The aim of this study was to obtain a critical evaluation of a simple method for labelling platelets with 111 In‐oxine. All experiments were carried out on healthy volunteers. 65 ± 7 (SD) % of the platelets in collected blood were labelled and reinjected. As compared to control experiments, only in response to a low final ADP concentration (1.0 μmol/l) did 111 In‐labelled platelets show reduced in vitro aggregability. The mean platelet volume for 111 In‐labelled platelets was slightly lower than the mean platelet volume in whole blood. The results for initial platelet recovery and platelet mean lifespan closely agreed with those of other studies in which considerably higher platelet extraction from whole blood was obtained. After injection, the splenic uptake and blood disappearance of 111 In‐labelled platelets followed a monoexponential function with almost identical rate constants. By compartmental analysis of the equilibration of platelets between blood and spleen, the splenic blood flow was estimated to be 4.8 ± 1.9 (SD) % of the total blood volume/min; the intrasplenic platelet transit time was 9.7 ± 1.6 (SD) min, and the exchangeable splenic platelet pool 31 ± 8 (SD) %. Highly significant relationships were present between the splenic blood flow and the splenic platelet pool size, as well as between the splenic blood flow and the initial platelet recovery. It is concluded that the requirements for adequate interpretation of platelet kinetics are well met with the present method for harvesting and labelling of platelets.
Background and Objectives We wanted to establish a permanent national database system, which can be utilized to study transfusion recipients and blood use in Finland. Materials and Methods A regularly updated register for permanent use was developed. To study the usability of the database, years 2002 and 2003 were further analysed. Database included all transfused patients in major blood‐transfusing hospitals from four university and five central hospital districts managing altogether 63% of Finnish inpatient hospital episodes. Results Audit of gathered data reveal 96·8% match in adult blood components with Finnish Red Cross, Blood Service sales figures. Model data set includes 59 535 transfused patients (44·3% men and 55·7% women) having received 529 104 blood components. Half of all blood units were transfused in connection with surgical operations. Most of the blood recipients were elderly (51·6% are over 64 years of age). Blood‐component use and transfusion‐related costs varied widely between hospitals. Conclusion Hospital data managing systems can be useful for creating a population‐based database system to monitor and compare transfusion practices. This record provides information about transfusion epidemiology for transfusion professionals, hospital management, and hospital administration.
Background: Paracetamol is a weak cyclo‐oxygenase inhibitor in vitro . A recent study in children has shown that high doses of paracetamol are effective and safe. We studied the effect of propacetamol on haemostasis in adult volunteers. Methods: Ten volunteers were investigated in a double‐blind, randomized, crossover study. They received propacetamol 60 mg kg −1 or ketorolac 0.4 mg kg −1 in saline i.v. (30 min) in two different sessions. Platelet function was evaluated before the test infusion (S‐0), two (S‐2) and 24 h (S‐24) after the start of the infusion. Coagulation parameters (PT, APTT, factor V and VII activities) were measured at S‐0, S‐24 and 48 h (S‐48). Results: One of the volunteers had no secondary platelet aggregation in S‐0 and was excluded from the final analysis. Two hours (S‐2) after propacetamol and ketorolac administration the adrenaline (0.9 μg ml −1 and 9.0 μg ml −1 ) induced maximal platelet aggregation was decreased compared with S‐0. At S‐2 platelet aggregation was inhibited more after ketorolac than after propacetamol. At 24 h after ketorolac, but not after propacetamol, there was still a decrease in the adrenaline‐induced maximal platelet aggregation. Propacetamol did not affect adenosine diphosphate (ADP)‐induced maximal platelet aggregation, whereas ketorolac decreased 3 and 6 μM ADP‐induced maximal platelet aggregation at S‐2 and S‐24. However, 2 h after both ketorolac and propacetamol, thromboxane B 2 (TxB 2 ) concentration decreased in platelet rich plasma after 5 min aggregation induced by 8 μM ADP. Coagulation was unaffected. Conclusion: Propacetamol 60 mg kg −1 i.v. causes reversible platelet dysfunction demonstrated by a decrease in maximal platelet aggregation and TxB 2 concentration. After 0.4 mg kg −1 ketorolac i.v. platelet aggregation and TxB 2 formation are inhibited more in comparison with propacetamol, and platelet dysfunction is still seen after 24 h.
Summary. During neonatal intensive care, blood components are often used in clinical situations where both their efficacy and safety lack solid justification. A practical system to continuously analyse actual transfusion practices is a prerequisite for improvements of quality in transfusion therapy. We hypothesized that such a system would reveal inappropriate variations in clinical decission making and offer a means for staff education and quality improvement and assurance. The study consisted of three 120–152‐day periods (P I, P II and P III) between January 2000 and October 2001 and involved 543 new patient admissions (141 patients with birth weight < 1501 g) and 6227 days of patient care at a single tertiary level NICU. P I was a control with no intervention, P II was after technically introducing the computer system and, the last period, P III was after presenting and discussing the results of P I and P II at a staff meeting. Upon an order of platelet or fresh frozen plasma (FFP) unit from the blood bank, a computer‐based audit system compared the last platelet count or prothrombin time [expressed as percentage of normal clotting activity, prothrombin time (PT‐%)] to predefined criteria. In the case of exceeding the preset thresholds, the system required additional information and recorded the pretransfusion laboratory values for later analysis. Thirty‐two per cent of platelet transfusions were given with pretransfusion platelet count >49 × 10 9 L −1 , and 60% of these transfusions (19% of all platelet transfusions) could not be clinically justified in retrospective chart review. There was no significant change in this practice from P II to P III. FFP transfusions were given with significantly different pretransfusion PT‐% values during P II and P III. The proportions of FFP transfusions with pretransfusion PT‐% > 49% were 7·8% and 0·9% during P II and P III, respectively ( P < 0·0001). In chart review, none of the FFP transfusions with pretransfusion PT‐% > 49% could be justified by clinical grounds. Inappropriate transfusions of both platelets and plasma remain a significant challenge for quality assurance of neonatal intensive care. Automated recording of pretransfusion platelet count and prothrombin time reliably identified the poorly justified transfusions and thus offered a practical resource‐saving tool for quality assurance of transfusion in the NICU. A significant shift towards more appropriate use of plasma was demonstrated after implementation of the audit system.
