Heavy i.v. sedation is often used in upper GI endoscopy. Sedation, however, creates the need for recovery facilities and precludes patients from returning to their normal daily activities. This is undesirable, since endoscopy is routinely performed as an out-patient procedure. Also the cost for medication and recovery facilities militate against the indiscriminate use of i.v. sedative premedication. The present study was undertaken in an attempt to establish what proportion of patients can benefit from oral premedication, and whether such an administration route can eliminate some of the disadvantages associated with i.v. sedation. Four hundred out-patients were randomized to receive orally either triazolam, 0.125 mg, or placebo. Of the patients, 359 were evaluable; 177 received placebo and 182 triazolam. All major aspects of the procedure were covered using visual analogue scale questionnaires for the endoscopist and patient. There were no differences in endoscopic experience, or sex and age distribution between the groups. Triazolam reduced patient discomfort, 38.6 +/- 25.6 vs 44.8 +/- 30.1 (p = 0.0379). Recollection of post-endoscopy information was the same in both groups. One patient complained of drowsiness following the procedure. No patient needed to stay in hospital to complete recovery. Endoscopy quality was identical in the two groups. Oral premedication has the potential to be of significant value, may optimize the use of endoscopy resources, and does not impair patient activities post-endoscopy.
Standardized intra-abdominal hemorrhage was induced in 7 anesthetized pigs. The resulting hypovolemic shock was treated with pneumatic anti-shock garment (PASG) followed by intra-aortic balloon occlusion. The effects of this treatment on circulation, lung mechanics and gas exchange were studied. Hemorrhage was induced by pulling out sutures introduced in the inferior caval vein. We found that the use of PASG partially restored mean arterial blood pressure from 44 ± 6 to 66 ± 6 mm Hg. When intra-aortic balloon occlusion was added, the arterial pressure returned to basal levels. Cardiac output fell severely due to the hemorrhage from 3.7 ± 0.2 to 1.3 ± 0.2 liters/min and could not be restored during the treatment. A severe fall in total lung compliance was recorded after inflation of the PASG from 18.6 ± 0.9 to 10 ± 0.7 ml/cm H2O, this was accompanied by a fall in alveolar ventilation. These findings emphasize the severe restriction in lung function that occurred during treatment with PASG. Both parameters returned to near normal values when the PASG was deflated and the intra-aortic balloon was inflated. Pulmonary vascular resistance increased by more than 400% and remained high during the study period. There was no change in arterial PO2, however the fall in mixed venous PO2, caused by hemorrhage was reversed at the end of the treatment. Indirect monitoring of cerebral function by continuous EEG showed a decreased voltage during the hemorrhage, this was reversed by the combined treatment. We conclude that the outlined treatment makes it possible to restore central hemodynamics and preserve cerebral function at least for a short period of time until definite surgical treatment can be performed. However, severe restriction on lung mechanics, especially when PASG was inflated, makes it probable that ventilatory support can be necessary in such cases.
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