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Indian Journal of Transfusion Medicine
  Indian Journal of Transfusion Medicine Indian Journal of Transfusion Medicine

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Critical Issues In Massive Blood Transfusion

                                                                                                      Dr. Niranjan Rathod

                  DM, MD, FACP (USA)

 INTRODUCTION

Large volume blood transfusions are increasingly  required in trauma patients and in patients with massive blood loss like hematemesis, post-partum  haemorrhage etc. Massive transfusion is defined as the replacement by transfusion of more than 50%  of a patient’s blood volume in 12 to 24 hours. It poses significant challenge and requires to be handled meticulously to prevent haemostatic and metabolic complications associated with it 1.

Selection of the appropriate amounts and types of blood components to be administered is very critical in massive transfusion and requires consideration of a number of important issues like volume status, tissue oxygenation, management of bleeding and coagulation abnormalities, as well as changes in ionized calcium, potassium, and acid-base balance. 

Volume Replacement: Red cell 

Crystalloid volume expanders will generally maintain  hemodynamic stability by correction of the deficit in blood volume, while red cells transfusion is used  to improve and maintain tissue oxygenation 2. Every unit of packed cells will raise the haematocrit by  roughly 3 to 4 percentage points in an adult unless there is continued bleeding. If intravascular volume   is maintained during bleeding and cardiovascular status is not impaired, oxygen delivery will  theoretically be adequate until the haematocrit falls below 10%. This is because adequate cardiac output  plus increased oxygen extraction can compensate for the decrease in arterial oxygen content.

Oxygen release by transfused red cells is reduced  as compared with normal red cells. Storage  decreases 2, 3-diphosphoglycerate (2, 3-DPG) levels, leading to a leftward shift of the  oxyhemoglobin dissociation curve. The transfused red cells regenerate 2, 3-DPG to normal levels within  six to 24 hours after transfusion.

In general, two units of packed red blood cells (PRBC) needs be transfused if hemodynamic fail to  improve after the administration of 2 to 3 litres (or more than 50 mL/kg) of crystalloid. Further transfusions   are given depending on the patient’s injuries and response to the initial transfusion.

Typed and cross-matched PRBCs are best, but may take considerable time to do. If the patient’s condition warrants, clinicians may consider to transfuse immediately using type O Rh-positive for males and type O Rh-negative for girls and women of child-bearing age, until type-specific or typed and cross-matched  blood is available. 

Coagulation system dysfunction: 

A patient requiring massive transfusion may present  with pre-existing coagulopathy (e.g., disseminated intravascular coagulation) due to activation of coagulation secondary to tissue trauma, prolonged hypoxia, hypothermia, massive head injury, or muscle damage3. It may be suspected in these patients when there is microvascular oozing, prolongation of the PT and aPTT in excess of that expected by dilution, along with significant thrombocytopenia, low fibrinogen levels, and increased levels of D-dimer4.

As packed red cell transfusions are devoid of plasma   and platelets, which are removed immediately after collection, massive transfusion leads to coagulation abnormalities without coagulopathy, induced by the dilutional effects of blood replacement on coagulation  proteins and the platelet count5. It leads to prolongation   of the prothrombin time (PT) and the activated partial thromboplastin time (aPTT). In an adult, there will be an approximate 10% decrease in the concentration of clotting proteins for each 500 mL of blood loss that is replaced. Additional bleeding based solely on dilution can occur when the level of coagulation proteins falls to 25% of normal. This usually requires eight to 10 units of red cells in an adult.

In some patients coagulopathy is caused by widespread tissue injury/trauma and associated physiologic changes (i.e., acidosis, hypothermia, consumption of coagulant proteins, and fibrinolysis) combined with extensive blood loss and dilutional effects of fluid replacement therapy6.

Acidosis specifically interferes with the assembly of  coagulation factor complexes involving calcium and negativelycharged phospholipids. The activity of the factor Xa/Va/ prothrombinase complex is reduced by 50, 70, and 90 % at  a pH of 7.2, 7.0, and 6.8, respectively. Hypothermia also reduces the enzymatic activity of plasma coagulation proteins, but has a greater effect by preventing the activation of platelets via traction on the glycoprotein Ib/IX/V complex by von Willebrand factor. 

Effect on Platelet count:

A similar dilutional effect on the  platelet concentration is also seen with  assive transfusion 7. In an adult, each 10 to 12 units of transfused red cells can produce a 50% fall in the platelet count. Hence significant   thrombocytopenia can be seen after 10 to 20 units of blood, with platelet counts below 50,000/microL. For replacement  therapy in this setting, six units of platelets should be givento an adult; each unit should increase the platelet count by 5,000 to 10,000/microL.

Monitoring recommendations :

 In the massively  transfused patient, assumptions about possible dilutional  effects should be confirmed by measurement of the PT, aPTT, and platelet count after the administration of every five to seven units of red cells. Replacement therapy should not be based upon any formula (e.g., one unit of fresh frozen plasma (FFP) for every four units of red cells), except perhaps in  patients with severe trauma. 

Metabolic complications Citrate toxicity:

Since blood is anticoagulated with sodium citrate and citric acid large amounts of citrate are given with massive blood  transfusion8. Metabolic alkalosis and a decline in the plasma free calcium concentration are the two potential complications of citrate infusion and accumulation. Metabolic alkalosis can occur if the renal ischemia or underlying renal disease prevents the excess bicarbonate from being excreted in the  urine. Citrate binding of ionized calcium can lead to a clinically  significant fall in the plasma free calcium concentration. This change can lead to paraesthesia and/or cardiac arrhythmias in some patients9. 

Prevention:

The maximum citrate infusion rate should be 0.02 mmol/kg per minute (since this represents the maximum rate of citrate metabolism) and the citrate concentration in whole blood is 15 mmol/L (0.015 mmol/mL). For a 50 kg  recipient with normal hepatic function and perfusion, the maximum rate of blood transfusion to avoid citrate toxicity is 66.5 mL/min, which is equal to 8.9 units of whole blood per hour (450 mL per unit) and 33.3 units of red cells per hour (approximately 120 mL per unit). Thus, significant

hypocalcaemia should not develop in this setting except under extreme circumstances. However, the risk is substantially greater in a patient with either pre-existing liver disease or ischemia-induced hepatic dysfunction. In such patients, the plasma ionized calcium concentration should be monitored and calcium replaced with either calcium chloride or calcium gluconate if ionized hypocalcaemia develops. 

Hypothermia:

Rapid transfusion of multiple units of chilled  blood may reduce the core temperature abruptly and can  lead to cardiac arrhythmias 10. Hence, during massive  transfusion, a blood warmer should be used to warm blood   toward body temperature during infusion particularly when  more than three units are transfused. 

Hyperkalaemia:

Plasma potassium levels in stored blood    increase by approximately 1 meq/L per day due to passive  leakage of potassium out of red cells. Loss of one unit (500 mL) of blood through bleeding results in the loss of 1.5 mEq  of potassium (five mEq/L x 0.3 L of plasma); transfusion of one unit of whole blood or red cells should provide  approximately 10 mEq of potassium, leading to a net gain of 8.5 mEq. This excess potassium does not usually lead to a  significant rise in the plasma potassium concentration due  to movement into the cells, urinary excretion, and dilution. However, infants and patients with renal impairment may develop hyperkalaemia.  

Prevention:

Selection of only blood collected less than five  days prior to transfusion. Other measures are washing immediately before infusion to remove extracellular potassium from the blood. 

Management of massive transfusion:

The management of the patient who is being massively  transfused requires careful and on-going  onsideration of various complex physiological relationships. The primary concern is correction of ischemia which can be accomplished at the outset by aggressive volume expansion to maintain perfusion pressure as blood is being readied for infusion. As volume is replaced, attention should be paid to several other parameters to allow successful resuscitation: Although the best approach to blood transfusion in trauma is unknown, transfusions are given based upon the patient’s injuries and response to the initial  ransfusions, with attention being paid  to any underlying cardiopulmonary disease. There is no clear

threshold to be followed beyond which blood use in patients requiring massive transfusion 11. The coagulation system  needs to be monitored with measurements of the PT, aPTT and platelet count, preferably after each five units of blood  replaced. If the PT and PTT exceed 1.5 times the control value, the patient should be transfused with two units of fresh frozen plasma. If the platelet count falls below  0,000/microL, six units of platelets should be given. A blood warmer should be used whenever more than three units are transfused. Hypothermia should be either avoided or minimized. Acid– base balance and the plasma ionized calcium and potassium levels should be periodically monitored, particularly in patients

with coexistent liver or renal disease or in those with massive  haemorrhage and low cardiac output 12. For the subset of patients who present with widespread tissue trauma and who present with  oagulopathy, a different  approach to transfusion therapy is recommended13: First issue  is rapid identification of  oagulopathic patients and frequent  use of recombinant human factor VIIa in patients with widespread bleeding. Simultaneously acidosis needs to be   treated aggressively and avoiding hypothermia. Unlike other  patients, these patients needs prompt initiation of 1:1:1 

References - 

  1. Collins, JA. Problems associated with the massive  References -  Collins, JA. Problems associated with the massive  transfusion of stored blood. Surgery 1974; 75:274.   
  2. Stehling, L. Fluid replacement in massive transfusion. Massive  Transfusion AABB 1994; 1. 
  3. Hardy, JF, De Moerloose, P, Samama, M. Massive transfusion  and coagulopathy: pathophysiology and implications for clinical management. Can J Anaesth 2004; 51:293.  
  4. Stainsby, D, MacLennan, S, Thomas, D, et al. Guidelines on the management of massive blood loss. Br J Haematol 2006;  135:634. 
  5. Miller, RD, Robbins, TO, Tong, MJ, Barton, SL. Coagulation defects associated with massive blood transfusions. Ann Surg 1971; 174:794.  
  6. Borgman, MA, Spinella, PC, Perkins, JG, et al. The ratio of blood products transfused affects mortality in patients  eceiving massive transfusions at a combat support hospital. J Trauma 2007; 63:805.  
  7. Reed, RL, Ciavarella, D, Heimbacch, DM, et al. Prophylactic platelet administration during massive transfusion. Ann Surg 1986; 203:48. 
  8. Dzik, WH, Kirkley, SA. Citrate toxicity during massive  transfusion. Transfus Med Rev 1988; 2:76. 
  9. 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. 
  10. Boyan, CP. Cold or warmed blood for massive transfusions. Ann Surg 1964; 160:282. 
  11. Como, JJ, Dutton, RP, Scalea, TM, et al. Blood transfusion  rates in the care of acute trauma. Transfusion 2004; 44:809. 
  12. 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. 
  13. Hess, JR. Blood and coagulation support in trauma care. Hematology Am Soc Hematol Educ Program 2007; 2007:187.
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Dr. NIRANJAN RATHOD
DM, MD, FACP (USA)
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