the transition from the retching phase to the expulsion phase. Similarly, when end-tidal CO2 was maintained higher than 4.6 +/- 0.7% in paralyzed, artificially ventilated decerebrate dogs, stimulation of abdominal vagal afferents induced fictive retching and fictive expulsion, which were identified from the characteristic discharge patterns of the motor nerves to the costal and hiatal parts of the diaphragm, the abdominal muscles and the digastric muscle. However, only fictive retching occurred at an end-tidal CO2 of less than 3.7 +/- 0.7%. Although end-tidal CO2 was at a low level, fictive retching was followed by fictive expulsion when artificial ventilation was interrupted during the fictive retching phase and when sinus nerve afferents were stimulated. Even after sino-aortic denervation, fictive retching and subsequent fictive expulsion could be induced by stimulation of either vagal afferents or the solitary tract and nucleus, but the threshold level of end-tidal CO2 which enabled the induction of fictive expulsion increased after denervation. These results indicate that the activity of arterial and/or central chemoreceptor afferents must exceed some critical level to induce the transition from the retching phase to the expulsion phase.
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PMID:Hypercapnia and hypoxia which develop during retching participate in the transition from retching to expulsion in dogs. 823 24

In six mongrel dogs under thiopental anesthesia, piezoelectric transducers and bipolar electromyographic (EMG) wires were installed onto left costal, medial crural and lateral crural segments of the diaphragm. During CO2 rebreathing, shortening and EMG activity increased significantly in all three regions of the diaphragm compared to resting breathing. During emesis, (1) both shortening and EMG activity significantly increased compared to resting in costal segment; however, (2) lateral crural shortening was not increased in spite of significant increase in EMG activity; furthermore, (3) the medial crural segment lengthened without any increased EMG activity. These results demonstrate a differential recruitment of costal and crural diaphragm segments, and an additional differential activity within the crural segment between medial and lateral crural regions, during emesis. This activity of the canine diaphragm is consistent with a central influence of emesis upon individual regions of the diaphragm.
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PMID:Differential function of the costal and crural diaphragm during emesis in canines. 846 43


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