Use of Blood Products in The Critically Ill - UpToDate

8/4/2018 Use of blood products in the critically ill - UpToDate
Authors: Addison K May, MD, John P Reilly, MD, MSCE

Section Editors: Scott Manaker, MD, PhD, Arthur J Silvergleid, MD
Deputy Editor: Geraldine Finlay, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2018. | This topic last updated: Sep 28, 2017.
INTRODUCTION — Transfusion of red blood cells or another blood product is common in the intensive care
unit (ICU). It has been estimated that greater than 40 percent of patients receive one or more red blood cell
transfusions while in the ICU, of which approximately 90 percent are provided in the context of stable anemia
[1-4].
The appropriate use of blood products requires that the potential benefits and risks be carefully weighed for
each patient. Indications and complications of blood product transfusion in the ICU are reviewed here, as well
as the various types of blood products. Other issues related to transfusion of blood products are discussed
separately. (See "Red blood cell transfusion in adults: Storage, specialized modifications, and infusion
parameters" and "Clinical use of plasma components" and "Clinical use of Cryoprecipitate" and "Initial
management of moderate to severe hemorrhage in the adult trauma patient" and "Clinical and laboratory
aspects of platelet transfusion therapy".)
RED BLOOD CELLS
RBC indications — Indications for the transfusion of packed red blood cells (RBCs) in critically ill patients
include the following [5,6]:
● Acute hemorrhage with hemodynamic instability (ie, hemorrhagic shock).
● Acute anemia with inadequate oxygen delivery (eg, cool vasoconstricted skin, obtundation or restlessness,
oliguria or anuria, lactic acidosis, an oxygen extraction ratio of greater than 0.3, and/or an oxygen delivery
of less than 10 to 12 mL/kg per minute). (See "Oxygen delivery and consumption".)
● Hemoglobin concentration of <7 to 8 g/dL, depending on patient characteristics [6,7].
Red blood cell transfusions were previously given routinely whenever the hemoglobin level was <10 g/dL. This
practice was based upon unproven physiological and clinical assumptions. However, a hemoglobin
concentration of <7 g/dL became the accepted threshold after the multicenter Transfusion Requirements in
Critical Care (TRICC) trial. The trial randomly assigned a broad population of 838 critically ill adults to either a
restrictive transfusion strategy (transfusion threshold of <7 g/dL) or a liberal transfusion strategy (threshold of
<10 g/dL) and found that the restrictive strategy decreased hospital mortality [8]. Among patients who were <55
years old or less acutely ill (APACHE II score ≤20), a restrictive strategy also reduced 30-day mortality. These
findings have been confirmed in subsequent meta-analysis of trials examining transfusion triggers [9,10].
Lower hemoglobin thresholds are also supported for specific subgroups of critically ill patients:
● Sepsis – The Transfusion Requirements in Septic Shock (TRISS) trial aimed to address divergent views on
transfusion in septic shock by determining the impact on mortality of a low versus high transfusion
threshold during septic shock treatment [11]. Investigators randomized 998 patients with septic shock to a
low transfusion threshold (<7 g/dL) versus a high transfusion threshold (<9 g/dL) and identified no
significant differences in 90 day mortality (43 versus 45 percent), despite patients in the low transfusion
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threshold group received 50 percent less red blood cell transfusions. This trial is discussed in detail
separately. (See "Evaluation and management of suspected sepsis and septic shock in adults", section on
'Red blood cell transfusions'.)
● Gastrointestinal bleeding – In patients with acute severe upper gastrointestinal (GI) bleeding, a lower
transfusion threshold is also supported by the evidence [12]. In one trial, 921 patients with acute upper GI
bleeding were randomly assigned to receive transfusion when hemoglobin fell below 7 g/dL versus 9 g/dL.
Patients in the lower trigger group (7 g/dL) had a higher probability of survival at six weeks, less ongoing
bleeding, and fewer complications relative to the liberal transfusion group. Importantly, patients with
massive exsanguinating bleeding were excluded from the trial.
Use of a lower hemoglobin concentration as the threshold for transfusion is also supported by several
observational studies that found that red blood cell transfusions were associated with adverse outcomes (eg,
increased risk of infection, acute respiratory distress, multiple organ dysfunction, and death) [2,13-16]. A pooled
analysis of randomized controlled trials comparing higher versus lower red blood cell transfusion thresholds
found decreased hospital mortality in the lower transfusion threshold groups. However, 60 day all-cause
mortality and intensive care unit mortality were not different between the two groups [9].
An important exception to the transfusion threshold of <7 g/dL is a patient who is having acute myocardial
ischemia (ie, acute myocardial infarction, unstable angina) [5,17]. The optimal transfusion threshold for such
patients is unknown because most clinical trials excluded such patients. However, in the TRICC trial, patients
with active ischemic cardiovascular disease had a trend toward improved clinical outcomes when a hemoglobin
level of <10 g/dL was used as the threshold for transfusion [14,18]. Although the improvements were not
statistically significant, the effect would be clinically important if real, indicating that larger trials are needed to
definitively confirm or exclude such an effect. In a secondary data analysis of Veterans Affairs intensive care
unit (ICU) episodes over a five year period, improved outcome was associated with a transfusion threshold
below 8.7 g/dL in patients with comorbid heart disease and near 10 g/dL in patients with an acute myocardial
infarction [7].
Additional indications for red blood cell transfusion that generally exist outside of the ICU are described
separately. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult".)
RBC preparations — Red blood cell transfusion may be performed using packed red blood cells, whole blood,
or salvaged autologous blood (see "Red blood cell transfusion in adults: Storage, specialized modifications, and
infusion parameters"):
● Packed red blood cells – Packed red cells are the preparation used in most clinical situations. Each unit of
packed red blood cells has a total volume of 300 mL, of which approximately 200 mL are red blood cells.
● Whole blood – Whole blood is rarely indicated and seldom is available. Its use should be considered only
in the context of massive blood transfusion. The rationale is that massive transfusion of only one blood
component (eg, red blood cells) will lead to dilutional deficiencies of the other components (eg, platelets,
coagulation factors). This can be avoided by transfusing whole blood. (See "Massive blood transfusion".)
● Autotransfusion – Autotransfusion refers to collection of a patient's blood during acute blood loss, followed
by transfusion of the blood back into the patient. It is the preferred technique whenever the collection
device is rapidly available or a large volume of blood loss can be anticipated (eg, certain surgeries) [19].
Autotransfusion facilitates rapid transfusion of immense quantities of blood, which is generally collected
from chest tubes or aspirated from the pleural and peritoneal cavities. It may be particularly valuable for
patients who have multiple alloantibodies that preclude the transfusion of donor blood. Autotransfusions
are acceptable to some Jehovah's Witnesses, as long as the blood does not leave the bedside for
processing [20]. Autotransfusion systems damage the red blood cells to some degree; therefore, it is
recommended that the volume of an autotransfusion be limited to less than 10 to 15 liters if possible. A
systematic review of the evidence confirmed that autotransfusion reduces the need for donor blood
transfusions [21]. (See "Surgical blood conservation: Blood salvage" and "The approach to the patient who
refuses blood transfusion".)
Red blood cell preparations that have undergone leukoreduction (ie, removal of leukocytes) are more costly;
however, they are preferred for chronically transfused patients, potential transplant recipients, patients with
previous transfusion reactions, patients undergoing cardiopulmonary bypass, and cytomegalovirus (CMV)
seronegative patients who are at risk for CMV infection and for whom seronegative components are not
available. (See "Leukoreduction to prevent complications of blood transfusion".)
RBC alternatives — Erythropoietin is an endogenously produced hormone that stimulates erythropoiesis,

provided that stores of vitamin B12, folate, and iron are adequate. Endogenous production of erythropoietin
normally increases with anemia and hypoxia, but this response is blunted during critical illness [22]. The use of
recombinant erythropoietin in critically ill patients has been studied in three randomized trials with conflicting
results [23-25]. Interpretation of the studies is confounded by variable dosing regimens and variable thresholds
for red cell transfusion. However, the preponderance of the evidence does not support the routine use of
erythropoietin in critically ill patients. The impact of recombinant erythropoietin on avoiding transfusions appears
to be small and there is insufficient evidence to determine if its benefits outweigh its risks. There may be a dose
response effect, but this is inadequately studied. Two trials have demonstrated a survival advantage within the
trauma subgroup of critically ill patients, despite no significant decrease in red cell transfusions [26]. The
explanation for this finding has not been established. (See "Oxygen carriers as alternatives to red blood cell
transfusion".)
RBC response — The transfusion of one unit of packed red cells can be expected to raise the hematocrit by
roughly 3 percent and the hemoglobin by approximately 1 g/dL, assuming that there is no ongoing bleeding.
RBC age — Similar to that observed in other populations, in critically ill patients, the age of transfused red cells
does not appear to affect outcomes including mortality, the details of which are discussed separately. (See "Red
blood cell transfusion in adults: Storage, specialized modifications, and infusion parameters".)
PLASMA PRODUCTS — Plasma is the portion of whole blood that remains after the cellular elements (ie, red
and white blood cells) and platelets have been removed by centrifugation.
Plasma indications — Indications for the transfusion of plasma in critically ill patients are less well established
than the indications for red blood cell transfusion. Generally speaking, transfusion of plasma is indicated
whenever hemostasis is inadequate and the benefit of correcting the insufficient hemostasis (ie, reduced
bleeding) is believed to outweigh the risks of the plasma transfusion. However, the benefit of plasma
administration remains controversial [27]. (See 'Complications' below.)
Examples of clinical situations in which plasma transfusions are often administered include the following:
● Active bleeding in the setting of known or strongly suspected coagulation abnormalities [28-32].
● Massive transfusion of packed red blood cells. The rationale is that massive transfusion of red blood cells
alone will lead to a dilutional deficiency of coagulation factors, which can be corrected via the transfusion of
plasma. This practice is supported by several studies of massively transfused trauma patients, in which
protocols with predefined ratios of plasma to red cell transfusions reduced total blood product use, reduced
organ dysfunction, and improved survival [33-35]. (See "Massive blood transfusion".)
● Prior to invasive and surgical procedures for which there is a HIGH risk of bleeding complications (eg,
thoracic, abdominal, spinal, intracranial, and some urologic surgeries), if the patient has ANY potentially
significant abnormality of their coagulation tests (ie, prothrombin time, international normalized ratio [INR],
or partial thromboplastin time). When deciding whether the abnormality is potentially significant, the
relationship between the severity of an abnormal coagulation test and the response to plasma should be
considered. (See 'Plasma response' below.)
● Prior to invasive procedures for which there is a LOW risk of bleeding complications (eg, endoscopy,
cardiac catheterization, central venous catheter insertion), if the patient has a SEVERE abnormality of their
coagulation tests (ie, prothrombin time >2-times control, INR >2, or partial thromboplastin time >2-times
control). Transfusion of plasma is not indicated prior to such procedures if the coagulation tests are only
mildly abnormal.
Generally speaking, there is a paucity of evidence regarding the transfusion of plasma prior to invasive and
surgical procedures; therefore, the related indications provided here are primarily based upon clinical
experience and biological rationale [27].
Plasma should not be transfused to reverse excessive (ie, "supra-therapeutic") warfarin effects, unless there is
active bleeding or an urgent invasive or surgical procedure is required. Four factor prothrombin complex
concentrates (4F-PCC) are recommended over fresh frozen plasma (FFP) in the setting of life-threatening
hemorrhage and therapeutic warfarin therapy [36,37]. The reason is that plasma products are only partially
effective, have short duration of action, and may cause hypervolemia (up to a liter of fresh frozen plasma may
be required to reverse the effects of excess warfarin) [31,32,38]. In addition, plasma products are not indicated
for the treatment of hypovolemia, malnutrition, or poor wound healing, and are of limited utility in the presence
of a clotting factor inhibitor. (See "Management of warfarin-associated bleeding or supratherapeutic INR".)
Additional indications for plasma transfusion that are generally seen outside of the ICU are described
separately. (See "Clinical use of plasma components", section on 'Indications'.)
Plasma preparations — Several different plasma preparations are available, including fresh frozen plasma,
thawed plasma, liquid plasma, cryoprecipitate, and factor concentrates:
● Fresh frozen plasma – FFP is separated from freshly drawn blood by removing the red blood cells, white
blood cells, and platelets. It is then frozen for storage and thawed when needed for transfusion. Once it has
thawed, the plasma must be transfused within 24 hours or the concentrations of factor V and factor VIII
begin to decline. FFP is the most commonly used plasma product, in part because it can ameliorate
deficiencies of any of the circulating coagulation factors. FFP needs to be ABO-compatible, but does not
require crossmatching or Rh typing.
● Thawed plasma – FFP becomes "thawed plasma" if it is not transfused within 24 hours of being thawed.
Thawed plasma can be transfused up to five days after being thawed, if stored at refrigerator temperature
(1 to 6ºC). (See "Clinical use of plasma components", section on 'Thawed Plasma'.)
● Cryoprecipitate – Cryoprecipitate is collected by thawing FFP at 4ºC and collecting the white precipitate. It
is rich in von Willebrand factor, factor VIII, factor XIII, and fibrinogen. The chief advantage to cryoprecipitate
is that it allows von Willebrand factor, factor VIII, factor XIII, and fibrinogen to be replaced using a much
smaller volume than if those factors were replaced by transfusing FFP. (See "Clinical use of
Cryoprecipitate".)
● Factor concentrates – A factor concentrate contains a large amount of a specific clotting factor that has
been produced with recombinant technology or collected from thousands of donors and pooled into a
highly concentrated product. PCCs comprise a group of products containing vitamin K dependent factors.
In the past, the major indication for these products is to replace specific factor deficiencies (eg, hemophilia
A and B) with minimal volume and without supplying extraneous proteins. Recombinant proteins also have
the advantage of being free from viral contamination. However, there has since been a paradigm shift in
the administration of 4F-PCC that has been approved for warfarin reversal by the US Food and Drug
Administration (FDA). 4F-PCCs rather than FFP are suggested the setting of life-threatening hemorrhage
and therapeutic warfarin therapy [36,37]. (See "Plasma derivatives and recombinant DNA-produced
coagulation factors", section on 'Coagulation factors'.)
● Liquid plasma – Liquid plasma is prepared by removing the red blood cells, white blood cells, and platelets
from previously stored whole blood. Its use is extremely rare because it has low levels of factor V.
However, it has some utility if FFP is unavailable and the coagulopathy is likely due to deficiencies of
factors other than factor V.
● Intravenous immunoglobulin – Intravenous immunoglobulin is the purified immunoglobulin fraction of

plasma pooled from several thousand donors. It is useful in the treatment of some autoimmune and
immunodeficiency states. (See "Overview of intravenous immune globulin (IVIG) therapy".)
Desmopressin (dDAVP) may also be useful in achieving hemostasis during the short-term management of
patients with certain types of von Willebrand disease, mild hemophilia A, or uremic platelet dysfunction, since
dDAVP induces the release of multimers of factor VIII and von Willebrand factor from endothelial cells.
Plasma response — The response to a plasma transfusion is directly proportional to the difference between
the patient's levels of coagulation factors and that of the infused plasma. Thus, patients with severe factor
deficiencies (manifested as severely abnormal coagulation tests) are more likely to see a significant decrease
in their INR than patients with mild factor deficiencies. In fact, patients with a mildly prolonged INR may see little
or no improvement, since the INR of a unit of plasma tends to be around 1.3. This was illustrated by a study in
which 121 patients with an INR between 1.1 and 1.85 received transfusions of FFP [39]. Only one patient's INR
corrected to normal and only 15 percent of patients corrected half way to normal. The median decrease in the
INR was only 0.07. (See "Clinical use of plasma components", section on 'Minimally elevated INR'.)
The response to transfusions of cryoprecipitate is more difficult to predict. However, transfusion of ten bags of
cryoprecipitate can be expected to raise the fibrinogen level approximately 70 mg/dL.
PLATELETS
Platelet indications — Indications for the transfusion of platelets in critically ill patients may be therapeutic (ie,
stop active bleeding) or prophylactic (ie, prevent bleeding) [29,31,40-42]:
● Patients with a platelet count <10 X 103 platelets/microliter. The purpose is to prevent spontaneous
hemorrhage.
● Patients with a platelet count <50 X 103 platelets/microliter who are actively bleeding, are scheduled to
undergo an invasive procedure, or have a qualitative intrinsic platelet disorder.
● Patients with a platelet count <100 X 103 platelets/microliter who have a central nervous system injury,
have multisystem trauma, are undergoing neurosurgery, or require an intrathecal catheter for anesthesia.
● Patients with a normal platelet count who have ongoing active bleeding and a reason for platelet
dysfunction, such as a congenital platelet disorder, chronic antiplatelet therapy, or uremia.
Additional indications for platelet transfusion that are generally seen outside of intensive care unit (ICU) are
described separately. (See "Clinical and laboratory aspects of platelet transfusion therapy", section on 'Specific
clinical scenarios'.)
Special considerations — Special consideration needs to be given to the indication for platelet transfusion
in the following conditions:
● Heparin-induced thrombocytopenia (HIT)
● Thrombotic thrombocytopenia purpura (TTP)
● Hemolytic-uremic syndromes (HUS)
● Disseminated intravascular coagulation (DIC)
● Thrombocytopenia associated with antiplatelet alloantibodies
● Immune thrombocytopenia (ITP)
In these conditions, platelet transfusion is typically reserved for life-threatening bleeding. This is because
platelet transfusion in this setting is often less effective (due to platelet consumption, eg, DIC) or associated
with clinical worsening (due to additional thrombosis, eg, TTP). Transfusion under specific clinical conditions
such as these is discussed separately. (See "Clinical and laboratory aspects of platelet transfusion therapy",
section on 'TTP or HIT' and "Clinical and laboratory aspects of platelet transfusion therapy", section on 'Immune
thrombocytopenia (ITP)' and "Management of heparin-induced thrombocytopenia", section on 'HIT with
bleeding' and "Acquired TTP: Initial treatment", section on 'Bleeding/platelet transfusion'.)
Platelet preparations — Platelets may be prepared for transfusion in a variety of ways (see "Clinical and
laboratory aspects of platelet transfusion therapy", section on 'Platelet collection'):
● Pooled concentrates from whole blood – Platelets may be separated from the other components of whole
blood by sequential steps that involve centrifugation at different speeds. While this technique is less
expensive than the alternative, more donors are required because the yield is lower. Six to 10 donors may
be required per platelet transfusion.
● Single donor apheresis concentrates – Platelets may also be obtained by apheresis, a procedure in which
the whole blood from a donor passes through a device that separates and collects the platelets, then
returns the remainder of the whole blood to the patient. This technique is more expensive, but the yield is
high and fewer donors are necessary. Only one donor is required per platelet transfusion.
Small amounts of donor erythrocytes, leukocytes, and plasma are transfused along with platelets, which may
sensitize the recipient and make subsequent red cell transfusions more difficult. ABO matching of platelets and
recipients is not essential, but it is preferred because ABO-incompatible platelets may have shortened survival
and incompatible donor plasma may produce a positive antiglobulin test and a small degree of hemolysis (acute
hemolytic reactions cannot occur). Rh-negative women of childbearing age should receive only Rh-negative
platelets, unless none are available. In those situations, they may be given Rh-positive platelets along with a
dose of Rh immune globulin appropriate for the amount of red blood cell (RBC) contamination.
Platelet response — Each unit of transfused platelets should increase the platelet count by 5 to 10 X 103
platelets/microliter in an average 70 kg adult. Thus, a transfusion of six units of platelets can be expected to
increase the platelet count by 30 X 103 platelets/microliter. Platelet destruction may decrease the response to a
platelet transfusion. When the platelet destruction is due to the presence of alloantibodies, single donor
platelets and HLA-matched platelets may be more effective. (See "Clinical and laboratory aspects of platelet
transfusion therapy", section on 'Ordering platelets'.)
COMPLICATIONS — A number of complications may result from transfusions of red blood cells (RBCs),
plasma, or platelets. Most of the complications increase in frequency and/or severity with greater transfusion
volumes. This section reviews the acute complications of blood product transfusions. The infectious risks are
discussed elsewhere. (See "Transfusion-transmitted bacterial infection" and "Risk of HIV from blood
transfusion".)
Immunologic reactions — Immunologic complications of blood product transfusions include acute hemolytic
reactions, delayed hemolytic reactions, febrile reactions, allergic reactions, acute lung injury, posttransfusion
purpura, and immunomodulation [2,16,43] (see "Immunologic transfusion reactions"):
● Acute hemolytic reactions – Acute hemolytic reactions (ie, the destruction of donor erythrocytes by
preformed recipient antibodies) are estimated to occur in 0.016 percent of red blood cell transfusions. Fatal
acute hemolytic reactions are estimated to complicate 0.003 percent of red cell transfusions and are almost
always the result of ABO incompatibility; clerical errors or improperly performed typing and crossmatching
are usually to blame. Acute hemolytic reactions present with pain at the infusion site, fever, chills, back and
substernal pain, mental status changes, dyspnea, hypotension, elevated jugular venous pressure,
cyanosis, or a bleeding diathesis due to disseminated intravascular coagulation. In the anesthetized and/or
critically ill patient, these reactions may be difficult to detect and should be suspected when unexplained
hypotension, hemoglobinuria, or a bleeding diathesis occurs during or shortly after transfusion. When an
acute hemolytic reaction is suspected, the transfusion should be stopped immediately and blood samples
collected for free hemoglobin, haptoglobin, and Coombs' testing. Crystalloid infusion to maintain the urine
output above 100 mL/h should be given, and other measures to protect against possible pigment
nephropathy (eg, mannitol, alkalinization of urine) should be considered. (See "Hemolytic transfusion
reactions", section on 'Acute hemolytic reactions'.)
● Delayed hemolytic reactions – Delayed hemolytic reactions are more common than acute hemolytic
reactions (approximately 0.025 percent of transfusions). They are often mild and may be undetected.
Patients who are pregnant or have received prior transfusions are at the greatest risk. Hemolysis of donor
erythrocytes is gradual and less severe than with acute hemolytic reactions, but may produce jaundice,
hemoglobinuria, and a falling hemoglobin concentration. Up to 35 percent of patients are asymptomatic.
Delayed hemolytic reactions generally require no specific therapy, but the compatibility of future
transfusions is altered because the reaction indicates that new alloantibodies are present. (See "Hemolytic
transfusion reactions", section on 'Delayed hemolytic reactions'.)
● Febrile nonhemolytic reactions – Febrile nonhemolytic reactions occur in up to 7 percent of red blood cell
transfusions. They are the consequence of antileukocyte antibodies (induced by previous blood exposure)
acting on donor leukocytes and/or the accumulation of cytokines in stored blood components. These
reactions are self-limited and patients are not at increased risk for repeat febrile nonhemolytic reactions
with future transfusions. Diagnosis requires that hemolysis be excluded, since both hemolytic and
nonhemolytic transfusion reactions manifest fever. Transfusions complicated by febrile nonhemolytic
reactions may be completed with antipyretics administered as needed. Future reactions may be avoided by
using leukoreduced blood components. (See "Immunologic transfusion reactions", section on 'Febrile
nonhemolytic reactions'.)
● Allergic reactions – Allergic reactions result from the infusion of an antigen to which the patient has
preexisting antibodies. Such reactions do not require previous blood exposure. The severity can range
from mild urticaria to anaphylaxis. Severe reactions require that the transfusion be stopped immediately.
Epinephrine may be required for hemodynamic support and to relieve bronchospasm. The use of extra-
washed cells for future transfusions may reduce recurrences. (See "Immunologic transfusion reactions",
section on 'Anaphylactic transfusion reactions' and "Immunologic transfusion reactions", section on
'Urticarial (allergic) reactions'.)
A subset of allergic transfusion reactions occurs in IgA deficient patients (approximately 0.13 percent of the
American population). Such patients may form IgE antibodies to IgA after being initially exposed to a blood
product and then proceed to develop anaphylaxis upon rechallenge with an IgA-containing blood product.
This possibility should be considered if dyspnea, bronchospasm, and hypotension occur in the absence of
fever after only a few milliliters of a blood product have been infused. For future transfusions, such patients
can be transfused with blood products that have been extra washed to remove any residual IgA. (See
"Immunologic transfusion reactions", section on 'Management and prevention of urticarial reactions'.)
● Immunomodulation – The immunosuppressive activity of allogeneic blood transfusion (transfusion-related

immunomodulation, TRIM), and its possible reduction with the use of leukoreduction is discussed
separately. (See "Leukoreduction to prevent complications of blood transfusion", section on
'Immunosuppression'.)
Volume overload — Infusion of any blood product will expand the intravascular volume, which has the
potential to cause pulmonary edema. This is particularly common among recipients who have diminished
cardiac or renal function. Fresh frozen plasma is particularly prone to causing pulmonary edema because it is
hyperoncotic, thereby promoting the movement of fluid from the interstitial to the intravascular space.
Hypothermia — Blood products that are stored at cold temperatures can produce profound hypothermia if they
are rapidly infused due to severe bleeding. Decreasing the core body temperature to below 32 to 35ºC (90 to
95ºF) can produce cardiac irritability and coagulation abnormalities. It can also cause peripheral
vasoconstriction, which limits tissue perfusion. Hypothermia should be prevented by using an external blood
warmer to infuse blood and other intravenous fluids. However, if it occurs, it may be corrected by rewarming
measures while maintaining an ambient temperature of 27ºC (80ºF) or greater. (See "Accidental hypothermia in
adults", section on 'Rewarming'.)
Coagulopathy — Coagulopathy may develop in patients who require significant packed red blood cell
transfusions (PRBCs), and is thought to be due to hemodilution from resuscitative fluids, and acidosis from
shock-induced tissue hypoxia. During resuscitation, when blood loss is matched by fluid and blood
replacement, the development of a coagulopathy is not predicted by estimations of blood loss or the number of
transfusions administered. During hemorrhagic shock, to limit the contributions of hemodilution and acidosis
from tissue hypoxia, data supports an approach that limits crystalloid resuscitation and provides replacement of
blood products approximating a 1:1:1 ratio of PRBCs, fresh frozen plasma (FFP), and platelets [34,44-53]. This
coagulopathic effect of massive transfusions is discussed in detail separately. (See "Massive blood transfusion",
section on 'Trauma'.)
Citrate toxicity — Citrate that is present in stored blood products may not be immediately metabolized when
massive amounts of blood are given. This can produce two complications: metabolic alkalosis (since
metabolism of the citrate generates bicarbonate) and a reduction in the plasma concentration of ionized calcium
(due to the calcium forming complexes with citrate). Ionized hypocalcemia can lead to tetany, myocardial
dysfunction, and/or hypotension.
To prevent this problem, calcium can be administered prophylactically during massive blood transfusions using
the following regimens. Ten to 20 mL of 10 percent calcium gluconate may be given intravenously per 500 mL
of blood product infused. Alternatively, 2 to 5 mL of 10 percent calcium chloride may be given intravenously per
500 mL of blood product infused. Ideally, the ionized calcium concentration should be monitored in order to
avoid administering too much calcium and inducing hypercalcemia. The calcium and blood products should be
administered into different veins to prevent clotting of the infused blood product. (See "Massive blood
transfusion", section on 'Complications of citrate infusion'.)
Acute lung injury — Alloreactive plasma antibodies or biologically active lipids contained within many blood
products (eg, red blood cell preparations, fresh frozen plasma or platelets) can lead to the agglutination and
activation of leukocytes, which may result in acute lung injury and noncardiogenic pulmonary edema (ie,
transfusion-related acute lung injury [TRALI]). Clinical findings range from mild increases in oxygen
requirements to severe acute respiratory distress syndrome (ARDS). The full extent of pulmonary dysfunction
may not manifest for hours to days after the transfusion was administered. (See "Transfusion-related acute lung
injury (TRALI)".)
Posttransfusion purpura — Posttransfusion purpura is a rare disorder in which thrombocytopenia develops

approximately 7 to 10 days after transfusion. It is the result of persons who lack the platelet antigen HPA-1a
(PlA1) becoming sensitized to the antigen when they are transfused with platelets expressing the protein. They
may subsequently destroy transfused platelets via an induced alloantibody, as well as their own platelets
through an undefined mechanism. Patients with this complication should receive only washed or HPA-1a
negative blood products and may benefit from treatment with high dose intravenous immunoglobulin. (See
"Immunologic transfusion reactions", section on 'Post-transfusion purpura'.)
SUMMARY AND RECOMMENDATIONS
● Transfusion of blood products is common in the intensive care unit (ICU). It has been estimated that
greater than 40 percent of patients receive one or more red blood cell transfusions while in the ICU. (See
'Introduction' above.)
● Indications for the transfusion of packed red blood cells in critically ill patients include acute hemorrhage
with hemodynamic instability (ie, hemorrhagic shock), acute hemorrhage with inadequate oxygen delivery,
and a hemoglobin concentration of <7 g/dL. High risk populations, such as those patients with acute
myocardial infarction may have higher thresholds. The transfusion may be performed using packed red
blood cells, whole blood, or salvaged autologous blood. The transfusion of one unit of packed red cells can
be expected to raise the hematocrit by roughly 3 percent and the hemoglobin by approximately 1 g/dL.
(See 'RBC indications' above and 'RBC preparations' above and 'RBC response' above.)
● Indications for transfusion of plasma in critically ill patients are less well established than the indications for
red blood cell transfusion. Examples of clinical situations in which plasma transfusions are often
administered include the following: active bleeding in the setting of known or strongly suspected
coagulation abnormalities, massive transfusion of packed red blood cells, prior to invasive and surgical
procedures for which there is a high risk of bleeding complications if the patient has a potentially significant
abnormality of their coagulation tests, and prior to invasive procedures for which there is a low risk of
bleeding complications if the patient has severely abnormal coagulation tests. (See 'Plasma indications'
above.)
● Plasma preparations available for transfusion include fresh frozen plasma, thawed plasma, cryoprecipitate,
factor concentrates, and liquid plasma. Patients with severe coagulopathy due to factor deficiencies are
more likely to see significant improvement of their coagulopathy than patients with mild factor deficiencies.
(See 'Plasma preparations' above and 'Plasma response' above.)
● Indications for the transfusion of platelets in critically ill patients include a platelet count <10 X 103
platelets/microliter; a platelet count <50 X 103 platelets/microliter in a patient who is actively bleeding,
scheduled to undergo an invasive procedure, or has a qualitative intrinsic platelet disorder; a platelet count
<100 X 103 platelets/microliter in a patient who has a central nervous system injury or multisystem trauma;
and, patients with a normal platelet count who have ongoing active bleeding and a reason for platelet
dysfunction, such as a congenital platelet disorder, chronic aspirin therapy, or uremia. Platelet transfusions
are contraindicated in the settings of heparin-induced thrombocytopenia (HIT), thrombotic
thrombocytopenia purpura (TTP), hemolytic-uremic syndromes (HUS), and disseminated intravascular

coagulation (DIC), unless life-threatening hemorrhage is present. (See 'Platelet indications' above.)
● Platelets may be prepared for transfusion as pooled concentrates from whole blood or single donor
apheresis concentrates. Each unit of transfused platelets should increase the platelet count by 5 to 10 X
103 platelets/microliter in an average 70 kg adult. (See 'Platelet preparations' above and 'Platelet response'
above.)
● Acute complications of blood product transfusions include immunologic reactions (eg, acute hemolytic
reaction, delayed hemolytic reaction, febrile nonhemolytic reaction, and immunomodulation), volume
overload, hypothermia, coagulopathy, citrate toxicity, acute lung injury, and posttransfusion purpura. (See
'Complications' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Nilam Mangalmurti, MD,
who contributed to an earlier version of this topic review.
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Topic 1615 Version 25.0


Use of Blood Products in The Critically Ill - UpToDate

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Authors: Addison K May, MD, John P Reilly, MD, MSCE

RED BLOOD CELLS

● Acute hemorrhage with hemodynamic instability (ie, hemorrhagic shock).

● Hemoglobin concentration of <7 to 8 g/dL, depending on patient characteristics [6,7].

RBC alternatives — Erythropoietin is an endogenously produced hormone that stimulates erythropoiesis,

● Intravenous immunoglobulin – Intravenous immunoglobulin is the purified immunoglobulin fraction of

● Heparin-induced thrombocytopenia (HIT)

● Thrombotic thrombocytopenia purpura (TTP)

● Hemolytic-uremic syndromes (HUS)

● Disseminated intravascular coagulation (DIC)

● Thrombocytopenia associated with antiplatelet alloantibodies

● Immune thrombocytopenia (ITP)

● Immunomodulation – The immunosuppressive activity of allogeneic blood transfusion (transfusion-related

Posttransfusion purpura — Posttransfusion purpura is a rare disorder in which thrombocytopenia develops

SUMMARY AND RECOMMENDATIONS

thrombocytopenia purpura (TTP), hemolytic-uremic syndromes (HUS), and disseminated intravascular

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Topic 1615 Version 25.0

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