Blood transfusion in the critically ill: does storage age matter?
Morphologic and biochemical changes occur during red cell storage prior to product expiry, and these changes may hinder erythrocyte viability and function following transfusion. Despite a relatively large body of literature detailing the metabolic and structural deterioration that occurs during red cell storage, evidence for a significant detrimental clinical effect related to the transfusion of older blood is relatively less conclusive, limited primarily to observations in retrospective studies. Nonetheless, the implication that the transfusion of old, but not outdated blood may have negative clinical consequences demands attention. In this report, the current understanding of the biochemical and structural changes that occur during storage, known collectively as the storage lesion, is described, and the clinical evidence concerning the detrimental consequences associated with the transfusion of relatively older red cells is critically reviewed. Although the growing body of literature demonstrating the deleterious effects of relatively old blood is compelling, it is notable that all of these reports have been retrospective, and most of these studies have evaluated patients who received a mixture of red cell units of varying storage age. Until prospective studies have been completed and produce confirmative results, it would be premature to recommend any modification of current transfusion practice regarding storage age. In 1917, Frances Payton Rous and J.R. Turner identified that a citrate-glucose solution allowed for the preservation of a whole blood unit for up to five days, thus facilitating the formative practice of blood banking. Later, Loutit and Mollison of Great Britain developed the first anticoagulant of the modern era, known as acid-citrate-dextrose (ACD). ACD extended the shelf life of refrigerated blood to 21 days, and ACD remained in wide spread usage until the 1960s, when it was replaced by citrate-phosphate-dextrose (CPD) and citrate-phosphate-dextrose-adenine (CPDA) solutions that increased shelf life to 35 days and 42 days respectively. More recently, additive solutions containing saline, adenine, and dextrose have been developed to augment red cell survival following transfusion, although without any direct increase in storage duration. It is now well appreciated, however, that a number of morphologic and biochemical changes occur during red cell storage prior to product expiry, and these changes may hinder erythrocyte viability and function following transfusion. Despite a relatively large body of literature detailing the metabolic and structural deterioration that occurs during red cell storage, evidence for a significant detrimental clinical effect related to the transfusion of older blood is relatively less conclusive, limited primarily to observations in retrospective studies. Nonetheless, the implication that the transfusion of old, but not outdated blood may have negative clinical consequences demands attention. The purpose of this report is to describe the current understanding of the biochemical and structural changes that occur during storage, known collectively as the storage lesion, and to critically review the clinical evidence concerning the detrimental consequences associated with the transfusion of relatively older red cells.
Vandromme
Marianne J
MJ
Department of Surgery, Center for Injury Sciences, University of Alabama at Birmingham, Birmingham, AL, USA. marianne.vandromme@ccc.uab.edu
McGwin
Gerald
G
Weinberg
Jordan A
JA
D001793:Blood Preservation / Q000379:methods*; D001803:Blood Transfusion; D016638:Critical Illness; D006801:Humans; D008421:Materials Management, Hospital; D013997:Time Factors
J Trauma. 2008 Oct;65(4):794-8
18849793
Vox Sang. 2000;78 Suppl 2:273-5
10938968
Transfus Apher Sci. 2004 Dec;31(3):185-9
15556465
Crit Care Med. 1997 May;25(5):726-32
9187588
Best Pract Res Clin Anaesthesiol. 2007 Jun;21(2):195-208
17650772
Vox Sang. 2009 Feb;96(2):93-103
19152602
Transplant Proc. 1973 Mar;5(1):253-9
4572098
Transfus Med Rev. 1988 Mar;2(1):40-7
2980078
Arch Surg. 2002 Jun;137(6):711-6; discussion 716-7
12049543
Transfusion. 1996 Nov-Dec;36(11-12):960-5
8937404
J Trauma. 2001 Mar;50(3):426-31; discussion 432
11265021
Am Surg. 2005 Sep;71(9):781-5
16468518
J Trauma. 2002 Jun;52(6):1224-5
12045660
Transfusion. 2000 Jan;40(1):101-9
10644819
J Trauma. 2002 Nov;53(5):1023-5
12435963
JAMA. 1993 Jun 16;269(23):3024-9
8501845
Transfusion. 1999 Jul;39(7):701-10
10413277
Can J Anaesth. 1997 Dec;44(12):1256-61
9429042
J Trauma. 2006 Jun;60(6 Suppl):S83-90
16763486
Shock. 2006 Oct;26(4):342-7
16980879
Anesth Analg. 2005 May;100(5):1433-1458
15845701
Crit Care Med. 2005 Jan;33(1):39-45; discussion 238-9
15644646
N Engl J Med. 2008 Mar 20;358(12):1229-39
18354101
Transfus Med. 2008 Aug;18(4):260-5
18783585
Vox Sang. 2007 Jul;93(1):12-8
17547560
Vox Sang. 2006 Jul;91(1):13-9
16756596
J Trauma. 2009 Jul;67(1):29-32
19590304
Am J Surg. 1999 Dec;178(6):570-2
10670874
Transfus Med. 2000 Dec;10(4):291-303
11123813
Chest. 2005 Jan;127(1):295-307
15653997
Crit Care Med. 2004 Feb;32(2):364-71
14758149
J Trauma. 2008 Aug;65(2):279-82; discussion 282-4
18695462