R Masuda1,2, T Iijima1,2, R Kondo3, Y Itoda3, M Matsuhashi1, S Hashimoto4, T Kohira4, N Kobayashi5, H Okazaki1. 1. Department of Transfusion Medicine, The University of Tokyo, Ohta, Japan. 2. Division of Anesthesiology, Department of Perioperative Medicine, School of Dentistry, Showa University, Tokyo, Japan. 3. Department of Cardiovascular Surgery, The University of Tokyo, Ohta, Japan. 4. Haemopoietic Stem Cell General Management Division, Blood Service Headquarters, Japanese Red Cross Society, Tokyo, Japan. 5. R&D Center, Nihon Kohden Corporation Co., Ltd., Shinjuku, Japan.
Abstract
BACKGROUND AND OBJECTIVES: Whether transfusion-associated circulatory overload arises as a simple result of over-transfusion or requires another trigger remains unclear. Here, we examined whether respiratory distress could be reproduced by massive transfusion alone in an animal model. MATERIALS AND METHODS: A total of 20 anaesthetized swine were equipped with monitors. Allogeneic blood was obtained from 10 donor swine. A 4-stage loading protocol with each stage equivalent to 25% of the blood volume (BV) in the recipient swine was then used to infuse crystalloid (CR), hydroxyethyl starch (HES) or allogeneic blood (TR) (n = 5 each). The five remaining animals were subjected to a haemorrhagic shock (HS) prior to an allogeneic blood transfusion (TRS). RESULTS: The PaO2 /FiO2 (P/F) ratio did not decrease to the level of respiratory distress in either the CR group or the HES group after loading with a volume corresponding to 100% of the recipient BV. However, the TRS and TR groups exhibited significant reductions in the P/F ratio after fluid overloading (227 ± 29 and 267 ± 133, respectively). Blood transfusion after HS expanded the blood volume, but over-transfusion alone did not. HS was accompanied by an increase in the white blood cell count. CONCLUSION: The lung and the heart can tolerate volume overloads with HES, CR and even transfused blood. However, a preceding HS may induce an inflammatory response, making the lung vulnerable to subsequent blood overloads. In this study, a preceding haemorrhagic shock mediated respiratory distress following massive transfusion in a swine model. (247 words).
BACKGROUND AND OBJECTIVES: Whether transfusion-associated circulatory overload arises as a simple result of over-transfusion or requires another trigger remains unclear. Here, we examined whether respiratory distress could be reproduced by massive transfusion alone in an animal model. MATERIALS AND METHODS: A total of 20 anaesthetized swine were equipped with monitors. Allogeneic blood was obtained from 10 donorswine. A 4-stage loading protocol with each stage equivalent to 25% of the blood volume (BV) in the recipient swine was then used to infuse crystalloid (CR), hydroxyethyl starch (HES) or allogeneic blood (TR) (n = 5 each). The five remaining animals were subjected to a haemorrhagic shock (HS) prior to an allogeneic blood transfusion (TRS). RESULTS: The PaO2 /FiO2 (P/F) ratio did not decrease to the level of respiratory distress in either the CR group or the HES group after loading with a volume corresponding to 100% of the recipient BV. However, the TRS and TR groups exhibited significant reductions in the P/F ratio after fluid overloading (227 ± 29 and 267 ± 133, respectively). Blood transfusion after HS expanded the blood volume, but over-transfusion alone did not. HS was accompanied by an increase in the white blood cell count. CONCLUSION: The lung and the heart can tolerate volume overloads with HES, CR and even transfused blood. However, a preceding HS may induce an inflammatory response, making the lung vulnerable to subsequent blood overloads. In this study, a preceding haemorrhagic shock mediated respiratory distress following massive transfusion in a swine model. (247 words).
Authors: Robert B Klanderman; Marije Wijnberge; Joachim J Bosboom; Joris J T H Roelofs; Dirk de Korte; Robin van Bruggen; Markus W Hollmann; Margreeth B Vroom; Denise P Veelo; Nicole P Juffermans; Bart F Geerts; Alexander P J Vlaar Journal: Vox Sang Date: 2021-08-15 Impact factor: 2.996
Authors: Alexander Ziebart; Moritz M Schaefer; Rainer Thomas; Jens Kamuf; Andreas Garcia-Bardon; Christian Möllmann; Robert Ruemmler; Florian Heid; Arno Schad; Erik K Hartmann Journal: PeerJ Date: 2019-08-16 Impact factor: 2.984
Authors: Robert B Klanderman; Joachim J Bosboom; Adrie A W Maas; Joris J T H Roelofs; Dirk de Korte; Robin van Bruggen; Jaap D van Buul; Coert J Zuurbier; Denise P Veelo; Markus W Hollmann; Margreeth B Vroom; Nicole P Juffermans; Bart F Geerts; Alexander P J Vlaar Journal: Transfusion Date: 2019-11-07 Impact factor: 3.157