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Aim:The purpose of the present study was to investigate the predictors of clinical deterioration soon after emergency department (ED) discharge. Methods:We undertook a case-control study using the ED database of the Nagano Municipal Hospital (Nagano, Japan) from January 2012 to December 2013. We selected adult patients with medical conditions who revisited the ED with deterioration within 2 days of ED discharge (deterioration group). The deterioration group was compared with a control group.Results: During the study period, 15,724 adult medical patients were discharged from the ED. Of these, 170 patients revisited the ED because of clinical deterioration within 2 days. Among the initial vital signs, respiratory rate was less frequently recorded than other vital signs (P < 0.001 versus all other vital signs in each group). The frequency of recording each vital sign did not differ significantly between the groups. Overall, patients in the deterioration group had significantly higher respiratory rates than those in the control group (21 AE 5/min versus 18 AE 5/min, respectively; P = 0.002). A binary logistic regression analysis revealed that respiratory rate was an independent risk factor for clinical deterioration (unadjusted odds ratio, 1.15; 95% confidence interval, 1.04À1.26; adjusted odds ratio, 1.15; 95% confidence interval, 1.01À1.29).Conclusions: An increased respiratory rate is a predictor of early clinical deterioration after ED discharge. Vital signs, especially respiratory rate, should be carefully evaluated when making decisions about patient disposition in the ED.

Some alterations in lipid metabolism in mice were observed by the intra-

Lipid peroxide formation and plasma membrane damage in mouse liver following the administration of Salmonella endotoxin were examined. The liver lipoperoxide level was markedly elevated in animals given endotoxin compared with that in the controls, and returned to its normal range after 2 days. On the other hand, superoxide dismutase activity was decreased by 18-48 hr after endotoxin injection, thereafter tending to increase. Glutathione reductase and glutathione peroxidase activities declined in the liver 18 hr after the injection. The endotoxin resulted in much lower lipoperoxide formation in the livers of tolerant mice than in those of the poisoned mice. The lipoperoxide level in endotoxin-poisoned mice after the administration of a-tocopherol was lower than that in the controls, and a-tocopherol administration prevented completely the membrane protein damage that arose from endotoxin challenge. After glutathione administration the membranes of the poisoned mice also returned to almost the· normal disk electrophoretic profile. These results suggest that lipid peroxide formation in the liver plasma membrane caused by free radicals might occur in a tissue ischemic state in endotoxicosis.

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