Official reprint from UpToDate

www.uptodate.com 2014 UpToDate

Massive blood transfusion
Author
John R Hess, MD, MPH

Section Editor
Arthur J Silvergleid, MD

Deputy Editor
Jennifer S Tirnauer, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2014. | This topic last updated: Apr 24, 2013.
INTRODUCTION 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, definitions such as five units over three hours are more effective in identifying
patients needing rapid issue of blood products for serious injuries because of uncontrolled hemorrhage.
Such transfusion episodes are associated with a number of hemostatic and metabolic complications [1].
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 Acute Trauma Life Support approach to massive transfusion with crystalloid fluids
and packed red cells is presented here [2,3], as is the damage control approach using red cells and
plasma in a 1:1 ratio [4]. 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 and management of shock in adult
trauma".)
EPIDEMIOLOGY The most common situation leading to massive transfusion is trauma. Other
situations leading to massive transfusion, such as ruptured abdominal aortic aneurism, liver transplant,
and obstetric catastrophes are less frequent. 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 [5]. 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
[6]. 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 forms of resuscitation and when to
use them. (See "Initial evaluation and management of shock in adult trauma".)
RED CELL AND VOLUME REPLACEMENT 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 [7,8]. 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 to 4 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

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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.
The American Society of Anesthesiologists recommends that hemoglobin below 6 g/dL be avoided in
healthy individuals, and notes that higher values are necessary in those with active cardiovascular
disease. In healthy medical student volunteers acutely cytapheresed to hemoglobin concentrations of
5.3 g/dL, equivalent to a hematocrit of 16 percent, correct answers to digit-symbol reversal questions
and the strength of retinal-evoked potentials were reduced, but promptly improved with return of their
own fresh or stored RBCs [9,10].
Oxygen release by transfused stored RBCs is diminished compared with normal RBCs. Storage reduces
2,3-bisphosphoglycerate (2,3-BPG) levels, leading to a leftward shift of the lower end of the
oxyhemoglobin dissociation curve (2,3-BPG binds to deoxyhemoglobin). This abnormality, however, has
not been shown to be clinically important, as the transfused RBCs regenerate 2,3-BPG to normal levels
within 6 to 24 hours after transfusion, and most oxygen delivery occurs from the unaffected upper end of
the oxygen binding curve. (See "Red blood cell transfusion in adults: Storage, specialized modifications,
and infusion parameters", section on '2,3 BPG concentration'.)
The above considerations, however, represent the optimal clinical response to massive RBC loss with
adequate volume replacement. An approach to the use of plasma and RBC transfusions in adult
patients suffering from shock due to loss of circulating blood volume secondary to hemorrhage is
presented below and separately. (See 'Trauma patients' below and "Initial evaluation and management
of shock in adult trauma", section on 'Transfusion of red blood cells'.)
ALTERATIONS IN THE COAGULATION SYSTEM A patient being massively transfused may have
coagulopathy because of activation and consumption of coagulation factors secondary to tissue trauma,
such as massive head injury or muscle damage, or have reduced activity of coagulation factors from
prolonged shock, hypoxia, hypothermia, or failure to clear activation peptides that act as competitive
inhibitors [11]. Such trauma-associated coagulopathy can be diagnosed as acute disseminated
intravascular coagulation (acute DIC) when there is microvascular oozing, prolongation of the PT and
aPTT in excess of that expected by dilution, together with significant thrombocytopenia, low fibrinogen
levels, and increased levels of D-dimer. (See "Pathogenesis and etiology of disseminated intravascular
coagulation", section on 'Trauma and extensive surgery' and "Clinical features, diagnosis, and treatment
of disseminated intravascular coagulation in adults", section on 'Acute (decompensated) DIC'.)
Even if coagulopathy diagnostic of acute DIC does not exist and coagulation parameters are normal
before blood is replaced, coagulation abnormalities may be induced by the dilutional effects of blood
replacement on coagulation proteins and the platelet count [12-14]. This occurs because packed red cell
transfusions are essentially devoid of plasma and platelets, which are removed after collection in the
blood component manufacturing process.
Many patients who suffer massive trauma present to a trauma center with a coagulopathy of trauma that
does not meet the diagnostic criteria for acute DIC or dilutional coagulopathy. This coagulopathy is
caused by widespread tissue injury/trauma and shock, and their associated physiologic changes (ie,
acidosis, hypothermia, consumption of coagulant proteins, and fibrinolysis) combined with extensive
blood loss and the dilutional effects of physiologic vascular refill and fluid replacement therapy [15].
Effects of acidosis and hypothermia Both acidosis and hypothermia interfere with the normal
functioning of the coagulation system. As examples:
Acidosis (ie, excess protons) specifically interferes with the assembly of coagulation factor
complexes involving calcium and negatively-charged phospholipids. As a result, the activity of the
factor Xa/Va/prothrombinase complex is reduced by 50, 70, and 80 percent at pHs of 7.2, 7.0,

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and 6.8, respectively [16]. The resulting delayed production and reduced concentrations of
generated thrombin lead to delayed fibrin production, altered fibrin structure, and increased
susceptibility to fibrinolysis [17]. The interaction of acidosis with coagulopathy to increased
trauma mortality has been widely recognized. (See "Coagulopathy associated with trauma",
section on 'Acidosis'.)
Hypothermia 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 [18]. 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.
This profound effect on platelet-mediated primary hemostasis means that massive bleeding in
conjunction with a core temperature of <30 C is rarely survived [19]. The onset of this effect is
seen at core temperatures of 34C and below.
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 (aPTT). In an adult, there will be an
approximate 10 percent 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 individual
coagulation proteins falls to 25 percent of normal. This usually requires 8 to 10 units of red cells in an
adult.
Thus, the PT, aPTT, and fibrinogen or a viscoelastic test of coagulation (also called point of care testing)
(table 1) should be monitored in patients receiving massive blood transfusions of this magnitude. (See
"Clinical use of coagulation tests", section on 'Evaluation of abnormal clotting times' and "Clinical use of
coagulation tests", section on 'Point-of-care testing'.)
Two to eight units of fresh frozen plasma (FFP) should be given if the values exceed 1.5 times control.
Each unit of FFP might be expected to increase the clotting protein levels by 10 percent in an adult, but
because of losses in product preparation, storage, and of transfused factors to the interstitial space,
typical increments are of the order of 2.5 percent [20]. Cryoprecipitate or, when available, virusinactivated fibrinogen concentrate, may be used when fibrinogen levels are critically low (ie, <100
mg/dL) [2]. (See "Clinical use of plasma components" and "Disorders of fibrinogen", section on
'Cryoprecipitate and FFP' and "Disorders of fibrinogen", section on 'Fibrinogen concentrate'.)
Platelet count A similar dilutional effect on the platelet concentration can be seen with massive
transfusion [21]. In an adult, each 10 to 12 units of transfused RBCs are associated with a 50 percent
fall in the platelet count; thus, 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 whole
blood derived platelets or one apheresis concentrate should be given to an adult; each unit should
increase the platelet count by 5000/microL or 30,000/microL for a full six unit adult dose. (See "Clinical
and laboratory aspects of platelet transfusion therapy", section on 'Massive blood loss'.)
Monitoring recommendations In the massively transfused patient, assumptions about possible
dilutional effects of RBC transfusion should be confirmed by measurement of the PT, aPTT, and platelet
count or a viscoelastic test after the administration of every five to seven units of red cells. Replacement
therapy should be based on these parameters rather than on any formula (eg, one unit of fresh frozen
plasma (FFP) for every four units of red cells), except in patients with severe trauma and possibly
obstetric hemorrhage. (See 'Obstetric hemorrhage' below.)
SPECIAL SCENARIOS
Trauma patients While replacement therapy with plasma, platelets, and red cells should not
generally be based upon any set formula, results from a number of observational studies suggest that
patients with severe trauma, massive blood replacement, and coagulopathy have improved survival

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when the ratio of transfused FFP (units) to transfused platelets (units) to red cells (units) approaches
1:1:1 (ie, the damage control approach) [22-29]. (See "Clinical and laboratory aspects of platelet
transfusion therapy", section on 'Massive blood loss' and "Initial evaluation and management of shock in
adult trauma", section on 'Transfusion of platelets'.)
The physiology supporting the 1:1:1 approach derives from the existence of the acute coagulopathy of
trauma and the dilute nature of conventional blood products. Patients who present with uncontrolled
hemorrhage and shock have typically lost 30 to 40 percent of their blood volume. Conventional
resuscitation with crystalloid will rapidly lead to greater than 50 percent dilution of coagulation factors
and a diminution of thrombin generation. Resuscitation with RBCs in additive solution, plasma, and
platelets at 1:1:1 unit ratios means that the actual blood being given has a hematocrit of 29 percent, a
coagulation factor concentration of 65 percent of normal, and a platelet count of 88 x 109/L. Because 10
percent of the RBC and 30 percent of the platelets administered will not circulate, the effective
concentrations are hematocrit of 26 percent, plasma coagulation factor concentration of 65 percent, and
platelet count of 55 x 109/L. Thus, giving blood products, and nothing but blood products, barely keeps
levels above conventional transfusion triggers. More of any one product merely dilutes the other two,
such that giving two units of RBC for every unit of plasma and platelets (2:1:1) leads to a hematocrit of
40 percent, plasma coagulation factor concentration of 52 percent, and platelet count of 55 x 109/L; and
after storage related losses, a hematocrit of 36 percent, plasma concentration of coagulation factors of
52 percent, and platelet count of 37 x 109/L. Any crystalloid solution administered will further dilute all
three blood components.
Clinical studies that have shown a benefit for the 1:1:1 approach in massively injured and rapidly
bleeding patients include:
A retrospective study of 246 patients who presented to an Army combat support hospital in Iraq
has produced some data to evaluate the merits of this regimen [22]. 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, 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).
In a retrospective study of 467 massively transfused trauma patients, 30-day 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) [23]. The combination of high plasma and high
platelet to RBC ratios was associated with decreased truncal hemorrhage and increased six-hour,
24-hour, and 30-day survivals, with no change in deaths due to multiple organ failure.
In a retrospective study of 694 massively transfused trauma patients who did not receive fresh
whole blood, those receiving a high ratio of apheresis platelets (equivalent to six units of pooled
platelets) per stored red cell unit (ie, ratio 1:8) had a higher 24-hour survival (95 percent)
compared with those receiving a medium (ie, ratio 1:16 to 1:8, 87 percent) or a low ratio (ie,
<1:16, 64 percent) [28]. 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.
Such 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 [22-29]. Since there
are only a limited number of retrospective studies in patients requiring massive transfusion, the value of
this approach is still controversial and remains to be proven. A multicenter, prospective, randomized
clinical trial is in progress [30]. (See 'Summary and recommendations' below and "Initial evaluation and
management of shock in adult trauma", section on 'Evaluation and management'.)

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For the subset of patients who present with widespread tissue trauma (as in combat injuries) and who
present with coagulopathy or the high likelihood of coagulopathy, an approach using plasma as the
primary resuscitation fluid has been advocated by the United States military. The treatment of such
patients is discussed in depth separately. (See "Coagulopathy associated with trauma", section on
'Treatment'.)
Obstetric hemorrhage Gravid and parturient women are hypercoagulable with compensatory
hyperfibrinolysis. When vascular disruption leads to massive bleeding, those with low fibrinogen are at
increased risk for bleeding [31]. (See "Placental abruption: Management", section on 'Treatment of
disseminated intravascular coagulation' and "Disseminated intravascular coagulation during
pregnancy".)
Liver disease Liver disease not only leads to the reduced production of normal coagulation factors,
but to the production of abnormal factors such as dysfunctional vitamin K-dependent factors and the
failure to clear activation fragments of coagulation factors, which can act as competitive inhibitors of
coagulation enzymes by occupying binding sites [32]. The presence of such inhibitors of coagulation can
reduce the effectiveness of conventional treatment. (See "Coagulation abnormalities in patients with
liver disease".)
COMPLICATIONS OF CITRATE INFUSION Large amounts of citrate are given with massive blood
transfusion, since blood is anticoagulated with sodium citrate and citric acid [33]. 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 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 3 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
[34,35]. (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 serum calcium
concentrations".) This change can lead to paresthesias and/or cardiac arrhythmias in some patients
[36]. (See "Clinical manifestations of hypocalcemia", section on 'Acute manifestations'.)
Recommendations for citrate infusion By extrapolation from animal studies, it is possible to
calculate the maximum transfusion rate that would permit a normal liver to metabolize excess citrate,
thereby avoiding hypocalcemia. 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). Thus:
Maximum citrate infusion rate (mmol/kg per min)
= (mmol citrate per mL of blood x mL of blood infused per min) wt (kg)
mL of blood infused per min = (0.02 0.015) x wt (kg) = 1.33 x wt (kg)
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 26.7 units of red cells per hour (approximately 150 mL per unit). Thus, significant hypocalcemia
should not develop in this setting except under extreme circumstances. However, the risk is substantially
greater in a patient with either preexisting liver disease or ischemia-induced hepatic dysfunction. In such

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patients, the plasma ionized calcium concentration should be monitored and calcium replaced with
either calcium chloride or calcium gluconate if ionized hypocalcemia develops:
If 10 percent calcium gluconate is used, 10 to 20 mL should be given intravenously (into another
vein) for each 500 mL of blood infused.
If 10 percent calcium chloride is used, only 2 to 5 mL per 500 mL of blood should be given.
Calcium chloride may be preferable to calcium gluconate in the presence of abnormal liver function,
since citrate metabolism is decreased, resulting in slower release of ionized calcium [2]. Care must be
taken to avoid administering too much calcium and inducing hypercalcemia, ideally by monitoring the
ionized calcium concentration.
PREVENTION OF HYPOTHERMIA A high capacity commercial blood warmer should be used to
warm blood components toward body temperature when more than three units are transfused.
Rapid transfusion of multiple units of chilled blood may reduce the core temperature abruptly and can
lead to cardiac arrhythmias [37]. Six units of RBCs at 4C will reduce the body temperature of a 70 kg
man by 1C. This heat loss can be additive with the evaporative heat loss associated with an open
abdomen or other body cavity which, by itself, can lead to a 1C decrease in core temperature in 40
minutes. Thus, 10 units of cold blood products and an hour of surgery can lead to a 3C drop in core
temperature and hypothermic coagulopathy.
PREVENTION OF HYPERKALEMIA Infants and patients with renal impairment may develop
hyperkalemia because of potassium leakage due to prolonged blood storage or irradiation [37]. (See
"Red blood cell transfusion in adults: Storage, specialized modifications, and infusion parameters",
section on 'Potassium leakage'.)
In storage, the supernatant of RBCs increases in [K+] by 1 mEq/day, increasing from approximately 3
mEq/L at the time of donation to 45 mEq/L during 42 days of storage. Irradiation can increase this rate to
1.5 mEq/day. Nevertheless, because the volume of suspending solution in a unit of red cells in additive
solution is small (150 mL), the actual amount of free K+ infused with a unit of RBC is only approximately
7 mEq, and this is rapidly pumped back into the cells as they warm. As a result, potassium is only a
problem when long-stored red cells are infused directly into the central circulation at high concentrations,
as occurs with blood-primed cardiopulmonary bypass machines, high volume transfusion devices, or
infants transfused through umbilical catheters.
In these patients, the following steps can be used to minimize the risk of hyperkalemia:
Select only red cells collected less than 5 or 10 days prior to transfusion.
Any unit of red cells can be washed immediately before infusion to remove extracellular
potassium.
SUMMARY AND RECOMMENDATIONS
The management of the patient who is being massively transfused requires careful and ongoing
consideration of a number of complex physiological relationships. There is no clear threshold for
hematocrit, platelet count, or coagulation factor deficiency below which blood use is futile. 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. (See
'Red cell and volume replacement' above and "Initial evaluation and management of shock in
adult trauma", section on 'Evaluation and management'.)
As volume is replaced, attention must be paid to coagulation parameters, platelet count, and
metabolic status. (See 'Alterations in the coagulation system' above and 'Complications of citrate
infusion' above.)

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 The coagulation system should be frequently monitored with measurements of the PT, aPTT,
fibrinogen concentration, and platelet count or a viscoelastic measure (also called point of care
testing) (table 1), preferably after each five units of blood replaced. If the PT and aPTT exceed
1.5 times the control value, the patient should be transfused with at least two units of fresh frozen
plasma. If the platelet count falls below 50,000/microL, six units of random donor platelets, or one
unit of apheresis platelets, should be given. (See 'Alterations in the coagulation system' above
and "Clinical use of coagulation tests", section on 'Evaluation of abnormal clotting times' and
"Clinical use of coagulation tests", section on 'Point-of-care testing'.)
The best approach to blood transfusion in trauma is unknown. Transfusions are given based
upon the patient's injuries and response to the initial transfusions, with attention being paid to any
underlying cardiopulmonary disease. In some cases where there is insufficient time to obtain
laboratory values to guide transfusion, it may be necessary to use the damage control approach
of transfusing red blood cells, platelets, and plasma in a set ratio. (See 'Trauma patients' above.)
For the subset of patients who present with widespread tissue trauma (as in combat injuries) and
who present with coagulopathy or the high likelihood of coagulopathy, an approach using plasma
as the primary resuscitation fluid has been advocated by the United States military. The treatment
of such patients is discussed in depth separately. (See "Coagulopathy associated with trauma",
section on 'Treatment'.)
Management of massive transfusion in other special scenarios (eg, obstetric hemorrhage, liver
disease) is discussed separately. (See "Coagulation abnormalities in patients with liver disease"
and "Placental abruption: Management".)
A blood warmer should be used whenever more than three units are transfused. Hypothermia
should be either avoided or minimized. (See 'Prevention of hypothermia' above.)
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
hemorrhage and low cardiac output [35]. (See 'Complications of citrate infusion' above and
'Prevention of hyperkalemia' above.)

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Topic 7931 Version 17.0

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GRAPHICS
Various types of thromboelastograms
Native TEG

Measures clot formation in the absence of a specific activator in either

untreated whole blood or in citrated whole blood after recalcification.

Rapid-TEG
(rTEG)

Tissue factor is used as the activator inducing clot formation via the
extrinsic pathway. Compared with native TEG, rTEG gives a readout of
clot characteristics within about 10 minutes. The corresponding RoTEM
test is the EXTEM.

Kaolin-TEG

Phospholipid and kaolin are used to induce activation via the intrinsic
pathway. The corresponding RoTEM test is the INTEM, which uses
phospholipid and ellagic acid as activators.

Heparinase
treatment

Simultaneous measurements can be performed comparing heparinasetreated blood with untreated blood to identify the effects of endogenous
heparan sulfates, exogenous heparin and heparinoids. The corresponding
RoTEM assay is the HEPTEM.

Platelet
mapping

Platelet mapping assesses platelet function via the cyclooxygenase and

ADP/P2 signaling pathways. The decrement in MA can be measured in the
presence of platelet antagonists such as acetylsalicylic acid, dipyridamole,
and clopidogrel and compared with the untreated MA.

Fibrin
function
testing

The RoTEM FIBTEM test activates the extrinsic pathway in the presence
of cytochalasin D, which is a cytoskeletal inhibitor of platelet activity. This
test qualitatively assesses fibrinogen levels since the clot formation in this
test is attributable to fibrin polymerization alone.

TEG: thromboelastogram; ADP/P2: adenosine diphosphate/P2 receptor; MA: maximal

amplitude.
Graphic 55087 Version 2.0

Disclosures
Disclosures: John R Hess, MD, MPH Nothing to disclose. Arthur J Silvergleid, MD Nothing to disclose. Jennifer S Tirnauer,
MD Employee of UpToDate, Inc.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting
through a multi-level review process, and through requirements for references to be provided to support the content.
Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
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