Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
Author
Steven Kleinman, MD
Section Editor
Arthur J Silvergleid, MD
Deputy Editor
Stephen A Landaw, MD, PhD
Last literature review version 18.2: mayo 2010 | This topic last updated: enero 26, 2010
but has a greater effect by preventing the activation of platelets via traction on the
glycoprotein Ib/IX/V complex by von Willebrand factor. In tests of shear-dependent
platelet activation, this pathway stops functioning in 50 percent of individuals at 30
C, and is markedly diminished in most of the rest.
Coagulation proteins The replacement of blood loss with red cells and a crystalloid
volume expander will result in gradual dilution of plasma clotting proteins, leading to
prolongation of the prothrombin time (PT) and the activated partial thromboplastin time
support hospital in Iraq has produced some data to evaluate the merits of this
regimen [9]. When patients who received massive transfusion were stratified by
transfusion therapy regimen, patients who received a high ratio of FFP to red cells
(median of 1:1.4) had a survival rate of 81 percent as compared with 66 percent for
those with an intermediate ratio (median 1:2.5) and 35 percent for those who
received a low ratio of FFP to red cells (median of 1:8).
survival was increased in patients transfused at a high plasma:RBC ratio (ie, 1:2)
as well as in those transfused at a high platelet:RBC ratio (ie, 1:2) [15]. The
combination of high plasma and high platelet to RBC ratios was associated with
decreased truncal hemorrhage and increased 6-hour, 24-hour, and 30-day survivals,
with no change in deaths due to multiple organ failure.
not receive fresh whole blood, those receiving a high ratio of apheresis platelets
(equivalent to 6 units of pooled platelets) per stored red cell unit (ie, ratio 1:8) had
a higher 24-hour survival (95 percent) as compared with those receiving a medium
(ie, ratio 1:16 to 1:8, 87 percent) or a low ratio (ie, <1:16, 64 percent) [18]. On
multivariate analysis, higher plasma:red cell ratios and higher apheresis platelets:red
cell ratios were both independently associated with improved survival at both 24
hours and 30 days.
These observations have led these and other authors to recommend that patients who have
sustained severe traumatic injuries and/or who are likely to require massive transfusion
receive a 1:1:1 ratio of FFP to platelets to RBCs at the outset of their resuscitation and
transfusion therapy [10,15,19-21]. Since there are only a limited number of studies in
patients requiring massive transfusion [22,23], the value of this approach is still
controversial and remains to be proven. (See 'Summary and recommendations' below and
"Management of shock in adult trauma", section on 'Evaluation and management'.)
COMPLICATIONS OF CITRATE INFUSION Large amounts of citrate are given
with massive blood transfusion, since blood is anticoagulated with sodium citrate and citric
acid [24]. Metabolic alkalosis and a decline in the plasma free calcium concentration are the
two potential complications of citrate infusion and accumulation.
Metabolic alkalosis The pH of a unit of blood at the time of collection is 7.10 when
measured at 37C (7.6 at 1 to 6C) due to citric acid present in the
anticoagulant/preservative in the collection bag. The pH then falls 0.1 pH unit/week due to
the production of lactic and pyruvic acids by the red cells. Acidosis does not develop in a
massively bleeding patient even if "acidic" blood is infused as long as tissue perfusion is
restored and maintained. In this setting, the metabolism of each mmol of citrate generates
three meq of bicarbonate (for a total of 23 meq of bicarbonate in each unit of blood). As a
result, metabolic alkalosis can occur if the renal ischemia or underlying renal disease
prevents the excess bicarbonate from being excreted in the urine. This may be accompanied
by hypokalemia as potassium moves into cells in exchange for hydrogen ions that move out
of the cells to minimize the degree of extracellular alkalosis [25]. (See "Potassium balance
in acid-base disorders".)
Free hypocalcemia Citrate binding of ionized calcium can lead to a clinically significant
fall in the plasma free calcium concentration. (See "Relation between total and ionized
plasma calcium concentration".) This change can lead to paresthesias and/or cardiac
arrhythmias in some patients [26].
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 hyperkalemia. In these patients, the following steps can be used to minimize the
risk of hyperkalemia:
Select only blood collected less than five days prior to transfusion.
are given based upon the patient's injuries and response to the initial transfusions,
with attention being paid to any underlying cardiopulmonary disease.
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
50,000/microL, six units of platelets should be given.
A blood warmer should be used whenever more than three units are
Acidbase balance and the plasma ionized calcium and potassium levels
Severe trauma and coagulopathy For the subset of patients who present with widespread
tissue trauma (as in combat injuries) and who present with coagulopathy, a different
approach to transfusion therapy has been advocated by the United States military. This
approach includes all of the following [10,19]:
universal donor AB plasma, and apheresis platelets, with conversion to fresh whole
blood as soon as this can be obtained. This ratio has not been universally adopted by
civilian hospitals. (See 'FFP, platelets, and red cells in trauma patients' above.)
Collins, JA. Problems associated with the massive transfusion of stored blood. Surgery 1974;
75:274.
Miller, RD, Robbins, TO, Tong, MJ, Barton, SL. Coagulation defects associated with massive
blood transfusions. Ann Surg 1971; 174:794.
Counts, RB, Haisch, C, Simon, TL, et al. Hemostasis in massively transfused trauma patients.
Ann Surg 1979; 190:91.
Mannucci, PM, Federici, AB, Sirchia, G. Hemostasis testing during massive blood replacement.
Vox Sang 1982; 42:113.
Borgman, MA, Spinella, PC, Perkins, JG, et al. The ratio of blood products transfused affects
9 mortality in patients receiving massive transfusions at a combat support hospital. J Trauma
2007; 63:805.
10
Hess, JR. Blood and coagulation support in trauma care. Hematology Am Soc Hematol Educ
Program 2007; 2007:187.
11
Kermode, JC, Zheng, Q, Milner, EP. Marked temperature dependence of the platelet calcium
signal induced by human von Willebrand factor. Blood 1999; 94:199.
Meng, ZH, Wolberg, AS, Monroe DM, 3rd, Hoffman, M. The effect of temperature and pH on
12 the activity of factor VIIa: implications for the efficacy of high-dose factor VIIa in
hypothermic and acidotic patients. J Trauma 2003; 55:886.
13
Reed, RL, Ciavarella, D, Heimbacch, DM, et al. Prophylactic platelet administration during
massive transfusion. Ann Surg 1986; 203:48.
15
Holcomb, JB, 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.
16
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.
Shaz, BH, Dente, CJ, Nicholas, J, et al. Increased number of coagulation products in
17 relationship to red blood cell products transfused improves mortality in trauma patients.
Transfusion 2010; 50:493.
18
Perkins, JG, Andrew, CP, 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.
19
Holcomb, JB, Jenkins, D, Rhee, P, et al. Damage control resuscitation: directly addressing the
early coagulopathy of trauma. J Trauma 2007; 62:307.
Yuan, S, Ziman, A, ANthony, MA, et al. How do we provide blood products to trauma
patients?. Transfusion 2009; 49:1045.
22
Schreiber, MA, Perkins, J, Kiraly, L, et al. Early predictors of massive transfusion in combat
casualties. J Am Coll Surg 2007; 205:541.
23
McLaughlin, DF, Niles, SE, Salinas, J, et al. A predictive model for massive transfusion in
combat casualty patients. J Trauma 2008; 64:S57.
24
Dzik, WH, Kirkley, SA. Citrate toxicity during massive transfusion. Transfus Med Rev 1988;
2:76.
25
Bruining, HA, Boelhouwer, RU, Ong, GK. Unexpected hypopotassemia after multiple blood
transfusions during operation. Neth J Surg 1986; 38:48.
26
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.
27 Boyan, CP. Cold or warmed blood for massive transfusions. Ann Surg 1964; 160:282.
28 Simon, GE, Bove, JR. The potassium load from blood transfusion. Postgrad Med 1971; 49:61.
29
Como, JJ, Dutton, RP, Scalea, TM, et al. Blood transfusion rates in the care of acute trauma.
Transfusion 2004; 44:809.
30
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.