Blood Bank and Transfusion

Blood transfusion
Blood transfusion is the process of transferring blood or blood-based products from one person
into the circulatory system of another. Blood transfusions can be life-saving in some situations,
such as massive blood loss due to trauma, or can be used to replace blood lost during surgery.
Blood transfusions may also be used to treat a severe anaemia or thrombocytopenia caused by a
blood disease. People suffering from hemophilia or sickle-cell disease may require frequent
blood transfusions. Early transfusions used whole blood, but modern medical practice commonly
uses only components of the blood.
Contents
1 History
o 1.1 Early attempts
o 1.2 First successful transfusion
o 1.3 The first successes
o 1.4 Development of blood banking
o 1.5 The modern era
2 Precautions
o 2.1 Compatibility
o 2.2 Transfusion transmitted infections
o 2.3 Processing of blood prior to transfusion
o 2.4 Neonatal transfusion
o 2.5 Terminology
3 Procedure
4 Blood donation
o 4.1 Risks to the recipient
o 4.2 Objections to blood transfusion
5 Animal blood transfusion
6 Blood transfusion substitutes
7 References
8 Further reading
9 External links
History
Early attempts
The first historical attempt at blood transfusion was described by the 17th century chronicler
Stefano Infessura. Infessura relates that, in 1492, as Pope Innocent VIII sank into a coma, the
blood of three boys was infused into the dying pontiff (through the mouth, as the concept of
circulation and methods for intravenous access did not exist at that time) at the suggestion of a
physician. The boys were ten years old, and had been promised a ducat each. However, not only
did the pope die, but so did the three children. Some authors have discredited Infessura's account,
accusing him of anti-papalism.
[1]

World War II syringe for direct inter-human blood transfusion
Beginning with Harvey's experiments with circulation of the blood, more sophisticated research
into blood transfusion began in the 17th century, with successful experiments in transfusion
between animals. However, successive attempts on humans continued to have fatal results.
The first fully documented human blood transfusion was administered by Dr. Jean-Baptiste
Denys, eminent physician to King Louis XIV of France, on June 15, 1667.
[2]
He transfused the
blood of a sheep into a 15-year old boy, who survived the transfusion.
[3]
Denys performed
another transfusion into a labourer, who also survived. Both instances were likely due to the
small amount of blood that was actually transfused into these people. This allowed them to
withstand the allergic reaction. Denys' third patient to undergo a blood transfusion was Swedish
Baron Bonde. He received two transfusions. After the second transfusion Bonde died.
[4]
In the
winter of 1667, Denys performed several transfusions on Antoine Mauroy with calf's blood, who
on the third account died.
[5]
Much controversy surrounded his death. Mauroy's wife asserted
Denys was responsible for her husband's death. But Mauroy's wife was accused of causing his
death. Though it was later determined that Mauroy actually died from arsenic poisoning, Denys'
experiments with animal blood provoked a heated controversy in France.
[4]
Finally, in 1670 the
procedure was banned. In time, the British Parliament and even the pope followed suit. Blood
transfusions fell into obscurity for the next 150 years.
First successful transfusion
Christian Zagado examined the effects of changes in blood volume on circulatory function and
developed methods for cross-circulatory study in animals, obviating clotting by closed
arteriovenous connections. His newly devised instruments eventually led to actual transfusion of
blood.
"Many of his colleagues were present. towards the end of February 1665 [when he] selected one
dog of medium size, opened its jugular vein, and drew off blood, until . . . its strength was nearly
gone . Then, to make up for the great loss of this dog by the blood of a second, I introduced
blood from the cervical artery of a fairly large mastiff, which had been fastened alongside the
first, until this latter animal showed . . . it was overfilled . . . by the inflowing blood." After he
"sewed up the jugular veins," the animal recovered "with no sign of discomfort or of
displeasure."
Lower had performed the first blood transfusion between animals. He was then "requested by the
Honorable [Robert] Boyle . . . to acquaint the Royal Society with the procedure for the whole
experiment," which he did in December of 1665 in the Societys Philosophical Transactions. On
15 June 1667 Denys, then a professor in Paris, carried out the first transfusion between humans
and claimed credit for the technique, but Lowers priority cannot be challenged.
[citation needed]

Six months later in London, Lower performed the first human transfusion in Britain, where he
"superintended the introduction in [a patients] arm at various times of some ounces of sheeps
blood at a meeting of the Royal Society, and without any inconvenience to him." The recipient
was Arthur Coga, "the subject of a harmless form of insanity." Sheeps blood was used because
of speculation about the value of blood exchange between species; it had been suggested that
blood from a gentle lamb might quiet the tempestuous spirit of an agitated person and that the
shy might be made outgoing by blood from more sociable creatures. Lower wanted to treat Coga
several times, but his patient refused. No more transfusions were performed. Shortly before,
Lower had moved to London, where his growing practice soon led him to abandon research.
[6]

The first successes
The science of blood transfusion dates to the first decade of the 19th century, with the discovery
of distinct blood types leading to the practice of mixing some blood from the donor and the
receiver before the transfusion (an early form of cross-matching).
In 1818, Dr. James Blundell, a British obstetrician, performed the first successful blood
transfusion of human blood, for the treatment of postpartum hemorrhage. He used the patient's
husband as a donor, and extracted four ounces of blood from his arm to transfuse into his wife.
During the years 1825 and 1830, Dr. Blundell performed 10 transfusions, five of which were
beneficial, and published his results. He also invented many instruments for the transfusion of
blood. He made a substantial amount of money from this endeavour, roughly $50 million (about
$2 million in 1827) real dollars (adjusted for inflation).
[citation needed]

In 1840, at St George's Hospital Medical School in London, Samuel Armstrong Lane, aided by
Dr. Blundell, performed the first successful whole blood transfusion to treat hemophilia.
In the novel "Dracula", by Bram Stoker, various incidences of blood transfusion were deliberated
upon. The book was published in 1897.
George Washington Crile is credited with performing the first surgery using a direct blood
transfusion at the Cleveland Clinic.
Many patients had died and it was not until 1901, when the Austrian Karl Landsteiner discovered
human blood groups, that blood transfusions became safer. Mixing blood from two individuals
can lead to blood clumping or agglutination. The clumped red cells can crack and cause toxic
reactions, which can have fatal consequences. Karl Landsteiner discovered that blood clumping
was an immunological reaction which occurs when the receiver of a blood transfusion has
antibodies (A, B, both A & B, or neither) against the donor blood cells. Karl Landsteiner's work
made it possible to determine blood groups (A, B, AB, O) and thus paved the way for blood
transfusions to be carried out safely. For this discovery he was awarded the Nobel Prize in
Physiology or Medicine in 1930.
Development of blood banking
See also: Blood bank
While the first transfusions had to be made directly from donor to receiver before coagulation, in
the 1910s it was discovered that by adding anticoagulant and refrigerating the blood it was
possible to store it for some days, thus opening the way for blood banks. The first non-direct
transfusion was performed on March 27, 1914 by the Belgian doctor Albert Hustin, who used
sodium citrate as an anticoagulant. The first blood transfusion using blood that had been stored
and cooled was performed on January 1, 1916. Oswald Hope Robertson, a medical researcher
and U.S. Army officer, is generally credited with establishing the first blood bank while serving
in France during World War I.
The first academic institution devoted to the science of blood transfusion was founded by
Alexander Bogdanov in Moscow in 1925. Bogdanov was motivated, at least in part, by a search
for eternal youth, and remarked with satisfaction on the improvement of his eyesight, suspension
of balding, and other positive symptoms after receiving 11 transfusions of whole blood.
In fact, following the death of Vladimir Lenin, Bogdanov was entrusted with the study of Lenin's
brain, with a view toward resuscitating the deceased Bolshevik leader. Bogdanov died in 1928 as
a result of one of his experiments, when the blood of a student suffering from malaria and
tuberculosis was given to him in a transfusion. Some scholars (e.g. Loren Graham) have
speculated that his death may have been a suicide, while others attribute it to blood type
incompatibility, which was not completely understood at the time.
[7]

The modern era
Following Bogdanov's lead, the Soviet Union set up a national system of blood banks in the
1930s. News of the Soviet experience traveled to America, where in 1937 Bernard Fantus,
director of therapeutics at the Cook County Hospital in Chicago, established the first hospital
blood bank in the United States. In creating a hospital laboratory that preserved and stored donor
blood, Fantus originated the term "blood bank". Within a few years, hospital and community
blood banks were established across the United States.
In the late 1930s and early 1940s, Dr. Charles R. Drew's research led to the discovery that blood
could be separated into blood plasma and red blood cells, and that the plasma could be frozen
separately. Blood stored in this way lasted longer and was less likely to become contaminated.
Another important breakthrough came in 1939-40 when Karl Landsteiner, Alex Wiener, Philip
Levine, and R.E. Stetson discovered the Rhesus blood group system, which was found to be the
cause of the majority of transfusion reactions up to that time. Three years later, the introduction
by J.F. Loutit and Patrick L. Mollison of acid-citrate-dextrose (ACD) solution, which reduces the
volume of anticoagulant, permitted transfusions of greater volumes of blood and allowed longer
term storage.
Carl Walter and W.P. Murphy, Jr., introduced the plastic bag for blood collection in 1950.
Replacing breakable glass bottles with durable plastic bags allowed for the evolution of a
collection system capable of safe and easy preparation of multiple blood components from a
single unit of whole blood. Further extending the shelf life of stored blood was an anticoagulant
preservative, CPDA-1, introduced in 1979, which increased the blood supply and facilitated
resource-sharing among blood banks.
As of 2006, there were about 15 million units of blood transfused per year in the United States.
[8]

Precautions
Compatibility
The key importance of the Rh group is its role in Hemolytic disease of the fetus and newborn.
When an Rh negative mother carries a positive fetus, she can become immunized against the Rh
antigen. This usually is not important during that pregnancy, but in the following pregnancies she
can develop an immune response to the Rh antigen. The mother's immune system can attack the
baby's red cells through the placenta. Mild cases of HDFN can lead to disability but some severe
cases are fatal. Rh-D is the most commonly involved red cell antigen in HDFN, but other red cell
antigens can also cause the condition. The "positive" or "negative" in heard blood types such as
"O positive" is the Rh-D antigen.
Transfusion transmitted infections
A number of infectious diseases (such as HIV, syphilis, hepatitis B and hepatitis C, among
others) can be passed from the donor to recipient.
Among the diseases that can be transmitted via transfusion are:
HIV-1 and HIV-2
Human T-lymphotropic virus (HTLV-1 and HTLV-2)
Hepatitis C virus (responsible for >90% of post-transfusion hepatitis)
Hepatitis B
Treponema pallidum
Malaria
Chagas Disease
variant Creutzfeldt-Jakob Disease or "Mad Cow Disease" has been shown to be
transmissible in blood products. No test exists for this, but various measures have been
taken to reduce risks.
When a person's need for a transfusion can be anticipated, as in the case of scheduled surgery,
autologous donation can be used to protect against disease transmission and eliminate the
problem of blood type compatibility. "Directed" donations from donors known to the recipient
were a common practice during the initial years of HIV. These kinds of donations are still
common in developing countries.
Processing of blood prior to transfusion
Donated blood is usually subjected to processing after it is collected, to make it suitable for use
in specific patient populations. Examples include:
Component separation: red cells, plasma and platelets are separated into different
containers and stored in appropriate conditions so that their use can be adapted to the
patient's specific needs. Red cells work as oxygen transporters, plasma is used as a
supplement of coagulation factors, and platelets are transfused when their number is very
scarce or their function severely impaired. Blood components are usually prepared by
centrifugation.
Leukoreduction, also known as Leukodepletion is the removal of white blood cells
from the blood product by filtration. Leukoreduced blood is less likely to cause
alloimmunization (development of antibodies against specific blood types), and less
likely to cause febrile transfusion reactions.
o Chronically transfused patients
o Potential transplant recipients
o Patients with previous febrile nonhemolytic transfusion reaction
o Patients with hereditary immune deficiencies
o Patients receiving blood transfusions from relatives in directed-donation programs
o Patients receiving large doses of chemotherapy, undergoing stem cell
transplantation, or with AIDS (controversial).
Tests for certain quality control issues such as disease or contamination.
Neonatal transfusion
To ensure the safety of blood transfusion to pediatric patients, hospitals are taking additional
precaution to avoid infection and prefer to use specially tested pediatric blood units that are
guaranteed negative for Cytomegalovirus. Most guidelines recommend the provision of CMV-
negative blood components and not simply leukoreduced components for newborns or low
birthweight infants in whom the immune system is not fully developed.
[9]
These specific
requirements place additional restrictions on blood donors who can donate for neonatal use.
Neonatal transfusions are usually top-up transfusions, exchange transfusions, partial exchange
transfusions. Top-up transfusions are for investigational losses and correction of mild degrees of
anemias, up to 5-15 ml/kg. Exchange transfusions are done for correction of anemia, removal of
bilirubin, removal of antibodies and replacement of red cells. Ideally plasma-reduced red cells
that are not older than 5 days are used.
[10]

Terminology
The terms type and screen are used for the testing that (1) determines the blood group (ABO
compatibility) and (2) screens for alloantibodies.
[11]
It takes about 45 minutes to complete
(depending on the method used). The blood bank technologist also checks for special
requirements of the patient (eg. need for washed, irradiated or CMV negative blood) and the
history of the patient to see if they have a previously identified antibody.
A positive screen warrants an antibody panel/investigation. An antibody panel consists of
commercially prepared group O red cell suspensions from donors that have been phenotyped for
commonly encountered and clinically significant alloantibodies. Donor cells may have
homozygous (e.g. K+k-), heterozygous (K+k+) expression or no expression of various antigens
(K-k+). The phenotypes of all the donor cells being tested are shown in a chart. The patient's
serum is tested against the various donor cells using an enhancement method, eg Gel or LISS.
Based on the reactions of the patient's serum against the donor cells, a pattern will emerge to
confirm the presence of one or more antibodies. Not all antibodies are clinically significant (i.e.
cause transfusion reactions, HDN, etc). Once the patient has developed a clinically significant
antibody it is vital that the patient receive antigen negative phenotyped red blood cells to prevent
future transfusion reactions. A direct antiglobulin test (DAT) is also performed as part of the
antibody investigation.
[12]

Once the type and screen has been completed, potential donor units will be selected based on
compatibility with the patient's blood group, special requirements (eg CMV negative, irradiated
or washed) and antigen negative (in the case of an antibody). If there is no antibody present or
suspected, the immediate spin or CAC (computer assisted crossmatch) method may be used.
In the immediate spin method, two drops of patient serum are tested against a drop of 3-5%
suspension of donor cells in a test tube and spun in a serofuge. Agglutination or hemolysis in the
test tube is a positive reaction and the unit should not be transfused.
If an antibody is suspected, potential donor units must first be screened for the corresponding
antigen by phenotyping them. Antigen negative units are then tested against the patient plasma
using an antiglobulin/indirect crossmatch technique at 37 degrees Celsius to enhance reactivity
and make the test easier to read.
If there is no time the blood is called "uncross-matched blood". Uncross-matched blood is O-
positive or O-negative. O-negative is usually used for children and women of childbearing age. It
is preferable for the laboratory to obtain a pre-transfusion sample in these cases so a type and
screen can be performed to determine the actual blood group of the patient and to check for
alloantibodies.
Procedure
Blood transfusions can be grouped into two main types depending on their source:
Homologous transfusions, or transfusions using the stored blood of others. These are
often called Allogeneic instead of homologous.
Autologous transfusions, or transfusions using the patient's own stored blood.
Donor units of blood must be kept refrigerated to prevent bacterial growth and to slow cellular
metabolism. The transfusion must begin within 30 minutes after the unit has been taken out of
controlled storage.
Blood can only be administered intravenously. It therefore requires the insertion of a cannula of
suitable caliber.
Before the blood is administered, the personal details of the patient are matched with the blood to
be transfused, to minimize risk of transfusion reactions. Clerical error is a significant source of
transfusion reactions and attempts have been made to build redundancy into the matching
process that takes place at the bedside.
A unit (up to 500 ml) is typically administered over 4 hours. In patients at risk of congestive
heart failure, many doctors administer a diuretic to prevent fluid overload, a condition called
Transfusion Associated Circulatory Overload or TACO. Acetaminophen and/or an antihistamine
such as diphenhydramine are sometimes given before the transfusion to prevent other types of
transfusion reactions.
Blood donation
Main article: Blood donation
Blood is most commonly donated as whole blood by inserting a catheter into a vein and
collecting it in a plastic bag (mixed with anticoagulant) via gravity. Collected blood is then
separated into components to make the best use of it. Aside from red blood cells, plasma, and
platelets, the resulting blood component products also include albumin protein, clotting factor
concentrates, cryoprecipitate, fibrinogen concentrate, and immunoglobulins (antibodies). Red
cells, plasma and platelets can also be donated individually via a more complex process called
apheresis.
In developed countries, donations are usually anonymous to the recipient, but products in a blood
bank are always individually traceable through the whole cycle of donation, testing, separation
into components, storage, and administration to the recipient. This enables management and
investigation of any suspected transfusion related disease transmission or transfusion reaction. In
developing countries the donor is sometimes specifically recruited by or for the recipient,
typically a family member, and the donation immediately before the transfusion.
Risks to the recipient
Main article: Transfusion reaction
There are risks associated with receiving a blood transfusion and these must be balanced against
the benefit which is expected. The most common adverse reaction to a blood transfusion is a
febrile non-hemolytic transfusion reaction, which consists of a fever which resolves on its own
and causes no lasting problems or side effects.
Hemolytic reactions include chills, headache, backache, dyspnea, cyanosis, chest pain,
tachycardia and hypotension.
Blood products can rarely be contaminated with bacteria; the risk of severe bacterial infection
and sepsis is estimated, as of 2002, at about 1 in 50,000 platelet transfusions, and 1 in 500,000
red blood cell transfusions.
[13]

There is a risk that a given blood transfusion will transmit a viral infection to its recipient. As of
2006, the risk of acquiring hepatitis B via blood transfusion in the United States is about 1 in
250,000 units transfused, and the risk of acquiring HIV or hepatitis C in the U.S. via a blood
transfusion is estimated at 1 in 2,000,000 (2 million) units transfused.
[citation needed]
These risks
were much higher in the past before the advent of second and third generation tests for
transfusion transmitted diseases. The implementation of Nucleic Acid Testing or "NAT" in the
early 2000s has further reduced risks, and confirmed viral infections by blood transfusion are
extremely rare in the developed world.
Transfusion-associated acute lung injury (TRALI) is an increasingly recognized adverse event
associated with blood transfusion. TRALI is a syndrome of acute respiratory distress, often
associated with fever, non-cardiogenic pulmonary edema, and hypotension, which may occur as
often as 1 in 2000 transfusions.
[14]
Symptoms can range from mild to life-threatening, but most
patients recover fully within 96 hours, and the mortality rate from this condition is less than
10%.
[15]
Although the cause of TRALI is not clear, it has been consistently associated with anti
HLA antibodies. Because anti HLA strongly correlate with pregnancy, several transfusion
organisations (Blood and Tissues Bank of Cantabria, Spain, National Health Service in Britain)
have decided to use only plasma from men for transfusion.
Other risks associated with receiving a blood transfusion include volume overload, iron overload
(with multiple red blood cell transfusions), transfusion-associated graft-vs.-host disease,
anaphylactic reactions (in people with IgA deficiency), and acute hemolytic reactions (most
commonly due to the administration of mismatched blood types).
Concerns about whether transfusion risks are heightened by storage time have also been
emerging, although there is no consensus on the significance of blood age.
[16]
Relatedly,
questions have been raised regarding the uncertain and inconsistent efficacy of transfusions for
certain vulnerable patient groups such as the critically ill.
[17]

Scientists working at the University of Copenhagen reported in the journal Nature Biotechnology
in April 2007 of discovering enzymes, which potentially enable blood from groups A, B and AB
to be converted into group O. These enzymes do not affect the Rh group of the blood
Objections to blood transfusion
Objections to blood transfusions may arise for personal, medical, or religious reasons. For
example, Jehovah's Witnesses object to blood transfusion primarily on religious grounds - they
believe that blood is sacred; although they have also highlighted possible complications
associated with transfusion.
Animal blood transfusion
Veterinarians also administer transfusions to animals. Various species require different levels of
testing to ensure a compatible match. For example, cats have 3 known blood types, cattle have
11, dogs have 12, pigs 16 and horses have 34. However, in many species (especially horses and
dogs), cross matching is not required before the first transfusion, as antibodies against non-self
cell surface antigens are not expressed constitutively - i.e. the animal has to be sensitized before
it will mount an immune response against the transfused blood.
The rare and experimental practice of inter-species blood transfusions is a form of xenograft.
Blood transfusion substitutes
Main article: Blood substitutes
As of 2009, there are no widely utilized oxygen-carrying blood substitutes for humans; however,
there are widely available non-blood volume expanders and other blood-saving techniques.
These are helping doctors and surgeons avoid the risks of disease transmission and immune
suppression, address the chronic blood donor shortage, and address the concerns of Jehovah's
Witnesses and others who have religious objections to receiving transfused blood.
A number of blood substitutes are currently in the clinical evaluation stage. Most attempts to find
a suitable alternative to blood thus far have concentrated on cell-free hemoglobin solutions.
Blood substitutes could make transfusions more readily available in emergency medicine and in
pre-hospital EMS care. If successful, such a blood substitute could save many lives, particularly
in trauma where massive blood loss results. Hemopure, a hemoglobin-based therapy, is approved
for use in South Africa.
References
1. ^ {"Vicars of Christ" - Peter de Rossa}
2. ^ "The First Blood Transfusion?". Heart-valve-surgery.com. 2009-01-03.
http://www.heart-valve-surgery.com/heart-surgery-blog/2009/01/03/first-blood-
transfusion. Retrieved 2010-02-09.
3. ^ "This Month in Anesthesia History".
http://www.anesthesia.wisc.edu/AHA/Calendar/June.html. Retrieved 2009-06-15.
4. ^
a

b
"Red Gold . Innovators & Pioneers . Jean-Baptiste Denis". PBS.
http://www.pbs.org/wnet/redgold/innovators/bio_denis.html. Retrieved 2010-02-09.
5. ^ "Mollisons Blood Transfusion in Clinical Medicine" by H.Klein, D. Anstee (2005),
p.406
6. ^ http://www.annals.org/cgi/reprint/132/5/420.pdf
7. ^ Bernice Glatzer Rosenthal. New Myth, New World: From Nietzsche to Stalinism,
Pennsylvania State University, 2002, ISBN 0-271-02533-6 pp. 161-162.
8. ^ Laura Landro (2007-01-10). "New rules may shrink ranks of blood donors". Wall
Street Journal. http://www.post-gazette.com/pg/07010/752655-28.stm.
9. ^ "Red blood cell transfusions in newborn infants: Revised guidelines". Canadian
Paediatric Society (CPS). http://www.cps.ca/english/statements/fn/fn02-
02.htm#What%20type%20of%20RBCs%20should%20be%20used. Retrieved 2007-02-
02.
10. ^ KM Radhakrishnan , Srikumar Chakravarthi , S Pushkala, J Jayaraju (2003 Aug).
"Component therapy". Indian J Pediatr 70 (8): 6616. doi:10.1007/BF02724257.
PMID 14510088.
11. ^ Blood Processing. University of Utah. Available at:
http://library.med.utah.edu/WebPath/TUTORIAL/BLDBANK/BBPROC.html. Accessed
on: December 15, 2006.
12. ^ D. Harmening, Modern Blood Banking and Transfusion Practices, 4th Ed. 1999
13. ^ Blajchman M (2007). "Incidence and significance of the bacterial contamination of
blood components". Dev Biol (Basel) 108: 5967. doi:10.2478/v10036-007-0007-1.
PMID 12220143.
14. ^ Silliman C, Paterson A, Dickey W, Stroneck D, Popovsky M, Caldwell S, Ambruso D
(1997). "The association of biologically active lipids with the development of
transfusion-related acute lung injury: a retrospective study". Transfusion 37 (7): 71926.
doi:10.1046/j.1537-2995.1997.37797369448.x. PMID 9225936.
15. ^ Popovsky M, Chaplin H, Moore S (1992). "Transfusion-related acute lung injury: a
neglected, serious complication of hemotherapy". Transfusion 32 (6): 58992.
doi:10.1046/j.1537-2995.1992.32692367207.x. PMID 1502715.
16. ^ Wang, Shirley S. (2009-12-01). "Focus on Age of Blood in Transfusions - WSJ.com".
Online.wsj.com.
http://online.wsj.com/article/SB10001424052748703939404574567771148801570.html.
Retrieved 2010-02-09.
17. ^ Marik PE, Corwin HL. Efficacy of red blood cell transfusion in the critically ill: a
systematic review of the literature. Crit Care Med 2008; 36:2667-2674.
Further reading
Transfusion, ISSN: 1537-2995 (electronic) 0041-1132 (paper)]
External links
Five Myths on Blood Transfusions, an information campaign by the New South Wales
Government.
Blood Transfusion Indications, information provide by Maharashtra State Blood
Transfusion Council.
[hide]
v d e
Transfusion medicine

General
concepts
Apheresis (plasmapheresis, plateletpheresis, leukapheresis) Blood transfusion
Coombs test (direct and indirect) Cross-matching Exchange transfusion
International Society of Blood Transfusion Intraoperative blood salvage ISBT 128
Transfusion reactions

Blood
group
systems
Blood
types
ABO Chido-Rodgers Colton Cromer Diego Dombrock Duffy Gerbich
GIL Hh Ii Indian JMH Kell (Xk) Kidd Knops LW Lewis Lutheran
MNS OK P Raph Rh and RHAG Scianna T-Tn Xg Yt Other

Blood
products
Blood donation Blood substitutes Cryoprecipitate Platelets Plasma Red blood
cells Whole blood Fresh frozen plasma Cryosupernatant
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Blood bank
A blood bank is a cache or bank of blood or blood components, gathered as a result of blood
donation, stored and preserved for later use in blood transfusions.
Contents
1 Transfusion
o 1.1 Short-term Storage
o 1.2 Long-term Storage
2 History
3 See also
4 Notes
5 External links
6 Headline text
[edit] Transfusion
Most hospital blood banks also perform testing to determine the blood type of patients and to
identify compatible blood products for blood transfusions, along with a battery of tests (e.g.
disease) and treatments (e.g. leukocyte filtration) to ensure and enhance quality. Some such
procedures can be done "upstream" by the collecting agency, or a contracted laboratory. The
increasingly-recognized problem of inadequate efficacy of transfusion and post-transfusion
complications
[1]
raises the importance of quality testing and screening; in fact, U.S. hospitals
spend more on dealing with the consequences of transfusion-related complications donors are
sometimes paid. In the U.S. and Europe, most blood for transfusion is collected from volunteers
while plasma (specifically plasma) for manufacturing is from paid donors.
In the US, certain standards are set for the collection and processing of each blood product.
"Whole blood" (WB) is the proper name for one defined product, specifically unseparated
venous blood with an approved preservative added. Most blood for transfusion is collected as
whole blood. Autologous donations are sometimes transfused without further modification,
however whole blood is typically separated (via centrifugation) into its components, with Red
Blood Cells (RBC) in solution being a commonly used product. Units of WB and RBC are both
kept refrigerated at 1-6 C, with maximum permitted storage periods (shelf lives) of 35 and 42
days respectively.
Red Blood Cell units can also be frozen when buffered with glycerol, but this is an expensive
and time consuming process, and is rarely done. Frozen red cells are given an expiration date of
3 years and are stored at -65C.
The less-dense blood plasma is made into a variety of frozen components, and is labeled
differently based on when it was frozen and what the intended use of the product is. If the plasma
is frozen promptly and is intended for transfusion, it is typically labeled as fresh frozen plasma.
If it is intended to be made into other products, it is typically labeled as recovered plasma or
plasma for fractionation. Cryoprecipitate can be made from other plasma components. These
components must be stored at -18C or colder, but are typically stored at -30C.
The layer between the red cells and the plasma is referred to as the buffy coat and is sometimes
removed to make platelets for transfusion. Platelets are typically pooled before transfusion and
have a shelf life of five days, or three days once the transfusion centre that collected them has
completed their tests. Platelets are stored at room temperature (20-24C) and must be agitated.
Since they are stored at room temperature in nutritive solutions, they are at high risk for growing
bacteria.
Some blood banks also collect products by apheresis. The most common component collected is
plasma via plasmapheresis, but red blood cells and platelet can be collected by similar methods.
These products have the same shelf life and storage conditions as their manually-produced
counterparts. An ongoing study allows platelets collected by apheresis to be kept for seven days,
but only with specific microbiological testing. The lack of a preservative solution makes a longer
shelf life of little use.
[edit] Short-term Storage
Routine blood storage is limited to several weeks (5 for WB, 6 for RBC), and involves
refrigeration but usually not freezing. There has been increasing controversy about whether the
age of blood is a factor in transfusion efficacy, specifically on whether older blood directly or
indirectly increases risks. complications.
[2]

[edit] Long-term Storage
Cryopreservation of red blood cells is done to store rare units, usually for up to 3 years. Very rare
units may be kept even longer
[3]
. The cells are incubated in a glycerol solution which acts as a
cryoprotectant ("antifreeze") within the cells. The units are then placed in special sterile
containers in a freezer at very cold temperatures. The exact temperature depends on the glycerol
concentration.
[edit] History
An early development leading to the establishment of blood banks occurred in 1915, when
Richard Lewison of Mount Sinai Hospital in New York City initiated the use of sodium citrate as
an anticoagulant. This discovery transformed the blood transfusion procedure from direct (vein-
to-vein) to indirect. In the same year, Richard Weil demonstrated the feasibility of refrigerated
storage of anticoagulated blood. The introduction of a citrate-glucose solution by Francis Peyton
Rous and JR Turner two years later permitted storage of blood in containers for several days,
thus opening the way for the first "blood depot" established in Britain during World War I.
Charles R. Drew researched in the field of blood transfusions, developing improved techniques
for blood storage, and applied his expert knowledge in developing large-scale blood banks early
in World War II. Oswald Hope Robertson, a medical researcher and U.S. Army officer who
established the depots, is now recognized as the creator of the first blood bank. The University of
Louisville is also credited for the Blood Bank.

Blood donation at the Royal Melbourne Hospital during the 1940s.
By the mid-1930s, the Soviet Union had set up a system of at least sixty large blood centers and
more than 500 subsidiary ones, all storing "canned" blood and shipping it to all corners of the
country. News of the Soviet experience traveled to America, where in 1937 Bernard Fantus,
director of therapeutics at the Cook County Hospital in Chicago, established the first hospital
blood bank in the United States.
[4]
In creating a hospital laboratory that preserved and stored
donor blood, Fantus originated the term "blood bank." Within a few years, hospital and
community blood banks were established across the United States. Willem Johan Kolff
organised the first blood bank in Europe (in 1940).
An important breakthrough came in 1939-40 when Karl Landsteiner, Alex Wiener, Philip
Levine, and R.E. Stetson discovered the Rh blood group system, which was found to be the
cause of the majority of transfusion reactions up to that time. Three years later, the introduction
by J.F. Loutit and Patrick L. Mollison of acid-citrate-dextrose (ACD) solution, which reduces the
volume of anticoagulant, permitted transfusions of greater volumes of blood and allowed longer
term storage.
Carl Walter and W.P. Murphy, Jr., introduced the plastic bag for blood collection in 1950.
Replacing breakable glass bottles with durable plastic bags allowed for the evolution of a
collection system capable of safe and easy preparation of multiple blood components from a
single unit of Whole Blood.
An anticoagulant preservative, CPDA-1 was introduced in 1979. It decreased wastage from
expiration and facilitated resource sharing among blood banks. Newer solutions contain adenine.
[edit] See also
Blood donation
Phlebotomist
Charles Richard Drew
Sergei Yudin
Medical technologist
[edit] Notes
1. ^ Marik PE, Corwin HL. Efficacy of red blood cell transfusion in the critically ill: a
systematic review of the literature. Crit Care Med 2008; 36:2667-2674.
2. ^
http://online.wsj.com/article/SB10001424052748703939404574567771148801570.html
3. ^ "Circular of Information for the use of Human Blood and Blood Components". AABB,
ARC, America's Blood Centers. pp. page 15.
http://www.aabb.org/Documents/About_Blood/Circulars_of_Information/coi0702.pdf.
4. ^ Morris Fishbein, M.D., ed (1976). "Blood Banks". The New Illustrated Medical and
Health Encyclopedia. 1 (Home Library Edition ed.). New York, N.Y. 10016: H. S.
Stuttman Co. pp. 220.
[hide]
v d e
Medicine: Pathology

Principles
of
pathology
Disease/Medical condition (Infection, Neoplasia) Hemodynamics (Ischemia)
Inflammation Wound healing
Cell death: Necrosis (Liquefactive necrosis, Coagulative necrosis, Caseous necrosis,
Fat necrosis) Apoptosis Pyknosis Karyorrhexis Karyolysis
Cellular adaptation: Atrophy Hypertrophy Hyperplasia Dysplasia Metaplasia
(Squamous, Glandular)
accumulations: pigment (Hemosiderin, Lipochrome/Lipofuscin, Melanin) Steatosis

Anatomical
pathology
Surgical pathology Cytopathology Autopsy Molecular pathology Forensic
pathology Dental pathology
Gross examination Histopathology Immunohistochemistry Electron
microscopy Immunofluorescence Fluorescent in situ hybridization

Clinical
pathology
Clinical chemistry Hematopathology Transfusion medicine Medical
microbiology Diagnostic immunology Immunopathology
Enzyme assay Mass spectrometry Chromatography Flow cytometry Blood
bank Microbiological culture Serology

Specific
conditions
Myocardial infarction

[edit] External links
Animated Venipuncture tutorial
Apheresis

Whole blood enters the centrifuge (1) and separates into plasma (2), leukocytes (3), and erythrocytes
(4). Selected components are then drawn off (5).
Apheresis (plural aphereses; also spelt aphaeresis, aphresis; from Ancient Greek
(aphairesis, a taking away)) is a medical technology in which the blood of a donor or patient is
passed through an apparatus that separates out one particular constituent and returns the
remainder to the circulation. It is thus an extracorporeal therapy.
Contents
1 Method
o 1.1 Continuous flow centrifugation (CFC)
o 1.2 Intermittent flow centrifugation
o 1.3 Centrifugation Variables
2 Types of apheresis
o 2.1 Donation
2.1.1 Donor Safety
2.1.1.1 Kit Problems
2.1.1.2 Plasticizer exposure
o 2.2 Therapy
3 Fluid replacement during apheresis
4 Intravenous immunoglobulin
5 See also
6 References
7 External links
[edit] Method
Depending on the substance that is being removed, different processes are employed in
apheresis. If separation by weight is required, centrifugation is the most common method. Other
methods involve absorption onto beads coated with an absorbent material and filtration.
The centrifugation method can be divided into two basic categories:
[edit] Continuous flow centrifugation (CFC)
Continuous flow centrifugation (CFC) historically required two venipunctures as the
"continuous" means the blood is collected, spun, and returned simultaneously. Newer systems
can use a single venipuncture. The main advantage of this system is the low extracorporeal
volume (calculated by volume of the apheresis chamber, the donor's hematocrit, and total blood
volume of the donor) used in the procedure, which may be advantageous in the elderly and for
children.
[edit] Intermittent flow centrifugation
Intermittent flow centrifugation works in cycles, taking blood, spinning/processing it and then
giving back the necessary parts to the donor in a bolus. The main advantage is a single
venipuncture site. To stop the blood from coagulating, anticoagulant is automatically mixed with
the blood as it is pumped from the body into the apheresis machine.
[edit] Centrifugation Variables
The centrifugation process itself has four variables that can be controlled to selectively remove
desired components. The first is spin speed and bowl diameter, the second is "sit time" in
centrifuge, the third is solutes added, and the fourth is not as easily controllable: plasma volume
and cellular content of the donor. The end product in most cases is the classic sedimented blood
sample with the RBC's at the bottom, the "buffy coat" of platelets and WBC's
(lymphocytes/granulocytes (PMN's, basophils, eosinophils/monocytes) in the middle and the
plasma on top.
[edit] Types of apheresis

Disinfect, insert the cannula, pull out the cannula, dress the wound. The blue pressure cuff is controlled
by the platelet apheresis machine in newer models.
There are numerous types of apheresis.

[edit] Donation
Blood taken from a healthy donor can be separated into its component parts during blood
donation, where the needed component is collected and the "unused" components are returned to
the donor. Fluid replacement is usually not needed in these type of collections. There are large
categories of component collections:
Plasmapheresis - blood plasma. Plasmapheresis is useful in collecting FFP (fresh frozen plasma)
of a particular ABO group. Commercial uses aside from FFP for this procedure include immune
globulin products, plasma derivatives, and collection of rare WBC and RBC antibodies.
Erythrocytapheresis- red blood cells. Erythrocytapheresis is the separation of erythrocytes from
whole blood. It is most commonly accomplished using the method of centrifugal sedimentation.
This process is used for red blood cell diseases such as sickle cell crises or severe malaria. The
automated red blood cell collection procedure for donating erythrocytes is referred to as
'Double Reds' or 'Double Red Cell Apheresis.'
[1]

Plateletpheresis (thrombapheresis, thrombocytapheresis) - blood platelets. Plateletpheresis, like
it sounds, is the collection of platelets by apheresis; while returning the RBC's, WBC's, and
component plasma. The yield is normally the equivalent of between six and ten random platelet
concentrates. Quality control demands the platelets from apheresis be equal to or greater than
3.0 x 10^11 in number and have a pH of equal to or greater than 6.2 in 90% of the products
tested and must be used within five days.
Leukapheresis - leukocytes (white blood cells). Leukopheresis is the removal of PMN's,
basophils, eosinophils for transfusion into patients whose PMN's are ineffective or traditional
therapy has failed. There is limited data to suggest the benefit of granulocyte infusion. The
complications of this procedure are the difficulty in collection and short shelf life (24 hours at 20
to 24 C). Since the "buffy coat" layer sits directly atop the RBC layer, HES, a sedimenting agent, is
employed to improve yield while minimizing RBC collection. Quality control demands the
resultant concentrate be 1.0 x 10^10 granulocytes in 75% of the units tested and that the
product be irradiated to avoid graft-versus-host disease (inactivate lymphocytes). Irradiation
does not affect PMN function. Since there is usually a small amount of RBC's collected, ABO
compatibility should be employed when feasible.
Stem cell harvesting - circulating bone marrow cells are harvested to use in bone marrow
transplantation.
[edit] Donor Safety
Single use kits - Apheresis is done using single-use kits, so there is no risk of infection from
blood-contaminated tubing or centrifuge.
Immune system effects - "the immediate decreases in blood lymphocyte counts and serum
immunoglobulin concentrations are of slight to moderate degree and are without known
adverse effects. Less information is available regarding long-term alterations of the immune
system"
[2]

[edit] Kit Problems
Two apheresis kit recalls were:
Baxter Healthcare Corporation (2005) in which "pinhole leaks were observed at the two-omega
end of the umbilicus (multilumen tubing), causing a blood leak. "
[3]

Fenwal Incorporated (2007) in which there were "two instances where the anticoagulant citrate
dextrose (ACD) and saline lines were reversed in the assembly process. The reversed line
connections may not be visually apparent in the monitor box, and could result in excessive ACD
infusion and severe injury, including death, to the donor."
[4]

[edit] Plasticizer exposure
Apheresis uses plastics and tubing, which come into contact with the blood. The plastics are
made of PVC in addition to additives such as a plasticizer, often DEHP. DEHP leaches from the
plastic into the blood, and people have begun to study the possible effects of this leached DEHP
on donors (as well as, obviously, transfusion recipients).
"current risk or preventive limit values for DEHP such as the RfD of the US EPA (20 g/kg/day)
and the TDI of the European Union (20-48 g/kg/day) can be exceeded on the day of the
plateletpheresis. . . . Especially women in their reproductive age need to be protected from
DEHP exposures exceeding the above mentioned preventive limit values."
[5]

"Commercial plateletpheresis disposables release considerable amounts of DEHP during the
apheresis procedure, but the total dose of DEHP retained by the donor is within the normal
range of DEHP exposure of the general population."
[6]

The Baxter company manufactured blood bags without DEHP, but there was little demand for
the product in the marketplace
[7]

"Mean DEHP doses for both plateletpheresis techniques (18.1 and 32.3 g/kg/day) were close to
or exceeded the reference dose (RfD) of the US EPA and tolerable daily intake (TDI) value of the
EU on the day of the apheresis. Therefore, margins of safety might be insufficient to protect
especially young men and women in their reproductive age from effects on reproductivity. At
present, discontinuous-flow devices should be preferred to avert conceivable health risks from
plateletpheresis donors. Strategies to avoid DEHP exposure of donors during apheresis need to
be developed."
[8]

[edit] Therapy

The assembly (A-D), operation (E) and disassembly (F) of the platelet apheresis machine which can be
configured to separate other components as well.
The various apheresis techniques may be used whenever the removed constituent is causing
severe symptoms of disease. Generally, apheresis has to be performed fairly often, and is an
invasive process. It is therefore only employed if other means to control a particular disease have
failed, or the symptoms are of such a nature that waiting for medication to become effective
would cause suffering or risk of complications.
LDL apheresis - removal of low density lipoprotein in patients with familial
hypercholesterolemia.
Photopheresis
Immunoadsorbtion with Staphylococcal protein A-agarose column - removal of allo- and
autoantibodies (in autoimmune diseases, transplant rejection, hemophilia) by directing plasma
through protein A-agarose columns. Protein A is a cell wall component produced by several
strains of Staphylococcus aureus which binds to the Fc region of IgG.
[edit] Fluid replacement during apheresis
It is important to remember that when the apheresis system is used for therapy the system is
removing relatively small amounts of fluid (not more than 10.5 mL/kg body weight). That fluid
must be replaced to keep correct intravascular volume. The fluid replaced is different at different
institutions. If a crystalloid like normal saline is used, the infusion amount should be triple what
is removed as the three to one ratio of NS for plasma is needed to keep up oncotic pressure.
Some institutions use normal serum albumin, but it is costly and can be difficult to find. Some
advocate using FFP or a similar blood product, but there are dangers including citrate toxicity
(from the anticoagulant), ABO incompatibility, infection, and cellular antigens.
[edit] Intravenous immunoglobulin
Intravenous immunoglobulin (IVIG) is a blood product administered intravenously. It contains
the pooled IgG immunoglobulins (antibodies extracted from the plasma of thousands of blood
donors). IVIG is given as a protein replacement therapy for immune deficient patients which
have decreased or abolished antibody production capabilities. IVIG is administered to maintain
adequate antibodies levels to prevent infections and confers a passive immunity. IVIG effects
last between 2 weeks and 3 months. It is mainly used as treatment in three major categories:
Immune deficiencies, such as X-linked agammaglobulinemia, hypogammaglobulinemia (primary
immune deficiencies), and acquired compromised immunity conditions (secondary immune
deficiencies), featuring low antibody levels;
Inflammatory and autoimmune diseases
Acute infections
[edit] See also
Leukoreduction
Venipuncture
[edit] References
1. ^ dtm double red cell
2. ^ http://www3.interscience.wiley.com/journal/113467388/abstract
3. ^ http://www.fda.gov/CbER/recalls/baxaphe013105.htm "Recall of Amicus Apheresis Kits,
Baxter Healthcare Corporation" , US FDA, Jan 31 2005
4. ^ http://www.fda.gov/CbER/recalls/aphfen062107.htm "Recall of CS3000 Apheresis Kits", US
Food and Drug Administration, June 21, 2007
5. ^ http://cat.inist.fr/?aModele=afficheN&cpsidt=17299235 Archives of toxicology ISSN 0340-
5761 CODEN ARTODN 2005, vol. 79, no12, pp. 689-693 [5 page(s) (article)] (1 p.1/4)
6. ^ http://www.ingentaconnect.com/content/bsc/trf/2003/00000043/00000008/art00019 "
Donor exposure to the plasticizer di(2-ethylhexyl)phthalate during plateletpheresis" , Source:
Transfusion, Volume 43, Number 8, August 2003 , pp. 1115-1120(6)
7. ^ http://www.highbeam.com/doc/1G1-56958320.html "SO FAR, PHTHALATE ALTERNATIVES
HAVEN'T INSPIRED MUCH DEMAND.", Article from: Plastics News ,October 25, 1999 , Toloken,
Steve
8. ^ http://cat.inist.fr/?aModele=afficheN&cpsidt=17286818 International journal of hygiene and
environmental health ISSN 1438-4639 , 2005, vol. 208, no6, pp. 489-498 [10 page(s) (article)] (2
p.) "Di(2-ethylhexyl)phthalate (DEHP) exposure of voluntary plasma and platelet donors yea"
R. Bambauer, R. Latza, M.R. Lentz (2009): Therapeutic Plasma Exchange and Selective Plasma
Separation Methods Fundamental Technologies, Pathology and Clinical Results. Pabst,
Lengerich/Berlin, 428 Seiten, ISBN 978-3-89967-458-3
[1]
Apheresis News
American Society for Apheresis
WebPath Apheresis page.
WebPath Blood Donation and Processing
Donating Platelet Apheresis: Facts and the FAQ
Baxter: Automated Component Collection
Haemonetics: PCS2 System
Haemonetics: MCS+ 9000 Dystem
CaridianBCT: Trima Automated Blood Collection System
[hide]
v d e

General
concepts
Apheresis (plasmapheresis, plateletpheresis, leukapheresis) Blood transfusion Coombs test
(direct and indirect) Cross-matching Exchange transfusion

Blood
group
systems
Blood
types
ABO Chido-Rodgers Colton Cromer Diego Dombrock Duffy Gerbich GIL Hh Ii
Indian JMH Kell (Xk) Kidd Knops LW Lewis Lutheran MNS OK P Raph Rh and
RHAG Scianna T-Tn Xg Yt Other

Blood Blood donation Blood substitutes Cryoprecipitate Platelets Plasma Red blood cells
products Whole blood Fresh frozen plasma Cryosupernatant

Coombs test
Coombs test (also known as Coombs' test, antiglobulin test or AGT) refers to two clinical
blood tests used in immunohematology and immunology. The two Coombs tests are the direct
Coombs test (also known as direct antiglobulin test or DAT), and the indirect Coombs test
(also known as indirect antiglobulin test or IAT).
In certain diseases or conditions an individual's blood may contain IgG antibodies that can
specifically bind to antigens on the red blood cell (RBC) surface membrane, and their circulating
red blood cells (RBCs) can become coated with IgG alloantibodies and/or IgG autoantibodies.
Complement proteins may subsequently bind to the bound antibodies. The direct Coombs test is
used to detect these antibodies or complement proteins that are bound to the surface of red blood
cells; a blood sample is taken and the RBCs are washed (removing the patient's own plasma) and
then incubated with antihuman globulin (also known as "Coombs reagent"). If this produces
agglutination of RBCs, the direct Coombs test is positive, a visual indication that antibodies
(and/or complement proteins) are bound to the surface of red blood cells.
The indirect Coombs test is used in prenatal testing of pregnant women, and in testing blood
prior to a blood transfusion. It detects antibodies against RBCs that are present unbound in the
patient's serum. In this case, serum is extracted from the blood, and the serum is incubated with
RBCs of known antigenicity. If agglutination occurs, the indirect Coombs test is positive.
[1]

Contents
1 Mechanism
2 Direct Coombs test
o 2.1 Examples of diseases that give a positive direct Coombs test
2.1.1 Examples of alloimmune hemolysis
2.1.2 Examples of autoimmune hemolysis
2.1.3 Drug-induced immune-mediated hemolysis
o 2.2 Laboratory method
3 Indirect Coombs test
o 3.1 Examples of clinical uses of the indirect Coombs test
3.1.1 Blood transfusion preparation
3.1.2 Antenatal antibody screening
o 3.2 Laboratory method
3.2.1 First stage
3.2.2 Second stage
3.2.3 Titrations
4 Coombs reagent
5 Enhancement media
6 History of the Coombs test
7 References
8 External links
[edit] Mechanism

Schematic showing the direct and indirect Coombs tests.
The two Coombs tests are based on the fact that anti-human antibodies, which are produced by
immunizing non-human species with human serum, will bind to human antibodies, commonly
IgG or IgM. Animal anti-human antibodies will also bind to human antibodies that may be fixed
onto antigens on the surface of red blood cells (also referred to as RBCs), and in the appropriate
test tube conditions this can lead to agglutination of RBCs. The phenomenon of agglutination of
RBCs is important here, because the resulting clumping of RBCs can be visualised; when
clumping is seen the test is positive and when clumping is not seen the test is negative.
Common clinical uses of the Coombs test include the preparation of blood for transfusion in
cross-matching, screening for atypical antibodies in the blood plasma of pregnant women as part
of antenatal care, and detection of antibodies for the diagnosis of immune-mediated haemolytic
anemias.
Coombs tests are done on serum from venous blood samples which are taken from patients by
venepuncture. The venous blood is taken to a laboratory (or blood bank), where trained scientific
technical staff do the Coombs tests. The clinical significance of the result is assessed by the
physician who requested the Coombs test, perhaps with assistance from a laboratory-based
hematologist.
[edit] Direct Coombs test
The direct Coombs test (also known as the direct antiglobulin test or DAT) is used to detect if
antibodies or complement system factors have bound to RBC surface antigens in vivo. The DAT
is not currently required for pre-transfusion testing but may be included by some laboratories.
[edit] Examples of diseases that give a positive direct Coombs test
The direct Coombs test is used clinically when immune-mediated hemolytic anemia (antibody-
mediated destruction of RBCs) is suspected. A positive Coombs test indicates that an immune
mechanism is attacking the patient's own RBC's. This mechanism could be autoimmunity,
alloimmunity or a drug-induced immune-mediated mechanism.
[edit] Examples of alloimmune hemolysis
Hemolytic disease of the newborn (also known as HDN or erythroblastosis fetalis)
o Rh D hemolytic disease of the newborn (also known as Rh disease)
o ABO hemolytic disease of the newborn (the indirect Coombs test may only be weakly
positive)
o Anti-Kell hemolytic disease of the newborn
o Rh c hemolytic disease of the newborn
o Rh E hemolytic disease of the newborn
o Other blood group incompatibility (RhC, Rhe, Kidd, Duffy, MN, P and others)
Alloimmune hemolytic transfusion reactions
[edit] Examples of autoimmune hemolysis
Warm antibody autoimmune hemolytic anemia
o Idiopathic
o Systemic lupus erythematosus
o Evans' syndrome (antiplatelet antibodies and hemolytic antibodies)
Cold antibody autoimmune hemolytic anemia
o Idiopathic cold hemagglutinin syndrome
o Infectious mononucleosis
o Paroxysmal cold hemoglobinuria (rare)
[edit] Drug-induced immune-mediated hemolysis
Methyldopa (IgG mediated type II hypersensitivity)
Penicillin (high dose)
Quinidine (IgM mediated activation of classical complement pathway and Membrane attack
complex, MAC)
(A memory device to remember that the DAT tests the RBCs and is used to test infants for
haemolytic disease of the newborn is: Rh Disease; R = RBCs, D = DAT.)
[edit] Laboratory method
The patient's red blood cells (RBCs) are washed (removing the patient's own serum) and then
incubated with antihuman globulin (also known as Coombs reagent). If immunoglobulin or
complement factors have been fixed on to the RBC surface in-vivo, the antihuman globulin will
agglutinate the RBCs and the direct Coombs test will be positive. (A visual representation of a
positive direct Coombs test is shown in the upper half of the schematic).
[edit] Indirect Coombs test
The indirect Coombs test (also known as the indirect antiglobulin test or IAT) is used to detect
in-vitro antibody-antigen reactions. It is used to detect very low concentrations of antibodies
present in a patient's plasma/serum prior to a blood transfusion. In antenatal care, the IAT is used
to screen pregnant women for antibodies that may cause hemolytic disease of the newborn. The
IAT can also be used for compatibility testing, antibody identification, RBC phenotyping, and
titration studies.
[edit] Examples of clinical uses of the indirect Coombs test
[edit] Blood transfusion preparation
Main articles: blood transfusion and cross-matching
The indirect Coombs test is used to screen for antibodies in the preparation of blood for blood
transfusion. The donor's and recipient's blood must be ABO and Rh D compatible. Donor blood
for transfusion is also screened for infections in separate processes.
Antibody screening
A blood sample from the recipient and a blood sample from every unit of donor blood are
screened for antibodies with the indirect Coombs test. Each sample is incubated against a wide
range of RBCs that together exhibit a full range of surface antigens (ie blood types).
Cross matching
The indirect Coombs test is used to test a sample of the recipient's serum against a sample of the
blood donor's RBCs. This is sometimes called cross-matching blood.
[edit] Antenatal antibody screening
The indirect Coombs test is used to screen pregnant women for IgG antibodies that are likely to
pass through the placenta into the fetal blood and cause haemolytic disease of the newborn.
[edit] Laboratory method
The IAT is a two-stage test. (A cross match is shown visually in the lower half of the schematic
as an example of an indirect Coombs test).
[edit] First stage
Washed test red blood cells (RBCs) are incubated with a test serum. If the serum contains
antibodies to antigens on the RBC surface, the antibodies will bind onto the surface of the RBCs.
[edit] Second stage
The RBCs are washed three or four times with isotonic saline and then incubated with antihuman
globulin. If antibodies have bound to RBC surface antigens in the first stage, RBCs will
agglutinate when incubated with the antihuman globulin (also known Coombs reagent) in this
stage, and the indirect Coombs test will be positive.
[edit] Titrations
By diluting a serum containing antibodies the quantity of the antibody in the serum can be
gauged. This is done by using doubling dilutions of the serum and finding the maximum dilution
of test serum that is able to produce agglutination of relevant RBCs.
[edit] Coombs reagent
Coombs reagent (also known as Coombs antiglobulin or antihuman globulin) is used in both
the direct Coombs test and the indirect Coombs test. Coombs reagent is antihuman globulin. It is
made by injecting human globulin into animals, which produce polyclonal antibodies specific for
human immunoglobulins and human complement system factors. More specific Coombs
reagents or monoclonal antibodies can be used.
[edit] Enhancement media
Both IgM and IgG antibodies bind strongly with their antigens. IgG antibodies are most reactive
at 37C. IgM antibodies are easily detected in saline at room temperature as IgM antibodies are
able to bridge between RBCs owing to their large size, efficiently creating what is seen as
agglutination. IgG antibodies are smaller and require assistance to bridge well enough to form a
visual agglutination reaction. Reagents used to enhance IgG detection are referred to as
potentiators. RBCs have a net negative charge called zeta potential which causes them to have a
natural repulsion for one another. Potentiators reduce the zeta potential of RBC membranes.
Common potentiators include low ionic strength solution (LISS), albumin, polyethylene glycol
(PEG), and proteolytic enzymes.
[edit] History of the Coombs test
The Coombs test was first described in 1945 by Cambridge immunologists Robin Coombs (after
whom it is named), Arthur Mourant and Rob Race.
[2]
Historically, it was done in test tubes.
Today, it is commonly done using microarray and gel technology.
[edit] References
1. ^ F. Rosen and R. Geha, Case Studies in Immunology, 4th ed., Garland Science, p.173.
2. ^ Coombs RRA, Mourant AE, Race RR. A new test for the detection of weak and "incomplete" Rh
agglutinins. Brit J Exp Path 1945;26:255-66.
Coombs testing - Institute for Transfusion Medicine.
Coombs test - direct - Medlineplus.org.
Coombs test - indirect - Medlineplus.org.
Acute Anemia - emedicine.com
Drugs that cause haemolytic anemia - Merck Manual.
MeSH Coombs'+Test

[show]
v d e

[show]
v d e
Operations/surgeries and other procedures of the hemic and lymphatic system (ICD-9-
CM V3 40-41)

Immunoprecipitation
Chromatin immunoprecipitation Immunodiffusion (Ouchterlony double
immunodiffusion, Radial immunodiffusion, Immunoelectrophoresis,
Counterimmunoelectrophoresis)

Immunoassay
ELISA Enzyme Multiplied Immunoassay Technique RAST test
Radioimmunoassay Immunofluorescence

Agglutination Hemagglutination/Hemagglutinin (Coombs test) Latex fixation test

Other
Nephelometry Complement fixation test Immunocytochemistry
Immunohistochemistry (Direct fluorescent antibody) Epitope mapping Skin
allergy test Patch test

M: LMC cell/phys/auag/auab imdf/ipig/tumr proc, drug(L3/4)
M: LMO anat(h,u,t,l)/phys lydi/spdi/thdi/thtu/vatu proc

Cross-matching
Cross-matching blood, in transfusion medicine, refers to the complex testing that is performed
prior to a blood transfusion, to determine if the donor's blood is compatible with the blood of an
intended recipient, or to identify matches for organ transplants. Cross-matching is usually
performed only after other, less complex tests have not excluded compatibility. Blood
compatibility has many aspects, and is determined not only by the blood types (O,A,B,AB), but
also by blood factors, (Rh, Kell, etc.)
Cross-matching is done by a certified laboratory technologist, in a laboratory. It can be done
electronically, with a computer database, or serologically. Simpler tests may be used to
determine blood type (only), or to screen for antibodies (only). (indirect Coombs test).
Contents
1 Types of cross-matching
o 1.1 Electronic cross-matching
o 1.2 Serological cross-matching
2 Emergencies
3 External links
[edit] Types of cross-matching
[edit] Electronic cross-matching
Electronic cross-matching is essentially a computer-assisted analysis of the data entered from
testing done on the donor unit and blood samples drawn from intended recipient. This includes
ABO/Rh typing of the unit and of the recipient, and an antibody screen of the recipient.
Electronic cross-matching can only be used if a patient has a negative antibody screen, which
means that they do not have any active red blood cell atypical antibodies, or they are below the
detectable level of current testing methods. If all of the data entered is compatible, the computer
will print a compatibility label stating that the unit is safe to transfuse.
[edit] Serological cross-matching
In serological cross-matching, red blood cells from the donor unit are tested against the plasma
of the patient in need of the blood transfusion. If the patients serum contains antibodies against
the antigens present on the donor red blood cells, agglutination will occur. Agglutination is
considered a positive reaction indicating that the donor unit is incompatible for that specific
patient. If no agglutination occurs the unit is deemed compatible and is safe to transfuse.
[edit] Emergencies
In the case of an emergency a physician can request "uncross-matched blood", or donor units of
blood that have not been cross-matched. It is thought that this lifesaving measure is of more
benefit than any risk of an antibody-mediated transfusion reaction. In addition, the risk of a
serious transfusion reaction can be minimized if the donor unit is both ABO-compatible and
Rhesus (Rh)-compatible. Type O and Rh negative blood can be given if the recipient's blood
group is not known, as may happen in an emergency. In an emergency, blood grouping can be
done easily and quickly in 2 or 3 minutes in the laboratory on glass slides with appropriate
reagents, by trained technical staff. This method depends on the presence or absence of
agglutination, which can usually be visualized directly, although occasionally a light microscope
may be needed. If laboratory services are not available, another system of deciding which type of
blood to use in an emergency is the bedside card method of blood grouping, where a drop of the
intended recipients' blood is added to dried reagents on a prepared card. This method may not be
as reliable as laboratory methods, which are preferable.
HealthAtoZ.com Blood typing and crossmatching
Nobelprize.org Interactive online game for blood typing and transfusion (Flash Player 5
required)
[hide]
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concepts

Blood
group
systems
Blood
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Blood
products
Retrieved from "http://en.wikipedia.org/wiki/Cross-matching"
Categories: Transfusion medicine | Hematology
Human blood group systems
The International Society of Blood Transfusion (ISBT) currently recognises 30 major blood
group systems (including the ABO and Rh systems).
[1]
Thus, in addition to the ABO antigens
and Rhesus antigens, many other antigens are expressed on the red blood cell surface membrane.
For example, an individual can be AB RhD positive, and at the same time M and N positive
(MNS system), K positive (Kell system), and Le
a
or Le
b
positive (Lewis system). Many of the
blood group systems were named after the patients in whom the corresponding antibodies were
initially encountered.
The ISBT definition of a blood group system is where one or more antigens are "controlled at a
single gene locus or by two or more very closely linked homologous genes with little or no
observable recombination between them".
[2]

Contents
1 Blood grouping procedure
2 Rare blood types
3 Blood group systems
4 References
5 External links
Blood grouping procedure
Blood is composed of cells suspended in a liquid. The liquid portion is the plasma, from which
therapeutic fractions and derivatives are made.
Suspended in the plasma are three types of cells:
Red cells carry oxygen
White cells fight infection
Platelets stop bleeding in injuries
The most common type of grouping is the ABO grouping. Red Blood Cells have a protein coat
on their surface which distinguishes them. According to this blood is divided into four groups:
A (A oligosaccharide is present)
B (B oligosaccharide is present)
AB (A and B oligosaccharides are present)
O (neither A nor B, only their precursor H oligosaccharide present)
There are subtypes under this grouping (listed as A1, A2, A1B or A2B) some of which are
quite rare. Apart from this there is a protein which plays an important part in the grouping of
blood. This is called the Rh factor. If this is present, the particular blood type is called positive. If
it is absent, it is called negative. Thus we have the following broad categories:
A1 Negative (A1 -ve)
A1 Positive (A1 +ve)
A1B Negative (A1B -ve)
A1B Positive (A1B +ve)
A2 Negative (A2 -ve)
A2 Positive (A2 +ve)
A2B Negative (A2B -ve)
A2B Positive (A2B +ve)
B Negative (B -ve)
B Positive (B +ve)
O Negative (O -ve)
O Positive (O +ve)
[3]

Rare blood types
A blood type is classified as rare when more than 200 donors have to be screened to find one
compatible donor with blood of that type.
[citation needed]
In the "ABO" system, all blood belongs to
one of four major group: A, B, AB, or O. But there are more than two hundred minor blood
groups that can complicate blood transfusions. These are known as rare blood types. About one
person in 1,000 will inherit a rare blood type.
[citation needed]
Whereas common blood types are
expressed in a letter or two, with maybe a plus or a minus, a fewer number of people express
their blood type in an extensive series of letters in addition to their 'ABO' type designation. For
example, AB +ve, O -ve, and A1 -ve are rare types.
[citation needed]

Blood group systems
ISBT
N
System
name
System
symbol
Epitope or carrier, notes Chromosome
001 ABO ABO
Carbohydrate (N-Acetylgalactosamine,
galactose). A, B and H antigens mainly
elicit IgM antibody reactions, although
anti-H is very rare, see the Hh antigen
system (Bombay phenotype, ISBT #18).
9
002 MNS MNS
GPA / GPB (glycophorins A and B).
Main antigens M, N, S, s.
4
003 P P1 Glycolipid. Antigen P1. 22
004 Rh RH
Protein. C, c, D, E, e antigens (there is no
"d" antigen; lowercase "d" indicates the
absence of D).
1
005 Lutheran LU
Protein (member of the immunoglobulin
superfamily). Set of 21 antigens.
19
006 Kell KEL
Glycoprotein. K
1
can cause hemolytic
disease of the newborn (anti-Kell), which
can be severe.
7
007 Lewis LE
Carbohydrate (fucose residue). Main
antigens Le
a
and Le
b
- associated with
tissue ABH antigen secretion.
19
008 Duffy FY
Protein (chemokine receptor). Main
antigens Fy
a
and Fy
b
. Individuals lacking
Duffy antigens altogether are immune to
malaria caused by Plasmodium vivax and
Plasmodium knowlesi.
1
009 Kidd JK
Protein (urea transporter). Main antigens
Jk
a
and Jk
b
.
18
010 Diego DI
Glycoprotein (band 3, AE 1, or anion
exchange). Positive blood is found only
among East Asians and Native
Americans.
17
011
Yt or
Cartwright
YT Protein (AChE, acetylcholinesterase). 7
012 XG XG Glycoprotein. X
013 Scianna SC Glycoprotein. 1
014 Dombrock DO
Glycoprotein (fixed to cell membrane by
GPI, or glycosyl-phosphatidyl-inositol).
12
015 Colton CO
Aquaporin 1. Main antigens Co(a) and
Co(b).
7
016
Landsteiner-
Wiener
LW
Protein (member of the immunoglobulin
superfamily).
19
017 Chido/Rodgers CH/RG C4A C4B (complement fractions). 6
018 Hh/Bombay H Carbohydrate (fucose residue). 19
019 Kx XK Glycoprotein. X
020 Gerbich GE GPC / GPD (Glycophorins C and D). 2
021 Cromer CROM
Glycoprotein (DAF or CD55, regulates
complement fractions C3 and C5,
attached to the membrane by GPI).
1
022 Knops KN
Glycoprotein (CR1 or CD35, immune
complex receptor).
1
023 Indian IN Glycoprotein (CD44 adhesion function?). 11
024 Ok OK Glycoprotein (CD147). 19
025 Raph MER2 Transmembrane glycoprotein. 11
026 JMH JMH Protein (fixed to cell membrane by GPI). 6
027 Ii I
Branched (I) / unbranched (i)
polysaccharide.
6
028 Globoside GLOB Glycolipid. Antigen P. 3
029 GIL GIL Aquaporin 3. 9
030
Rh-associated
glycoprotein
RHAG Rh-associated glycoprotein. 6
References
1. ^ "Table of blood group systems". International Society of Blood Transfusion. October
2006.
http://blood.co.uk/ibgrl/ISBT%20Pages/ISBT%20Terminology%20Pages/Table%20of%
20blood%20group%20systems.htm. Retrieved 2006-11-14.
2. ^ ISBT Committee on Terminology for Red Cell Surface Antigens. "Terminology Home
Page".
http://ibgrl.blood.co.uk/ISBT%20Pages/ISBT%20Terminology%20Pages/Terminology%
20Home%20Page.htm. Retrieved 2009-02-13.
3. ^ Information Courtesy: Indian Red Cross Society, Tamil Nadu Branch.
External links
ISBT Table of blood group antigens within systems Updated August 2008.
BGMUT NCBI Blood Group Antigen Gene Mutation Database.
Blood group The Faculty of Applied Sciences, University of the West of England.
Distribution of Blood Types, Behavioral Sciences Department, Palomar College.
[hide]
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concepts

Blood
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Blood
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Blood type

Blood type (or blood group) is determined, in part, by the ABO blood group antigens present on
red blood cells.
A blood type (also called a blood group) is a classification of blood based on the presence or
absence of inherited antigenic substances on the surface of red blood cells (RBCs). These
antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the blood
group system. Some of these antigens are also present on the surface of other types of cells of
various tissues. Several of these red blood cell surface antigens that stem from one allele (or very
closely linked genes), collectively form a blood group system.
[1]
Blood types are inherited and
represent contributions from both parents. A total of 30 human blood group systems are now
recognized by the International Society of Blood Transfusion (ISBT).
[2]

Many pregnant women carry a fetus with a different blood type from their own, and the mother
can form antibodies against fetal RBCs. Sometimes these maternal antibodies are IgG, a small
immunoglobulin, which can cross the placenta and cause hemolysis of fetal RBCs, which in turn
can lead to hemolytic disease of the newborn, an illness of low fetal blood counts which ranges
from mild to severe.
[3]

Contents
1 Blood group systems
o 1.1 ABO blood group system
o 1.2 Rh blood group system
o 1.3 ABO and Rh distribution by country
o 1.4 Other blood group systems
2 Clinical significance
o 2.1 Blood transfusion
o 2.2 Hemolytic disease of the newborn (HDN)
3 Compatibility
o 3.1 Blood products
o 3.2 Red blood cell compatibility
o 3.3 Plasma compatibility
o 3.4 Universal donors and universal recipients
4 Blood group genotyping
5 Conversion
6 History
7 Cultural beliefs and other claims
8 References
9 Further reading
10 External links
[edit] Blood group systems
A total of 30 human blood group systems are now recognized by the International Society of
Blood Transfusion (ISBT).
[2]
A complete blood type would describe a full set of 30 substances
on the surface of RBCs, and an individual's blood type is one of the many possible combinations
of blood-group antigens. Across the 30 blood groups, over 600 different blood-group antigens
have been found,
[4]
but many of these are very rare or are mainly found in certain ethnic groups.
Almost always, an individual has the same blood group for life, but very rarely an individual's
blood type changes through addition or suppression of an antigen in infection, malignancy, or
autoimmune disease.
[5][6][7][8]
An example of this rare phenomenon is the case of Demi-Lee
Brennan, an Australian citizen, whose blood group changed after a liver transplant.
[9][10]
Another
more common cause in blood-type change is a bone marrow transplant. Bone-marrow transplants
are performed for many leukemias and lymphomas, among other diseases. If a person receives
bone marrow from someone who is a different ABO type (e.g., a type A patient receives a type O
bone marrow), the patient's blood type will eventually convert to the donor's type.
Some blood types are associated with inheritance of other diseases; for example, the Kell antigen
is sometimes associated with McLeod syndrome.
[11]
Certain blood types may affect susceptibility
to infections, an example being the resistance to specific malaria species seen in individuals
lacking the Duffy antigen.
[12]
The Duffy antigen, presumably as a result of natural selection, is
less common in ethnic groups from areas with a high incidence of malaria.
[13]

ABO blood group system

ABO blood group system - diagram showing the carbohydrate chains that determine the ABO
blood group
Main article: ABO blood group system
The ABO system is the most important blood-group system in human-blood transfusion. The
associated anti-A antibodies and anti-B antibodies are usually "Immunoglobulin M", abbreviated
IgM, antibodies. ABO IgM antibodies are produced in the first years of life by sensitization to
environmental substances such as food, bacteria, and viruses. The "O" in ABO is often called "0"
(zero/null) in other languages.
[14]

Phenotype Genotype
A AA or AO
B BB or BO
AB AB
O OO
[edit] Rh blood group system
Main article: Rh blood group system
The Rh system is the second most significant blood-group system in human-blood transfusion
with currently 50 antigens. The most significant Rh antigen is the D antigen because it is the
most likely to provoke an immune system response of the five main Rh antigens. It is common
for D-negative individuals not to have any anti-D IgG or IgM antibodies, because anti-D
antibodies are not usually produced by sensitization against environmental substances. However,
D-negative individuals can produce IgG anti-D antibodies following a sensitizing event: possibly
a fetomaternal transfusion of blood from a fetus in pregnancy or occasionally a blood transfusion
with D positive RBCs.
[15]
Rh disease can develop in these cases.
[16]

[edit] ABO and Rh distribution by country
ABO and Rh blood type distribution by nation (population averages)
Country Population
[17]
O+ A+ B+ AB+
O-

A-

B-

AB-

Australia
[18]
21,262,641 40% 31% 8% 2% 9% 7% 2% 1%
Austria
[19]
8,210,281 30% 33% 12% 6% 7% 8% 3% 1%
Belgium
[20]
10,414,336 38% 34% 8.5% 4.1% 7% 6% 1.5% 0.8%
Brazil
[21]
198,739,269 36% 34% 8% 2.5% 9% 8% 2% 0.5%
Canada
[22]
33,487,208 39% 36% 7.6% 2.5% 7% 6% 1.4% 0.5%
Denmark
[23]
5,500,510 35% 37% 8% 4% 6% 7% 2% 1%
Estonia
[24]
1,299,371 30% 31% 20% 6% 4.5% 4.5% 3% 1%
Finland
[25]
5,250,275 27% 38% 15% 7% 4% 6% 2% 1%
France
[26]
62,150,775 36% 37% 9% 3% 6% 7% 1% 1%
Germany
[27]
82,329,758 35% 37% 9% 4% 6% 6% 2% 1%
Hong Kong SAR
[28]
7,055,071 40% 26% 27% 7% 0.31% 0.19% 0.14% 0.05%
Iceland
[29]
306,694 47.6% 26.4% 9.3% 1.6% 8.4% 4.6% 1.7% 0.4%
India
[30]
1,166,079,217 36.5% 22.1% 30.9% 6.4% 2.0% 0.8% 1.1% 0.2%
Ireland
[31]
4,203,200 47% 26% 9% 2% 8% 5% 2% 1%
Israel
[32]
7,233,701 32% 34% 17% 7% 3% 4% 2% 1%
Netherlands
[33]
16,715,999 39.5% 35% 6.7% 2.5% 7.5% 7% 1.3% 0.5%
New Zealand
[34]
4,213,418 38% 32% 9% 3% 9% 6% 2% 1%
Norway
[35]
4,660,539 34% 42.5% 6.8% 3.4% 6% 7.5% 1.2% 0.6%
Poland
[36]
38,482,919 31% 32% 15% 7% 6% 6% 2% 1%
Portugal
[37]
10,707,924 36.2% 39.8% 6.6% 2.9% 6.0% 6.6% 1.1% 0.5%
Saudi Arabia
[38]
28,686,633 48% 24% 17% 4% 4% 2% 1% 0.23%
South Africa
[39]
49,320,000 39% 32% 12% 3% 7% 5% 2% 1%
Spain
[40]
40,525,002 36% 34% 8% 2.5% 9% 8% 2% 0.5%
Sweden
[41]
9,059,651 32% 37% 10% 5% 6% 7% 2% 1%
Turkey
[42]
76,805,524 29.8% 37.8% 14.2% 7.2% 3.9% 4.7% 1.6% 0.8%
United Kingdom
[43]
61,113,205 37% 35% 8% 3% 7% 7% 2% 1%
United States
[44]
307,212,123 37.4% 35.7% 8.5% 3.4% 6.6% 6.3% 1.5% 0.6%
Population-weighted
mean
(total population
= 2,261,025,244)
36.44% 28.27% 20.59% 5.06% 4.33% 3.52% 1.39% 0.45%
[show]Racial & Ethnic Distribution of ABO (without Rh) Blood Types
[45]

(This table has more entries than the table above but does not distinguish between Rh types.)
PEOPLE GROUP O (%) A (%) B (%)
AB
(%)
Aborigines 61 39 0 0
Abyssinians 43 27 25 5
Ainu (Japan) 17 32 32 18
Albanians 38 43 13 6
Grand Andamanese 9 60 23 9
Arabs 34 31 29 6
Armenians 31 50 13 6
Asian (in USA - General) 40 28 27 5
Austrians 36 44 13 6
Bantus 46 30 19 5
Basques 51 44 4 1
Belgians 47 42 8 3
Blackfoot (N. Am. Indian) 17 82 0 1
Bororo (Brazil) 100 0 0 0
Brazilians 47 41 9 3
Bulgarians 32 44 15 8
Burmese 36 24 33 7
Buryats (Siberia) 33 21 38 8
Bushmen 56 34 9 2
Chinese-Canton 46 23 25 6
Chinese-Peking 29 27 32 13
Chuvash 30 29 33 7
Czechs 30 44 18 9
Danes 41 44 11 4
Dutch 45 43 9 3
Egyptians 33 36 24 8
English 47 42 9 3
Eskimos (Alaska) 38 44 13 5
Eskimos (Greenland) 54 36 23 8
Estonians 34 36 23 8
Fijians 44 34 17 6
Finns 34 41 18 7
French 43 47 7 3
Georgians 46 37 12 4
Germans 41 43 11 5
Greeks 40 42 14 5
Gypsies (Hungary) 29 27 35 10
Hawaiians 37 61 2 1
Hindus (Bombay) 32 29 28 11
Hungarians 36 43 16 5
Icelanders 56 32 10 3
Indians (India - General) 37 22 33 7
Indians (USA - General) 79 16 4 1
Irish 52 35 10 3
Italians (Milan) 46 41 11 3
Japanese 30 38 22 10
Jews (Germany) 42 41 12 5
Jews (Poland) 33 41 18 8
Kalmuks 26 23 41 11
Kikuyu (Kenya) 60 19 20 1
Koreans 28 32 31 10
Lapps 29 63 4 4
Latvians 32 37 24 7
Lithuanians 40 34 20 6
Malaysians 62 18 20 0
Maori 46 54 1 0
Mayas 98 1 1 1
Moros 64 16 20 0
Navajo (N. Am. Indian) 73 27 0 0
Nicobarese (Nicobars) 74 9 15 1
Norwegians 39 50 8 4
Papuas (New Guinea) 41 27 23 9
Persians 38 33 22 7
Peru (Indians) 100 0 0 0
Filipinos 45 22 27 6
Poles 33 39 20 9
Portuguese 35 53 8 4
Romanians 34 41 19 6
Russians 33 36 23 8
Sardinians 50 26 19 5
Scots 51 34 12 3
Serbians 38 42 16 5
Shompen (Nicobars) 100 0 0 0
Slovaks 42 37 16 5
South Africans 45 40 11 4
Spanish 38 47 10 5
Sudanese 62 16 21 0
Swedes 38 47 10 5
Swiss 40 50 7 3
Tartars 28 30 29 13
Thais 37 22 33 8
Turks 43 34 18 6
Ukrainians 37 40 18 6
USA (US blacks) 49 27 20 4
USA (US whites) 45 40 11 4
Vietnamese 42 22 30 5
Mean 43.91 34.80 16.55 5.14
Standard deviation 16.87 13.80 9.97 3.41
Blood group B has its highest frequency in Northern India and neighboring Central Asia, and its
incidence diminishes both towards the west and the east, falling to single digit percentages in
Spain.
[46][47]
It is believed to have been entirely absent from Native American and Australian
Aboriginal populations prior to the arrival of Europeans in those areas.
[47][48]

Blood group A is associated with high frequencies in Europe, especially in Scandinavia and
Central Europe, although its highest frequencies occur in some Australian Aborigine populations
and the Blackfoot Indians of Montana.
[49][50]

[edit] Other blood group systems
Main article: Human blood group systems
The International Society of Blood Transfusion currently recognizes 30 blood-group systems
(including the ABO and Rh systems).
[2]
Thus, in addition to the ABO antigens and Rh antigens,
many other antigens are expressed on the RBC surface membrane. For example, an individual
can be AB, D positive, and at the same time M and N positive (MNS system), K positive (Kell
system), Le
a
or Le
b
negative (Lewis system), and so on, being positive or negative for each blood
group system antigen. Many of the blood group systems were named after the patients in whom
the corresponding antibodies were initially encountered.
Rh blood group system
The Rh blood group system is one of the currently 30 human blood group systems. It is the
clinically most important blood group system besides ABO. The Rh blood group system
currently consists of 50 defined blood group antigens among which the 5 antigens D, C, c, E, and
e are the most important ones. The commonly used terms Rh factor, Rh positive and Rh negative
refer to the D antigen only. Besides its role in blood transfusion, the Rh blood group system, in
particular the strongest D antigen, is a relevant cause of the hemolytic disease of the newborn for
which prevention is key.
Contents
1 Rh factor
2 History of discoveries
3 Rh nomenclature
4 Rh system antigens
5 Hemolytic disease of the newborn
6 Population data
7 Inheritance
8 Function
9 Origin of RHD polymorphism
10 Weak D
11 Other Rh group antigens
12 References
13 External links
[edit] Rh factor
Individuals either have, or do not have, the "Rh factor" on the surface of their red blood cells.
This term strictly refers only to the most immunogenic D antigen of the Rh blood group system.
This is usually indicated by Rh positive (does have the D antigen) or Rh negative (does not have
the D antigen) suffix to the ABO blood type. However, other antigens of this blood group system
are also clinically relevant. These antigens are listed separately (see nomenclature below). In
contrast to ABO, immunization against Rh can generally only occur through blood transfusion or
placental exposure during pregnancy.
[edit] History of discoveries
In 1939, Drs. Philip Levine and Rufus Stetson published in a first case report the clinical
consequences of non-recognized Rh factor, hemolytic transfusion reaction and hemolytic disease
of the newborn in its most severe form.
[1]
It was recognized that the serum of the reported
woman agglutinated with red blood cells of about 80% of the people although the then known
blood groups, in particular ABO were matched. No name was given to this then for the first time
described agglutinin. In 1940, Drs. Karl Landsteiner and Alexander S. Wiener reported a serum
that also reacted with about 85% of different human red blood cells.
[2]
This serum was produced
by immunizing rabbits with red blood cells from Rhesus macaque. The antigen that induced this
immunization was designated by them as Rh factor "to indicate that rhesus blood had been used
for the production of the serum."
[3]

Based on the serologic similarities Rh factor was later also used for antigens, and anti-Rh for
antibodies, found in humans such as the previously described by Levine and Stetson. Although
differences between these two sera were shown already in 1942 and clearly demonstrated in
1963, the already widely used term "Rh" was kept for the clinically described human antibodies
which are different to the ones related to the Rhesus ape. This real factor found in Rhesus
macaque was classified in the Landsteiner-Wiener antigen system (antigen LW, antibody anti-
LW) in honor to the discoverers.
[4][5]
It was recognized that the Rh factor was just one in a
system of various antigens. Based on different models of genetic inheritance, two different
terminologies were developed; both of them are still in use (see below).
The clinical significance of this highly immunizing D antigen (i.e. Rh factor) was soon realized.
Some keystones were to recognize its importance for blood transfusion including reliable
diagnostic tests, and hemolytic disease of the newborn including exchange transfusion and very
importantly the prevention of it by screening and prophylaxis.
[edit] Rh nomenclature
The Rh blood group system has two sets of nomenclatures, one developed by Fisher and Race
and one by Wiener. Both systems reflected alternative theories of inheritance. The Fisher-Race
system, which is more commonly in use today, uses the CDE nomenclature. This system was
based on the theory that control the product of the corresponding antigen (e.g., a "D gene"
produces D antigen, and so on). However, the d gene was hypothetical, not actual.
The Wiener system used the Rh-Hr nomenclature. This system was based on the theory that there
was one gene at a single locus on each chromosome of the pair which controls production of
multiple antigens. In this theory a gene R is supposed to give rise to the blood factors Rho, rh,
and hr and the gene r to produce hr and hr.
Notations of the two theories are used interchangeably in blood banking (e.g., Rho(D)). Wieners
notation is more complex and cumbersome for routine use. Because it is simpler to explain, the
Fisher-Race theory is more widely used.
DNA testing has shown that both theories are partially correct.
[citation needed]
There are in fact two
linked genes (RHCE and RHD), one with multiple specificities and one with a single specificity.
Thus, Wiener's postulate that a gene could have multiple specificities (something many did not
give credence to originally) has been proven correct. On the other hand, Wiener's theory that
there is one gene has proven incorrect, as has the Fischer-Race theory that there are three genes.
[edit] Rh system antigens
The proteins which carry the Rh antigens are transmembrane proteins, whose structure suggest
that they are ion channels[1]. The main antigens are D, C, E, c and e, which are encoded by two
adjacent gene loci, the RHD gene which encodes the RhD protein with the D antigen (and
variants) [2] and the RHCE gene which encodes the RhCE protein with the C, E, c and e antigens
(and variants) [3]. There is no d antigen. Lowercase "d" indicates the absence of the D antigen
(the gene is usually deleted or otherwise nonfunctional).
Rhesus genotypes
Genotype symbol Rh(D) status
cde/cde rr Negative
CDe/cde R
1
r Positive
CDe/CDe R
1
R
1
Positive
cDE/cde R
2
r Positive
CDe/cDE R
1
R
2
Positive
cDE/cDE R
2
R
2
Positive
Rh Phenotypes in Patients and Donors
[6]

Rh Phenotype CDE Patients (%) Donors (%)
R
1
r CcDe 37.4 33.0
R
1
R
2
CcDEe 35.7 30.5
R
1
R
1
CDe 5.7 21.8
rr ce 10.3 11.6
R
2
r cDEe 6.6 10.4
R
0
R
0
cDe 2.8 2.7
R
2
R
2
cDE 2.8 2.4
rr cEe 0.98
R
Z
R
Z
CDE 0.03
rr Cce 0.8
Hemolytic disease of the newborn
This condition occurs when there is an incompatibility between the blood types of the mother
and the fetus. These terms do not indicate which specific antigen-antibody incompatibility is
implicated. The disorder in the fetus due to Rh D incompatibility is known as erythroblastosis
fetalis.
Hemolytic comes from two words: hemo (blood) and lysis (destruction) or breaking down of red
blood cells
Erythroblastosis refers to the making of immature red blood cells
Fetalis refers to the fetus
When the condition is caused by the Rh D antigen-antibody incompatibility, it is called Rh D
Hemolytic disease of the newborn (often called Rhesus disease or Rh disease for brevity).
Here, sensitization to Rh D antigens (usually by feto-maternal transfusion during pregnancy)
may lead to the production of maternal IgG anti-D antibodies which can pass through the
placenta. This is of particular importance to D negative females of or below childbearing age,
because any subsequent pregnancy may be affected by the Rhesus D hemolytic disease of the
newborn if the baby is D positive. The vast majority of Rh disease is preventable in modern
antenatal care by injections of IgG anti-D antibodies (Rho(D) Immune Globulin). The incidence
of Rhesus disease is mathematically related to the frequency of D negative individuals in a
population, so Rhesus disease is rare in East Asians, South Americans, and Africans, but more
common in Caucasians.
Symptoms and signs in the fetus:
o Enlarged liver, spleen, or heart and fluid buildup in the fetus' abdomen seen via
ultrasound.
Symptoms and signs in the newborn:
o Anemia which creates the newborn's pallor (pale appearance).
o Jaundice or yellow discoloration of the newborn's skin, sclera or mucous membrane.
This may be evident right after birth or after 2448 hours after birth. This is caused by
bilirubin (one of the end products of red blood cell destruction).
o Enlargement of the newborn's liver and spleen.
o The newborn may have severe edema of the entire body.
o Dyspnea or difficulty breathing.
[edit] Population data
The frequency of Rh factor blood types and the RhD neg allele gene differs in various
populations.
Population data for the Rh D factor and the RhD neg allele
[7]

Population Rh(D) Neg Rh(D) Pos
Rh(D) Neg
alleles
European Basque
approx
35%
[citation needed]

65% approx 60%
other Europeans 16% 84% 40%
African American approx 7% 93% approx 26%
Native Americans approx 1% 99% approx 10%
African descent less 1% over 99% 3%
Asian less 1% over 99% 1%
[edit] Inheritance
The D antigen is inherited as one gene (RHD) (on the short arm of the first chromosome,
1p36.13-p34.3) with various alleles. Very much simplified one can think of alleles that are
positive or negative for the D antigen. The gene codes for the RhD protein on the red cell
membrane. D- individuals who lack a functional RHD gene do not produce the D antigen, and
may be immunized by D+ blood.
The epitopes for the next 4 most common Rh antigens, C, c, E and e are expressed on the highly
similar RhCE protein that is genetically encoded in the RHCE gene. It has been shown that the
RHD gene arose by duplication of the RHCE gene during primate evolution. Mice have just one
RH gene.
[8]

[edit] Function
The structure homology data suggest that the product of RHD gene, the RhD protein, acts as an
ion pump of uncertain specificity (CO
2
or NH
3
) and unknown physiological role
[9]

[10]
. Three
recent studies
[11]

[12]

[13]
have reported a protective effect of the RhD-positive phenotype,
especially RhD heterozygosity, against the negative effect of latent toxoplasmosis on
psychomotor performance of infected subjects. RhD-negative compared to RhD-positive subjects
without anamnestic titres of anti-Toxoplasma antibodies have shorter reaction times in tests of
simple reaction times. And conversely, RhD-negative subjects with anamnestic titres (i.e. with
latent toxoplasmosis) exhibited much longer reaction times than their RhD-positive counterparts.
The published data suggested that only the protection of RhD-positive heterozygotes was long
term in nature; the protection of RhD-positive homozygotes decreased with duration of the
infection while the performance of RhD-negative homozygotes decreased immediately after the
infection.
[edit] Origin of RHD polymorphism
For a long time, the origin of RHD polymorphism was an evolutionary enigma
[14]

[15]

[16]
. Before
the advent of modern medicine, the carriers of the rarer allele (e.g. RhD-negative women in a
population of RhD positives or RhD-positive men in a population of RhD negatives) were at a
disadvantage as some of their children (RhD-positive children born to preimmunised RhD-
negative mothers) were at a higher risk of fetal or newborn death or health impairment from
hemolytic disease. It was suggested that higher tolerance of RhD-positive heterozygotes against
Toxoplasma-induced impairment of reaction time
[17]

[18]
and Toxoplasma-induced increase of
risk of traffic accident
[19]
could counterbalance the disadvantage of the rarer allele and could be
responsible both for the initial spread of the RhD allele among the RhD-negative population and
for a stable RhD polymorphism in most human populations. It was also suggested that
differences in the prevalence of Toxoplasma infection between geographical regions (095%)
could also explain the striking variation in the frequency of RhD-negative alleles between
populations. According to some parasitologists
[20]
it is possible that the better psychomotor
performance of RhD-negative subjects in the Toxoplasma-free population could be the reason for
spreading of the d allele (deletion) in the European population. In contrast to the situation in
Africa and certain (but not all) regions of Asia, the abundance of wild cats (definitive hosts of
Toxoplasma gondii) in the European territory was very low before the advent of domestic cat.
[edit] Weak D
In serologic testing, D positive blood is easily identified. Units which are D negative are often
retested to rule out a weaker reaction. This was previously referred to as D
u
, which has been
replaced.
[21]
In some cases, this phenotype occurs because of an altered surface protein that is
more common in people of African descent. The testing is difficult, since using different anti-D
reagents, especially the older polyclonal reagents, may give different results.
The practical implication of this is that people with this sub-phenotype will have a product
labeled as "D positive" when donating blood. When receiving blood, they are sometimes typed
as a "D negative", though this is the subject of some debate. Most "Weak D" patients can receive
"D positive" blood without complications.
[22]
However, it is important to correctly identify the
ones that have to considere D+ or D-. This is important, since most blood banks have a limited
supply of "D negative" blood and the correct transfusion is clinically relevant. In this respect,
genotyping of blood groups has much simplified this detection of the various variants in the Rh
blood group system.
[edit] Other Rh group antigens
Currently, 50 antigens have been described in the Rh group system, among the here described D,
C, c, E and e antigens are the most important one. The others are much less frequently
encountered or are rarely clinically significant. Each is given a number, though the highest
assigned number (CEST or RH57 according to the ISBT terminology) is not an accurate
reflection of the antigens encountered since many (e.g. Rh38) have been combined, reassigned to
other groups, or otherwise removed.
[23]

[edit] References
1. ^ Levine P, Stetson RE (1939). "An unusual case of intragroup agglutination". JAMA 113: 126
127.
2. ^ Landsteiner K, Wiener AS (1940). "An agglutinable factor in human blood recognized by
immune sera for rhesus blood". Proc Soc Exp Biol Med 43: 2234.
3. ^ Landsteiner K, Wiener AS (1941). "Studies on an agglutinogen (Rh) in human blood reacting
with anti-rhesus sera and with human isoantibodies". J Exp Med 74 (4): 309320.
4. ^ Avent ND, Reid ME (2000). "The Rh blood group system: a review". Blood 95 (2): 375387.
5. ^ Scott ML (2004). "The complexities of the Rh system". Vox sang 87 ((Suppl. 1)): S58-S62.
6. ^ Canatan, Duran; Nilgn Acar & Banu Kili (1999). "Rh Subgroups and Kell Antigens in Patients
With Thalassemia and in Donors in Turkey" (PDF). Turkish Journal of Medical Sciences (Tbitak)
29: 1557. http://journals.tubitak.gov.tr/medical/issues/sag-99-29-2/sag-29-2-15-98073.pdf.
7. ^ Mack, Steve (March 21, 2001). "Re: Is the RH negative blood type more prevalent in certain
ethnic groups?". MadSci Network.
http://www.madsci.org/posts/archives/mar2001/985200157.Ge.r.html.
8. ^ Wagner FF, Flegel WA (Mar 2002). "RHCE represents the ancestral RH position, while RHD is
the duplicated gene". Blood 99 (6): 22723. doi:10.1182/blood-2001-12-0153. PMID 11902138.
http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=11902138.
9. ^ Kustu S, Inwood W (2006). "Biological gas channels for NH
3
and CO
2
: evidence that Rh (rhesus)
proteins are CO
2
channels". Transfusion Clinique et Biologique 13: 103110.
10. ^ Biver S, Scohy S, Szpirer J, Szpirer C, Andre B, Marini AM (2006). "Physiological role of the
putative ammonium transporter RhCG in the mouse.". Transfusion Clinique et Biologique 13:
167168.
11. ^ Novotna M, Havlicek J, Smith AP, Kolbekova P, Skallova A, Klose A, Gasova Z, Pisacka M,
Sechovska M, Flegr J (2008). "Toxoplasma and reaction time: Role of toxoplasmosis in the origin,
preservation and geographical distribution of Rh blood group polymorphism". Parasitology 135:
12531261. http://natur.cuni.cz/flegr/pdf/rh.pdf.
12. ^ Flegr J, Novotna M, Lindova J, Havlicek J (2008). "Neurophysiological effect of the Rh factor.
Protective role of the RhD molecule against Toxoplasma-induced impairment of reaction times
in women". Neuroendocrinology Letters 29: 475481. http://natur.cuni.cz/flegr/pdf/rh2.pdf.
13. ^ Flegr, J., Klose, J., Novotna, M., Berenreitterov, M. Havlicek, J. (2009). "Increased incidence of
traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule
revealed by a large-scale prospective cohort study.". BMC Infect. Dis. 9: 72.
http://www.biomedcentral.com/1471-2334/9/72.
14. ^ Haldane JBF (1942). "Selection against heterozygosis in Man.". Eugenics 11: 333-340.
15. ^ Fisher RA, Race RR, Taylor GL. (1944). "Mutation and the Rhesus reaction". Nature 153: 106.
16. ^ Li CC (1953). "Is the Rh facing a crossroad? A critique of the compensation effect.". Am
Naturalist. 87: 257261.
18. ^ Flegr J, Novotna M, Lindova J, Havlicek J (2008). "Neurophysiological effect of the Rh factor.
Protective role of the RhD molecule against Toxoplasma-induced impairment of reaction times
in women". Neuroendocrinology Letters 29: 475481. http://natur.cuni.cz/flegr/pdf/rh2.pdf.
19. ^ Flegr, J., Klose, J., Novotna, M., Berenreitterov, M. Havlicek, J. (2009). "Increased incidence of
traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule
revealed by a large-scale prospective cohort study.". BMC Infect. Dis. 9: 72.
http://www.biomedcentral.com/1471-2334/9/72.
21. ^ Mark E. Brecher (2005). Technical Manual (15th ed.). Bethesda MD: American Association of
Blood Banks. pp. 322. ISBN 1-56395-196-7.
Rh at BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH
Rare Blood Types, A database and information on Rare Blood Types.
[hide]
v d e

General
concepts

Blood
group
systems
Blood
types

Blood
products
Blood donation Blood substitutes Cryoprecipitate Platelets Plasma Red blood cells
Whole blood Fresh frozen plasma Cryosupernatant

[edit] Clinical significance
[edit] Blood transfusion
Main article: Blood transfusion
Transfusion medicine is a specialized branch of hematology that is concerned with the study of
blood groups, along with the work of a blood bank to provide a transfusion service for blood and
other blood products. Across the world, blood products must be prescribed by a medical doctor
(licensed physician or surgeon) in a similar way as medicines. In the USA, blood products are
tightly regulated by the U.S. Food and Drug Administration.

Main symptoms of acute hemolytic reaction due to blood type mismatch.
[51][52]

Much of the routine work of a blood bank involves testing blood from both donors and recipients
to ensure that every individual recipient is given blood that is compatible and is as safe as
possible. If a unit of incompatible blood is transfused between a donor and recipient, a severe
acute hemolytic reaction with hemolysis (RBC destruction), renal failure and shock is likely to
occur, and death is a possibility. Antibodies can be highly active and can attack RBCs and bind
components of the complement system to cause massive hemolysis of the transfused blood.
Patients should ideally receive their own blood or type-specific blood products to minimize the
chance of a transfusion reaction. Risks can be further reduced by cross-matching blood, but this
may be skipped when blood is required for an emergency. Cross-matching involves mixing a
sample of the recipient's serum with a sample of the donor's red blood cells and checking if the
mixture agglutinates, or forms clumps. If agglutination is not obvious by direct vision, blood
bank technicians usually check for agglutination with a microscope. If agglutination occurs, that
particular donor's blood cannot be transfused to that particular recipient. In a blood bank it is
vital that all blood specimens are correctly identified, so labeling has been standardized using a
barcode system known as ISBT 128.
The blood group may be included on identification tags or on tattoos worn by military personnel,
in case they should need an emergency blood transfusion. Frontline German Waffen-SS had
blood group tattoos during World War II.
Rare blood types can cause supply problems for blood banks and hospitals. For example Duffy-
negative blood occurs much more frequently in people of African origin,
[53]
and the rarity of this
blood type in the rest of the population can result in a shortage of Duffy-negative blood for
patients of African ethnicity. Similarly for RhD negative people, there is a risk associated with
travelling to parts of the world where supplies of RhD negative blood are rare, particularly East
Asia, where blood services may endeavor to encourage Westerners to donate blood.
[54]

[edit] Hemolytic disease of the newborn (HDN)
Main article: Hemolytic disease of the newborn
A pregnant woman can make IgG blood group antibodies if her fetus has a blood group antigen
that she does not have. This can happen if some of the fetus' blood cells pass into the mother's
blood circulation (e.g. a small fetomaternal hemorrhage at the time of childbirth or obstetric
intervention), or sometimes after a therapeutic blood transfusion. This can cause Rh disease or
other forms of hemolytic disease of the newborn (HDN) in the current pregnancy and/or
subsequent pregnancies. If a pregnant woman is known to have anti-D antibodies, the Rh blood
type of a fetus can be tested by analysis of fetal DNA in maternal plasma to assess the risk to the
fetus of Rh disease.
[55]
One of the major advances of twentieth century medicine was to prevent
this disease by stopping the formation of Anti-D antibodies by D negative mothers with an
injectable medication called Rho(D) immune globulin.
[56][57]
Antibodies associated with some
blood groups can cause severe HDN, others can only cause mild HDN and others are not known
to cause HDN.
[3]

[edit] Compatibility
[edit] Blood products
In order to provide maximum benefit from each blood donation and to extend shelf-life, blood
banks fractionate some whole blood into several products. The most common of these products
are packed RBCs, plasma, platelets, cryoprecipitate, and fresh frozen plasma (FFP). FFP is
quick-frozen to retain the labile clotting factors V and VIII, which are usually administered to
patients who have a potentially fatal clotting problem caused by a condition such as advanced
liver disease, overdose of anticoagulant, or disseminated intravascular coagulation (DIC).
Units of packed red cells are made by removing as much of the plasma as possible from whole
blood units.
Clotting factors synthesized by modern recombinant methods are now in routine clinical use for
hemophilia, as the risks of infection transmission that occur with pooled blood products are
avoided.
[edit] Red blood cell compatibility
Blood group AB individuals have both A and B antigens on the surface of their RBCs,
and their blood serum does not contain any antibodies against either A or B antigen.
Therefore, an individual with type AB blood can receive blood from any group (with AB
being preferable), but can donate blood only to another type AB individual.
Blood group A individuals have the A antigen on the surface of their RBCs, and blood
serum containing IgM antibodies against the B antigen. Therefore, a group A individual
can receive blood only from individuals of groups A or O (with A being preferable), and
can donate blood to individuals with type A or AB.
Blood group B individuals have the B antigen on the surface of their RBCs, and blood
serum containing IgM antibodies against the A antigen. Therefore, a group B individual
can receive blood only from individuals of groups B or O (with B being preferable), and
can donate blood to individuals with type B or AB.
Blood group O (or blood group zero in some countries) individuals do not have either A
or B antigens on the surface of their RBCs, but their blood serum contains IgM anti-A
antibodies and anti-B antibodies against the A and B blood group antigens. Therefore, a
group O individual can receive blood only from a group O individual, but can donate
blood to individuals of any ABO blood group (i.e. A, B, O or AB). If anyone needs a
blood transfusion in a dire emergency, and if the time taken to process the recipient's
blood would cause a detrimental delay, O Negative blood can be issued.

RBC Compatibility chart
In addition to donating to the same blood group; type O blood donors can give to A, B and AB;
blood donors of types A and B can give to AB.
Red blood cell compatibility table
[58][59]

Recipient
[1]
Donor
[1]

O O+ A A+ B B+ AB AB+
O

O+

A

A+

B

B+

AB

AB+

Table note
1. Assumes absence of atypical antibodies that would cause an incompatibility between donor and recipient blood,
as is usual for blood selected by cross matching.
An Rh D-negative patient who does not have any anti-D antibodies (never being previously
sensitized to D-positive RBCs) can receive a transfusion of D-positive blood once, but this
would cause sensitization to the D antigen, and a female patient would become at risk for
hemolytic disease of the newborn. If a D-negative patient has developed anti-D antibodies, a
subsequent exposure to D-positive blood would lead to a potentially dangerous transfusion
reaction. Rh D-positive blood should never be given to D-negative women of child bearing age
or to patients with D antibodies, so blood banks must conserve Rh-negative blood for these
patients. In extreme circumstances, such as for a major bleed when stocks of D-negative blood
units are very low at the blood bank, D-positive blood might be given to D-negative females
above child-bearing age or to Rh-negative males, providing that they did not have anti-D
antibodies, to conserve D-negative blood stock in the blood bank. The converse is not true; Rh
D-positive patients do not react to D negative blood. This same matching is done for other
antigens of the Rh system as C, c, E and e and for other blood group systems with a known risk
for immunization such as the Kell system in particular for females of child-bearing age or
patients with known need for many transfusions.
[edit] Plasma compatibility

Plasma compatibility chart
In addition to donating to the same blood group; plasma from type AB can be given to A, B and
O; plasma from types A and B can be given to O.
Recipients can receive plasma of the same blood group, but otherwise the donor-recipient
compatibility for blood plasma is the converse of that of RBCs: plasma extracted from type AB
blood can be transfused to individuals of any blood group; individuals of blood group O can
receive plasma from any blood group; and type O plasma can be used only by type O recipients.
Plasma compatibility table
[59]

Recipient Donor
[1]

O A B AB
O

A

B

AB

Table note
1. Assumes absence of strong atypical antibodies in donor plasma
Rh D antibodies are uncommon, so generally neither D negative nor D positive blood contain
anti-D antibodies. If a potential donor is found to have anti-D antibodies or any strong atypical
blood group antibody by antibody screening in the blood bank, they would not be accepted as a
donor (or in some blood banks the blood would be drawn but the product would need to be
appropriately labeled); therefore, donor blood plasma issued by a blood bank can be selected to
be free of D antibodies and free of other atypical antibodies, and such donor plasma issued from
a blood bank would be suitable for a recipient who may be D positive or D negative, as long as
blood plasma and the recipient are ABO compatible.
[citation needed]

[edit] Universal donors and universal recipients
With regard to transfusions of whole blood or packed red blood cells, individuals with type O Rh
D negative blood are often called universal donors, and those with type AB Rh D positive blood
are called universal recipients; however, these terms are only generally true with respect to
possible reactions of the recipient's anti-A and anti-B antibodies to transfused red blood cells,
and also possible sensitization to Rh D antigens. Exceptions include individuals with hh antigen
system (also known as the Bombay blood group) who can only receive blood safely from other
hh donors, because they form antibodies against the H substance.
[60][61]

Blood donors with particularly strong anti-A, anti-B or any atypical blood group antibody are
excluded from blood donation. The possible reactions of anti-A and anti-B antibodies present in
the transfused blood to the recipients RBCs need not be considered, because a relatively small
volume of plasma containing antibodies is transfused.
By way of example: considering the transfusion of O Rh D negative blood (universal donor
blood) into a recipient of blood group A Rh D positive, an immune reaction between the
recipient's anti-B antibodies and the transfused RBCs is not anticipated. However, the relatively
small amount of plasma in the transfused blood contains anti-A antibodies, which could react
with the A antigens on the surface of the recipients RBCs, but a significant reaction is unlikely
because of the dilution factors. Rh D sensitization is not anticipated.
Additionally, red blood cell surface antigens other than A, B and Rh D, might cause adverse
reactions and sensitization, if they can bind to the corresponding antibodies to generate an
immune response. Transfusions are further complicated because platelets and white blood cells
(WBCs) have their own systems of surface antigens, and sensitization to platelet or WBC
antigens can occur as a result of transfusion.
With regard to transfusions of plasma, this situation is reversed. Type O plasma, containing both
anti-A and anti-B antibodies, can only be given to O recipients. The antibodies will attack the
antigens on any other blood type. Conversely, AB plasma can be given to patients of any ABO
blood group due to not containing any anti-A or anti-B antibodies.
[edit] Blood group genotyping
In addition to the current practice of serologic testing of blood types, the progress in molecular
diagnostics allows the increasing use of blood group genotyping. In contrast to serologic tests
reporting a direct blood type phenotype, genotyping allows the prediction of a phenotype based
on the knowledge of the molecular basis of the currently known antigens. This allows a more
detailed determination of the blood type and therefore a better match for transfusion, which can
be crucial in particular for patients with needs for many transfusions to prevent allo-
immunization.
[62][63]

Conversion
In April 2007 a method was discovered to convert blood types A, B, and AB to O, using
enzymes. This method is still experimental and the resulting blood has yet to undergo human
trials.
[64][65]
The method specifically removes or converts antigens on the red blood cells, so other
antigens and antibodies would remain. This does not help plasma compatibility, but that is a
lesser concern since plasma has much more limited clinical utility in transfusion and is much
easier to preserve.
History
The two most significant blood group systems were discovered by Karl Landsteiner during early
experiments with blood transfusion: the ABO group in 1901
[66]
and in co-operation with
Alexander S. Wiener the Rhesus group in 1937.
[67]
Development of the Coombs test in 1945,
[68]

the advent of transfusion medicine, and the understanding of hemolytic disease of the newborn
led to discovery of more blood groups, and now 30 human blood group systems are recognized
by the International Society of Blood Transfusion (ISBT),
[2]
and across the 30 blood groups, over
600 different blood group antigens have been found,
[4]
many of these are very rare or are mainly
found in certain ethnic groups. Blood types have been used in forensic science and in paternity
testing, but both of these uses are being replaced by genetic fingerprinting, which provides
greater certainty.
[69]

Cultural beliefs and other claims
The Japanese blood type theory of personality is a popular belief that a person's ABO blood type
is predictive of their personality, character, and compatibility with others. This belief is also
widespread in South Korea.
[70]
Deriving from ideas of historical scientific racism, the theory
reached Japan in a 1927 psychologist's report, and the militarist government of the time
commissioned a study aimed at breeding better soldiers.
[70]
The fad faded in the 1930s due to its
unscientific basis. The theory has long since been rejected by the scientists, but it was revived in
the 1970s by Masahiko Nomi, a broadcaster who had no medical background.
[70]

[edit] References
1. ^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson,
Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and
Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1.
2. ^
a

b

c

d
"Table of blood group systems". International Society of Blood Transfusion.
October 2008.
http://ibgrl.blood.co.uk/isbt%20pages/isbt%20terminology%20pages/table%20of%20blo
od%20group%20systems.htm. Retrieved 2008-09-12.
3. ^
a

b
E.A. Letsky; I. Leck, J.M. Bowman (2000). "Chapter 12: Rhesus and other
haemolytic diseases". Antenatal & neonatal screening (Second ed.). Oxford University
Press. ISBN 0-19-262827-7.
4. ^
a

b
"American Red Cross Blood Services, New England Region, Maine, Massachusetts,
New Hampshire, Vermont". American Red Cross Blood Services - New England Region.
2001. http://www.newenglandblood.org/medical/rare.htm. Retrieved 2008-07-15. "there
are more than 600 known antigens besides A and B that characterize the proteins found
on a person's red cells"
5. ^ Dean, Laura. "The ABO blood group". Blood Groups and Red Cell Antigens. online:
NCBI.
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=rbcantigen&part=ch05ABO. "A
number of illnesses may alter a person's ABO phenotype"
6. ^ Stayboldt C, Rearden A, Lane TA (1987). "B antigen acquired by normal A1 red cells
exposed to a patient's serum". Transfusion 27 (1): 414. PMID 3810822.
7. ^ Matsushita S, Imamura T, Mizuta T, Hanada M (November 1983). "Acquired B
antigen and polyagglutination in a patient with gastric cancer". The Japanese Journal of
Surgery 13 (6): 5402. PMID 6672386.
8. ^ Kremer Hovinga I, Koopmans M, de Heer E, Bruijn J, Bajema I (2007). "Change in
blood group in systemic lupus erythematosus". Lancet 369 (9557): 1867; author reply
187. doi:10.1016/S0140-6736(07)60099-3. PMID 17240276.
9. ^ Demi-Lee Brennan has changed blood types and immune system Kate Sikora, The
Daily Telegraph, January 25, 2008
10. ^ Aust doctors hail teen's transplant 'miracle' Sean Rubinsztein-Dunlop, ABC News
(Australia), January 24, 2008
11. ^ CHOWN B, LEWIS M, KAITA K (October 1957). "A new Kell blood-group
phenotype". Nature 180 (4588): 711. PMID 13477267.
12. ^ Miller LH, Mason SJ, Clyde DF, McGinniss MH (August 1976). "The resistance factor
to Plasmodium vivax in blacks. The Duffy-blood-group genotype, FyFy". The New
England Journal of Medicine 295 (6): 3024. PMID 778616.
13. ^ Kwiatkowski DP (August 2005). "How malaria has affected the human genome and
what human genetics can teach us about malaria". American Journal of Human Genetics
77 (2): 17192. doi:10.1086/432519. PMID 16001361. "The different geographic
distributions of thalassemia, G6PD deficiency, ovalocytosis, and the Duffy-negative
blood group are further examples of the general principle that different populations have
evolved different genetic variants to protect against malaria".
14. ^ "Your blood a textbook about blood and blood donation" (PDF). pp. 63.
http://www.bloddonor.dk/fileadmin/Fil_Arkiv/PDF_filer/Andre/Your_Blood__June_200
6.pdf. Retrieved 2008-07-15.
15. ^ Talaro, Kathleen P. (2005). Foundations in microbiology (5th ed.). New York:
McGraw-Hill. pp. 5101. ISBN 0-07-111203-0.
16. ^ Moise KJ (July 2008). "Management of rhesus alloimmunization in pregnancy".
Obstetrics and Gynecology 112 (1): 16476. doi:10.1097/AOG.0b013e31817d453c.
PMID 18591322.
17. ^ CIA World Factbook
18. ^ Blood Types - What Are They?, Australian Red Cross
19. ^ Austrian Red Cross - Blood Donor Information
20. ^ Rode Kruis Wielsbeke - Blood Donor information material
21. ^ Tipos Sanguneos
22. ^ Types & Rh System, Canadian Blood Services
23. ^ Frequency of major blood groups in the Danish population.
24. ^ Veregruppide esinemissagedus Eestis
25. ^ Suomalaisten veriryhmjakauma
26. ^ "Les groupes sanguins (systme ABO)" (in French). Centre Hospitalier Princesse
GRACE - Monaco. C.H.P.G. MONACO. 2005.
http://www.chpg.mc/go/article.php3?id_article=111. Retrieved 2008-07-15.
27. ^ de:Blutgruppe#Hufigkeit der Blutgruppen
28. ^ Blood Donation, Hong Kong Red Cross
29. ^ Blflokkar
30. ^ Indian Journal for the Practising Doctor
31. ^ "Irish Blood Transfusion Service - Irish Blood Group Type Frequency Distribution".
Irish Blood Transfusion Service.
http://www.ibts.ie/All_About_Blood/Blood_Group_Basics/. Retrieved 2009-11-07.
32. ^ The national rescue service in Israel
33. ^ "Voorraad Erytrocytenconcentraten Bij Sanquin" (in Dutch).
http://www.sanquin.nl/Sanquin-nl/erygrafiek.nsf/All/Voorraad-Erytrocytenconcentraten-
Bij-Sanquin.html. Retrieved 2009-03-27.
34. ^ What are Blood Groups? - NZ Blood
35. ^ Norwegian Blood Donor Organization
36. ^ Regionalne Centrum Krwiodawstwa i Krwiolecznictwa we Wroclawiu
37. ^ Portuguese Blood Institute (assuming Rh and AB antigens are independent)
38. ^ Fequency of ABO blood groups in the eastern region of Saudi Arabia
39. ^ South African National Blood Service - What's Your Type?
40. ^ Federacin Nacional de Donantes de Sangre/La sangre/Grupos
41. ^ Frequency of major blood groups in the Swedish population.
42. ^ Turkey Blood Group Site.
43. ^ Frequency of major blood groups in the UK.
44. ^ Blood Types in the U.S.
45. ^ RACIAL & ETHNIC DISTRIBUTION of ABO BLOOD TYPES,
BLOODBOOK.COM
46. ^ Blood Transfusion Division, United States Army Medical Research Laboratory (1971).
Selected contributions to the literature of blood groups and immunology. 1971 v. 4.
United States Army Medical Research Laboratory, Fort Knox, Kentucky.
http://books.google.com/books?id=ALilcA7Acd0C. "... In northern India, in Southern
and Central China and in the neighboring Central Asiatic areas, we find the highest
known frequencies of B. If we leave this center, the frequency of the B gene decreases
almost everywhere ..."
47. ^
a

b
Encyclopaedia Britannica (2002). The New Encyclopaedia Britannica.
Encyclopaedia Britannica, Inc.. ISBN 0852297874.
http://books.google.com/books?id=fpdUAAAAMAAJ. "... The maximum frequency of
the B gene occurs in Central Asia and northern India. The B gene was probably absent
from American Indians and Australian Aborigines before racial admixture occurred with
the coming of the white man ..."
48. ^ Carol R. Ember, Melvin Ember (1973). Anthropology. Appleton-Century-Crofts.
http://books.google.com/books?id=fvpFAAAAMAAJ. "... Blood type B is completely
absent in most North and South American Indians ..."
49. ^ Laura Dean, MD (2005). Blood Groups an Red Cell Antigens. National Center for
Biotechnology Information, United States Government. ISBN 1932811052.
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=rbcantigen. "... Type A is common
in Central and Eastern Europe. In countries such as Austria, Denmark, Norway, and
Switzerland, about 45-50% of the population have this blood type, whereas about 40% of
Poles and Ukrainians do so. The highest frequencies are found in small, unrelated
populations. For example, about 80% of the Blackfoot Indians of Montana have blood
type A ..."
50. ^ (PDF) Technical Monograph No. 2: The ABO Blood Group System and ABO
Subgroups. Biotec. March 2005.
http://www.biotec.com/pdf/Technical%20Monograph%20No.%202%20-
%20ABO%20system%20and%20subgroups.pdf. "... The frequency of blood group A is
quite high (25-55%) in Europe, especially in Scandinavia and parts of central Europe.
High group A frequency is also found in the Aborigines of South Australia (up to 45%)
and in certain American Indian tribes where the frequency reaches 35% ..."
51. ^ Possible Risks of Blood Product Transfusions from American Cancer Society. Last
Medical Review: 03/08/2008. Last Revised: 01/13/2009
52. ^ 7 ADVERSE REACTIONS TO TRANSFUSION Pathology Department at University
of Michigan. Version July 2004, Revised 11/5/08
53. ^ Nickel RG, Willadsen SA, Freidhoff LR, et al. (August 1999). "Determination of Duffy
genotypes in three populations of African descent using PCR and sequence-specific
oligonucleotides". Human Immunology 60 (8): 73842. doi:10.1016/S0198-
8859(99)00039-7. PMID 10439320.
54. ^ Bruce, MG (May 2002). "BCF - Members - Chairman's Annual Report". The Blood
Care Foundation. http://www.bloodcare.org.uk/html/resources_chairman_2001.htm.
Retrieved 2008-07-15. "As Rhesus Negative blood is rare amongst local nationals, this
Agreement will be of particular value to Rhesus Negative expatriates and travellers"
55. ^ Daniels G, Finning K, Martin P, Summers J (September 2006). "Fetal blood group
genotyping: present and future". Annals of the New York Academy of Sciences 1075: 88
95. doi:10.1196/annals.1368.011. PMID 17108196.
56. ^ "Use of Anti-D Immunoglobulin for Rh Prophylaxis". Royal College of Obstetricians
and Gynaecologists. May 2002. http://www.rcog.org.uk/index.asp?PageID=1972.
57. ^ "Pregnancy - routine anti-D prophylaxis for D-negative women". NICE. May 2002.
http://www.nice.org.uk/guidance/TA41/?c=91520.
58. ^ "RBC compatibility table". American National Red Cross. December 2006.
http://chapters.redcross.org/br/northernohio/INFO/bloodtype.html. Retrieved 2008-07-15.
59. ^
a

b
Blood types and compatibility bloodbook.com
60. ^ Fauci, Anthony S.; Eugene Braunwald, Kurt J. Isselbacher, Jean D. Wilson, Joseph B.
Martin, Dennis L. Kasper, Stephen L. Hauser, Dan L. Longo (1998). Harrison's
Principals of Internal Medicine. New York: McGraw-Hill. pp. 719.. ISBN 0-07-020291-
5.)
61. ^ Universal acceptor and donor groups
62. ^ Anstee DJ (2009). "Red cell genotyping and the future of pretransfusion testing". Blood
114 (2): 24856. doi:10.1182/blood-2008-11-146860. PMID 19411635.
63. ^ Avent ND (2009). "Large-scale blood group genotyping: clinical implications". Br J
Haemat 144 (1): 313. doi:10.1111/j.1365-2141.2008.07285.x. PMID 19016734.
64. ^ "Blood groups 'can be converted'". BBC News. 2007-04-02.
http://news.bbc.co.uk/1/hi/health/6517137.stm. Retrieved 2008-07-15.
65. ^ Liu Q, Sulzenbacher G, Yuan H, Bennett E, Pietz G, Saunders K, Spence J, Nudelman
E, Levery S, White T, Neveu J, Lane W, Bourne Y, Olsson M, Henrissat B, Clausen H
(2007). "Bacterial glycosidases for the production of universal red blood cells". Nat
Biotechnol 25 (4): 454. doi:10.1038/nbt1298. PMID 17401360.
66. ^ Landsteiner K. Zur Kenntnis der antifermentativen, lytischen und agglutinierenden
Wirkungen des Blutserums und der Lymphe. Zentralblatt Bakteriologie 1900;27:357-62.
67. ^ Landsteiner K, Wiener AS. An agglutinable factor in human blood recognized by
immune sera for rhesus blood. Proc Soc Exp Biol Med 1940;43:223-224.
68. ^ Coombs RRA, Mourant AE, Race RR. A new test for the detection of weak and
"incomplete" Rh agglutinins. Brit J Exp Path 1945;26:255-66.
69. ^ Johnson P, Williams R, Martin P (2003). "Genetics and Forensics: Making the National
DNA Database". Science Studies 16 (2): 2237. PMID 16467921.
70. ^
a

b

c
Associated Press (2005-05-06). "Myth about Japan blood types under attack". AOL
Health.
http://aol.mediresource.com/channel_health_news_details.asp?news_id=6661&news_cha
nnel_id=11&channel_id=11. Retrieved 2007-12-29.
[edit] Further reading
Dean, Laura. "Blood Groups and Red Cell Antigens, a guide to the differences in our
blood types that complicate blood transfusions and pregnancy." (HTML, also PDF, Flash
and PRC versions). National Center for Biotechnology Information.
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=rbcantigen. Retrieved September
15, 2006.
Mollison PL, Engelfriet CP and Contreras M. Blood Transfusion in Clinical Medicine.
1997. 10th edition. Blackwell Science, Oxford, UK. ISBN 0-86542-881-6.
BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH has details of
genes and proteins, and variations thereof, that are responsible for blood types
Online 'Mendelian Inheritance in Man' (OMIM) 110300 (ABO)
Online 'Mendelian Inheritance in Man' (OMIM) 111680 (Rhesus D)
Farr AD (April 1979). "Blood group serology--the first four decades (1900--1939)".
Medical History 23 (2): 21526. PMID 381816.
"Blood group test, Gentest.ch" (HTML, JavaScript). Gentest.ch GmbH.
http://www.gentest.ch/index.php?content=bloodtype&langchange=en. Retrieved 2006.
"Blood typing systems other than ABO". BloodBook.com. 2005-09-10.
http://www.bloodbook.com/type-sys.html. Retrieved 2008-07-15.
"Blood Facts". LifeShare Blood Centers. http://www.lifeshare.org/facts/raretraits.htm.
Retrieved September 15, 2006.
"Modern Human Variation: Distribution of Blood Types". Dr. Dennis O'Neil, Behavioral
Sciences Department, Palomar College, San Marcos, California. 2001-06-06. Archived
from the original on 2006-02-21.
http://web.archive.org/web/*/http://anthro.palomar.edu/vary/vary_3.htmhttp://web.archiv
e.org/web/*/http://anthro.palomar.edu/vary/vary_3.htm. Retrieved November 23, 2006.
"Racial and Ethnic Distribution of ABO Blood Types - BloodBook.com, Blood
Information for Life". bloodbook.com. http://www.bloodbook.com/world-abo.html.
Retrieved September 15, 2006.
"Molecular Genetic Basis of ABO". http://abobloodgroup.googlepages.com/home.
Retrieved July 31, 2008.
Blood Type Calculator -The calculator is used to determine the blood type of child when
the blood type of parents are known.
Blood Care Foundation - A charity delivering properly screened blood all over the world.
[show]
v d e
Human group differences

[show]
v d e
Certain conditions originating in the perinatal period / fetal disease (P, 760-779)

Respiratory Intrauterine hypoxia Infant respiratory distress syndrome Transient
tachypnea of the newborn Meconium aspiration syndrome pleural disease
(Pneumothorax, Pneumomediastinum) Wilson-Mikity syndrome
Bronchopulmonary dysplasia

Cardiovascular Pneumopericardium Persistent fetal circulation

Haemorrhagic
and
haematological/
hematologic
disease
Vitamin K deficiency (Haemorrhagic disease of the newborn)
HDN (ABO Anti-Kell Rh c Rh D Rh E) Hydrops fetalis
Hyperbilirubinemia (Kernicterus, Neonatal jaundice)
Velamentous cord insertion

Digestive
system
Ileus Necrotizing enterocolitis Meconium peritonitis

Integument and
temperature
regulation
Erythema toxicum

Nervous system Periventricular leukomalacia

Musculoskeletal
system
Gray baby syndrome muscle tone (Congenital hypertonia, Congenital
hypotonia)

M: OBS phys mthr/fetu/infc, epon proc, drug(2A/G2C)

Blood product
A blood product is any component of the blood which is collected from a donor for use in a
blood transfusion. Whole blood is uncommonly used in transfusion medicine at present; most
blood products consist of specific processed components such as red blood cells, blood plasma,
or platelets.
[hide]
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General
concepts

Blood
group
systems
Blood
types

Blood
products

Fresh frozen plasma
The term fresh frozen plasma (FFP) refers to the liquid portion of human blood which has been
frozen and preserved quickly after a blood donation and will be used for blood transfusion. The
capitalized term Fresh Frozen Plasma is the proper name in the United States for the fluid
portion of one unit of human blood that has been centrifuged, separated, and frozen solid at
18 C (0.4 F) (or colder) within 8 hours of collection. Other single-donor plasma units, either
frozen or liquid, are substituted for FFP. Indications for these products are similar to those for
FFP with the exception heat-sensitive proteins in the plasma, such as factor V, and the term
"FFP" is often used to mean any transfused plasma product.
The use of plasma and its products has evolved over a period of four decades. The use of FFP
has increased tenfold within the past 10 years and reached almost 2 million units annually in the
United States. This trend may be attributable to multiple factors, possibly including decreased
availability of whole blood due to widespread acceptance of the concept of component therapy.
FFP contains the labile as well as the stable components of the coagulation, fibrinolytic and
complement systems; the proteins that maintain oncotic pressure and modulate immunity; and
other proteins that have diverse activities. In addition, fats, carbohydrates and minerals are
present in concentrations similar to those in circulation. Although well-defined indications exist
for the use of FFP in single or multiple coagulation deficiencies, indications for many of its other
uses may be empiric.
Contents
1 Indications
o 1.1 Replacement of isolated factor deficiencies
o 1.2 Reversal of warfarin effect
o 1.3 Massive blood transfusion (>1 blood volume within several hours)
o 1.4 Use in antithrombin III deficiency
o 1.5 Treatment of immunodeficiencies
o 1.6 Treatment of thrombotic thrombocytopenic purpura
2 Risks
3 Alternatives
4 Effectiveness
5 External links
[edit] Indications
Few specific indications for the use of FFP exist. These indications generally are limited to the
treatment of deficiencies of coagulation proteins for which specific factor concentrates are
unavailable or undesirable. In addition, circumstances exist in which FFP has been employed and
is believed to be of therapeutic value, but data supporting its efficacy are limited or unavailable
(e.g. multiple coagulation protein deficiencies in the uncontrollably bleeding patient). Because
such patients are often critically ill and satisfactory alternative therapy may not be at hand, FFP
may be appropriate.
Indications for the use of FFP include the following:
[edit] Replacement of isolated factor deficiencies
FFP is efficacious for treatment of deficiencies of factors II, V, VII, IX, X, and XI when specific
component therapy is neither available nor appropriate. Requirements for FFP vary with the
specific factor being replaced. For example, hemostatic levels of factor IX in a patient with
severe deficiency are difficult to achieve with FFP alone, whereas patients with severe factor X
deficiency require factor levels of about 10 percent to achieve hemostasis and are easily treated
with FFP.
[edit] Reversal of warfarin effect
Patients who are anticoagulated with warfarin are deficient in the functional vitamin K
dependent coagulation factors II, VII, IX, and X, as well as proteins C and S. These functional
deficiencies can be reversed by the administration of vitamin K. However, for anticoagulated
patients who are actively bleeding or who require emergency surgery, FFDP (or single-donor
plasma) can be used to achieve immediate hemostasis
[edit] Massive blood transfusion (>1 blood volume within several hours)
Use of FFP in massive blood transfusion, for which there is less credible evidence of efficacy,
appears to have increased in frequency in the past decade, possibly due in part to the relative
unavailability of whole blood. Pathological hemorrhage in the massively transfused patient is
caused more frequently by thrombocytopenia than by depletion of coagulation factors. The
empiric use of FFP to reverse hemostatic disorders should be confined to those patients in whom
factor deficiencies are presumed to be the sole or principal derangement. There is no evidence
that the prophylactic administration of FFP decreases transfusion requirements in multiply
transfused patients who do not have documented coagulation defects.
It is however exceedingly common for patients to have documented blood clotting abnormalities
(Prolonged APTT, INR) after large blood loss requiring for example 4 units or more of packed
red blood cells, so FFP is commonly required in these settings. In urgent situations it is
unacceptable to wait hours for a lab test before blood products are requested from a blood bank.
Clearly a trial to document efficacy of this vs not giving FFP would be unethical.
[edit] Use in antithrombin III deficiency
FFP can be used as a source of antithrombin III in patients who are deficient in this inhibitor and
are undergoing surgery or who require heparin for treatment of thrombosis.
[edit] Treatment of immunodeficiencies
FFP is useful in infants with secondary immunodeficiency associated with severe protein-losing
enteropathy and in whom total parenteral nutrition is ineffectual. FFP also can be used as a
source of immunoglobulin for children and adults with humoral immunodeficiency. However,
the development of a purified immune globulin for intravenous use largely has replaced FFP.
[edit] Treatment of thrombotic thrombocytopenic purpura
FFP may be beneficial for the treatment of thrombotic thrombocytopenic purpura.
[edit] Risks
The risks of FFP include disease transmission, anaphylactoid reactions, alloimmunization, and
excessive intravascular volume, but also Transfusion Associated Lung Injury (TRALI) and
increase in infections (including surcical wound infections). The potential viral infectivity of FFP
probably is similar to that of whole blood and red blood cells. The rate of posttransfusion
hepatitis depends on many factors, including donor selection. In rare instances, human
immunodeficiency virus (HIV) is transmitted by blood transfusions and possibly by FFP.
Allergic or anaphylactoid reactions can occur in response to FFP administration and may vary
from hives to fatal noncardiac pulmonary edema. The potential for alloimmunization is present,
as demonstrated by the infrequent formation of Rh antibodies. As with any intravenously
administered fluid, excessive amounts of FFP may result in hypervolemia and cardiac failure.
[edit] Alternatives
Evidence indicates that other plasma components (e.g., single-donor plasma) that do not meet the
criteria of FFP may have adequate levels of coagulation factors and are suitable for patients in
whom FFP is indicated. Single-donor plasma is efficacious in the treatment of mild deficiencies
of stable clotting factors. It also is of value in treatment of multiple deficiencies as in reversal of
warfarin effects or in liver disease.
Safe and effective alternative treatment often exists so that FFP is no longer the therapy of choice
in many conditions. Cryoprecipitate should be used when fibrinogen or von Willebrand factor is
needed. For treatment of hemophilia A, cryoprecipitate or factor VIII concentrates, heated or
unheated, are available. For treatment of severe hemophilia B, factor IX complex is preferable.
Both of these concentrates are prepared from pooled plasma, and the risk of virus transmission is
negligible as there hasn't been an infection since 1985 when techniques were developed to kill of
viruses including HIV. The factor IX concentrate carries the additional hazard of
thrombogenicity.
Crystalloid, colloid solutions containing human serum albumin or plasma protein fraction,
hydroxyethyl starch, and dextran are preferable to FFP for volume replacement. The practice of
administering both packed red cells and FFP to the same patient should be discouraged, as this
adds to the cost and doubles the infection rate. When conditions are appropriate, whole blood
should be given.
For nutritional support, amino acid solutions and dextrose are available.
The most important alternative to the use of FFP is a comprehensive program of blood
conservation. This includes measures such as autologous donation before elective surgery, the
infusion of shed blood, and the realization that in many patients normovolemic anemia is not an
indication for transfusion.
[edit] Effectiveness
There is little scientific evidence to support the increasing use of FFP in clinical medicine purely
for volume expansion. While FFP is a reliable solution for intravascular volume replacement in
acute blood loss, alternative therapies are equally satisfactory and considerably safer. There is no
documentation that FFP has a beneficial effect when used as part of the transfusion management
of patients with massive hemorrhage
[citation needed]
. FFP contains the major plasma proteins,
including the labile coagulation factors (V and VIII), but in clinical practice other blood
components or derivatives usually provide greater efficacy.
Nevertheless, in augmenting replacement of whole blood lost in catastrophic haemorrhage, FFP
replacement must be considered along with replacement of packed red blood cells.
NIH Consensus Development Program: Fresh Frozen Plasma: Indications and Risks
(public domain)
Circular of Information describing intended uses of transfusion products in the United
States

[hide]
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Blood
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systems
Blood
types

Blood
products
Cryoprecipitate
Cryoprecipitate, also called "Cryoprecipitated Antihemophilic Factor", "Cryoprecipitated
AHF", and most commonly just "cryo", is a frozen blood product prepared from plasma.
It is often transfused as a four to six unit pool instead of as a single product. Many uses of the
product have been replaced by factor concentrates, but it is still routinely stocked by many
hospital blood banks.
Like fresh frozen plasma, compatibility testing is not strictly necessary, but cryo is given as ABO
compatible when possible. Compatibility is reversed for plasma products: AB type is the
universal plasma donor and O type is the universal plasma recipient. Type AB plasma contains
no A or B antibodies, whereas type O plasma has both A and B antibodies.
Contents
1 Composition
2 Indications
3 Manufacture
4 History
5 References
[edit] Composition
Each 15 mL unit typically contains 100 IU of factor VIII, and 250 mg of fibrinogen. It also
contains von Willebrand factor (vWF) and factor XIII.
US standards require manufacturers to test at least four units each month, and the products must
have an average of 150 mg or more of fibrinogen and 80 IU of factor VIII.
[1]
Individual products
may actually have less than these amounts as long as the average remains above these
minimums. Typical values for a unit are substantially higher, and aside from infants it is rare to
transfuse just one unit.
[edit] Indications
Indications for giving cryoprecipitate include:
[2]

Haemophilia - Used for emergency back up when factor concentrates are not available.
von Willebrands's disease - Not currently recommended unless last reserve. dDAVP is
first line, followed by factor concentrates.
Hypofibrinogenaemia (low fibrinogen levels), as can occur with massive transfusions
Bleeding from excessive anticoagulation - FFP contains most of the coagulation factors,
and is a much better choice when anticoagulation has to be quickly reversed.
Massive haemorrhage - RBCs and volume expanders are preferred therapies.
Disseminated intravascular coagulation
[edit] Manufacture
The product is manufactured by slowly thawing a unit of FFP at temperatures just above freezing
(1-6 C), typically in a water bath or a refrigerator. The product is then centrifuged to remove the
majority of the plasma, and the precipitate is resuspended in the remaining plasma or in sterile
saline. The product may be pooled and frozen or frozen as individual units.
[edit] History
The first publication of the method of concentrating clotting factors from plasma was by Judith
Graham Pool at Stanford University in 1964, writing in Nature.
[3]

Cryoprecipitate was originally known as "Cryoprecipitate AHF", where AHF stands for "Anti-
hemophiliac factor." AHF is now known as Factor VIII.
According to Dr. Charles Abildgaard, who was a Stanford medical resident at the time:
They obtained frozen plasma in very large containers that they got from Japan. They would thaw
that and send her [Pool] samples of the liquid parts to assay. She wasn't really finding very much
Factor VIII activity, and then someone mentioned to her that when they thawed this large amount
of plasma, there was always some mucky stuff at the bottom of it, and she said, "Well, send me
some of that, too." She found that at least half of the Factor VIII activity was in the residue.
What was happening that, because of the large volume, as the mass thawed, it stayed cold. So
this was cryoprecipitate.
[4]

Others had been close to discovering cryoprecipitate but failed to make the connection between
the lack of plasma clotting activity after thawing and the precipitate. According to Dr. Frederick
Rickles:
I made a mistake in an experiment, and instead of putting frozen plasma back in the freezer at the
end of the day's experiment, I instead stuck it in the refrigerator. When I came in the next
morning, there was all this junk in the bottom of the tube which I spun out, and I used the plasma
for my experiment. My experiment didn't work because there was no Factor VIII in it. And I
went back and fished the junk out of the trash and assayed the junk and got these outrageously
high values for Factor VIII in the junk, and neither Charlie nor I believed it, and so it was one of
those things. And sure enough, about a year later Judith Graham Pool discovered
cryoprecipitate.
[4]

[edit] References
1. ^ "Circular of Information For the Use of Human Blood and Blood Components" (PDF).
http://www.fda.gov/cber/gdlns/crclr.pdf. Retrieved 2008-02-28.
2. ^ Erber WN, Perry DJ (2006). "Plasma and plasma products in the treatment of massive
haemorrhage". Best Pract Res Clin Haematol 19 (1): 97112.
doi:10.1016/j.beha.2005.01.026. PMID 16377544.
3. ^ Pool JG, Gershgold EJ, Pappenhagen AR (18 July 1964). "High-Potency
Antihaemophilic Factor Concentrate Prepared from Cryoglobulin Precipitate". Nature
203: 312. doi:10.1038/203312a0. PMID 14201780.
http://www.nature.com/nature/journal/v203/n4942/abs/203312a0.html.
4. ^
a

b
Resnik, Susan (1999). Blood Saga: Hemophilia, AIDS, and the Survival of a
Community. Berkeley: University of California Press. pp. 4041. ISBN 0520211952.
[hide]
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group
systems
Blood
types

Blood
products
Whole blood
Whole Blood is the term used in transfusion medicine for human blood from a standard blood
donation. The blood is typically combined with an anticoagulant during the collection process,
but is generally otherwise unprocessed. In the US, the capitalized "Whole Blood" means a
specific standardized product for transfusion or further processing, where "whole blood" is any
unmodified collected blood.
Contents
1 Processing
2 Transfusion
3 Storage
4 Sources
[edit] Processing
Historically, blood was transfused as Whole Blood without further processing. Most blood banks
now split the Whole Blood into two or more components, typically red blood cells and a plasma
component such as Fresh Frozen Plasma. Platelets for transfusion can also be prepared from a
unit of Whole Blood. Some blood banks have replaced this with platelets collected by
Plateletpheresis because whole blood Platelets, sometimes called "random" platelets, must be
pooled from multiple donors to get enough for a therapeutic dose.
The collected blood is generally separated into components by one of three methods. A
centrifuge can be used in a "hard spin" which separates Whole Blood into plasma and red cells or
for a "soft spin" which separates it into plasma, buffy coat (used to make platelets), and red blood
cells. The third method is sedimentation: the Whole Blood simply sits overnight and the red cells
and plasma are separated by gravity.
[edit] Transfusion
Whole Blood has similar risks to a transfusion of Red Blood Cells and must be cross-matched to
avoid hemolytic transfusion reactions. Most of the indications for use are identical to those for
RBCs, and Whole Blood is not used because the extra plasma can contribute to transfusion
associated circulatory overload (TACO), a potentially dangerous complication.
Whole Blood is sometimes "recreated" from stored red blood cells and FFP for neonatal
transfusions. This is done to provide a final product with a very specific hematocrit (percentage
of red cells) with type O red cells and type AB plasma to minimize the chance of complications.
[edit] Storage
Whole Blood is typically stored under the same conditions as Red Blood Cells and can be kept
up to 35 days if collected with CPDA-1 storage solution or 21 days with other common storage
solutions such as CPD.
If the blood will be used to make platelets, it is kept at room temperature until the process is
complete. This must be done quickly to minimize the warm storage of RBCs in the unit.
[edit] Sources
Circular of Information for Blood Products
Mark E. Brecher, MD, Chair and Editor. Technical Manual. 2005. 15th Edition. AABB,
Bethesda, MD, United States.
[hide]
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systems
Blood
types

Blood
products
Red blood cell

Human red blood cells
Red blood cells (also referred to as erythrocytes) are the most common type of blood cell and
the vertebrate organism's principal means of delivering oxygen (O
2
) to the body tissues via the
blood flow through the circulatory system. They take up oxygen in the lungs or gills and release
it while squeezing through the body's capillaries.
These cells' cytoplasm is rich in hemoglobin, an iron-containing biomolecule that can bind
oxygen and is responsible for the blood's red color.
In humans, mature red blood cells are flexible biconcave disks that lack a cell nucleus and most
organelles. The cells develop in the bone marrow and circulate for about 100120 days in the
body before their components are recycled by macrophages. Each circulation takes about 20
seconds. Approximately a quarter of the cells in the human body are red blood cells.
[1][2]

Red blood cells are also known as RBCs, red blood corpuscles (an archaic term), haematids,
erythroid cells or erythrocytes (from Greek erythros for "red" and kytos for "hollow", with cyte
translated as "cell" in modern usage). The capitalized term Red Blood Cells is the proper name
in the US for erythrocytes in storage solution used in transfusion medicine.
[3]

Contents
1 History
2 Vertebrate erythrocytes
o 2.1 Nucleus
o 2.2 Secondary functions
3 Mammalian erythrocytes
4 Human erythrocytes
o 4.1 Life cycle
4.1.1 Erythropoiesis
4.1.2 Functional lifetime
4.1.3 Senescence
o 4.2 Membrane composition
4.2.1 Membrane lipids
4.2.2 Membrane proteins
o 4.3 Separation and blood doping
o 4.4 Artificially grown red blood cells
5 Diseases and diagnostic tools
6 See also
7 References
8 External links
[edit] History
The first person to describe red blood cells was the young Dutch biologist Jan Swammerdam,
who had used an early microscope in 1658 to study the blood of a frog.
[4]
Unaware of this work,
Anton van Leeuwenhoek provided another microscopic description in 1674, this time providing
a more precise description of red blood cells, even approximating their size, "25,000 times
smaller than a fine grain of sand".
In 1901 Karl Landsteiner published his discovery of the three main blood groups - A, B, and C
(which he later renamed to O). Landsteiner described the regular patterns in which reactions
occurred when serum was mixed with red blood cells, thus identifying compatible and
conflicting combinations between these blood groups. A year later Alfred von Decastello and
Adriano Sturli, two colleagues of Landsteiner, identified a fourth blood group - AB.
In 1959, by use of X-ray crystallography, Dr. Max Perutz was able to unravel the structure of
hemoglobin, the red blood cell protein that carries oxygen.
[5]

[edit] Vertebrate erythrocytes

There is an immense size variation in vertebrate erythrocytes, as well as a correlation between
cell and nucleus size. Mammalian erythrocytes, which do not contain nuclei, are considerably
smaller than those of most other vertebrates.
[6]

Erythrocytes consist mainly of hemoglobin, a complex metalloprotein containing heme groups
whose iron atoms temporarily bind to oxygen molecules (O
2
) in the lungs or gills and release
them throughout the body. Oxygen can easily diffuse through the red blood cell's cell membrane.
Hemoglobin in the erythrocytes also carries some of the waste product carbon dioxide back from
the tissues; most waste carbon dioxide, however, is transported back to the pulmonary capillaries
of the lungs as bicarbonate (HCO
3
-
) dissolved in the blood plasma. Myoglobin, a compound
related to hemoglobin, acts to store oxygen in muscle cells.
[7]

The color of erythrocytes is due to the heme group of hemoglobin. The blood plasma alone is
straw-colored, but the red blood cells change color depending on the state of the hemoglobin:
when combined with oxygen the resulting oxyhemoglobin is scarlet, and when oxygen has been
released the resulting deoxyhemoglobin is of a dark red burgundy color, appearing bluish
through the vessel wall and skin. Pulse oximetry takes advantage of this color change to directly
measure the arterial blood oxygen saturation using colorimetric techniques.
The sequestration of oxygen carrying proteins inside specialized cells (rather than having them
dissolved in body fluid) was an important step in the evolution of vertebrates as it allows for less
viscous blood, higher concentrations of oxygen, and better diffusion of oxygen from the blood to
the tissues. The size of erythrocytes varies widely among vertebrate species; erythrocyte width is
on average about 25% larger than capillary diameter and it has been hypothesized that this
improves the oxygen transfer from erythrocytes to tissues.
[8]

The only known vertebrates without erythrocytes are the crocodile icefishes (family
Channichthyidae); they live in very oxygen rich cold water and transport oxygen freely dissolved
in their blood.
[9]
While they don't use hemoglobin anymore, remnants of hemoglobin genes can
be found in their genome.
[10]

[edit] Nucleus
Erythrocytes in mammals are anucleate when mature, meaning that they lack a cell nucleus. In
comparison, the erythrocytes of other vertebrates have nuclei; the only known exceptions are
salamanders of the Batrachoseps genus and fish of the Maurolicus genus with closely related
species.
[11][12]

[edit] Secondary functions
When erythrocytes undergo shear stress in constricted vessels, they release ATP which causes
the vessel walls to relax and dilate so as to promote normal blood flow.
[13]

When their hemoglobin molecules are deoxygenated, erythrocytes release S-nitrosothiols which
also acts to dilate vessels,
[14]
thus directing more blood to areas of the body depleted of oxygen.
It has been recently demonstrated that erythrocytes can also synthesize nitric oxide
enzymatically, using L-arginine as substrate, just like endothelial cells.
[15]
Exposure of
erythrocytes to physiological levels of shear stress activates nitric oxide synthase and export of
nitric oxide,
[16]
which may contribute to the regulation of vascular tonus.
Erythrocytes can also produce hydrogen sulfide, a signalling gas that acts to relax vessel walls. It
is believed that the cardioprotective effects of garlic are due to erythrocytes converting its sulfur
compounds into hydrogen sulfide.
[17]

Erythrocytes also play a part in the body's immune response: when lysed by pathogens such as
bacteria, their hemoglobin releases free radicals which break down the pathogen's cell wall and
membrane, killing it.
[18][19]

[edit] Mammalian erythrocytes

Typical mammalian erythrocytes: (a) seen from surface; (b) in profile, forming rouleaux; (c)
rendered spherical by water; (d) rendered crenate by salt. (c) and (d) do not normally occur in the
body.
Mammalian erythrocytes are unique among the vertebrates as they are non-nucleated cells in
their mature form. These cells have nuclei during early phases of erythropoiesis, but extrude
them during development as they mature in order to provide more space for hemoglobin. In
mammals, erythrocytes also lose all other cellular organelles such as their mitochondria, golgi
apparatus and endoplasmic reticulum. As a result of not containing mitochondria, these cells use
none of the oxygen they transport; instead they produce the energy carrier ATP from glucose by
a glycolysis pathway that ends with lactic acid production. Furthermore, red blood cells do not
have an insulin receptor and thus their glucose uptake is not regulated by insulin. Because of the
lack of nuclei and organelles, mature red blood cells do not contain DNA and cannot synthesize
any RNA, and consequently cannot divide and have limited repair capabilities.
[20]

Mammalian erythrocytes are typically shaped as biconcave disks: flattened and depressed in the
center, with a dumbbell-shaped cross section, and a torus-shaped rim on the edge of the disk.
This distinctive biconcave shape optimises the ow properties of blood in the large vessels, such
as maximization of laminar flow and minimization of platelet scatter, which suppresses their
atherogenic activity in those large vessels.
[21]
However, there are some exceptions concerning
shape in the artiodactyl order (even-toed ungulates including cattle, deer, and their relatives),
which displays a wide variety of bizarre erythrocyte morphologies: small and highly ovaloid
cells in llamas and camels (family Camelidae), tiny spherical cells in mouse deer (family
Tragulidae), and cells which assume fusiform, lanceolate, crescentic, and irregularly polygonal
and other angular forms in red deer and wapiti (family Cervidae). Members of this order have
clearly evolved a mode of RBC development substantially different from the mammalian
norm.
[6][22]
Overall, mammalian erythrocytes are remarkably flexible and deformable so as to
squeeze through tiny capillaries, as well as to maximize their apposing surface by assuming a
cigar shape, where they efficiently release their oxygen load.
[23]

In large blood vessels, red blood cells sometimes occur as a stack, flat side next to flat side. This
is known as rouleaux formation, and it occurs more often if the levels of certain serum proteins
are elevated, as for instance during inflammation.
The spleen acts as a reservoir of red blood cells, but this effect is somewhat limited in humans. In
some other mammals such as dogs and horses, the spleen sequesters large numbers of red blood
cells which are dumped into the blood during times of exertion stress, yielding a higher oxygen
transport capacity.

Scanning electron micrograph of blood cells. From left to right: human erythrocyte, thrombocyte
(platelet), leukocyte.
[edit] Human erythrocytes

Two drops of blood are shown with a bright red oxygenated drop on the left and a deoxygenated
drop on the right.

An animation of a typical human red blood cell cycle in the circulatory system. This animation
occurs at real time (20 seconds of cycle) and shows the red blood cell deform as it enters
capillaries, as well as changing color as it alternates in states of oxygenation along the circulatory
system.
A typical human erythrocyte has a disk diameter of 68 m and a thickness of 2 m, being much
smaller than most other human cells. These cells have a volume of about 90 fL with a surface of
about 136 m
2
, and can swell up to a sphere shape containing 150 fL, without membrane
distension.
Adult humans have roughly 23 10
13
(20-30 trillion) red blood cells at any given time,
comprising approximately one quarter of the total human body cell number (women have about 4
to 5 million erythrocytes per microliter (cubic millimeter) of blood and men about 5 to 6 million;
people living at high altitudes with low oxygen tension will have more). Red blood cells are thus
much more common than the other blood particles: there are about 4,00011,000 white blood
cells and about 150,000400,000 platelets in each microliter of human blood.
Human red blood cells take on average 20 seconds to complete one cycle of circulation.
[1][2][24]

As red blood cells contain no nucleus, protein biosynthesis is currently assumed to be absent in
these cells, although a recent study indicates the presence of all the necessary biomachinery in
human red blood cells for protein biosynthesis.
[20]

The blood's red color is due to the spectral properties of the hemic iron ions in hemoglobin. Each
human red blood cell contains approximately 270 million of these hemoglobin biomolecules,
each carrying four heme groups; hemoglobin comprises about a third of the total cell volume.
This protein is responsible for the transport of more than 98% of the oxygen (the remaining
oxygen is carried dissolved in the blood plasma). The red blood cells of an average adult human
male store collectively about 2.5 grams of iron, representing about 65% of the total iron
contained in the body.
[25][26]
(See Human iron metabolism.)
[edit] Life cycle
Human erythrocytes are produced through a process named erythropoiesis, developing from
committed stem cells to mature erythrocytes in about 7 days. When matured, these cells live in
blood circulation for about 100 to 120 days. At the end of their lifespan, they become senescent,
and are removed from circulation.
[edit] Erythropoiesis
Erythropoiesis is the development process in which new erythrocytes are produced, through
which each cell matures in about 7 days. Through this process erythrocytes are continuously
produced in the red bone marrow of large bones, at a rate of about 2 million per second in a
healthy adult. (In the embryo, the liver is the main site of red blood cell production.) The
production can be stimulated by the hormone erythropoietin (EPO), synthesised by the kidney.
Just before and after leaving the bone marrow, the developing cells are known as reticulocytes;
these comprise about 1% of circulating red blood cells.
[edit] Functional lifetime
This phase lasts about 100120 days, during which the erythrocytes are continually moving by
the blood flow push (in arteries), pull (in veins) and squeezing through microvessels such as
capillaries as they compress against each other in order to move.
[edit] Senescence
The aging erythrocyte undergoes changes in its plasma membrane, making it susceptible to
selective recognition by macrophages and subsequent phagocytosis in the reticuloendothelial
system (spleen, liver and bone marrow), thus removing old and defective cells and continually
purging the blood. This process is termed eryptosis, or erythrocyte programmed cell death. This
process normally occurs at the same rate of production by erythropoiesis, balancing the total
circulating red blood cell count. Much of the resulting important breakdown products are
recirculated in the body. The heme constituent of hemoglobin are broken down into Fe
3+
and
biliverdin. The biliverdin is reduced to bilirubin, which is released into the plasma and
recirculated to the liver bound to albumin. The iron is released into the plasma to be recirculated
by a carrier protein called transferrin. Almost all erythrocytes are removed in this manner from
the circulation before they are old enough to hemolyze. Hemolyzed hemoglobin is bound to a
protein in plasma called haptoglobin which is not excreted by the kidney.
[27]

[edit] Membrane composition
The membrane of the red blood cell plays many roles that aid in regulating their surface
deformability, flexibility, adhesion to other cells and immune recognition. These functions are
highly dependent on its composition, which defines its properties. The red blood cell membrane
is composed of 3 layers: the glycocalyx on the exterior, which is rich in carbohydrates; the lipid
bilayer which contains many transmembrane proteins, besides its lipidic main constituents; and
the membrane skeleton, a structural network of proteins located on the inner surface of the lipid
bilayer. In human erythrocytes, like in most mammal erythrocytes, half of the membrane mass is
represented by proteins and the other half are lipids, namely phospholipids and cholesterol.
[28]

[edit] Membrane lipids

The most common erythrocyte cell membrane lipids, schematically disposed as they are
distributed on the bilayer. Relative abundances are not at scale.
The erythrocyte cell membrane comprises a typical lipid bilayer, similar to what can be found in
virtually all human cells. Simply put, this lipid bilayer is composed of cholesterol and
phospholipids in equal proportions by weight. The lipid composition is important as it defines
many physical properties such as membrane permeability and fluidity. Additionally, the activity
of many membrane proteins is regulated by interactions with lipids in the bilayer.
Unlike cholesterol which is evenly distributed between the inner and outer leaflets, the 5 major
phospholipids are asymmetrically disposed, as shown below:
Outer monolayer
Phosphatidylcholine (PC);
Sphingomyelin (SM).
Inner monolayer
Phosphatidylethanolamine (PE);
Phosphoinositol (PI) (small amounts).
Phosphatidylserine (PS);
This asymmetric phospholipid distribution among the bilayer is the result of the function of
several energy-dependent and energy-independent phospholipid transport proteins. Proteins
called Flippases move phospholipids from the outer to the inner monolayer while others called
floppases do the opposite operation, against a concentration gradient in an energy dependent
manner. Additionally, there are also scramblase proteins that move phospholipids in both
directions at the same time, down their concentration gradients in an energy independent manner.
There is still considerable debate ongoing regarding the identity of these membrane maintenance
proteins in the red cell membrane.
The maintenance of an asymmetric phospholipid distribution in the bilayer (such as an exclusive
localization of PS and PIs in the inner monolayer) is critical for the cell integrity and function
due to several reasons:
Macrophages recognize and phagocytose red cells that expose PS at their outer surface.
Thus the confinement of PS in the inner monolayer is essential if the cell is to survive its
frequent encounters with macrophages of the reticuloendothelial system, especially in the
spleen.
Premature destruction of thallassemic and sickle red cells has been linked to disruptions
of lipid asymmetry leading to exposure of PS on the outer monolayer.
An exposure of PS can potentiate adhesion of red cells to vascular endothelial cells,
effectively preventing normal transit through the microvasculature. Thus it is important
that PS is maintained only in the inner leaflet of the bilayer to ensure normal blood flow
in microcirculation.
Both PS and phosphatidylinositol-4,5-bisphosphate (PIP2) can regulate membrane
mechanical function, due to their interactions with skeletal proteins such as spectrin and
protein 4.1R. Recent studies have shown that binding ofspectrin to PS promotes
membrane mechanical stability. PIP2 enhances the binding of protein band 4.1R to
glycophorin C but decreases its interaction with protein band 3, and thereby may
modulate the linkage of the bilayer to the membrane skeleton.
The presence of specialized structures named "lipid rafts" in the erythrocyte membrane have
been described by recent studies. These are structures enriched in cholesterol and sphingolipids
associated with specific membrane proteins, namely flotillins, stomatins (band 7), G-proteins,
and -adrenergic receptors. Lipid rafts that have been implicated in cell signaling events in
nonerythroid cells have been shown in erythroid cells to mediate 2-adregenic receptor signaling
and increase cAMP levels, and thus regulating entry of malarial parasites into normal red
cells.
[29][30]

[edit] Membrane proteins

Red blood cell membrane proteins separated by SDS-Page and silverstained
[31]

The proteins of the membrane skeleton are responsible for the deformability, flexibility and
durability of the red blood cell, enabling it to squeeze through capillaries less than half the
diameter of the erythrocyte (7-8 m) and recovering the discoid shape as soon as these cells stop
receiving compressive forces, in a similar fashion to an object made of rubber.
There are currently more than 50 known membrane proteins, which can exist in a few hundred
up to a million copies per erythrocyte. Approximately 25 of these membrane proteins carry the
various blood group antigens, such as the A, B and Rh antigens, among many others. These
membrane proteins can perform a wide diversity of functions, such as transporting ions and
molecules across the red cell membrane, adhesion and interaction with other cells such as
endothelial cells, as signaling receptors, as well as other currently unknown functions. The blood
types of humans are due to variations in surface glycoproteins of erythrocytes. Disorders of the
proteins in these membranes are associated with many disorders, such as hereditary
spherocytosis, hereditary elliptocytosis, hereditary stomatocytosis, and paroxysmal nocturnal
hemoglobinuria.
[28][29]

The red blood cell membrane proteins organized according to their function:

Red Blood Cell membrane major proteins
Transport
Band 3 - Anion transporter, also an important structural component of the erythrocyte cell
membrane, makes up to 25% of the cell membrane surface, each red cell contains
approximately one million copies. Defines the Diego Blood Group;
[32]

Aquaporin 1 - water transporter, defines the Colton Blood Group;
Glut1 - glucose and L-dehydroascorbic acid transporter;
Kidd antigen protein - urea transporter;
RhAG - gas transporter, probably of carbon dioxide, defines Rh Blood Group and the
associated unusual blood group phenotype Rh
null
;
Na
+
/K
+
- ATPase;
Ca
2+
- ATPase;
Na
+
K
+
2Cl
-
- cotransporter;
Na
+
-Cl
-
- cotransporter;
Na-H exchanger;
K-Cl - cotransporter;
Gardos Channel.
Cell adhesion
ICAM-4 - interacts with integrins;
BCAM - a glycoprotein that defines the Lutheran blood group and also known as Lu or
laminin-binding protein.
Structural role - The following membrane proteins establish linkages with skeletal proteins and
may play an important role in regulating cohesion between the lipid bilayer and membrane
skeleton, likely enabling the red cell to maintain its favorable membrane surface area by
preventing the membrane from collapsing (vesiculating).
Ankyrin-based macromolecular complex - proteins linking the bilayer to the membrane
skeleton through the interaction of their cytoplasmic domains with Ankyrin.
o Band 3 - also assembles various glycolytic enzymes, the presumptive CO
2

transporter, and carbonic anhydrase into a macromolecular complex termed a
metabolon, which may play a key role in regulating red cell metabolism and ion
and gas transport function);
o RhAG - also involved in transport, defines associated unusual blood group
phenotype Rh
mod
.
Protein 4.1R-based macromolecular complex - proteins interacting with Protein 4.1R.
o Protein 4.1R - weak expression of Gerbich antigens;
o Glycophorin C and D - glycoprotein, defines Gerbich Blood Group;
o XK - defines the Kell Blood Group and the Mcleod unusual phenotype (lack of
Kx antigen and greatly reduced expression of Kell antigens);
o RhD/RhCE - defines Rh Blood Group and the associated unusual blood group
phenotype Rh
null
;
o Duffy protein - has been proposed to be associated with chemokine clearance;
[33]

o Adducin - interaction with band 3;
o Dematin- interaction with the Glut1 glucose transporter.
[28][29]

[edit] Separation and blood doping
Red blood cells can be obtained from whole blood by centrifugation, which separates the cells
from the blood plasma. During plasma donation, the red blood cells are pumped back into the
body right away and the plasma is collected. Some athletes have tried to improve their
performance by blood doping: first about 1 litre of their blood is extracted, then the red blood
cells are isolated, frozen and stored, to be reinjected shortly before the competition. (Red blood
cells can be conserved for 5 weeks at 79 C.) This practice is hard to detect but may endanger
the human cardiovascular system which is not equipped to deal with blood of the resulting higher
viscosity.
[edit] Artificially grown red blood cells
In 2008 it was reported that human embryonic stem cells had been successfully coaxed into
becoming erythrocytes in the lab. The difficult step was to induce the cells to eject their nucleus;
this was achieved by growing the cells on stromal cells from the bone marrow. It is hoped that
these artificial erythrocytes can eventually be used for blood transfusions.
[34]

[edit] Diseases and diagnostic tools

Affected by Sickle-cell disease, red blood cells alter shape and threaten to damage internal
organs.
Blood diseases involving the red blood cells include:
Anemias (or anaemias) are diseases characterized by low oxygen transport capacity of the
blood, because of low red cell count or some abnormality of the red blood cells or the
hemoglobin.
Iron deficiency anemia is the most common anemia; it occurs when the dietary
intake or absorption of iron is insufficient, and hemoglobin, which contains iron,
cannot be formed
Sickle-cell disease is a genetic disease that results in abnormal hemoglobin
molecules. When these release their oxygen load in the tissues, they become
insoluble, leading to mis-shaped red blood cells. These sickle shaped red cells are
rigid and cause blood vessel blockage, pain, strokes, and other tissue damage.
Thalassemia is a genetic disease that results in the production of an abnormal ratio
of hemoglobin subunits.
Spherocytosis is a genetic disease that causes a defect in the red blood cell's
cytoskeleton, causing the red blood cells to be small, sphere-shaped, and fragile
instead of donut-shaped and flexible.
Pernicious anemia is an autoimmune disease wherein the body lacks intrinsic
factor, required to absorb vitamin B12 from food. Vitamin B12 is needed for the
production of hemoglobin.
Aplastic anemia is caused by the inability of the bone marrow to produce blood
cells.
Pure red cell aplasia is caused by the inability of the bone marrow to produce only
red blood cells.

Effect of osmotic pressure on blood cells
Hemolysis is the general term for excessive breakdown of red blood cells. It can have
several causes and can result in hemolytic anemia.
The malaria parasite spends part of its life-cycle in red blood cells, feeds on their
hemoglobin and then breaks them apart, causing fever. Both sickle-cell disease
and thalassemia are more common in malaria areas, because these mutations
convey some protection against the parasite.
Polycythemias (or erythrocytoses) are diseases characterized by a surplus of red blood
cells. The increased viscosity of the blood can cause a number of symptoms.
In polycythemia vera the increased number of red blood cells results from an
abnormality in the bone marrow.
Several microangiopathic diseases, including disseminated intravascular coagulation and
thrombotic microangiopathies, present with pathognomonic (diagnostic) RBC fragments
called schistocytes. These pathologies generate fibrin strands that sever RBCs as they try
to move past a thrombus.
Inherited hemolytic anemias caused by abnormalities of the erythrocyte membrane
comprise an important group of inherited disorders. These disorders are characterized by
clinical and biochemical heterogeneity and also genetic heterogeneity, as evidenced by
recent molecular studies.
The Hereditary spherocytosis (HS) syndromes are a group of inherited disorders
characterized by the presence of spherical-shaped erythrocytes on the peripheral
blood smear. HS is found worldwide. It is the most common inherited anemia in
individuals of northern European descent, affecting approximately 1 in 1000-2500
individuals depending on the diagnostic criteria. The primary defect in hereditary
spherocytosis is a deficiency of membrane surface area. Decreased surface area
may produced by two different mechanisms: 1) Defects of spectrin, ankyrin, or
protein 4.2 lead to reduced density of the membrane skeleton, destabilizing the
overlying lipid bilayer and releasing band 3-containing microvesicles. 2) Defects
of band 3 lead to band 3 deficiency and loss of its lipid-stabilizing effect. This
results in the loss of band 3-free microvesicles. Both pathways result in
membrane loss, decreased surface area, and formation of spherocytes with
decreased deformability. These deformed erythrocytes become trapped in the
hostile environment of the spleen where splenic conditioning inflicts further
membrane damage, amplifying the cycle of membrane injury.
Hereditary elliptocytosis
Hereditary pyropoikilocytosis
Hereditary stomatocytosis
[35]

Hemolytic transfusion reaction is the destruction of donated red blood cells after a
transfusion, mediated by host antibodies, often as a result of a blood type mismatch.
Several blood tests involve red blood cells, including the RBC count (the number of red blood
cells per volume of blood), the hematocrit (percentage of blood volume occupied by red blood
cells), and the erythrocyte sedimentation rate. The blood type needs to be determined to prepare
for a blood transfusion or an organ transplantation.
[edit] See also
Hemoglobin-based oxygen carriers
Packed red blood cells
Blood serum
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Sickle Cell and Thalassemic Disorders. Accessed 22 September 2007.
27. ^ Fller M, Huber SM, Lang F (October 2008). "Erythrocyte programmed cell death".
IUBMB Life 60 (10): 6618. doi:10.1002/iub.106. PMID 18720418.
28. ^
a

b

c
Yazdanbakhsh K, Lomas-Francis C, Reid ME (October 2000). "Blood groups and
diseases associated with inherited abnormalities of the red blood cell membrane".
Transfusion Medicine Reviews 14 (4): 36474. doi:10.1053/tmrv.2000.16232.
PMID 11055079.
29. ^
a

b

c
Mohandas N, Gallagher PG (November 2008). "Red cell membrane: past, present,
and future". Blood 112 (10): 393948. doi:10.1182/blood-2008-07-161166.
PMID 18988878.
30. ^ Rodi PM, Trucco VM, Gennaro AM (June 2008). "Factors determining detergent
resistance of erythrocyte membranes". Biophysical Chemistry 135 (1-3): 148.
doi:10.1016/j.bpc.2008.02.015. PMID 18394774.
31. ^ Hempelmann E, Gtze O (1984). "Characterization of membrane proteins by
polychromatic silver staining". Hoppe Seyler's Z Physiol Chem 365: 241242.
32. ^ Iolascon A, Perrotta S, Stewart GW (March 2003). "Red blood cell membrane defects".
Reviews in Clinical and Experimental Hematology 7 (1): 2256. PMID 14692233.
33. ^ Denomme GA (July 2004). "The structure and function of the molecules that carry
human red blood cell and platelet antigens". Transfusion Medicine Reviews 18 (3): 203
31. doi:10.1016/j.tmrv.2004.03.006. PMID 15248170.
34. ^ First red blood cells grown in the lab, New Scientist News, 19 August 2008
35. ^ An X, Mohandas N (May 2008). "Disorders of red cell membrane". British Journal of
Haematology 141 (3): 36775. doi:10.1111/j.1365-2141.2008.07091.x. PMID 18341630.
[show]
v d e
Myeloid lineage - Blood (WBC and RBC)

Myeloid/
Myeloblast
CFU-
GEMM
CFU-
GM
CFU-G:
Granulocytes
Band cell Neutrophil

CFU-M:
Monocytes
Macrophages
Histiocytes Kupffer cells Alveolar macrophage
Microglia Osteoclasts Epithelioid cells giant
cells (Langhans giant cells, Foreign-body giant
cell, Touton giant cells)

CFU-DL Dendritic cells Langerhans cell

Common Myelomonocyte

CFU-
Baso
Granulocytes (Basophil)

CFU-
Eos
Granulocytes (Eosinophil)

MEP
CFU-
Meg
Megakaryoblast Megakaryocyte Platelets

CFU- Reticulocyte Normoblast
E

CFU-
Mast
Mast cell precursors

M: MYL cell/phys (coag, heme,
gran)
rbmg/mogr/tumr,
sysi/epon
drug (B1/2/3+5+6), btst

Cryosupernatant
The term cryosupernatant (also called cryo-poor or plasma, cryoprecipitate depleted) refers to
plasma from which the cryoprecipitate has been removed. The resulting plasma has reduced
levels of Factor VIII (FVIII), von Willebrand factor (VWF), Factor XIII (FXIII), fibronectin and
fibrinogen. While the levels of FVIII are greatly reduced, levels of fibrinogen can be as much as
70% of original levels. Cryosupernatant plasma can be used when replacement of FVIII is not
required
[1]
, and is indicated for plasma exchange for patients with thrombotic thrombocytopenic
purpura (TTP) as well as for treatment of hemolytic-uremic syndrome (HUS) by plasma
exchange, when plasma exchange is indicated
[2]
.
[edit] References
1. ^ Shehata, N., Blajchman, M. & Heddle, N. (21 Dec 2001). "Coagulation factors in fresh frozen
plasma (FFP) and cryosupernatant (CSP) plasma (Abstract, in Abstracts of papers presented at
the Joint Scientific Conference of the Canadian Society for Transfusion Medicine and Canadian
Blood Services, 10-13 May 2001)". Transfusion Medicine 11 (5): 391401. doi:10.1046/j.1365-
3148.2001.00115.x.
2. ^ Canadian Blood Services (2004). "F. Cryosupernatant, Leucocytes Reduced (LR)". 2004 Circular
of Information. p. 49.
http://www.bloodservices.ca/CentreApps/Internet/UW_V502_MainEngine.nsf/resources/COI/$
file/Circular-of-Information_SF_E.pdf. Retrieved December 2, 2009.
[hide]
v d e

General
concepts

Blood
group
systems
Blood
types

Blood
products

International Society of Blood Transfusion
The International Society of Blood Transfusion (ISBT), is a scientific society, founded in
1935, which aims to promote the study of blood transfusion, and to spread the know-how about
the manner in which blood transfusion medicine and science best can serve the patient's interests.
The society's central office is in Amsterdam, and there are around 1500 members in more than
90 countries
[1]
. As of May 2008, the President is Professor Erhard Seifried. Past notable
Presidents include Geoffrey Tovey.
[2]

The society organizes every even year an international congress and in odd years two regional
congresses, one in Europe and one in Asia. The Society advocates standardisation and
harmonisation in the field of blood transfusion. A recent example is a standardized bar coding
system for blood for transfusion: the ISBT 128 standard for blood products. Blood banks in the
United States have been expected to use this standard as of May 2008 to meet AABB
Standards
[3]
. It is also used in the United Kingdom
[4]
, Germany
[5]
, and other countries.
The other major impact on the transfusion community is the classification of various Human
blood group systems under a common nomenclature. ISBT's coordination also extends to
obtaining donors with rare antigens, a process that often involves international searches, and a
common terminology is critical to that process.
ISBT also collects and distributes funds for research involving blood and transfusion activities,
including research in developing countries
[6]
. Through Wiley-Blackwell publishing the society
manages a research journal entitled Vox Sanguinis, often cited as "Vox Sang"
[7]
.
ISBT website
Vox Sanguinis
ISBT 128 Standardized bar coding
Classification of blood group systems
[edit] See also
World Health Organization
AABB
Transfusion
[edit] References
1. ^ Isbt-Web.Org
2. ^ http://www.telegraph.co.uk/news/obituaries/1365785/Geoffrey-Tovey.html
3. ^ Association Bulletin #05-12 - ISBT 128 Implementation
4. ^ Professional guidelines for transfusion and for the collection, testing, processing of blood
5. ^ http://old.roteskreuz.at/show_medium.php?mid=6003
6. ^ Isbt-Web.Org
7. ^ Vox Sanguinis - Journal Information
[hide]
v d e

General
concepts

Blood
group
systems
Blood
types

Blood
products

Exchange transfusion
An exchange transfusion is a medical treatment in which apheresis is used to remove one
person's red blood cells or platelets and replace them with transfused blood products. Exchange
transfusion is used in the treatment of a number of diseases, including:
Sickle cell disease
Thrombotic thrombocytopenic purpura (TTP)
Hemolytic disease of the newborn
Contents
[hide]
1 Description
2 Why the Procedure is Performed
3 Risks
4 Recovery
5 See also
[edit] Description
An exchange transfusion requires that the patient's blood can be removed and replaced. In most
cases, this involves placing one or more thin tubes, called catheters, into a blood vessel. The
exchange transfusion is done in cycles: each one usually lasts a few minutes.
The patients blood is slowly withdrawn (usually about 5 to 20 mL at a time, depending on the
patients size and the severity of illness). An equal amount of fresh, prewarmed blood or plasma
flows into the patient's body. This cycle is repeated until the correct volume of blood has been
replaced.
After the exchange transfusion, catheters may be left in place in case the procedure needs to be
repeated.
In diseases such as sickle cell anemia, blood is removed and replaced with donor blood.
In conditions such as neonatal polycythemia, a specific amount of the childs blood is removed
and replaced with a normal saline solution, plasma, or albumin (the clear liquid portion of
blood). This decreases the total number of red blood cells in the body and makes it easier for
blood to flow through the body.
[edit] Why the Procedure is Performed
An exchange transfusion may be needed to treat the following conditions:
Neonatal polycythemia
Rh-induced hemolytic disease of the newborn
Severe disturbances in body chemistry
Severe newborn jaundice that does not respond to phototherapy with bili lights
Severe sickle cell crisis
Toxic effects of certain drugs
[edit] Risks
General risks are the same as with any transfusion. Other possible complications include:
Blood clots
Changes in blood chemistry (high or low potassium, low calcium, low glucose, change in acid-
base balance in the blood )
Heart and lung problems
Infection (greatly decreased risk due to careful screening of blood)
Shock due to inadequate replacement of blood
[edit] Recovery
The infant may need to be monitored for several days in the hospital after the transfusion, but the
length of stay generally depends on the condition for which the exchange transfusion was
performed.
[edit] See also
Plasmapheresis
[hide]
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General
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Blood
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Blood
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Blood
products

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