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Currently, donated blood products are not screened for
Dengue in the United States [46] nor most other developed
countries due to the general mildness of disease. This may
change over the coming decades as mosquito grounds expand
and cases become more prevalent.
Like Dengue, Zika virus infection initially begins with an
asymptomatic viremia that usually results in a mild u-like
illness. Infection can result in a Guillian Barre-like syndrome
or can cause miscarriage or congenital defects of pregnancy
[42, 47]. Transmission may occur via mosquito, sexual contact, and blood transfusion. The FDA currently requires
nucleic acid amplication testing (NAT) or the use of
pathogen- reduced products in an attempt to limit the transmission risk [46].
Babesia Species
Babesiosis is a tick-borne protozoan illness endemic to the
Northeastern and Midwestern United States [42]. Clinical
manifestations range from asymptomatic to potentially fatal
severe hemolytic disease. The most common species identied in the United States is Babesia microti. All known
Babesia species can be transmitted through tick bite and red
blood cell transfusion. The FDA recommends selective testing of blood donations for Babesia parasites in endemic
regions. RNA NAT donor screening assays are currently
available for testing, but only identify a limited number of
Babesia species, including B. microti [42, 46].
Creutzfeldt–Jakob Disease (CJD)
CJD is a fatal neurodegenerative spongiform encephalitis
resulting from abnormally folded proteins (prions). The
majority of cases are due to sporadic mutations, with genetic
and iatrogenic causes making up the remainder (6–16% of
cases combined) [48]. Transmission has been identied in
certain forms of transplant including corneal and human dura
mater grafts, from the use of previously contaminated neurosurgical equipment or the use of human pituitary growth factor [7]. There have been no identied cases of CJD
transfusion-transmission, but the risk remains theoretical
[46]. Since 2000, the FDA has recommended permanent
donor deferral based on risk factor screening for CJD as there
are no commercially available tests or treatments [42, 48].
Pathogen Reduction Technology (PRT)
The FDA recommends PRT to aid in the reduction of infectious risk of some blood products. Blood donor screening
and testing reduce the risk of transfusion-transmitted infections, but cannot address all asymptomatic yet viremic infec-
tion windows or screen for the disease in the absence of a
developed test. It is also logistically and scally unrealistic
to screen every donor unit for every known infectious risk
[49]. PRT, however, reduces the need for extensive testing by
eliminating bacteria and certain virus reproduction.
PRT uses a photochemical compound that is excited by
light to cause nucleic acid cross-linking [50]. This crosslinking results in the inability of a pathogen to replicate.
Babesia microti, Dengue, Zika virus, and other arboviruses
are effectively inactivated using PRT, signicantly decreasing their transmission risk [44, 50]. This treatment is also
effective in reducing the transmission risk of other known
bacteria, viruses, and protozoa [44]. Additionally, the technology disables leukocyte proliferation, reducing the need
for irradiation while still decreasing the risk of TA-GVHD
[51]. This technology may allow for the discontinuation of
some currently required infectious disease testing in the
future, helping to offset the costs associated with pathogen
reduction.
PRT is approved for use on plasma and platelet products
in the United States. Technologies for red blood cells and
whole blood unit pathogen reduction are currently in trials.
PRT has been especially benecial in reducing transmission
risk in platelet products. Due to platelet storage conditions
(20–24 °C with continuous agitation for 5–7 days (see
Chapter 3), bacterial proliferation is a known hazard.
Transfusion services are currently required to have methods
to detect or inactivate bacteria for these reasons [6]. As an
alternative, the FDA allows the use of PRT.
PRT does have its limitations. Prion diseases are not
affected by nucleic acid cross-linking and PRT is not as
effective at inactivating non-enveloped viruses [50]. PRT
platelets have lower corrected count increments following
transfusion, more frequent transfusion failures and platelet
refractoriness, and more platelet transfusions required per
patient with shorter transfusion time intervals in between.
There were no differences found in signicant bleeding or
adverse outcomes however when comparing PRT to nonPRT platelets [46].
Conclusion
Blood banking and transfusion medicine is a complex and
evolving discipline. Familiarity with red blood cell and
human leukocyte antigen (HLA) systems is essential to
understand the impact of alloimmunization in clinical settings. Transfusion practices have adapted in an era of limited
inventory. Blood donation campaigns have begun to target the
younger generations, in an attempt to reinvigorate donors and
protect long-term supplies, but an era of conservation and
limited availability may be the new norm of modern blood
banking. Clinicians who transfuse must be aware of modern
transfusion topics to include evidence-based transfusion
18
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L. Helander and C. R. Alquist
guidelines, shelf-life limitations, the use of O-positive red
blood cells and thawed group A plasma in emergency transfusions, platelet product splitting, the effect of ordering practices on product availability, and the potential impact of
emerging infections and PRT on transfusion risk. As always,
your clinical pathology and transfusion medicine colleagues
remain an available resource in this changing eld.
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Blood Component Therapy
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ChristineT.Vo andPamelaR.Roberts
3
Introduction
In the United States, the US Food and Drug Administration
(FDA) Center for Biologics Evaluation and Research sets the
standards regarding collection of blood components and
whole blood. All entities that collect, prepare, store, process,
or distribute blood products must be registered with the FDA
and inspected by them at dened intervals. Many institutions
that collect or prepare blood products also get accreditation
by the American Association of Blood Banks (AABB) since
this organization sets standards that help maintain quality
and safety of blood banking and transfusion practices. Other
parts of the world have similar entities.
Combat history and related medical care during the last
century contributed much of what we know about treatment
of trauma and principles of resuscitation and contributed to
blood banking technology. From the 1940s through 1960s,
the military program mostly used whole blood. But following the Vietnam War, interest grew in the civilian medical
arena to conserve blood and focus on treating specic component deciencies resulting in the predominance of component therapy in the 1970s–1990s [1–3]. Component therapy
allowed longer storage times and lower rates of infection. By
the mid-2000s, persistent coagulopathy was recognized as
contributing to deaths from severe trauma. [4] In 2012,
Pidcoke and colleagues published a large retrospective
cohort study of patients injured in Operation Iraqi Freedom
and Operation Enduring Freedom and reported that use of a
1:1:1 ratio of red blood cells (RBCs), platelets, and fresh frozen plasma conveyed a signicant survival benet as opposed
C. T. Vo
University of Oklahoma College of Medicine, Department of
Anesthesiology, Oklahoma City, OK, USA
e-mail: christine-vo@ouhsc.edu
P. R. Roberts (
Department of Anesthesiology, University of Oklahoma College
of Medicine, Oklahoma City, OK, USA
e-mail: pamela-roberts@ouhsc.edu
*)
to transfusion of then traditional large volumes of packed
RBCs [5]. Over the last decade, clinical studies of improved
outcomes with whole blood for hemorrhaging patients led to
renewed interest in utilizing whole blood for transfusion of
critically injured trauma patients or those with severe hemorrhaging. Massive transfusion strategies are covered elsewhere in this book. This chapter will focus on specics of
blood components derived from blood donation.
PRBCs
Provision of packed red blood cells (PRBCs) or red blood
cell (RBC) units relies on donation of blood from volunteers.
These donors rst undergo screening of their medical history
which specically addresses risk factors for infectious diseases or other complications. For example, women that have
been pregnant should be screened as they may have developed HLA antibodies and therefore convey a risk of a recipient developing transfusion associated acute lung injury
(TRALI). Then, all donated blood undergoes laboratory testing for specic infectious organisms and viruses. Details of
all elements of screening and laboratory testing are beyond
the scope of this chapter, but have led to signicant reduction
of transmission of disease via blood transfusion. However,
the risk of new emerging infections is a constant potential
threat to our blood supply, as was seen most recently with
Zika virus and West Nile virus.
Most commonly a unit of whole blood with a volume of
500–600 mL is donated and undergoes routine centrifugation to separate it into components including RBCs, platelets, and plasma. Alternatively, RBC units can be obtained
via apheresis; in the United States, about 20% of RBC units
are collected via apheresis [6]. For apheresis, a donor with an
adequate hematocrit is connected to an apheresis machine
which separates other constituents from the RBCs and
returns the other cellular and plasma constituents to the
donor. Typically, this type of apheresis will yield twounits of
© Springer Nature Switzerland AG 2021
A. D. Kaye, S. Leavitt (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_3
21
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RBCs. However, some apheresis systems can collect a single
unit of RBCs along with a unit of platelets and/or plasma.
The number of RBCs in an RBC unit from donated whole
blood will vary based on the donor’s hemoglobin level. In
contrast, apheresis units are collected in a manner that provides more standardized numbers of RBCs per unit. Both
types of RBC units provide sufcient RBCs for transfusion.
In the early 1960s, bags made of polyvinyl chloride
became available for storage of blood products, permitting
separation of collected products into components in a sterile,
closed environment. The plasticizer used in bags for RBC
storage is di-2-ethylhexylphthalate (DEHP) and it is key to
preservation of the integrity of the RBC membrane during
prolonged storage. It is believed that small amounts of DEHP
leak into the stored unit but no deleterious effects of DEHP
have been found from transfused RBCs in patients. That
said, concerns of potential exposure to DEHP from other
medical devices are extended to RBC recipients and in particular neonates who may be vulnerable to related adverse
effects of DEHP or toxic metabolites. Due to these concerns,
efforts are underway to develop an alternative plasticizer that
is also capable of stabilizing red cell membrane integrity [7].
Preservation of blood requires an anticoagulantpreservative (A-P) solution. It was a major breakthrough in
the 1940s when acid citrate dextrose was developed as the
rst A-P solution allowing storage for up to 21days. Since
then, other A-P solutions were developed: citrate phosphate
dextrose (CPD) with 21-day storage, CDP-adenine with
35-day storage, and current generation additive solutions
with 42-day storage. There are several additive formulations
used in the United States from different manufacturers
denoted as AS-1, AS-3, and AS-5. A solution similar to AS-1
is used in Europe and it is saline, adenine, glucose, mannitol
(SAGM). These additive solutions maintain the pH and other
essential parameters for RBC shelf life [6]. This has resulted
in less loss of RBC units due to being outdated. Less additive
is used than the volume of plasma that was removed resulting in a higher hematocrit and lower volume than in the original unit of whole blood. See Table3.1 for expected volumes
and hematocrits of RBCs obtained from the methods
described. Whole blood is collected into an anticoagulant
solution and the additive preservative solution is added to the
RBC units through an integral bag system soon after collection and component preparation. Apheresis-derived RBCs
undergo similar procedures depending on the apheresis
device.
Table 3.1 Practical differences of RBCs from current common
methodologies
Type of storage or additive Final volume (mL) Hematocrit (%)
CPD-adenine (CPD-A1) 225–350 65–80
AS formulations 300–400 55–65
Apheresis-derived 175–200 55–60
Table 3.2 Populations that should receive leukocyte-reduced blood
components [
History of a previous febrile nonhemolytic transfusion reaction
Undergoing cardiac surgery [
Recipients or potential recipients of solid organ or hematopoietic cell
transplants [
Acute leukemias and probably other malignancies
Chronically transfused
CMV seronegative at risk patients if they are not given seronegative
components
8]
9]
10]
Leukocytes are naturally collected along with other cellular elements during blood donation. A unit of whole blood
or packed RBCs has about 2–5 billion leukocytes and these
are believed to convey risk of adverse effects such as human
leukocyte antigen (HLA) alloimmunization, febrile nonhemolytic reactions, transmission of cytomegalovirus (CMV)
or intracellular organisms, and potentially other immunologic and inammatory mediated events. Leukocyte depletion or reduction refers to the process of ltering the blood to
remove leukocytes and can be done before storage or at the
time of transfusion. Leukoreduction prior to storage is preferred since it results in removal of more leukocytes as well
as better quality control and standardization of the process.
Such processes decrease the leukocyte load by approximately 99.9%, thereby signicantly decreasing adverse
events. Leukoreduction decreases the hemoglobin concentration by up to 15%. Some clinical populations are at higher
risk of leukocyte-related adverse reactions, so it is recommended that they receive leukocyte-reduced blood components when transfused [8] (See Table 3.2). Currently,
universal leukoreduction is a standard practice in many
developed countries. In the United States, more than 80% of
institutions provide universally leukoreduced RBCs with an
estimated 85% of these using pre-storage leukoreduction
processes [6]. When ordering transfusions, one needs to be
familiar with local processes such as leukoreduction so that
ordering for at-risk patients is clinically appropriate. If RBC
units are not universally leukoreduced, this should be specically requested for selected patients. In general, pre-storage
leukoreduction is preferable to bedside leukoreduction; bedside leukoreduction is preferable to transfusion of nonleukoreduced RBC units. Of note, leukoreduction techniques
do not prevent transfusion-associated graft versus host disease (TAGVHD) since even a small number of cells can contribute to this disorder. Susceptible patients should receive
irradiated blood to prevent graft versus host disease.
Irradiation of RBC units prior to transfusion is sufcient
to inactivate lymphocytes that can attack recipient cells in
immunologically impaired individuals resulting in
TAGVHD.All hematopoietic cells as well as other tissues
can be targets of TAGVHD.Bone marrow aplasia as well as
other fatal complications can occur from
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23
Table 3.3 Populations that should receive irradiated blood compo-
11]
nents [
Premature neonates and recipients of intrauterine or neonatal
exchange transfusion
Recipients of autologous or allogeneic hematopoietic stem cell
transplants
Individuals with any stage of Hodgkin lymphoma
Individuals receiving treatment with potent immune-suppressing
therapies (e.g., some monoclonal antibodies, antithymocyte
globulin); may include those with hematologic malignancies and
non-Hodgkin lymphoma
Individuals at risk for partial HLA-matching with the donor due to
directed donations, HLA-matched products, or genetically
homogenous populations
Table 3.4 Populations that should receive CMV-negative blood com-
ponents if they are not CMV-positive
Low birth weight neonates
Pregnant women
HIV-infected individuals
Recipients of solid organ transplants
Recipients of hematopoietic stem cell transplants
TAGVHD.Randomized trials have not been performed to
establish which patients must be given irradiated blood and
recommendations are based on observational evidence and
attempts to predict the degree of immunosuppression of populations. Table3.3 lists patient populations for which irradiated components are recommended; some of these are
lifelong needs while others may be time-limited [11]. In the
United States, each hospital typically develops its own policy regarding which patient populations should be given irradiated products [12]. Society guidelines should be consulted
for specic recommendations.
Cytomegalovirus (CMV) seronegative components have
tested negative for the presence of CMV using antibody testing. Enough units are typically tested for CMV so that an
adequate supply of CMV-negative units is available to be
administered to individuals at risk of clinically serious CMV
infection (See Table3.4). In the general adult population, at
least 40% have been exposed to CMV; however, exposure
varies geographically. Individuals that are immunocompetent generally do not need CMV-negative blood as they can
mount their own immune responses. However, immunocompromised individuals that are CMV-negative can develop
serious CMV infections if given a unit of CMV-positive
blood. Conversely, if they are already CMV-positive, they
can likely receive CMV-positive units [6]. Of note, leukoreduction is considered to be of equivalent safety to administering CMV-negative components for individuals at risk of
severe CMV infections and may be an alternative to transfusion of seronegative units.
RBC units must be stored at controlled refrigeration temperatures of 1–6°C to preserve viability and prevent bacterial growth. During transport between facilities such as from
a blood collection facility to a hospital, temperatures of
1–10°C must be sustained. Similarly, during transport from
a blood bank to a patient care area for transfusion, these
same transport temperatures must be maintained. Changes to
RBCs during storage include depletion of ATP, membrane
changes, oxidative damage to lipids and proteins, leakage of
potassium, and loss of the ability to change shape for ow in
the microvasculature.
In the United States, RBCs can be stored up to 42days;
average storage of RBC units is estimated to be between
15–19 days [
6]. Numerous randomized clinical trials have
evaluated whether longer storage times result in more recipient morbidity or not. These have demonstrated similar outcomes from transfusion of fresh compared to longer or
standard issue RBCs. These include the ARIPI trial (Age of
Red Blood Cells in Premature Infants), the TOTAL trial in
children (Tissue Oxygenation by Transfusion in Severe
Anemia with Lactic Acidosis), the RECESS trial in cardiac
surgery patients (Red Cell Storage Duration Study), and the
TRANSFUSE trial (Standard Issue Transfusion versus
Fresher Red-Cell Use in Intensive Care) [
13–16].
Additionally, a meta-analysis by Alexander et al. also conrmed lack of clinical benet of use of RBC units with
shorter storage times [17].
RBC units can be frozen in 40% glycerol and are approved
by the United States FDA and AABB to be stored at -80°C
for up to ten years. The major reasons for freezing RBC units
is to maintain a supply of very rare blood group phenotypes
(e.g., Bombay phenotype) or for those who have developed
numerous alloantibodies directed against common RBC
blood group antigens [18]. A randomized trial of 57 trauma
patients comparing refrigerated RBC units to frozen then
deglycerolized RBC units did not demonstrate signicant
differences in effects on hematocrit, thromboelastography
parameters, or clinical outcomes [19]. However, preparing
RBCs for freezing, thawing, then removing the glycerol is
time consuming and thus delays transfusion as well as
increases the costs, so is not utilized unless necessary.
Administration of RBC units should start with informed
consent except in emergency situations where consent cannot be immediately obtained. Care must be taken to assure
the intended unit is given to the intended recipient to prevent
transfusion reactions (e.g., acute hemolytic transfusion reactions due to ABO mismatch). Data do not support routine pre
medication with acetaminophen or antihistamines for prevention of allergic transfusion or febrile nonhemolytic reactions. The unit should be visually inspected for any
abnormalities. RBC units must be transfused through a 170–
260 micron lter to remove clots or aggregates of cellular
components. Patients at risk of hypothermia or those with
autoimmune cold-induced hemolysis can receive blood
warmed to near body temperature but no higher than 40°C
as heat can cause hemolysis.
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C. T. Vo and P. R. Roberts
As a general rule, uids containing calcium should not be
administered through the same tubing concurrently with
RBCs as the calcium may chelate the citrate and thus overcome the anticoagulant effect of citrate and clotting may
occur in the tubing. Compatible uids for concurrent transfusion include 0.9% sodium chloride, plasma, and albumin.
Generally, use of Ringer’s lactate is prohibited as it contains
calcium, although some have advocated it for emergency
trauma cases due to immediate needs of therapy [6]. The
safety of this practice has not been veried and we recommend the safety of avoiding Ringer’s lactate in this circumstance. Dextrose containing intravenous uids should not be
administered through the same tubing concurrently as the
dextrose can be taken up rapidly by the RBCs which will
then uptake water and then lyse. When transfusing via a
multi-lumen central line, other meds may be administered
simultaneously via other lumens. When concurrently administered with RBC units, it can be challenging to distinguish
potential adverse effects of medications versus transfusion
reactions. If the same lumen is to be used for medications
before or after a transfusion, the lumen should be ushed
with normal saline both before and after a medication.
RBC units should be given at rates that are efcient but
that do not increase risk of volume overload. Typically, a rate
of 1–2mL/min over the rst 15minutes followed by a faster
rate as tolerated is adequate. One RBC unit should be transfused over no more than 4hours. For patients at higher risk
of circulatory overload, slower rates using partial units may
be indicated to avoid complications. Concomitant diuretics
may be helpful in preventing circulatory overload in some
patients.
Indications for RBC unit transfusions include symptomatic anemias and acute blood loss. Physiologic triggers
include shock with marginal hemoglobin levels, orthostatic
hypotension, and evidence of end-organ damage from inadequate tissue oxygenation to maintain vital organ function.
For example, symptomatic anemia may manifest as dyspnea
or fatigue with exercise. Anemia itself warrants investigation
into its cause, so appropriate diagnostic studies and treatment can be administered. Historically, RBC transfusion was
guided by a “10/30 rule” which aimed to maintain a hemoglobin of 10g/dL and a hematocrit of 30%. Along with this
goal, it was a historic standard practice to transfuse two or
more RBC units per transfusion [20]. Over the last 20years,
clinical concerns of risks of transfusions led to recognition of
the need to establish indications that provide greater benet
than risk to patients receiving RBC unit transfusions.
Multiple randomized trials in varied populations demonstrated either noninferiority or superiority of restrictive
transfusion strategies (aimed for hemoglobin levels of 7–8g/
dL) versus more liberal ones [21]. The Choosing Wisely
Campaign started in the United States in 2012 and now
includes participating clinical groups from over 20 countries
on ve continents. Single unit transfusions followed by reassessment and treating iron deciency anemia with iron
instead of transfusion in patients that are hemodynamically
stable are both strategies promoted in the Choosing Wisely
recommendations from the American Society of Hematology,
the AABB, and the Canadian Society for Transfusion
Medicine [22]. Further, it is recommended that a restrictive
threshold of 7–8g/dL hemoglobin be used for most hospitalized stable patients without evidence of inadequate tissue
oxygenation. For patients with pre existing cardiovascular
disease, they note that evidence supports a threshold of 8g/
dL.The recommendations also make the point that a decision to transfuse should include assessment of symptoms as
well as hemoglobin level.
An international consensus statement recommends that
anesthesia providers take a lead role with pre operative assessment using strategies aimed at reducing need for peri operative transfusions starting with assessment and treatment of
pre operative anemia. They even recommend delay of major
non urgent surgery to allow diagnosis and treatment of anemia and iron deciency [23]. A recent meta-analysis by
Chong et al. compared studies using restrictive vs liberal
transfusion strategies for critically ill vs surgical patients [24].
These authors reported that restrictive strategies led to better
outcomes which included reduced risk of stroke, transfusion
reactions, packed RBC exposure, hospital length of stay, and
30-day mortality in critically ill patients. For surgical patients,
the restrictive compared to a liberal strategy was associated
with an opposite direction effect on mortality which was
reported as a potentially increased risk or no difference
between strategies. Both populations were exposed to lower
RBC units with restrictive strategies. Caution should be taken
at over extrapolation of this meta-analysis as future studies
are required to target specic goals for different perioperative
stages of care as well as varied surgical populations.
Improved donor questionnaires and sophisticated laboratory screenings for infectious diseases has signicantly
reduced infectious complications of transfusions.
Noninfectious serious complications of blood transfusions
are now more common than infectious ones [25]. Transfusion
reactions include febrile, hemolytic, septic, allergic, urticarial, and anaphylactic reactions. Other complications such as
mistransfusion, TRALI, transfusion-associated circulatory
overload (TACO), TAGVHD, alloimmunization, iron overload, and metabolic derangements to name a few.
Complications of RBC transfusions are covered in detail
elsewhere in this book. Some strategies to reduce complications are obvious such as avoiding unnecessary transfusions
and others employ use of electronic systems to help assure
patient identication and appropriate blood matching to the
patient [26]. Appropriate use of RBC units and attention to
details of administration are vital to provide safe delivery of
this vital resource to patients.
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Fresh Frozen Plasma
Fresh Frozen Plasma (FFP) is obtained from whole blood or
apheresis donations using a centrifugal process. Citratecontaining anticoagulants and preservatives are added to
whole blood prior to separation into its components to
increase its shelf life and reduce biochemical changes. Blood
separates into its components via centrifugation, with plasma
precipitating to the top, leukocytes and platelets to the middle, and RBCs to the bottom. Essentially, platelet-rich plasma
is expressed after the rst centrifugation step. It is further
separated into plasma and platelet concentrates with a second, higher speed centrifugation. Within eight hours of collection, plasma is immediately frozen to –18 °C or colder
and stored for up to one year. FFP can be further processed
to produce cryoprecipitate [27]. When plasma is frozen
greater than 8hours from collection, but less than 24hours,
this is termed plasma frozen within 24hours of phlebotomy
(PF24). The clinical efcacy of clotting factors in PF24 are
similar to FFP except for a mild decrease in the labile clotting factors VIII and protein C when thawed [28]. To prevent
contamination, FFP is thawed at 33 °C and 37 °C in a
vacuum- sealed overwrap bag. Once thawed, FFP should be
transfused within fourhours as long as maintained in temperatures at approximately 22±2°C. If transfusion is not
going to be immediate, thawed FFP may be stored up to a
maximum of 120hours at 4±2°C [29].
Often, when clinicians order FFP, there is not a clear designation of the “type” of plasma being released from the
blood bank. In fact, most plasma that is transfused is PF24
and not actually FFP. Studies have shown that integrity of
most clotting factors are maintained in PF24. However, the
clinician should keep in mind that factor VIII is 15–20%
lower in thawed PF24 compared to FFP but factors V, VII,
and VIII decrease over time in thawed plasma [28, 30]. The
drop in factor VIII can be greater than 50%, and the drop in
factor V and VII can be by approximately 20% activity by
day 5 [31]. FFP can also be processed with solvent detergents or methylene blue to reduce pathogen contamination.
But doing so results in loss of clotting factors and natural
anticoagulants [32].
FFP contains the following: all coagulation factors
except platelets, factors II, V, VII, VIII, IX, X, XI.FFP contains brinogen (400–900 mg/unit), albumin, protein C,
protein S, antithrombin, tissue factor pathway inhibitor, and
vWF [33]. A standard dose of 10–20mL FFP/kg (4–6units
FFP in adults) will raise factor levels by approximately
20%. An increase of approximately 10% of several factors is
enough to effect hemostasis. When accounting for brinogen levels of at least 75–100mg/dL with no other inhibiting
agent such as heparin, increasing coagulation factors to
25–30% of normal is enough to obtain hemostasis. Infusing
approximately one-fourth to one-third of the patient’s total
Table 3.5 Transfusion reactions and associated signs and symptoms
Reaction Signs and symptoms
Acute hemolytic
transfusion
reaction
Allergy Urticaria, hives, ushing
Anaphylaxis Dyspnea, wheezing, coughing, nausea/vomiting,
TAC O Acute dyspnea, hypoxia, pulmonary edema,
TRALI Sudden dyspnea, pulmonary edema, hypoxemia,
Jaundice, hemoglobinuria, hypotension,
disseminated intravascular coagulation, feeling
of impending doom, fever, and chills
hypotension, loss of consciousness,
cardiopulmonary collapse
possible elevated systolic pressure, enlarged
heart, increased BNP, signicant response to
diuretic
bilateral pulmonary inltrates, occurs within
6hours of transfusion
plasma volume, or 10–15mL/kg, should achieve this effect
[34].
Fresh frozen plasma (FFP) is often used to treat conditions in which a quantitative or qualitative decit in coagulation factors is present. This includes disseminated
intravascular coagulation, severe liver disease, and massive
bleeding/trauma. It can also be used in the reversal of vitamin K deciency and warfarin-induced coagulopathy if sufcient time for vitamin K repletion is not an option. This
could be due to urgent surgery in which massive blood loss
is anticipated, trauma or hemodynamic instability. FFP may
be indicated in rare coagulation disorders when a specic
factor concentrate or recombinant product is not readily
available.
Transfusion of any blood product is not without risks.
ABO compatibility must be considered due to the presence
of alloantibodies in plasma. Failure to screen for ABO compatibility could result in an acute hemolytic transfusion reaction. Other reactions include allergy, anaphylaxis, TACO,
and TRALI [35]. Common symptoms of transfusion reactions are shown in Table3.5. TRALI is now the leading cause
of transfusion associated mortality in the United States, with
FFP the most frequently implicated blood product [36].
Occurrence of infection is low but not zero. Processes to
reduce these risks include nucleic acid testing, donor-retested
plasma, or pathogen-inactivated/reduced plasma.
Platelets
Platelets can be obtained from whole blood donations by two
different methods. Platelet-rich plasma is preferred in the
United States whereas the buffy coat method is primarily
utilized in Europe. To generate platelet-rich plasma, whole
blood undergoes a low-speed centrifugation or “soft” spin
that separates the RBCs from the platelet-rich plasma. The
platelet-rich plasma then undergoes a higher centrifugation
or “hard” spin to separate platelets from plasma. In the buffy
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coat method, whole blood is subjected to high-speed centrifugation to separate red blood cells, plasma, and a buffy
coat that contains mostly platelets with a small amount of
RBCs and leukocytes. Buffy coats from 4–6 whole blood
donations are then added to a unit of plasma from one donation. After that, a low-speed centrifugation yields plateletrich plasma which is then removed for potential transfusion.
Platelets are obtained from whole blood or apheresis in a
similar fashion to FFP. Each donation of approximately
500mL of whole blood is collected in a citrate preservative
solution within 8hours of donation. From 500mL of whole
blood, approximately 5–7×1010 platelets are extracted as a
volume of about 50mL in 50–70 mL of plasma for a total
volume of about 100–120mL. The plasma helps maintain
the pH greater than or equal to 6.2.
A single unit of platelets from one unit of whole blood is
not enough to raise platelet counts to hemostatic levels in
clinical practice. Typically, 4–6units are pooled from multiple donors to provide adequate platelet counts for clinical
purposes. Alternatively, apheresis uses specialized equipment that selectively removes plasma and platelets from a
single donor and returns RBCs and leukocytes to the donor.
This allows extraction of approximately 200mL of platelets
suspended in about 200mL of plasma from one donor. A unit
of pooled platelets or one unit of apheresis platelets is
expected to raise the platelet count by approximately 30,000–
50,000/microL in a 70kg adult. In an infant, administration
of 10–15mL platelets/kg should increase the platelet count
by 50,000–100,000/microL.
Platelets are stored at room temperature (20–24°C) with
continuous gentle agitation to extend their clinical lifespan.
Platelets that are cooled to 4°C have shown poor survival
due to an irreversible clustering of alpha subunits of glycoprotein Ib on the platelet surface. Chilled platelets undergo
rapid clearance by phagocytosis from the circulation when
transfused. Once collected, platelets must be transfused
within vedays of collection. Once platelets are processed
via pooling or washing, it must be transfused within
fourhours. A standard 170–260 micron lter should be used
to transfuse platelets since a smaller lter could remove
platelets from the transfusion. Caution should be taken to
avoid infusing platelets through extreme heat (i.e., temperature greater than 43°C) due to the risk of altering cytoskeletal membrane components and impairing aggregation [37].
There is not much data available to recommend for or against
infusion through standard OR warming devices.
Platelet transfusion is indicated when platelet dysfunction
exists or in the presence of signicant thrombocytopenia.
When a patient with thrombocytopenia is actively bleeding,
transfusion to maintain platelet counts above 50,000/microL
is recommended for most circumstances. Recommended
platelet counts for safe performance of common perioperative procedures are shown in Table3.6. Platelets may also be
transfused prophylactically in preparation for invasive proce-
Table 3.6 Recommended platelet counts for common perioperative
procedures
Type of procedure
Major surgery and/or actively
bleeding
Neurosurgery, ocular, and
cardiopulmonary bypass
Central line placement 20,000 [
Epidural placement 80,000 [
Pre-procedure platelet count
goal/microL
39]
50,000 [
100,000 [
39]
40]
41]
dures. Platelet transfusion is contraindicated for both thrombotic thrombocytopenic purpura and heparin-induced
thrombocytopenia due to risk of further thrombosis and associated morbidity [38].
Platelet transfusions have risks for complications.
Bacterial contamination is highest with platelet transfusions
compared to other blood components due to storage conditions. The rate of bacterial contamination of platelets is
approximately1:2000 as compared to RBC units at 1:30,000
[42]. Because platelets contain plasma, the risks are similar
between components with regards to TRALI, TACO, allergic
and anaphylactic reactions. Post transfusion purpura is
unique to transfusion of platelets or platelet containing products. Lingering leukocytes may cause febrile non hemolytic
transfusion reactions, alloimmunization, and TAGVHD [43].
Although ABO compatibility does not apply to platelets,
consideration should be given to RhD-negative women of
childbearing age due to the risk for development of alloimmunization to RBC antigens that are potentially present in
platelet units. If ABO compatibility cannot be attained due to
scarcity of resources, then Rho(D) immune globulin should
be given after transfusion [44].
Cryoprecipitate
Cryoprecipitate contains specic products from fresh frozen
plasma. These include brinogen, factor VIII, factor XIII,
von Willebrand factor, and bronectin. Each unit of cryoprecipitate is expected to raise brinogen concentration by
7–10mg/dL.Cryoprecipitate is typically pooled to include
either ve or ten units. Normal brinogen levels range from
150 to 400 mg/dL. The minimum level of brinogen to
maintain hemostasis is 100 mg/dL. Although the recommended goal is higher at 150–200 mg/dL for individuals
with signicant risks of bleeding, such as intracerebral hemorrhage [45].
Cryoprecipitate is prepared by thawing FFP at 4°C to precipitate out the higher molecular weight proteins, called cryoproteins. The thawed and cooled FFP is then separated by
centrifugal forces and after removal of the supernatant the
cryoprecipitate is stored with a small volume of plasma
at –20 °C [46]. One unit (~10–20 ml) of cryoprecipitate is
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27
produced from one unit of FFP (~250 ml). Cryoprecipitate
can be stored for up to 12 months. It should be noted that
cryoprecipitate cannot be derived from PF24 due to the
decreased availability of labile clotting factors in PF24 as
compared to FFP.In particular, factor VIII is mild to moderately reduced in PF24. If transfusion is indicated, cryoprecipitate takes approximately 10–30 minutes to thaw. And
once a unit has been thawed, it must be transfused within
six hours. If pooled with other units, it must be transfused
within fourhours.
Administration of cryoprecipitate is indicated when a
deciency in specic clotting factors VIII, XIII, vWF, or
brinogen exists. It is commonly used for acquired hypobrinogenemia states instead of inherited deciencies due to
the availability and safety of commercial brinogen concentrates, recombinant or plasma-derived factor concentrates
[47]. Currently, the use of brinogen concentrates is limited
to inherited disorders in the United States. Factor VIII and
von Willebrand’s factor are now produced as puried recombinant concentrates making cryoprecipitate dedicated to the
treatment of hypo- or dysbrogenemia, It was once thought
of as a “last resort” to treat a trauma-induced coagulopathy
but now is deployed as the desired rst component to treat
trauma resuscitative coagulopathy, especially in scenarios
where whole blood is not utilized for massive transfusions.
Fibrinogen levels are commonly low upon arrival to the
trauma emergency room. Cryoprecipitate is a part of many
massive transfusion protocols. Cryoprecipitate may also be
used in patients with liver disease, disseminated intravascular coagulation, and uremic bleeding. The decision to replace
brinogen with cryoprecipitate, brinogen concentrate, or
FFP is based on clinical judgment and availability.
Risks associated with cryoprecipitate include potential
pathogen transmission since viral inactivation can result in a
signicant decrease in available brinogen. ABO compatibility must be considered since it is suspended in plasma.
The risks are similar to those with plasma, although likely
lower depending on rate and volume infused. The process of
thawing can be a problematic rate-limiting step, especially
when massive bleeding necessitates expedient availability of
blood components [46].
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