Resuscitation
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Seventy-seven consecutive hypotensive (mean arterial pressure (MAP) less than 80 mmHg) surgical emergency patients were resuscitated according to either physicians' individual orders (38 patients) or an algorithm (39 patients). The shock was mainly caused by accidental injuries or acute gastrointestinal bleeding. The patients of the algorithm group were given more plasma expanders than the patients of the control group, while the total amount of fluids administered was similar in both groups. ⋯ Renal failure was somewhat more common in the control group and the renal function disturbances were significantly more severe among the control patients. The results suggest that the physicians in some extent altered their practices in fluid resuscitation when the algorithm was put to use, and that this change, perhaps, produced the somewhat better outcome of the patients. The authors recommend the algorithm to be used as a basis of shock treatment and particularly in those emergency departments where the resuscitation of hypotensive patients is performed by junior or inexperienced physicians.
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A lethal case of Adult Respiratory Distress Syndrome (ARDS) consequent to meningococcal septicemia is clinically and physiologically described. Very high levels of eosinophil cationic protein and lactoferrin in bronchoalveolar lavage were observed in spite of peripheral eosinopenia and neutropenia. These findings provide support for the hypothesis that activated granulocytes are involved in the pathogenesis of septic-induced ARDS.
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This study examined the effect of carbon dioxide, lidoflazine and deferoxamine therapy upon the 10-day survival incidence and subsequent neurologic function of rats subjected to 7 min of cardiorespiratory arrest with resuscitation. Cardiac arrest (asystole) was induced at time zero by injection of cold, 1% KCl into the left ventricle of ketamine-anesthetized rats pretreated with succinylcholine. Positive pressure ventilation was discontinued at time zero. ⋯ At 2 days postresuscitation, 75% of treated rats vs. 25% of control rats were alive (CHI2 = 10.0, d.f. = 1, P less than 0.01), and at 10 days, 60% of treated rats vs. 25% of control rats were alive (CHI2 = 5.01, d.f. = 1, P less than 0.05). There was no detectable neurologic deficit among survivors in either group at 15 days. The combination of carbon dioxide, lidoflazine and deferoxamine, administered after return of spontaneous circulation, is a simple and easily administered treatment regimen that improves the survival incidence without neurologic deficits in this animal model of cardiorespiratory arrest and CPR.