Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Massive blood transfusion

John R Hess, MD, MPH
Section Editor
Arthur J Silvergleid, MD
Deputy Editor
Jennifer S Tirnauer, MD


Massive transfusion, historically defined as the replacement by transfusion of 10 units of red cells in 24 hours, is a response to massive and uncontrolled hemorrhage. With more rapid and effective therapy, alternative definitions such as three units over one hour are more sensitive in identifying patients needing rapid issue of blood products for serious injuries because of uncontrolled hemorrhage [1]. Such transfusion episodes are associated with a number of hemostatic and metabolic complications [2]. Massive transfusion involves the selection of the appropriate amounts and types of blood components to be administered, and requires consideration of a number of issues including volume status, tissue oxygenation, management of bleeding and coagulation abnormalities, as well as changes in ionized calcium, potassium, and acid-base balance.

An overview of the Advanced Trauma Life Support approach to massive transfusion with crystalloid fluids and packed red cells is presented here [3,4], as is the “damage control” approach using red cells and plasma in a 1:1 ratio [5]. Other issues related to the use of blood products are discussed separately. (See "Use of blood products in the critically ill" and "Indications and hemoglobin thresholds for red blood cell transfusion in the adult" and "Red blood cell transfusion in adults: Storage, specialized modifications, and infusion parameters" and "Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock".)


The most common situation leading to massive transfusion is cardiac surgery, but trauma, where physical injury and blood loss combine, remains the best-studied example [6]. Other situations leading to massive transfusion, such as ruptured abdominal aortic aneurism, liver transplant, and obstetric catastrophes are less frequent [7]. In a review of experience in a major trauma center during the year 2000, 8 percent of all admitted patients were given red cells, 3 percent received more than 10 units of red cells during their admission, and 1.7 percent received 10 units in the first 24 hours [8]. More recently, an NIH-sponsored collaboration of trauma centers studying the cytokine response to massive transfusion and other groups reported that the fraction of all patients receiving red cells who go on to receive 10 units of red cells has decreased by 40 percent as more plasma and platelets are given earlier [9]. Taken together, these data suggest that most injured patients never need massive transfusion and can be treated based on physical assessment and laboratory tests, but approximately 1.7 percent of the most severely injured will require more prompt treatment of coagulopathy, which in turn reduces total blood use in some of them. Appropriate care requires knowing both "classic" and "hemorrhage-control" forms of resuscitation and when to use them. (See "Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock".)


Correction of the deficit in blood volume with crystalloid volume expanders will generally maintain hemodynamic stability, while transfusion of red cells is used to improve and maintain tissue oxygenation [10,11]. Each unit of packed red blood cells (RBCs) contains approximately 200 mL of red cells and, in an adult, will raise the hematocrit by roughly 3 percentage points unless there is continued bleeding. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult".)

At rest, oxygen delivery is normally four times oxygen consumption, indicating the presence of an enormous reserve. Thus, if intravascular volume is maintained during bleeding and cardiovascular status is not impaired, oxygen delivery will theoretically be adequate until the hematocrit (packed cell volume) falls below 10 percent. This is because adequate cardiac output plus increased oxygen extraction can compensate for the decrease in arterial oxygen content. However, increasing cardiac work to increase output requires more oxygen, so the “critical point” where oxygen consumption becomes delivery dependent is higher.

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: Oct 18, 2017.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Savage SA, Sumislawski JJ, Zarzaur BL, et al. The new metric to define large-volume hemorrhage: results of a prospective study of the critical administration threshold. J Trauma Acute Care Surg 2015; 78:224.
  2. Collins JA. Problems associated with the massive transfusion of stored blood. Surgery 1974; 75:274.
  3. British Committee for Standards in Haematology, Stainsby D, MacLennan S, et al. Guidelines on the management of massive blood loss. Br J Haematol 2006; 135:634.
  4. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support (ATLS) Student Course Manual, 9th ed, American College of Surgeons, Chicago 2012.
  5. Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma 2007; 62:307.
  6. Dzik WS, Ziman A, Cohen C, et al. Survival after ultramassive transfusion: a review of 1360 cases. Transfusion 2016; 56:558.
  7. Halmin M, Chiesa F, Vasan SK, et al. Epidemiology of Massive Transfusion: A Binational Study From Sweden and Denmark. Crit Care Med 2016; 44:468.
  8. Como JJ, Dutton RP, Scalea TM, et al. Blood transfusion rates in the care of acute trauma. Transfusion 2004; 44:809.
  9. Kautza BC, Cohen MJ, Cuschieri J, et al. Changes in massive transfusion over time: an early shift in the right direction? J Trauma Acute Care Surg 2012; 72:106.
  10. Stehling L. Fluid replacement in massive transfusion. Massive Transfusion AABB 1994; 1.
  11. Lundsgaard-Hansen P. Treatment of acute blood loss. Vox Sang 1992; 63:241.
  12. Weiskopf RB, Kramer JH, Viele M, et al. Acute severe isovolemic anemia impairs cognitive function and memory in humans. Anesthesiology 2000; 92:1646.
  13. Weiskopf RB, Feiner J, Hopf H, et al. Fresh blood and aged stored blood are equally efficacious in immediately reversing anemia-induced brain oxygenation deficits in humans. Anesthesiology 2006; 104:911.
  14. Hardy JF, De Moerloose P, Samama M, Groupe d'intérêt en Hémostase Périopératoire. Massive transfusion and coagulopathy: pathophysiology and implications for clinical management. Can J Anaesth 2004; 51:293.
  15. Miller RD, Robbins TO, Tong MJ, Barton SL. Coagulation defects associated with massive blood transfusions. Ann Surg 1971; 174:794.
  16. Counts RB, Haisch C, Simon TL, et al. Hemostasis in massively transfused trauma patients. Ann Surg 1979; 190:91.
  17. Mannucci PM, Federici AB, Sirchia G. Hemostasis testing during massive blood replacement. A study of 172 cases. Vox Sang 1982; 42:113.
  18. Hess JR. Blood and coagulation support in trauma care. Hematology Am Soc Hematol Educ Program 2007; :187.
  19. Meng ZH, Wolberg AS, Monroe DM 3rd, Hoffman M. The effect of temperature and pH on the activity of factor VIIa: implications for the efficacy of high-dose factor VIIa in hypothermic and acidotic patients. J Trauma 2003; 55:886.
  20. Cosgriff N, Moore EE, Sauaia A, et al. Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidoses revisited. J Trauma 1997; 42:857.
  21. Kermode JC, Zheng Q, Milner EP. Marked temperature dependence of the platelet calcium signal induced by human von Willebrand factor. Blood 1999; 94:199.
  22. Jurkovich GJ, Greiser WB, Luterman A, Curreri PW. Hypothermia in trauma victims: an ominous predictor of survival. J Trauma 1987; 27:1019.
  23. Stanworth SJ, Walsh TS, Prescott RJ, et al. A national study of plasma use in critical care: clinical indications, dose and effect on prothrombin time. Crit Care 2011; 15:R108.
  24. Reed RL Jr, Ciavarella D, Heimbach DM, et al. Prophylactic platelet administration during massive transfusion. A prospective, randomized, double-blind clinical study. Ann Surg 1986; 203:48.
  25. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma 2007; 63:805.
  26. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg 2008; 248:447.
  27. Cotton BA, Au BK, Nunez TC, et al. Predefined massive transfusion protocols are associated with a reduction in organ failure and postinjury complications. J Trauma 2009; 66:41.
  28. Shaz BH, Dente CJ, Nicholas J, et al. Increased number of coagulation products in relationship to red blood cell products transfused improves mortality in trauma patients. Transfusion 2010; 50:493.
  29. Inaba K, Lustenberger T, Rhee P, et al. The impact of platelet transfusion in massively transfused trauma patients. J Am Coll Surg 2010; 211:573.
  30. de Biasi AR, Stansbury LG, Dutton RP, et al. Blood product use in trauma resuscitation: plasma deficit versus plasma ratio as predictors of mortality in trauma (CME). Transfusion 2011; 51:1925.
  31. Perkins JG, Cap AP, Spinella PC, et al. An evaluation of the impact of apheresis platelets used in the setting of massively transfused trauma patients. J Trauma 2009; 66:S77.
  32. Johansson PI, Stensballe J, Rosenberg I, et al. Proactive administration of platelets and plasma for patients with a ruptured abdominal aortic aneurysm: evaluating a change in transfusion practice. Transfusion 2007; 47:593.
  33. Kornblith LZ, Howard BM, Cheung CK, et al. The whole is greater than the sum of its parts: hemostatic profiles of whole blood variants. J Trauma Acute Care Surg 2014; 77:818.
  34. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA 2015; 313:471.
  35. Delaney M, Stark PC, Suh M, et al. Massive Transfusion in Cardiac Surgery: The Impact of Blood Component Ratios on Clinical Outcomes and Survival. Anesth Analg 2017; 124:1777.
  36. Simon L, Santi TM, Sacquin P, Hamza J. Pre-anaesthetic assessment of coagulation abnormalities in obstetric patients: usefulness, timing and clinical implications. Br J Anaesth 1997; 78:678.
  37. Monroe DM, Hoffman M. The coagulation cascade in cirrhosis. Clin Liver Dis 2009; 13:1.
  38. Dzik WH, Kirkley SA. Citrate toxicity during massive blood transfusion. Transfus Med Rev 1988; 2:76.
  39. Lier H, Krep H, Schroeder S, Stuber F. Preconditions of hemostasis in trauma: a review. The influence of acidosis, hypocalcemia, anemia, and hypothermia on functional hemostasis in trauma. J Trauma 2008; 65:951.
  40. Bruining HA, Boelhouwer RU, Ong GK. Unexpected hypopotassemia after multiple blood transfusions during an operation. Neth J Surg 1986; 38:48.
  41. Howland WS, Schweizer O, Carlon GC, Goldiner PL. The cardiovascular effects of low levels of ionized calcium during massive transfusion. Surg Gynecol Obstet 1977; 145:581.
  42. Smith HM, Farrow SJ, Ackerman JD, et al. Cardiac arrests associated with hyperkalemia during red blood cell transfusion: a case series. Anesth Analg 2008; 106:1062.