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11 Ultrasound forBleeding Disorders
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Complications ofBlood Transfusion
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12
As any procedure in medicine, the transfusion of blood products to the patient involves benets and risks. The benets of
increased oxygen carrying capacity with the ability to deliver
oxygen to the tissue are clear in the setting of severe hemorrhage. The risks are not as clear. While patients are mainly
concerned with infectious risks, there are other risks that
must be considered by the provider.
Transfusion-Related Acute Lung Injury
Transfusion-related acute lung injury (TRALI) is an acute
lung injury that occurs within 6hours of blood transfusion;
the entity was rst described in 1951 [1]. The actual syndrome and its link to the administration of blood products
did not occur until 1983. In a case series of 3130 consecutive
blood transfusions, ve patients developed respiratory distress in close association to the transfusion [2]. The lung
injury was linked to the transfusion with term TRALI being
used. TRALI occurs in both women and men and occurs in
patients of any age, except neonates. The reason for the concern with TRALI is the signicant morbidity and mortality.
Survival from TRALI is estimated at 50%. All plasma-containing blood and blood components have been implicated in
the development of TRALI. A common theme to the cases of
TRALI is the receipt of blood products 6 hours prior to the
development of pulmonary symptoms. Other symptoms that
also may occur include fever and hypotension.
A consensus panel was convened in 2004 to establish the
criteria for the diagnosis of TRALI [3]. TRALI was dened
as a new acute lung injury that occurred during or within
6 hours of a completed transfusion that was not related to
another cause for the lung injury. While the diagnosis
requires the administration of the blood products within 6
J. Cassis (*) · R. Gaiser
University of Kentucky, Department of Anesthesiology,
Lexington, KY, USA
e-mail: Jsca246@uky.edu; Robert.gaiser@uky.edu
hours, the overwhelming majority of patients will have the
onset of symptoms within 1–2hours following the transfusion. The diagnosis was to be based upon clinical symptoms
combined with a radiographic diagnosis. The diagnostic criteria for TRALI are outlined in Table12.1. The chest x-ray
should show bilateral inltrates that may be patchy or diffuse
suggestive of alveolar or interstitial disease [4].
Possible TRALI is a diagnosis used when it is difcult to
determine whether the actual etiology of the lung injury is
TRALI or another cause of the acute lung injury [5].
Sometimes it is difcult to determine whether the lung injury
is from the blood transfusion. In patients meeting the diagnosis of TRALI but with another reason to explain the acute
lung injury, the alternative diagnosis of “possible TRALI” is
used. Possible TRALI refers to transfusion-related lung
injury in a patient with a preexisting lung injury prior to the
transfusion. This term is not universally accepted, with many
feeling that possible TRALI is simply ARDS or TRALI type
II (TRALI in a patient with risk factor for ARDS) [6].
Postmortem tissue examination of patients with TRALI
demonstrates pulmonary edema, diffuse alveolar damage,
and granulocytes in the alveoli. The pulmonary vasculature
contains neutrophil aggregates when examined postmortem.
The major nding in patients with TRALI is increased pulmonary microvascular permeability with protein in the uid.
Patients with TRALI have chest x-rays that demonstrate
bilateral inltrates that suggest cardiac failure with no evidence for cardiac causes of the ndings.
The pathogenesis is poorly understood. The most common theory for TRALI is the two hit model in the transfused
donor [1]. In this theory, a patient who had an increase in
Table 12.1 Diagnostic criteria for TRALI
1. Abrupt onset
2. No evidence of left atrial hypertension
3. Bilateral inltrates on chest x-ray
4. Hypoxemia as dened PaO2/FiO2≤300mmHg or oxygen
saturation≤90% on room air
© Springer Nature Switzerland AG 2021
C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_12
113
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Table 12.2 Risk Factors for Development of TRALI
Cardiac Surgery
Mechanical ventilation with increased peak airway pressure
Chronic alcohol use
Current smoker
End-stage liver disease
Liver transplantation
Hematologic malignancy
neutrophil responsiveness receives a stimulus from the transfusion itself. The possible risk factors (Table12.2) that may
cause the rst hit include chronic alcohol abuse, sepsis,
mechanical ventilation, shock, surgery, smoking, inammation, and uid overload. The inammatory proteins that are
elevated in patients with TRALI include interleukin-6 and
interleukin-8 as well as protein C-reactive protein. The
second hit comes from the antibodies in the transfused blood
products. In the two-hit model, a certain threshold from the
initial insult must be present in a patient who receives a sufcient amount of volume and titer of antibody. If the amount
of antibody is insufcient to initiate antibody-antigen activation, TRALI will not occur. In the critically ill patient, the
neutrophils are primed and ready to be activated from the
antibodies in the transfused blood, which leads to pulmonary
edema.
Approximately 80% of cases of TRALI are due to the
presence of donor antibodies such as antihuman leukocyte or
antihuman neutrophil antibodies. The implicated antibodies
include cognate anti-HLA-Class II and anti-human neutrophil antigen (HNA)-positive antibodies. Antibodies are the
second hit for TRALI.Antibodies to leukocyte antigen Class
I or II or neutrophil antigen can be detected in the transfused
blood of patients who develop TRALI. These antibodies in
the donor product activate neutrophils in the recipient lung
causing pulmonary damage and capillary leak. Donors have
developed these antibodies when the immune system comes
into contact with foreign HNA or HLA during pregnancy,
transfusion, or transplantation [7].
The remaining 20% of cases of TRALI are related to biolipids of the blood products or components from aging blood.
These microparticles occur in blood products and activate
inammatory mediators resulting in plasma leak within the
lung. The microparticles may be generated from any cell,
including platelets, red blood cells, and white blood cells.
The exact mechanism for TRALI from this etiology is poorly
understood [7].
Given the role of human leukocyte antigen antibodies in
the development of TRALI, blood banks have moved toward
the use of male-predominant plasma. Multiparous women
have a high exposure to fetal HLA antigens and other
granulocyte- borne antigens from the fetus. This knowledge
has led to the practice of eliminating donor plasma from
multiparous women or the screening of female donors for
HLA antibodies. This practice was instituted in 2004. Prior
to this change, the estimated incidence of TRALI was 1in
5000 blood and blood components, 1 in 2000 plasmacontaining components, 1 in 7900 units of fresh frozen
plasma, and 1in 432units of whole blood-derived platelets
[8]. Since the introduction of male-predominant plasma, the
incidence of TRALI has decreased. The University of Texas
Health Science Center in Houston evaluated the incidence of
TRALI as this center uses plasma in the setting of trauma,
and the use is early and aggressive [9]. Over a 10-year period,
a total of 714,757units of blood products were transfused
with seven cases of TRALI, giving an incidence of 1 in
102,000. As compared to the screening and discarding of
blood based on the presence of antibodies, another approach
is the use of pooled solvent-detergent-treated plasma instead
of fresh frozen plasma. This treatment with solvent and
detergent was done to inactivate lipid-enveloped viruses.
This approach has been shown to be effective in eliminating
the antibodies [10].
No specic treatment exists for TRALI. The provision of
increased concentrations of oxygen is required in all, and
mechanical ventilation is required in most [7]. Given the
lung injury component of TRALI, it is recommended that
lung protective strategies be used for ventilation. Also, these
patients should not be treated with diuretics as uid overload
is not the precipitating factor. TRALI may be differentiated
from transfusion-associated circulatory overload by obtaining a B-type natriuretic peptide level, which is elevated in
overload. Other factors that differentiate TRALI from transfusion-associated circulatory overload include the elevated
pulmonary capillary wedge pressure and the positive
response to diuretics in overload. Given the two-hit theory,
managing the patient’s underlying risk factors as well as
decreasing transfusion would decrease the incidence of
TRALI.
Transfusion-Associated Circulatory Overload
Transfusion-associated circulatory overload (TACO) is the
most common type of transfusion-related pulmonary complication with an estimated incidence estimate of 1–8%
(although some estimating it to be as high as 11%) [11].
TACO was rst observed in the 1930s, but became recognized as a distinct clinical entity in the 1990s [12]. The incidence of TACO varies by study, with data from passive
surveillance showing a very low incidence while studies with
active surveillance reporting a higher incidence. This point
highlights the general consensus that TACO is vastly underreported and lacks a clear, established dening set of criteria,
as evidenced by the variation in the reported incidence
among studies with active surveillance. Data from the
Serious Hazards of Transfusion UK reporting system suggest
12 Complications ofBlood Transfusion
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115
that the understanding of TACO has improved as reports of
TACO increased each year between 2007 and 2013 [13].
TACO was more likely to occur with the transfusion of
packed red blood cells (1/8000), as compared to plasma
(1/15,000) or platelets (1/48,000) [14]. Various other studies
have supported this relationship between volume transfused
and TACO although the impact of the rate of transfusion on
the incidence remains unknown.
TACO is dened as acute cardiogenic pulmonary edema
associated with volume overload occurring within 6hours of
receiving a blood transfusion [15]. This temporal relationship between transfusion of blood products and pulmonary
edema is a key feature of TACO (as well as TRALI) distinguishing it from other forms of pulmonary edema. The pulmonary edema caused by TACO is thought to be due to
increased hydrostatic pressure (i.e., cardiogenic pulmonary
edema) as opposed to capillary leak (i.e., noncardiogenic
pulmonary edema), the latter being associated with transfusion-related acute lung injury [16]. Although there is no consensus on standardized criteria for TACO, the Centers for
Disease Control’s Hemovigilance Module Surveillance
Protocol proposed possible criteria for recognizing and diagnosing TACO (Table12.3) [17]. The CDC criteria state that
a patient must have 3 or more of the following ndings
within 6hours of cessation of transfusion:
• Acute respiratory distress
• Elevated brain natriuretic peptide(BNP)
• Elevated CVP
• Evidence of left heart failure
• Evidence of positive uid balance
• Radiographic evidence of pulmonary edema
Table 12.3 Comparison of diagnostic criteria transfusion-associated
circulatory overload based upon organization
CDC
Biovigilance
Surveillance
Protocol
Timing/onset Within 6hours
Criteria based
on observed
signs/
symptoms or
measured
values
of cessation of
transfusion
Three or more
of the
following:
Acute
respiratory
distress
Radiographic
evidence of
pulmonary
edema
Evidence of left
heart failure
Evidence of
positive uid
balance
Elevated brain
natriuretic
peptide
Elevated CVP
International Society of Blood
Transfusion
During/up to 12hours
Acute or worsening respiratory
distress and/or evidence of
pulmonary edema and three or
more of the following criteria:
Acute or worsening respiratory
distress
Evidence of acute or worsening
pulmonary edema (based on
physical exam, CXR, or
echocardiogram
Evidence of cardiovascular system
changes that are unrelated to their
underlying condition (HTN,
tachycardia, JVD, Enlarged
cardiac silhouette, peripheral
edema, widened pulse pressure
Evidence of uid overload:
Positive uid balance, change in
weight in the peri-transfusion
period, response to diuretic
therapy(medication or dialysis)
Biomarker: increase in BNP or
NT-pro BNP above age-adjusted
reference range and greater than
1.5 times pretransfusion value.
Normal BNP level most
transfusion is not consistent with
TACO diagnosis
Since TACO is a form of cardiogenic pulmonary edema
related to the transfusion of blood products, understanding
the pathophysiology of pulmonary edema will aide in the
management of TACO. In the normal lung, uid that is ltered out of circulation into the alveolar interstitial space
does not enter the alveoli due to tight junctions that prevent
passage; this uid is removed via the lymphatics. The hydrostatic force for uid ltration between the capillaries and
alveoli microcirculation is roughly equal, with the osmotic
pressure of the capillaries tipping the balance slightly in
favor of capillary circulation [14]. In TACO, the hydrostatic
pressure increases due to the rapid increase in circulatory
volume resulting in an imbalance. There is an increase in
uid ltration (edema into the interstitial space), and the
tight junctions of the epithelium are overcome allowing protein poor uid to enter the alveolar space thus causing pulmonary edema.
There are multiple risk factors for TACO, with age, cardiovascular dysfunction, and renal disease being the major
risk factors. Although TACO can occur at any age, advanced
age appears to be the greatest risk with most studies reporting the highest incidence in patients aged greater than
70years. Patients with cardiovascular dysfunction also have
a higher incidence of TACO. In particular, patients with CHF
(especially NYHA Class 4), atrial brillation, a history of
coronary artery disease, use of diuretics (and lack of use
when there is evidence of TACO), and amiodarone all have a
higher risk of developing TACO [16]. Chronic renal failure
has also been shown to be a risk factor. Other risk factors
include positive uid status (uids other than blood products
can contribute to TACO), number of units transfused, type of
product transfused (likely related to volume), rate of transfusion, preexisting pulmonary disease, female sex (although
the evidence is not conclusive), patients of small stature,
shock, anemia, and hospitalized patients (especially OR and
ICU) [12, 14, 15]. Many of the risk factors lend credence to
the hypothesis that TACO occurs when the body’s ability to
manage intravascular volume status is overwhelmed, especially when intravascular volume is increased by a large
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J. Cassis and R. Gaiser
amount or at higher infusion rates. For example, the incidence of TACO correlates with the number of units of blood
products transfused, and there is evidence that higher rates of
infusion lead to higher incidence of TACO [12, 18].
Respiratory distress/worsening pulmonary status within
6hours of receiving a blood transfusion is the principle manifestation of TACO. A patient’s respirations, oxygen saturation, heart rate, temperature, blood pressure, and uid
balance should all be monitored closely during transfusion.
Increasing oxygen requirement and decreasing oxygen saturation on pulse oximetry should warrant further investigation
including a chest x-ray and physical exam. Consideration
should be given to close monitoring for 24hours after transfusion as multiple studies show clear evidence that active
surveillance yields higher rates of recognition of TACO.
Supplemental oxygen which is common in the OR and ICU
can mask evidence for worsening pulmonary status, especially if the patient is intubated. Arterial blood gas monitoring measures the ratio of the partial pressure of oxygen to
fractional inspired oxygen (PaO2/FiO2) which is used in
ARDS and TRAILI and could prove useful in TACO. [14]
Potential respiratory manifestations include the following:
• Dyspnea
• Tachypnea
• Hypoxia
• Pulmonary edema– CXR (possible enlarged cardiac sil-
houette, pleural effusions, enlarged vascular pedicle, dis-
tribution of edema is even/central
• Orthopnea
• Crackles
In addition to respiratory status, patients should be monitored for cardiac dysfunction before, during, and after transfusion. Hypertension is sometimes, though not always, a
distinguishing feature from the noncardiogenic pulmonary
edema associated with TRALI.Physical examination of the
patient may reveal jugular venous distention and peripheral
edema. A patient’s uid balance should be determined before
a transfusion is started as studies demonstrating overall positive volume status contribute to the development of TACO.
Chart review, urine output, patient’s weight, response to
diuretics, and volume removed through dialysis can all be
used to determine uid balance. Bedside echocardiography
may be utilized to determine cardiac function as well as volume status.
B-type natriuretic peptide (BNP) and NT-pro-BNP have
been studied as a way to diagnose TACO and differentiate it
from TRALI to aide in clinical decision making.
Unfortunately, the evidence is mixed as to whether or not
BNP is an effective biomarker for distinguishing TACO from
TRALI. The evidence is weaker for differentiating TACO
from other forms of pulmonary edema [19]. The most signicant problem with these biomarkers is the vast differen-
tial and large number of factors that can explain elevations.
Heart failure, renal dysfunction, age, gender, sepsis, and
ACE inhibitors affect BNP and NT-pro-BNP levels.
Management of TACO is essentially the same as managing patients with other causes of cardiogenic pulmonary
edema. If TACO is suspected, the initial step in treatment is
to stop the transfusion. Treatment should begin with supplemental oxygen and elevating the head of the bed to 30
degrees. Supplemental oxygen may be delivered via nasal
canula; however, positive pressure may be required if the
pulmonary edema is severe; BiPap or high ow nasal canula
can be useful. Diuretic use has shown a signicant decrease
in not only the incidence of TACO but also the mortality
when it occurs. In cases of severe renal failure, CRRT or
hemodialysis is used to reduce volume overload. Reduction
of afterload as tolerated by the patient may also prove useful
in decreasing workload and increasing cardiac output. In the
most severe cases, intubation, vasopressors, and inotropes
are necessary.
Transfusion Reactions
The understanding of the antigen/antibody cause for the
blood group system was developed by Dr. Karl Landsteiner
when he noted that mixing red blood cells with different
plasma and different patterns of agglutination was obtained
[20]. He termed the rst pattern A and the second pattern
B.There were other individuals who did not achieve any pattern of agglutination, which was termed C.The rst two patterns led to the nomenclature of Type A and Type B; it was
the lack of a pattern of agglutination that led to Type O.
Furthermore, it was these observations that led Dr.
Landsteiner to postulate that whichever ABO antigens are
lacking on a red blood cell will result in the corresponding
antibody. This theory has been termed Landsteiner’s Law.
The antigens for the ABO system are produced by various
enzymes that add sugars to the oligosaccharide chain. The
source of the antibodies is less clear; it may due to inherited
antibodies or due to classical immune-mediated reactions.
When ABO incompatible blood is administered, hemolysis
may occur.
For the transfusion of red blood cells, patients may receive
group O red blood cells as these cells lack A and B antigens
and are compatible with plasma. For plasma, all patients may
receive AB plasma as these lack anti-A and anti-B antibodies. Of note, while ABO compatibility is vital for red blood
cells to prevent a fatal acute hemolytic transfusion reaction,
it is not vital and frequently not followed for plasma and
platelets. Although plasma may contain anti-A or anti-B
antibodies, the presence of A and B antigens on endothelial
cells, dilution in the patient blood volume, and the presence
of soluble A and B antigen in the plasma of secretors provide
protection [21].
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The presence of D antigen on the donor and recipient also
must be considered. Antibody to the D antigen is not naturally occurring, requiring exposure to develop the antibody.
Exposure to D+ red blood cells in a D- patient will result in
the development of antibodies in 1 out of every 5 exposures.
The formation of D antibodies is most important in women
of childbearing age where the antibody may complicate the
pregnancy. As such, men and women who are beyond childbearing typically receive D+ packed red blood cells, due to
the shortage of D- blood. In fact, D- blood has become so
low that many transfusion services provide D+ blood, even
for women of childbearing age [21].
A febrile nonhemolytic transfusion reaction is dened as
an increase in temperature of 1 degree Celsius above 37
degrees that occurs during or after the transfusion of blood
products. This reaction is the most common during transfusion. The reaction may occur without the symptoms of
chills, rigors, and rash or may occur with it. The most common blood product to produce a non-hemolytic transfusion
reaction is platelets. Initially, it was felt that the reaction
was due to the presence of white blood cells in the patient’s
plasma that reacted with the white cells in the blood product. This explanation mainly applies to red blood cells;
platelets have a different explanation. The reaction is more
likely to occur the older the platelets are. Within the stored
platelets, there is the generation of cytokines during storage. These cytokines are responsible for the reaction [22].
The most important point when a patient develops a febrile
response to a transfusion is to insure that it is not due to an
acute hemolytic reaction or transfusion of a contaminated
product.
There is always the risk of administering the wrong blood
product to the patient. While infectious disease transmission
has decreased, mistransfusion remains a constant risk to the
patient [23]. In an effort to prevent this error of incompatible blood products, an institution conducted a quality
improvement project with the introduction of a cognitive
aid. This cognitive aid was a simple card that was worn with
the participants’ badge, as demonstrated in Table 12.4.
Based upon a quiz, there was a marked improvement in
ABO compatibility.
Table 12.4 ABO compatibility based upon blood product type
Group O B A AB
ABO group of compatible RBCs
AB • • • •
A • •
B • •
O •
ABO group of compatible FFP
AB •
A • •
B • •
O • • • •
Hemolytic transfusion reactions occur when the antibodies within the recipient react to the antigens on the red
blood cell surface. These reacts are classied as acute or
delayed. An acute reaction occurs during the transfusion,
while a delayed reaction occurs within days or weeks of
transfusion. The most common reason for a hemolytic
transfusion reaction is misidentication of the patient or
mislabeling the blood sample. When the IgM antibody
binds to the antigen, the red cell membrane is destroyed
resulting in the release of contents within the red blood cell
into the circulation. The free hemoglobin damages the kidney, while the complement activation leads to disseminated
intravascular coagulation [24]. Management includes stopping the transfusion and administering uids, vasopressors,
and blood products for the coagulopathy. A delayed reaction occurs from antibodies developed from a previous
transfusion. These antibodies are not present in a detectable
level at the time of the testing and appear days after the
transfusion. Typical manifestations of a delayed reaction
include anemia and jaundice.
Infectious Complications
Transfusion-transmitted infection due to viral and bacterial
contamination decreased dramatically with the transition to
closed, sterile systems for collection and storage. John Elliott
developed the rst vacuum bottle for blood collection in 1940
[25, 26]. In addition, the testing of blood donations has further contributed to a dramatic reduction in transfusiontransmitted infections. By 1947, every unit of blood collected
was tested for syphilis followed by hepatitis B in 1971, hepatitis C in 1990, and HIV-1 and 2 by 1992 [26]. Over time viral
infections related to transfusion have seen a signicant drop;
transfusion-transmitted bacterial infection has not seen the
same reduction over the last 30years. According to studies
from the US FDA, French Hemovigilance study, and the
British SHOT study, the incidence for bacterial contamination/sepsis has not decreased (in fact, has not changed) to the
same degree as viral infection [25].
Bacterial contamination is the most common cause of
transfusion-transmitted infection, with an estimated overall
prevalence of 0.2% [27, 28]. Bacterial infection is more
common than viral or fungal infection. It is estimated that
bacterial contamination is approximately 1 in 3000 units
[29]. Transfusion-transmitted bacterial infections accounted
for the most reports transfusion-related fatality, accounting
for 20% of fatalities (second to ABO errors) [25, 30]. The
actual incidence of transfusion-transmitted bacterial infection varies based on the study (Table12.5). This variation is
likely due to differences in the processing and storage of
blood products [30]. The FDA reports mortality from
transfusion-related infections to range from 1in 6,000,000 to
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Table 12.5 Risk of Bacterial Transmission Through Transfusion
French Bacthem
Case-Control Study [
Summary of Transfusiontransmitted Bacterial
Infection Incidence Rates
Blood Products Rate Blood Products Rate
Packed red blood
cells (PRBCs)
Pooled Platelets 71.8 Single Unit Platelets 9.98
Single Unit
Platelets
Apheresis Platelets 31.8
FFP 7.4
Total Units Transfused:
5,423,597
Transfusion-transmitted bacterial
4]
infection in the US [5]
Rate of transfusion-transmitted
bacteremia (in events/million units)
5.8 PRBCs 0.21
9.4 Pooled Platelets 10.64
Patients who received gram negative
bacteria were at greatest risk of death
Transfusion-transmitted bacterial
infections accounted for the most reports
transfusion related fatality after
hemolytic reactions (>10% from
1985–1999)
1in 9,000,000 when examining all blood products together
and 1in 1,000,000 for platelets [30].
Though the incidence of bacterial contamination and
transfusion-transmitted bacterial infections varies, the highest risk of contamination and infection occurs with platelets.
This incidence is due to storage as platelets are stored at
room temperature, allowing bacteria to grow that would otherwise remain dormant at lower levels with refrigeration. In
countries where platelets are screened using BacT/ALERT
culture system, the incidence of transfusion-transmitted bacterial infections is lower [31]. The detection of bacterial contamination in platelet samples is largely dependent on
bacterial concentration as tests where resampling of a previously positive BacT/ALERT screenings has yielded negative
results [32]. Unlike viruses, bacteria have the ability to multiply during storage making the duration of their storage
another factor in the incidence of transfusion-related bacterial infection. One study found that the incidence of contamination and the bacterial levels measured were both
signicantly less for units transfused in under 4days compared with units that were 5days and older [33].
The infectious concern with the transfusion of red blood
cells is primarily viral. The risk depends upon which testing
is performed. Current testing of red blood cells includes
Hepatitis B (antibody in 1987; nucleic acid in 2009),
Hepatitis C (antibody in 1990; nucleic acid in 1999), Human
Immunodeciency Virus (antibody in 1985; nucleic acid in
2000), West Nile Virus, and Zika Virus [34]. The risk of viral
infection occurs when a virus emerges in which testing does
not occur, as happened with Zika Virus, which was added in
2016 [35]. Currently, blood is not tested for Hepatitis A,
malaria, or new variants of Creutzfeld-Jacob disease prions.
Conclusion
The transfusion of blood products has risk to the patient. There
is always the risk of misidentication resulting in the administration of the wrong blood product. Even when the patient is
properly cross-matched, there are infectious risks from both
known and unknown agents. There is also the risk of transfusion-related acute lung injury and transfusion- associated circulatory overload. While the risks may be mitigated, they
cannot be removed completely. These concerns help one
understand the continually evolving transfusion thresholds
and administer products only when truly indicated.
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16. Bolton-Maggs PH, Cohen H. Serious Hazards of Transfusion
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Diseases oftheCoagulation System:
https://t.me/medicina_free
Hemophilia, Von Willebrands Disease,
Cryoglobulinemia, and Inborn Errors
ofFactor Synthesis
PierreAlexCasthely andShruthimaThangada
13
Hemophilia A
There are three major types of hemophilias, A, B, and
C. They are classied based on their decient coagulation
factor. Hemophilias A and B are X-linked recessive disorders
caused by a mutation in the long arm of chromosome X at
the F8 and F9 genes. Males are affected, and females are carriers [1]. Hemophilia A is the most common X-linked genetic
disease and the second most common factor deciency after
von Willebrand disease (vWD). The worldwide incidence of
hemophilia A is approximately 1 out of 5000 males [2]. The
exact number of people living with hemophilia A is not
known [3]. The prevalence of hemophilia A varies by country and ranges 5.4–14.5 cases per 100,000 males. In the
United States, the prevalence of hemophilia A is 20.6 cases
per 100,000 males, and the number of people in the United
States with hemophilia was estimated to be about 20,000in
2016 [4].
Etiology ofHemophilia A
Hemophilia A can be caused by a factor VIII deciency, dysfunctional factor VIII, or even factor VIII inhibitors leading
to the disruption of the normal intrinsic coagulation cascade.
Any defect or absence in factor VIII will cause a decrease in
thrombin production by FIXa and FVIIIa in the intrinsic
pathway of the coagulation cascade. The factor VIII gene is
large and comprises 0.1% of the DNA in the X chromosome.
A defect in the normal factor VIII coding sequence caused
by a mutation can result in an inability to properly transcribe
P. A. Casthely · S. Thangada (*)
NYU Langone Medical Center, NYU Department of
Anesthesiology, Perioperative Care, & Pain Medicine,
New York, NY, USA
e-mail: casthp02@nyulmc.org;
Shruthima.Thangada@nyulangone.org
the complete, normal factor VIII protein, resulting in the loss
of its normal function [4].
Signs andSymptoms
Bleeding is the number one sign of hemophilia A.The severity of symptoms depends on the amount of factor VIII in the
plasma. Normal plasma levels of factor VIII range from 50%
to 150% (0.5–1.5IU/ml). Levels below 50%, or half of what
is needed to form a clot, determine a person’s symptoms.
Those with mild hemophilia have 6–49% of factor VIII.These
account for 25% of all cases. They generally experience
bleeding only after serious injury, trauma, or surgery. In
many cases, mild hemophilia is not diagnosed until after an
injury has occurred and results in prolonged bleeding.
Women with mild hemophilia often experience heavy menstrual periods and are at risk for hemorrhage during childbirth [5].
Patients with moderate hemophilia A have 1–5% of factor
VIII in the blood. This accounts for 15% of all cases. They
may have bleeding episodes after injuries, but rarely bleed
spontaneously.
Severe hemophilia A occurs in patients with less than 1%
of factor VIII and accounts for 60% of cases. In addition to
bleeding following an injury, they may experience frequent
spontaneous bleeding into their joints (hemarthrosis) and
muscles [5]. Chronic bleeding into the joints, particularly the
knees, elbows, and ankles, can lead to decreased range of
motion, contractures, and muscle hypertrophy. Over time,
degenerative joint disease, osteoarthritis, and osteophyte formation can occur, necessitating surgery [6].
In addition to bleeding into the joint space, bleeding can
also occur in the gastrointestinal tract. Infections such as
Helicobacter pylori can increase the frequency of GIB in
patients with hemophilia [7]. Intracranial hemorrhage is a
rare occurrence, but a serious cause of morbidity and mortality in patients with hemophilia, thirty percent, result in death.
© Springer Nature Switzerland AG 2021
C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_13
121
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