ASAIO journal : a peer-reviewed journal of the American Society for Artificial Internal Organs
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The impact of dialysis intensity on erythropoietin (EPO) requirements is unclear. Previous work suggests that increased dialysis is associated with increased erythropoietin responsiveness (ERSP), but average dialysis intensity has increased since those publications. We hypothesized that ERSP would be independent of delivered Kt/V(urea) at current intensities of hemodialysis. ⋯ We found no relationship between erythropoietin responsiveness and intensity of hemodialysis in this population of patients with a mean delivered Kt/V(urea) of 1.6. This may indicate a threshold effect beyond which more dialysis will not improve ERSP. However, markers of an underlying inflammatory state and of secondary hyperparathyroidism were associated with decreased response to erythropoietin.
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We performed this study to identify predictors of mortality in critically ill patients treated with continuous venovenous hemodiafiltration (CVVHDF) for acute renal failure in an intensive care setting. It was an uncontrolled, observational study that took place in a general intensive care unit in a university hospital. Forty-one patients undergoing CVVHDF for acute renal failure in a consecutive sample of 1,018 ICU treatments were studied. ⋯ The crucial factors in predicting outcome of critically ill patients undergoing CVVHDF for renal failure are elevated serum bilirubin and lactate levels at the onset of CVVHDF. Presence of hepatic failure, defined as both jaundice and coagulopathy, may also worsen outcome of critically ill patients undergoing CVVHDF for renal failure. The cut-off value set at bilirubin levels > 10 mg/dl or arterial lactate levels > 3.5 mmol/L may serve as beneficial predictors of hospital mortality.
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Nitric oxide (NO) is an inhibitor of platelet aggregation. We analyzed the effect of direct infusion of NO into adult blood oxygenators on local clot formation. Nonheparinized calves in a control group (n = 3) and NO group (n = 4) were connected to a jugulocarotid cardiopulmonary bypass (CPB; centrifugal pump) for 6 hours. ⋯ However, general coagulation parameters were not modified by local NO administration. The activated coagulation time remained stable between 110 and 150 seconds in both groups (p = not significant [ns]), and there were no differences in hematocrit, thrombin time, partial thromboplastin time, or fibrinogen between groups during the 6 hours of CPB. Thus, the mixed infusion of a continuous low dose of NO into adult oxygenators during prolonged CPB prevented local clot formation, whereas the general coagulation pattern remained unchanged.
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The study objective was to determine whether a phosphodiesterase III inhibitor, olprinone chlorate, is effectively removed by continuous venovenous hemodiafiltration (CVVHDF) in a patient with cardiac and renal failure. The patient was a 73 year old man who had undergone coronary artery bypass grafting for ischemic heart disease and who developed cardiac and renal failure postoperatively. A 0.2 microg/kg per minute dosage of olprinone chlorate was administered intravenously for 120 minutes while the patient was treated with CVVHDF. ⋯ The olprinone chlorate clearance of CVVHDF approximates only 10% of total clearance in this case. CVVHDF may not produce significant reduction in the serum olprinone chlorate level. It is recommended that the infusion dosage of olprinone chlorate should be reduced when given to patients with renal failure even if treated with CVVHDF.
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Cardiopulmonary bypass (CPB) is known to induce an inflammatory response in association with neutrophil mediated lung injury. P-Selectin has been reported to be involved in the initiation of this inflammatory response by promoting the adhesion of neutrophils to endothelial cells in postcapillary venules. However, the role of P-selectin in the inflammatory response induced by CPB has never been clarified. ⋯ The RI value increased in a pattern similar to that of the inflammatory cytokines and was significantly lower in group P. These data demonstrate that the addition of an anti-rat specific monoclonal antibody inhibits the abnormal release of inflammatory cytokines and attenuates CPB induced lung injury in rats. Thus, P-selectin may play a role in the augmentation of CPB induced inflammatory response, and the use of its inhibitory monoclonal antibody seems to be a promising strategy for the treatment of CPB induced lung injury.