The Ohio State University Medical Center
Transfusion Service
On-Call Manual
GENERAL INFORMATION:
The on-call resident pathologist will be responsible for the medical consultation of the
Transfusion Service, Monday through Friday from 5:00pm until the day shift Transfusion
Service Pathology Resident assumes responsibility in the morning at 8:30am and twentyfour hour coverage on weekends and holidays. Between 7:30 and 8:30am weekdays, the
attending Transfusion Medicine physician is responsible for answering calls. Your primary
responsibility will be directed consultation with the medical house staff concerning blood
component usage, patient problems and apheresis procedures.
Listed below are the typical hours of operation for each department within the Transfusion
Service:
1.
Main Laboratory- is open twenty-four hours, 365 days per year.
2.
Reference/Prenatal Laboratory- is open Monday through Friday, excluding holidays
from 8:00am through 4:30pm.
3.
Apheresis Department- is open Monday through Friday, excluding holidays from
8:00am through 4:00pm.
The Transfusion Service has additional staff available on an on-call basis:
1.
Main/Reference/Prenatal Laboratory- a lead medical technologist is on call 365
days per year. Their function is to assist with serological problem resolution, after
hours testing and staff coverage.
a. They can be reached via either their home phone number or beeper 7317989. Home phone numbers are located in the Transfusion Service (2938467).
2.
Apheresis- an apheresis nurse is on call for urgent after-hours and weekend
procedures. They can be reached via beeper 730-7817. All other procedures
should be scheduled during normal working hours. If for some reason the apheresis
nurse on call cannot be reached by the beeper, home telephone numbers are
located in the Transfusion Service and Apheresis Unit.
Before leaving for the evening, it is recommended that the on-call resident
pathologist checks with the Transfusion Service day resident or the Transfusion
Service evening lead medical technologist or designated shift supervisor to be
advised of any particular patient problems and/or blood inventory shortages.
Likewise, the resident pathologist on-service for Transfusion Service should check
the shift-to-shift communication log and with the morning shift lead medical
technologist or designated shift supervisor, upon arriving in the morning. Also,
check with the Apheresis Unit in case a late patient or emergency patient is
anticipated.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
TRANSFUSION SERVICE PANIC VALUES:
The physician or person responsible for taking care of a patient must be notified
immediately by laboratory personnel or the on-call resident pathologist of the following
conditions:
1.
Positive direct antiglobulin test on a cord blood and/or heelstick specimen.
2.
Results of a transfusion reaction investigation, including gram stain and culture
results (conveyed by the on-call resident pathologist).
3.
Any clerical or technical error discovered after a blood component was issued for
transfusion.
4.
Delayed hemolytic transfusion reaction when the patient has been transfused within
the last three months and developed a positive direct antiglobulin test or new
alloantibody.
5.
When blood components requested are not available because of inventory
problems, serological problems and/or any other reasons.
6.
Results of Kleihauer Betke test indicating a fetal maternal bleed.
7.
An antibody titer of 1:32 or greater in a pregnant woman.
8.
Results of Delta OD 450.
9.
Results of ABO/Rh(D) on Lifeline of Ohio Organ Procurement specimens.
10. Results of subsequent compatibility testing on patients when blood was sent
uncrossmatched.
11. Clerical or technical errors that involve patient reports or blood components.
DISASTER PLAN:
Modified Disaster Alert:
This is a disaster of limited scope and only requires partial
mobilization of Medical Center resources to be used for
expansion of emergency services for the increased victims from
one incident.
Full Disaster Alert:
This could involve the utilization of all community hospitals in
the Columbus/Franklin County area.
In order to ensure the appropriate utilization of the facilities resources while providing the
best care to all our patients, the Medical Center has developed a two-tiered disaster plan.
The tiered approach identifies a limited activation as well as a full activation of resources.
The Transfusion Service responds to all disaster alerts (Code D).
When the notification of a disaster is received, note the time of call, number of individuals
involved and disaster status. The on-call Transfusion Service lead medical technologist is
immediately notified. The on-call lead medical technologist will notify the on-call resident
pathologist, determine increased staffing needs, coordinate blood and/or blood component
inventory and transfusions and call-in needed personnel. The on-call resident pathologist
must notify the attending pathologist and the Director of Clinical Laboratories.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
During a disaster, there will be prioritizing of blood and blood components released from
the Transfusion Service to patient care areas. Criteria for blood release at this time will be
acutely hemodynamically unstable patients or patients with life threatening hemorrhage.
Routine transfusions could be delayed until additional personnel become available in the
Transfusion Service.
a. Internal – an event in which only the Medical center is involved such as a fire, power
outage or explosion.
b. External – an event in which the Medical Center is not directly involved, but where
the Emergency Department would receive a greater number of victims than can be
treated under normal conditions.
MAIN/REFERENCE/PRENATAL LABORATORY SPECIMEN REQUIREMENTS:
The following are specimen requirements for serological testing:
All of the following serological tests are performed routinely, twenty-four hours per day,
365 days per year. NOTE: All specimens and Transfusion Service requisitions must be
signed (with physician’s pager number), dated and timed by the M.D., R.N. or Transfusion
Service approved designee.
1.
Type/Screen/Crossmatch-
Two 5ml lavender (EDTA) tubes, unless the
request is for greater than six units of packed
red blood cells or the patient has atypical alloantibodies, three 5-ml lavender (EDTA) tubes.
Transfusion Service specimen requisition.
2.
Direct Antiglobulin Test-
This request should also include a type and
screen for evaluation of the indirect antiglobulin
test (antibody screen). Two 5-ml lavendar
(EDTA) tubes. General consult listing patient’s
diagnosis, reason for consultation and current
medications.
3.
Cord Blood Workup-
One lavender clearly marked “cord” blood.
Transfusion Service specimen requisition.
4.
Heelstick Workup-
One brick heelstick bullet tube and
Transfusion Service specimen requisition.
5.
Rh Immune Globulin Evaluation- Two 5-ml lavender (EDTA) tubes and the
Transfusion Service specimen requisition.
the
The following serological tests are performed routinely Monday through Friday form
8:00am through 4:30pm, excluding holidays:
1.
Cold Agglutinin Titer-
One cherry tube and a general consult. (Titers are
done on Thursdays only.) Specimen is routed
through the Central Processing Area.
2.
Antibody Titer-
Three 5-ml lavender (EDTA) tubes.
Transfusion Service specimen requisition.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
(*) 3.
Kleihauer Betke-
One lavender (EDTA) tube, a general consult
listing the primary problem, gestational age and
blood type if known. If the patient is in-house, it is
recommended to have the patient type/screened.
Kleihauer Betke’s are done on outpatients and
specimen received from other facilities Monday
through Friday, 8:00am through 3:30pm.
4.
ABO Titer-
One brick tube on the recipient and one yellow
(ACD) tube on the donor. General consult.
5.
Immunogenetic Markers-
One yellow (ACD) tube on both the recipient and
the donor. General consult.
Delta OD 450-
Amniotic fluid and Delta OD 450 consult.
Cordocentesis/IUT-
One lavender (EDTA) and 1-4 lavendar bullet
tubes and amniotic fluid. Delta OD 450 consult.
(*) 6.
7.
(*)The Kleihauer Betke and the Delta OD 450 can be performed after hours on patients if
clinically indicated. Refer to pages 37-38 for after-hour Kleihauer Betke/Delta OD 450
criteria.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
HLA AND PLATELET SPECIMEN REQUIREMENTS:
A. HLA/DR TYPING:
1. HLA/DR TYPING FOR ALL PATIENTS is done by the Clinical Histocompatibility
Laboratory located in N-935 Doan Hall, (293-8554), 7:00am to 5:00pm. Below are
guidelines for specimen collection, although you should contact Tissue Typing prior
to having a specimen drawn.
Diagnosis/Suspected Disorder
Test(s) To Order
Bone Marrow Malignancy
1. HLA-A, B, C
Platelet Transfusion Refractory
Neonatal Alloimmune
Thrombocytopenia (NAIT)
(Sent out test: Coordinate with
Transfusion Service)
2. HLA-A, B
1. Platelet
Phenotyping (mother
and father).
2. Serum platelet
Antibody (mother)
Post-Transfusion Purpura (PTP)
(Send out test: Coordinate with
Transfusion Service)
3. Platelet antibody
identification
1. Platelet antibody
identification
2. Platelet phenotyping
Sample Requirements
WBC 500-1000
Drawn 40ml Sodium
Heparin (green)
WBC 1000-3000
Draw 30ml Sodium
Heparin (green)
WBC >3000
Draw 20ml Sodium
Heparin (green)
30ml
EDTA
from
mother and father
2. & 3. 5ml of serum from
the mother
1. 5ml of serum as soon
as possible after the
onset of thrombocytopenia
2. EDTA sample
(The volume guidelines are valid if a differential blood count reveals a lymphocyte value of
greater than twenty percent. If there will be a greater than 24 hour delay in delivery,
specimen(s) should be drawn in acd (yellow).
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
B. HLA/ ANTIBODY SCREEN
HLA antibody screening is used to identify the presence of antibody(ies) directed
against HLA antigens occurring on cells such as lymphocytes and platelets for platelet
transfusion. The method used is flow cytometry.
Unlike the HLA antigens on lymphocytes, which are intrinsically expressed, it is felt that
HLA antigens on platelets are acquired due to the absorption of circulating, soluble
HLA antigens. Sensitization to HLA antigens resulting from platelet transfusion support
can contribute to immune clearance of transfused platelets and poor platelet
transfusion response.
This test is useful in identifying cases of platelet refractoriness due to an immune
mechanism. For those patients exhibiting poor transfusion response as measured by
the ten minute-one hour post transfusion increment, the HLA antibody screen confirm
the presence of HLA incompatibility.
Testing is done by the Clinical Histocompatibility Laboratory (293-8554), 7:00am to
5:00pm. Draw a 10ml brick top tube. The specimen should be drawn preferably at least
24 hrs post platelet transfusion.
Transfusions are selected on the basis of HLA using the following definitions:
1. A match- identity of all HLA-A and –B antigens are identical.
2. BU match- two or three HLA antigens identical to the recipient with blanks in the
balance of the phenotype.
3. BX match- two or three antigens identical, the remaining cross-reactive.
4. C match- three donor antigens match the recipient or are cross-reactive, while the
fourth is mismatched.
5. D match- two or more donor antigens are non-identical to the recipient.
C. PLATELET ANTIBODY SPECIMEN REQUIREMENTS
Anti-platelet antibody and platelet-associated antibody are routinely done in Cellular
Immunology. These tests must be scheduled through Cellular Immunology (293-8326),
7:30am to 2:00pm. Testing for heparin-induced thrombocytopenia is routinely done in
the Coagulation Laboratory (688-6501), Monday through Friday, 7:30am to 2:00pm.
The platelet antibody test is used for patients suspected of having allo- or autoimmune
platelet antibodies (NAIT or ITP). It is also used as a rule-out for immunothrombocytopenia when other causes are suspected.
Cases of suspected post transfusion purpura (PTP) are also investigated using the
serum platelet antibody test. Platelet antibody, usually having anti-PLA1 specificity, can
be detected in more than 90% of cases. Platelet phenotyping of the patient can be
used additionally, to support a diagnosis of PTP.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
D. NEUTROPHIL ANTIBODY ASSAY
Both auto and allo-neutrophil antibody assays are sent to a Reference Laboratory
through Central Processing Area. Central Processing Area (293-8375) is responsible
for shipping the specimen(s).
E. PLATELET CROSSMATCHING
Platelet crossmatching should be attempted first (prior to HLA-matching) as a method
to find compatible donors for patients refractory to platelet transfusion. Using a solidphase red cell adherence assay, the patient’s serum is tested against a panel of donor
platelets. Even if a patient is broadly allo-immunized, compatible donors may still be
found using this test, although the chance may be low.
Platelet crossmatching involves mixing patient/recipient serum with donor platelets and
assessing compatibility. This is believed to be more indicative of in vivo compatibility
than is HLA-matching. In the absence of an existing HLA-antigen type of the patient,
platelet crossmatching should be performed.
Platelet-crossmatching specimen requirements:
1. Need 10ml of EDTA plasma from the patient.
2. Use the American Red Cross Platelet Testing Request form.
NOTE:
*If
crossmatching with family member is requested, the American Red Cross
needs an additional lavender (EDTA) tube from each family member to be
crossmatched.
F. PLATELET PHENOTYPING
Neonatal alloimmune thrombocytopenia (NAIT) is the result of the destruction of fetal
platelets by transplacentally acquired maternal antibody directed against paternal alloantigens. PLA1 incompatibility between the mother and the fetus accounts for 80-90%
of NAIT cases. Platelet phenotyping of the mother and father often reveals that the
mother is PLA1 negative and the father is PLA1positive, providing presumptive evidence
for this diagnosis.
Additionally, platelet antibody identification and a crossmatch of the maternal serum
against the father’s platelets can be used to establish this diagnosis.
Ideally, if the fetus/neonate should require platelet transfusion, the mother’s platelets,
washed and suspended in saline, can be administered. This will require consultation
with the medical director at the American Red Cross. If the mother is unable to donate,
the American Red Cross will recruit a suitable platelet donor.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
POLICY ON TRANSFUSION AND TURNAROUND TIME:
All blood and/or blood component transfusion request(s) require the completion of the
Transfusion Service Blood and/or Blood Component Order form.
1. Routine: The patient is on a regular nursing care unit, hemodynamically stable, but
requires a blood transfusion as part of therapeutic regimen.
2. ASAP: The patient is bleeding, but hemodynamically stable, has a low hemoglobin
or low platelet count. This also includes patients to be provided service on a priority
basis (outpatient clinic and dialysis).
3. STAT: The patient is bleeding and hemodynamically unstable, or has the potential
for sudden extensive blood loss or is having surgery within two hours.
4. TAT
If a current specimen is available, the response time for a STAT order is 10-15
minutes. If no current specimen is available:

Uncrossmatched group O Rh(D) negative red blood cells will be available within
5-10 minutes of receiving an order.

Uncrossmatched type specific red blood cells will be available within 15-20
minutes of receiving the proper specimen and order.

Complete type and screen and crossmatch will be done within 45-60 minutes of
receipt of specimen.
ASAP (Definition as above)
Type and screen and crossmatch(es) will be completed within 2 hours of receiving the
specimen.
ROUTINE (Definition as above)
Response time is 6-10 hours from time of specimen collection to administration of the
blood component.
ALLO-ANTIBODY IDENTIFICATION: 4-6 hours after receipt of the specimen.
ALLO-ANTIBODY IDENTIFICATION WITH A POSITIVE DIRECT ANTIGLOBULIN
TEST: routinely, 6-8 hours after receipt of the specimen.
WARM AUTOABSORPTION: 12-16 hours after receipt of the specimen.
ORDERS TO BE CLEARED BY THE ON-CALL RESIDENT PATHOLOGIST:
NOTE: (Also refer to the current Transfusion Service Procedure Manual)
The Transfusion Service technologists are required to intercept unusual orders and obtain
the on-call resident pathologist approval before issuing the requested blood and/or blood
components. The following is a list of unusual orders and recommendations:
1. Fresh Frozen Plasma (FFP) (see Transfusion Guidelines):
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
When the physician wants to transfuse more than four units of fresh frozen
plasma/day to any patient or indications for transfusion are outside audit criteria and
there is no medical indication, the Transfusion Service technologist will contact the
on-call resident pathologist. The on-call resident pathologist should contact the
ordering physician and determine if coagulation studies are abnormal or if there is
other justification for transfusion. Hemorrhage, single/multiple coagulation factor
deficiencies and DIC are some indications for fresh frozen plasma or pooled plasma
solvent detergent treated transfusion.
The Transfusion Service technologists normally attempts to obtain the laboratory
results of the PT, INR, PTT, Fibrinogen, BUN, Creatinine, Platelet Count and Hgb,
the patient’s diagnostic information and the name and beeper number of the
ordering physician before calling the on-call resident pathologist. However, when
the Transfusion Service technologist(s) are busy, the on-call resident
pathologist may have to obtain all the information.
2. Cryoprecipitate AHF – (see Transfusion Guidelines):
Cryoprecipitate is indicated for the treatment of hypofibrinogenemia,
dysfibrinogenemia, congenital fibrinogen deficiency and consumptive coagulopathy.
The Transfusion Service technologist will contact the on-call resident pathologist in
ALL cases of orders for cryoprecipitate. Typically, 6 units of cryoprecipitate (cryo
“pool”) are given to patients who have a dilutional coagulopathy due to massive
transfusion. Uremic patients can also be given cryoprecipitate to aid in exposing the
Von Willebrands factor for platelet adhesion, although this is not the first choice of
therapy. Dialysis and DDAVP are more effective and should be used first. Estrogen
therapy has been used in uremia with a more prolonged hemostatic effect. Single
unit cryoprecipitate is used for fibrin surgical adhesive. Cryoprecipitate transfusions
are indicated if the fibrinogen level is less than 100 mg/dL in bleeding patients.
3. Platelet Concentrates/Plateletpheresis (see Transfusion Guidelines):
If the platelet count falls below 10,000 in a non-bleeding hematology or oncology
patient or below 50,000 for surgical patients, platelet transfusion is indicated.
Platelet counts of 5,000-10,000 (Lancet 338:1223, 1991) may be satisfactory in
stable patients. This also allows for more judicious use of scarce/difficult-to-obtain
platelet components.
When more than 8 units of single, random donor platelet concentrates (2 platelet
pools or 2 plateletpheresis) per day are requested for a patient, the Transfusion
Service technologist will contact the on-call resident pathologist for approval. If the
pre and 10 minute-up-to one hour post transfusion counts have not been done, the
ordering physician should be encouraged to obtain pre and post transfusion platelet
counts. If the post transfusion platelet count shows refractoriness to ABO matched
random donor platelet apheresis on at least two occasions, the ordering physician
should be encouraged to order crossmatched platelets (see page 39 and 40).
4. Other Situations Where The Transfusion Service May Request The On-Call
Resident Pathologist Assistance:
Massive Transfusion – Not Enough ABO/Rh(D) Identical Red Blood Cells:
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
When a massively transfused patient is using large amounts of red blood cell
components (10 units in 24 hours), the Transfusion Service may not be able to
continue providing ABO/Rh(D) identical red blood cells. Transfusing non-identical,
but compatible ABO blood type red blood cells is not a major problem. Almost all of
our red blood cells are collected in AS-1 (ADSOL) and have very little remaining
plasma. A Transfusion Medicine physician’s approval is not required.
However, having to give Rh(D) positive red blood cells to an Rh(D) negative patient
requires the consent of the on-call resident pathologist.
Rh(D) negative women of childbearing age (usually, but not exclusively, 45 years
old) are never given Rh(D) positive red blood cells unless it is the only blood
available and the medical condition (life-saving) warrants (see pages 33-35).
5. Not Enough Rh(D) Negative Platelet Concentrates and/or Plateletpheresis
Available:
Shortage of Rh(D) negative platelets occurs more frequently than shortage of Rh(D)
negative red blood cells. When the patient in question is a hematology, oncology or
bone marrow transplant patient requiring long-term platelet support, the Transfusion
Service technologist will contact the on-call resident pathologist for the initial platelet
transfusion of Rh(D) positive platelets.
When the patient in question is a non-hematology or oncology patient, whose
platelet transfusion support is not long-term, the on-call resident pathologist may
approve transfusing Rh(D) positive platelets. If indicated, one vial of Rh Immune
Globulin is enough to cover the transfusion of up to 30 Rh(D)-positive platelet
concentrates or 6 plateletpheresis (see pages 33-35).
6. Massive Transfusion:
When a patient is using a large number of red blood cells, but no fresh frozen
plasma, cryoprecipitate and/or platelets, the Transfusion Service technologist will
contact the on-call resident pathologist for assistance. The on-call resident
pathologist should urge the patient’s physician to consider fresh frozen plasma and
platelets, and to order appropriate coagulation studies. On the basis of the
coagulation studies, the on-call resident pathologist may recommend fresh frozen
plasma, cryoprecipitate and/or platelets to correct the dilutional coagulopathy.
7. Transfusion Reaction Complications:
When a patient has an acute and/or delayed hemolytic transfusion reaction, the
Transfusion Service technologist will contact the on-call resident pathologist. The
on-call resident pathologist will notify the patient’s physician of the transfusion
reaction. If the patient has signs and symptoms of an allergic, anaphylactic and/or
febrile transfusion reaction, the Transfusion Service technologist will call the on-call
resident pathologist with results of the initial transfusion reaction investigation. The
on-call resident pathologist will advise the technologist if any additional testing is
required (ABO, Rh(D), gram stain, culture, etc). The on-call resident pathologist
should consult with the patient’s physician and advise medication and offer advise
regarding clinical management (see pages 23-26).
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
8. CMV Negative/Irradiated Blood Components:
The first time a patient is requested to be given CMV negative and/or irradiated
blood components, the on-call resident pathologist’s approval is required. Refer to
guidelines on pages 30-31.
9. Blood Warmer:
Refer to guidelines on page 30.
WHEN CONSULTING WITH AN ORDERING PHYSICIAN AND A MODIFICATION IS
MADE OF THE INITIAL ORDER, REMIND THE PHYSICIAN TO MODIFY THE
ORDER. COMMUNICATE TO THE TRANSFUSION SERVICE THE DECISION
REGARDING TRANSFUSION.
ANTIBODY SCREEN (INDIRECT ANTIGLOBULIN TEST):
Allo-antibodies are found in people who through pregnancy, previous transfusion, or
injections have been exposed to foreign red blood cell antigens. Some people with no
known immune stimulus may have unexpected antibodies, usually reacting at low
temperature.
Unexpected antibodies may be responsible for the following:
1. A discrepancy between ABO forward and reverse typing.
2. A positive antibody screening test.
3. An incompatible crossmatch.
4. A transfusion reaction.
5. Jaundice in a newborn.
6. A positive direct antiglobulin test.
7. A positive autocontrol.
Antibodies stimulated by red cell antigens usually react in a predictable manner,
depending on the specificity of the antigen. Some of the antigens stimulate the production
of IgM and other IgG. The IgM antibodies react by agglutinating the red blood cells, while
the IgG antibodies bind to the red blood cells, which then can be agglutinated by
antiglobulin serum. Some antibodies (all IgM and some IgG) are able to activate
complement. If the bound complement proceeds to completion of the sequence, the red
blood cells will be lysed. If the sequence is not completed, the cell-bound components can
be detected with polyspecific or monospecific anti-C3 antiglobulin serum.
Routine antibody testing at The Ohio State University Medical Center is done by PEGantiglobulin method using immediate spin, 15 minute 37C incubation and the indirect
antiglobulin test technique or Capture-R (solid phase adherence) technique. Capture-R is
based on a modified solid phase technique using red cell adherence to detect IgG blood
group allo-antibodies in the patient sera. Antibody screen red cells are bound and dried in
a monolayer to the surface of polystyrene strip wells. The membrane antigens are used to
capture red cell specific IgG antibodies. Following a brief incubation period, unbound
residual immunoglobulins are rinsed from the wells and replaced with a suspension of antiIgG coated indicator red cells. Red cells for antibody screen are selected to have as many
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
antigens as possible. Antibodies reacting only at temperatures lower than 37C are
generally considered to be clinically insignificant. If the antibody screen is negative by
routine testing, only an immediate spin crossmatch is required.
If a patient has a positive antibody screen, a complete routine panel is performed to
identify the allo-antibody(ies). Antibody panels are composed of selected group O red
blood cells from several donors who have been tested for as many of the common
antigenic determinants as possible. These cells are different from each other and negative
for several antigens. In addition to performing the antibody panel, the following additional
tests are performed:
1. Direct antiglobulin test and autocontrol.
2. A test for the antigen(s) corresponding to the antibody(ies) suspected, unless the
patient has been recently transfused.
When ruling out alloantibodies, the following general principles apply:
1. Antibodies known to show dosage should be ruled out on the basis of homozygous
cells. These include, but are not limited to, anti-Fya, Fyb, E, Jka, Jkb, M, C, S and s.
Exceptions: Anti-E with anti-c, anti-S with anti-M, anti-C and anti-E with anti-D and
anti-C with anti-e can be ruled out with heterozygous cells, because homozygous
cells are rare.
2. Antibodies to low incidence antigens (Cw,Kpa, Jsa and Lua) need not be ruled out,
rather rely on “crossmatch-compatible” blood.
If a single and/or multiple antibody is suspected in a patient’s serum, at least 3 antigen
positive panel cells must be shown to react. At least 3 antigen negative panel cells must
be shown to be non-reactive.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
Positive Antibody Screen Flow Chart
Negative Panel
Positive Panel
Repeat Antibody Screen
Identify Antibody(ies)
Repeat ABSCR Positive
Repeat ABSCR Negative
Same phase and strength
no additional testing required:
Inconclusive Antibody
No additional testing required
Contamination
Positive Crossmatch with Negative Antibody Screen Flow Chart
1. Obtain a new donor segment.
2. Check ABO of patient and donor.
3. Consider possibility of Anti-A1.
Direct Antiglobulin Test on Donor Segment
Negative
Positive
Repeat ABSCR and Xmatch
Withdraw unit,
Return to blood supplier
All Negative
Repeat ABSCR and panel
Negative, Xmatch Positive
No additional testing
Frequency Antibody or Antibody Showing Dosage
ESTIMATING BLOOD COMPATIBILITY:
The frequency of blood group antigens can be used to calculate the probability of finding
antigen-negative red blood cells. The calculation is relatively simple for a patient with a
single blood group antibody. For example, if the serum of an individual contains anti-JK9
and the frequency of individuals lacking the JK9 antigen in the population is 23%, then
approximately 23% or one out of every four ABO group specific red blood cells would be
compatible.
If more than one antibody is involved, it is necessary to multiply the frequencies of antigennegative donors. For example, if a Group A patient has anti-c, anti-JK9 and anti-Kell, the
probability of finding compatible antigen-negative red blood cells:
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
0.20 = probability of c negative
0.23 = probability of JK9 negative
0.90 = probability of K negative
0.40 = probability of A
0.54 = probability of O
0.11 = probability of B
0.04 = probability of AB
To determine the probability, multiply the individual antigen frequencies and frequency of
ABO compatibility.
0.20 X 0.23 X 0.90 X 0.40 = 0.01656 X 100 = 1.7%
Frequency in A’s
0.20 X 0.23 X 0.90 X 0.54 = 0.022356 X 100 = 2.2%
Frequency in O’s
0.20 X 0.23 X 0.90 X 0.94 (A’s + O’s) = 0.038916 X 100 = 3.89% Frequency in A’s and O’s
If six red blood cells were needed for this patient, it would be necessary to screen 154
donor units of the compatible ABO type to find six compatible red cell. (see below)
N = number of donor to be tested
3.89 = 6
100 N
N = 600
3.89
= 154 units
Once the degree of difficulty of the donor unit search is calculated, a rational approach to
addressing the patient’s transfusion needs can be established and communicated to the
medical housestaff.
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
RED CELL ANTIBODIES:
Antibody
% Compatible
D
C
E
c
e
Cw
V
G
f
K
k
Kp
Kp
Jsa
Jsb
Fya
Fyb
Jka
Jkb
M
N
S
s
U
Lea
Leb
P/P1(Tja)
Pla
Lua
Lub
Xga
Dia
I
i
W = White
B = Black
15
30
70
20
3
98
100W 82B
15
33
90
0.2
98
<0.1
99W 80B
0W<0.1B
33W 89B
20W 77B
25
25
22
28
45
11
0W 1B
78W 82B
22W 40B
0.1
20W 5B
92
1
36M 13F
99
0.1
99
M = Male
F = Female
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
Associated withb
Donor (%)
Antibody
Anti-A
Anti-B
Anti-A1
Anti-A,B
Anti-D
Anti-C
Anti-Cw
Anti-E
Anti-c
Anti-e
Anti-M
Anti-N
Anti-S
Anti-s
Anti-U
Anti-P1
Anti-P
Anti-PP1pk
Anti-Lua (Lutheran)
Anti-Lub (Lutheran)
Anti-K (Kell)
Anti-k (Chilo)
Anti-Kpa
Anti-Kpb
Anti-Jsa
Anti-Jsb
Anti-Lea (Lewisa)
Anti-Leb (Lewisb)
Anti-Fya (Duffya)
Anti-Fyb (Duffyb)
Anti-Jka (Kidda)
Anti-Jkb (Kiddb)
Anti-Xga (x-linked
Antigen)
Anti-Dia (Diegoa)
Anti-Dib (Diegob)
Anti-Yta (Cartwrighta)
Anti-Ytb (Cartwrightb)
Anti-Doa (Dombrocka)
Anti-Dob (Dombrockb)
Anti-Coa (Coltona)
Anti-Cob (Coltonb)
Anti-Sc1 (Scianna1)
Anti-Sc2 (Scianna2)
Anti-Ch (Chido)
Anti-Rg (Rodgers)
Anti-Kna (Knopsa)
Anti-Knb (Knopsb)
Anti-Yka (Yorka)
Anti-SLa (McCoya)
HDN
HTR
Yes
Yes
Yes
Yes
?
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Few
Few
Rare
?
Yes
Yes
Yes
Yes
Yes
Yes
No
Rare
No
?
Rare
?
No
?
Mild
Yes
Yes
Yes
Yes
Yes
Yes
Yes
?
Yes
?
Yes
?
No
Few
No
?
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
No report
Yes
Yes
Yes
Yes
No
Yes
No Report
?
Yes
No Report
Yes
?
No Report
No Report
No Report
No
Yes
No
No
No
No
No
No
No
No
No
No
Compatible
White
Black
56
69
85
76
53
52
45
49
15
8
30
68
99
100
70
98
20
1
2
2
22
30
28
26
45
69
11
3
0
<1
21
6
Extremely Rare
Extremely Rare
92
0.15
91
98
0.2
Rare
97.7
100
Rare
0
100
80
0
1
78
77
28
45
34
22
17
77
23
9
28
57
M, 34
F,11
100
0
0.2
92
33
17
0.3
89
Very rare
99.7
-
Data are from the American Association of Blood Banking Technical Manual (1985).
HDN: Hemolytic Disease of the Newborn; HTR: Hemolytic Disease Transfusion Reaction
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CROSSMATCH/COMPATIBILITY TEST:
Routinely an immediate spin major crossmatch, testing of donor cells with the recipient’s
serum, is performed on all patient specimens with a negative antibody screen. If the
patient’s serum has a clinically significant antibody, a complete major crossmatch
(immediate spin – AHG) is performed, which requires a 15-minute 37C incubation.
Antibody
Anti-D,C,E,c,e,
Jka,Jkb,S,s,K,k
Crossmatch
Fya,Fyb,
Donor red blood cells must be antigen negative.
Complete major crossmatch.
Anti-A1,P1,Lea,Leb
Donor red blood cells do not have to be antigen
negative. Rely on complete major crossmatch.
Anti-M,N
If antibody reactive at 37C and/or AHG, the donor
red blood cells must be antigen negative.
Otherwise, rely on complete major crossmatch.
Anti-Jsa,Wra, Lua,
Cw,Kpa,V
Donor red blood cells do not have to be antigen
negative. Rely on complete major crossmatch.
The crossmatch will not:
1. Guarantee normal donor red cell survival.
2. Prevent recipient alloimmunization.
3. Detect all ABO grouping errors.
4. Detect Rh(D) typing errors.
5. Detect all unexpected red blood cell antibodies in the recipient serum.
All red blood cell containing components (i.e., packed red blood cells, whole blood,
granulocytes) must be crossmatched before being administered. Platelets usually contain
less than .5ml of red blood cells and, therefore, do not require crossmatching. “Bloody”
platelets should be returned to the supplier.
Selection of Red Blood Cells for Crossmatch:
1. Select older red blood cells for patients with transfusion orders, and fresher red
blood cells for surgical patients.
2. Infants should receive CPDA-1/CPD red blood cells, generally less than 14 days old
and CMV negative. Adsol has been used for neonatal transfusion (Children’s
Hospital).
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Selection Of Blood Components When ABO Identical Donors Are Not Available
ABO GROUP OF
RECIPIENT
ACCEPTABLE
BLOOD GROUP OF
DONORS
Red Blood Cells
O
A
B
AB
None
A,O
B,O
AB, A, B or O
ABO and Rh(D) must
be compatible with the
recipient’s plasma.
Fresh Frozen Plasma
O
A
B
AB
O, A, B, or AB
A, AB
B, AB
None
ABO should be
compatible with the
recipient’s red cells.
Rh(D) typing need not
be a consideration.
Platelet Concentrate*
O
A
B
AB
O, B, A, or AB
A, B, AB, or O
B, A, AB, or O
AB, A, B
Although all ABO
groups are
acceptable, ABO
identical components
are preferred. Platelet
compatibility with
recipient’s plasma is
preferred. HLA match
and platelet
crossmatched are
given regardless of
ABO type. If more
than 350 ml of
incompatible plasma,
the component should
be plasma reduced.
Cryoprecipitate
O
A
B
AB
O, A, B, or AB
O, A, B or AB
O, A, B or AB
O, A, B, or AB
All ABO and Rh(D)
groups are acceptable
since the volume
administered is small,
unless volume
exceeds 350 ml of
ABO compatible
plasma.
COMPONENT
RATIONAL
NOTE: Type O packed red blood cells ADSOL (AS-1) are considered safe for transfusion for patients of any
blood type. The concern for plasma incompatibility is unwarranted in view of the small amount of plasma
remaining in an ADSOL (AS-1) pack red blood cell.
*Platelet
Concentrates/Pheresis: Every effort should be made to give ABO/Rh(D) identical platelets or at
minimum ABO compatible platelets.
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On-Call Manual
DIRECT ANTIGLOBULIN (COOMBS) TEST (DAT):
The direct antiglobulin test (DAT) is used to detect the in vivo sensitization of red blood
cells with IgG and/or complement.
The DAT is useful for:
1. Diagnosis of hemolytic disease of the newborn.
2. Diagnosis of autoimmune hemolytic anemia and cold agglutinin disease.
3. Investigation of red blood cell sensitization caused by drugs.
4. Investigation of transfusion reactions.
Positive Direct Antiglobulin Flow Chart
Positive Polyspecific DAT
Monospecific Testing
DAT Positive IgG with
DAT Positive C3 only
or without C3
No More Testing
Patient not transfused
past 3 months
Patient transfused
within past 3 months
DAT Positive 1st
time this admission
Positive DAT previously
during this admission
Eluate
No Eluate Needed
When interpreting a positive DAT, consideration must be given to the medication history,
diagnosis, obstetrical history and transfusion history of the patient.
1. Polyspecific positive, monospecific negative:
This situation is seen in patients with an increased reticulocyte count and in some
cases due to the weak, synergetic effect of anti-IgG and anti-C3 in weak
sensitization due to both IgG and C3.
2. Polyspecific positive, C3 only positive:
a. Patients with Cold Hemagglutinin Disease. The antibody screen should show
the presence of a cold autoagglutinin.
b. 10-20% of Warm Autoimmune Hemolytic Anemias.
c. Numerous medications cause in vivo complement binding on red cells
(significant hemolysis seen with 3rd generation cephalosphorins).
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d. C3 alone coated on the red cells in various neoplastic and collagen-vascular
disease.
3. Polyspecific positive, monospecific positive:
a. If a positive direct antiglobulin test is due to IgG, with or without a C3
component, an eluate must be performed.
b. Both anti-IgG and anti-C3 are positive in 40-50% of cases of warm autoimmune
hemolytic anemia.
ELUTION:
Red cell elution is the process of dissociating coated antibody from the membrane of
the red blood cells. This makes the antibody available in a medium in which it can be
tested for specificity.
Interpretation of Eluate Results:
1. Eluate Nonreactivea. Drug induced (i.e. penicillin).
b. Inadequate coating of antibody.
2. Eluate Reactive with all Cellsa. Drug induced (Aldomet, i.e., alpha-methyldopa).
b. Warm autoantibody.
3. Eluate Reactive With only A and/or B Cellsa. Transfusion of ABO incompatible plasma (i.e. previous transfusion of platelets).
b. Hemophiliacs (factor concentrate).
4. Eluate Reactive with Certain Cellsa. Antibody production (delayed transfusion reaction).
b. Non-specific reactivity.
c. IVIG (Anti-D and Anti-Kell have been reported).
Drugs That Have Been Reported To Induce RBC Drug-Independent Antibodies (i.e.,
Autoantibodies)
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Group 1a
Methyldopa
Levodopa
Mefenamic acid
Procainamide
Catergenb
Chaparralb
Cyclofenilb
Ibuprofenb
a These
b
Group IIc
Azapropazone
Carbimazole
Cefoxitin
Chlorinated hydrocarbons
Cianidanol
Diclofenac
Galfenine
Latamoxef
Nomifensine
Phenacetin
Streptomycin
Teniposide
Tolmetin
drugs induce drug-independent antibodies only.
More evidence is needed to prove that these drugs really can induce RBC autoantibodies
c These
drugs induce drug-independent antibodies together with antibodies reacting by
different mechanisms.
Associated With Antibodies Showing Characteristics Of More Than One Mechanisms a
Drug
Mechanisma
a
Chlorinated hydrocarbons
AA + DA + IC
Phenacerin
AA + IC
Streptomycin
AA + DA
Azapropazone
AA + DA
Teniposide
AA + IC
Galfenine
AA + IC
Latamoxef
AA + IC
Nomifensine
AA + IC
Cianidanol
AA + DA + IC
Diclofenac
AA + IC
Carbimazole
AA + IC
Tolmetin
AA + IC
Zomepirac
AA + IC
Cefotaxime
AA + IC
Ceftazidime
AA + IC
Cefotetan
AA + DA and DA + IC
Mechanisms are those described in the literature as (1) autoantibody (AA), (2) drugabsorption (DA), (3) “immune complex” (IC).
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Drugs That Have Caused Immune Hemolytic Anemia and/or Positive Direct Antiglobulin
Test (DAT)
Acetaminophen
Amephotericin B
Ampicilin
Antazoline
Apronal
Butizide
Carbenicillin
Carbimazole
Cabromal
Cefamandole
Cefazolin
Cefotetan
Cefoxitin
Ceftazidime
Deftriaxone
Cephalexin
Cephaloridine
Cephalothin
Chlorinated hydrocarbons
(insecticides)
Chlorpropamide
Chlorpromazine
Cianidanol
Cisplatin
Cyclofenil
Diglycoaldehyde
Dipppyrone
Crythromycin
Fenoprofen
Fluorouracil (5-FU)
Floursemide
Glafenine
Hydralazine
Hydrochlorothiazide
9-Hydroxy=methylEllipticinium
Ibuprofen
Insulin
Isoniazid
Latamoxef
Levodopa
Mefenamic acid
Melphalan
Methadone
Methicillin
Methotrexate
Methyldopa
Methysergide
Nafcillin
Nomifensine
p-aminosalicylic
acid
Penicillin G
Phenacetin
Podophyllotoxin
Probenecid
Procainamide
Pyramidon
Quinidine
Quinine
Ranitidine
Rifampicin
Sodium Pentothal
Streptomycin
Sulphamides
Teniposide
Tetracycline
Thiopental
Tolbutamide
Tolmetin
Triamterene
Trimellitic
anhydride
Zomepirac
Drugs were included only when reasonable evidence was presented in the literature to
support that they caused the immune reaction. There are many more reported, but the
evidence that they caused a positive DAT or drug-induced hemolytic anemia is often
minimal or totally lacking.
Adapted from AABB Technical Manual, Principles of Transfusion Medicine (Rossi, et al),
DAT Workshop.
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WARM AUTOABSORPTION:
In cases of warm autoimmune hemolytic anemia and warm autoagglutinins induced by
drugs, such as Aldomet, not only may the direct antiglobulin test be strongly positive due to
IgG or IgG/C3 but a warm autoagglutinin may be demonstrable in the serum.
This antibody usually reacts with all donor and panel cells tested. In these cases, it is
essential to know if there is an alloantibody being masked by the autoagglutinin. This can
be accomplished by eluting some of the autoantibody off the patient’s red cells and then
using these cells to absorb the autoagglutinin from the patient’s serum.
Important consideration:
1. This procedure is performed with heterologous cells if the patient has been
transfused in the past three months. The results of the autoabsorption studies
should be interpreted with caution. Misleading negative results with the absorped
serum may occur if the transfused cells possess the relevant antigen and have
absorbed an alloantibody from the test serum. The American Red Cross can
perform a heterologous absorption in problem/transfused cases.
NOTE: Heterologous absorption can absorb out high-incidence antibodies.
COLD AUTOAGGLUTININS:
Cold autoagglutinins are present to a greater or lesser extent in all human sera. Under
certain circumstances (i.e., monoclonal/polyclonal gammopathies, viral and/or
pneumococcal infection), cold agglutinins may become extremely high titered. Most of the
specificity of these antibodies is directed against antigens of the I system or related
antigen systems. In the Transfusion Service, a cold agglutinin can cause all ABO and
Rh(D) typing tests to be agglutinated with a positive reaction in the immediate spin phase
of the antibody screen and/or crossmatches. The reaction is usually weaker at 37C.
Most non-pathological cold agglutinins are primarily reactive below 32C and cause
serological problems by binding complement. The presence or absence of clinically
significant alloantibodies can be demonstrated by doing a regular pre-warm antibody
screen. The pre-warm technique eliminates the carryover of the immediate spin
agglutination into the indirect antiglobulin tests. If a pre-warm crossmatch is required for a
resolution of a positive antibody due to cold agglutinins, any blood components given must
be given through a blood warmer (see page 30).
Most cold IgM antibodies will bind complement to red cells. This binding occurs best at
4C, but may also occur at room temperature.
TRANSFUSION REACTIONS:
A transfusion reaction is any unfavorable event occurring in a patient during or following
transfusion of blood components that can be related to the transfusion. Since compatibility
testing is performed for the detection of antibodies to red blood cell antigens, adverse
effects of transfusion are most commonly caused by leukocytes, platelets, and plasma
proteins. The most common causes of an acute hemolytic transfusion reaction are clerical
errors and lack of proper patient identification.
After completing the clerical check, DAT and hemolytic check, the Transfusion Service
technologist will consult the on-call resident pathologist if more detailed serological work-
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up is required or if the remaining blood and/or blood component needs to be gram stained
and cultured.
Acute Hemolytic Transfusion Reaction:
Hemolysis of transfused red blood cells occurs infrequently but may cause a severe
reaction accompanied by hemoglobinemia, hemoglobinuria, hypotension, DIC, acute renal
failure and death. Initial symptoms are not diagnostic of hemolysis and often consist of
fever, chills, flushing, a feeling of apprehension, chest or back pain, and nausea or
vomiting. During anesthesia, the development of diffuse bleeding may be the only
evidence of hemolytic reaction. Red blood cell destruction may be primarily intravascular,
as seen in ABO incompatible red blood cell infusion or predominately extravascular as in
Rh incompatibility. The Transfusion Service will perform a direct antiglobulin test, visual
inspection for hemolysis, and a clerical check. In the event of a hemolytic transfusion
reaction, the on-call resident pathologist should immediately call the on-call attending
pathologist. If the reaction results in death, the FDA must be notified within 24 hours of
ascertaining the transfusion was causal to the dealth.
Recommend these tests to the patient’s physician, if clinically indicated:
Test
Specimen Times
Serum Hemoglobin
1. Pre-transfusion
2. Immediate Post
Serum Haptoglobin
1. Pre-transfusion
2. Immediate Post
Serum Bilirubin
1. Immediate Post
2. 24-Hour Post
Urine Hemoglobin
1. Immediate Post
BUN/Creatinine
1. Immediate Post
2. Daily
DIC Workup
1. Immediate Post
Febrile Non-Hemolytic Reactions:
Febrile non-hemolytic reactions, often preceded by chills, constitute the bulk of the
transfusion reactions. These reactions are generally considered to be a result of
cytotoxic or agglutinating antibodies in either the donor or recipient plasma directed
against antigens present on lymphocyte, granulocyte or platelet membranes. While
reactions are usually mild and result principally in recipient anxiety and discomfort, a
hemolytic transfusion reaction must be ruled out. Pre-medication with antipyretics may
modify reactions in some recipients. Leukocyte-reduced red blood cells and platelets
help prevent these reactions.
A febrile non-hemolytic reaction is a temperature rise of 1C or 2F or more occurring
during transfusion or up to 2-4 hours following transfusion and without other
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explanation. The fever may be caused by the infusion of bacterially contaminated
blood. Psychrophilic gram negative bacteria (e.g. Yersinia) can cause severe reactions
characterized by high fever. If indicated, specimens are sent to the Clinical
Microbiology Laboratory for culture and sensitivity and a STAT gram stain. Between
3:00pm – 7:00am, the Critical Care Laboratory will perform and read the gram stain.
Allergic Reactions:
Allergic reactions following blood or plasma transfusion occur in about 1% of patients
and are usually relatively mild. Most consist of local erythema, hives and itching,
usually without a fever. An allergic reaction can easily be treated and/or prevented by
administration of antihistamines; rarely, solucortef is required.
Anaphylactic Transfusion Reactions:
Most anaphylactic transfusion reactions have unknown etiology. Rarely, this form of
transfusion reaction may be encountered in a patient who is IgA deficient and has
made IgG antibodies. IV steroids and antihistamines are given. Some patients also
require bronchodilators and blood pressure support.
Delayed Hemolytic Transfusion Reaction:
Delayed hemolytic transfusion reactions usually result in extravascular removal of
transfused cells from the circulation days to weeks following transfusion. Rarely, abrupt
intravascular hemolysis may occur with certain antibodies, such as anti-Jka and antiJkb. Red blood cells that were compatible at the time of transfusion may be destroyed
following antibody formation (anamnestic response). The direct antiglobulin test is
usually positive although the indirect antiglobulin test may be negative until all
transfused red blood cells have been eliminated from the circulation. Nearly all delayed
transfusion reactions, except for the very uncommon transfusion reactions, which
produce intravascular hemolysis, tend to be asymptomatic and are only manifest by a
mild, gradual anemia and transiently positive direct antiglobulin test.
TRALI:
Transfusion-related acute lung injury (TRALI) should be considered whenever a
transfusion recipient experiences acute respiratory insufficiency, chills, fever, cyanosis,
hypotension and/or when an x-ray finding is consistent with pulmonary edema, but
without evidence of cardiac failure. The severity of the respiratory distress is
disproportional to the volume of blood infused. Donor antibodies to HLA or neutrophil
antigens may react with the recipient’s leukocytes, which cause permeability of the
pulmonary microcirculation and fluid enters the alveolar spaces. If specific antibodies
are absent, TRALI may result from complement activation to generate anaphylatoxins
C3a and C5a; direct aggregation of granulocytes into a leukoemboli or transfusion of
cytokines that have accumulated in stored blood. Treatment typically consists of O 2
therapy and ventilatory assistance and intravenous steroids. Patients recover
adequate pulmonary function in 2-4 days.
Circulatory Overload:
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On-Call Manual
Rapid transfusion or transfusion in a fluid-overloaded patient may cause acute
pulmonary edema due to volume overload. Infusion of 25% albumin, which shifts large
volumes of interstitial fluid into the vascular space, may cause circulatory overload.
Circulatory overload should be considered if dyspnea, cyanosis, orthopnea, severe
headaches, hypertension or congestive heart failure occur during or following
transfusion.
Graft versus Host Disease:
T lymphocytes present in cellular blood components may cause transfusion-associated
graft-vs-disease (GVHD), which results in some or all of the following findings: fever,
dermatitis or erythroderma, hepatitis, enterocolitis, pancytopenia, and immunodeficiency. At present, there is no effective treatment for transfusion-associated
GVHD. Gamma irradiation (minimum 1500 rads) of cellular blood components prevent
transfusion-associated GVHD.
Citrate Toxicity:
When larger volumes of fresh frozen plasma, whole blood or platelet concentrates are
transfused with rates exceeding 100 ml/minute, plasma citrate levels may rise and
hypocalcemia may occur. Unless a patient has a predisposing condition that hinders
citrate metabolism, hypocalcemia due merely to citrate overload requires no treatment
other than slowing or discontinuing the transfusion. If a patient remains symptomatic,
the patient may require careful intravenous infusion of 10% calcium gluconate.
Calcium should not be administered through the access line for transfusion as the
blood may clot.
Cytokines:
Leukocyte reduction has been used with considerable success to prevent febrile nonhemolytic transfusion reactions, but in many cases even near complete removal of the
leukocytes is ineffective. It is known that cytokines are generated during storage, even
at 1-6C but to a much greater extent at 20-24C. Cytokine levels rise in direct
proportion to the number of leukocytes. The variety of cytokines produce a combined
effect including fever, hypotension, mobilization of neutrophils from the bone marrow,
activation of endothelial cells to express adhesion molecules and procoagulant activity,
activation of T and B lymphocytes and priming of neutrophils.
ESTIMATED RISKS OF TRANSFUSION:
1.
Hepatitis B transmission per screened unit – 1:600,000
2.
Hepatitis C transmission per screened unit – 1:1,200,000
3.
HIV transmission per screened unit – 1:2,000,000
4.
HTLV I/II transmission per screened unit – 1:641,000
HTLV infection – 4% lifetime risk of associated disease (adult T-cell leukemia,
tropical spastic paraparesis).
5.
Acute hemolytic transfusion reaction – 1:25,000
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6.
Non-hemolytic transfusion reaction – 1:200
7.
Chills – 1:200
8.
Fever – 1:200
9.
Formation of allo-antibodies – 1:100
10. Non-Enveloped Viruses (Hepatitis A, Parvovirus B19): the risk of transmission is
not determined. Parvovirus B19 can cause bone marrow hypoplasia.
11. Other risks –
a. Circulation overload
b. Bacterial contamination
c. Iron overload
12. Other diseases: Yersinia, Malaria, Babesiosis, Chagas – 1:1,000,000 each.
Overall: risk that blood recipient will have a serious or fatal transfusion transmitted
disease – 1:20,000
RISK OF MASSIVE TRANSFUSION:
1.
Hypothermia (RBC massive transfusion)
2.
Air emboli if blood component transfused under pressure
3.
Citrate toxicity (predominantly with FFP administration)
4.
Metabolic alkalosis
5.
Hypokalemia
6.
Coagulation defect (predominantly dilutional coagulopathies)
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TRANSFUSION REACTIONS
Symptoms*
Lab Findings*
Treatment
Hives
None
Antihistamines
(Benadryl 50 mg
p.o. or i.v.)
Anaphylactic
Laryngeal edema
Bronchoconstriction
Rarely, IgA
deficiency or none
Corticosteroids
Febrile
Non Hemolytic
Fever, chills, shortness of breathe,
tachycardia, flushing
Usually none.
Sometimes leukoagglutinin or
lymphocytotoxic
antibodies
Antipyretics
(Tylenol)
Antipyretics leuko
reduced
Fever, chills,
shock, acute renal
failure
Clerical errors,
hemolysis, positive
direct antiglobulin
test. Elevated
serum and urine
bilirubin
Fluids, diuretics
(Lasix). Monitor
renal output
Careful identification
of blood specimens
and blood
components
Fever, chills,
jaundice, dropping
H/H. Sometimes no
symptoms
Positive direct antiglobulin test, and
antibody screen
(Hemolysis rare).
Increased bilirubin.
Monitor renal
function
Rarely can be
prevented
Shortness of
breath, cough,
pulmonary edema
Chest x-ray
Slow or stop
infusion, patient
sitting position,
diuretics
Use packed red blood
cells. Avoid
unnecessary
transfusion of plasma
Shortness of breath,
pulmonary edema
without cardiac failure
Neutrophil or HLA
antibodies
Reaction Type
Allergic
Acute Hemolytic
Delayed Hemolytic
Circulatory
Overload
TRALI
*Any
Prevention
Give antihistamine
Support patient.
Antihistamines
Avoid unnecessary
transfusion. Report
donor to blood
supplier
one of any combination
BLOOD ADMINISTRATION:
1. Recommended Needle Gauge to Maintain Red Blood Cell Integrity:
Needles or catheters used for blood transfusion should be large enough to allow
appropriate flow rates. An 18-gauge needle provides good flow rates for cellular
components without excessive discomfort to the patient.
A. Red blood cells/whole blood: 22-gauge or larger.
B. Other blood components: 22-gauge or larger.
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2. IV Solution Compatibility:
A. Normal saline (0.9 NaCl) is the only acceptable fluid.
DO NOT USE: 5% dextrose/water (D5/W) – water causes the red blood cells to
swell and rupture, hemolysis.
Lactated Ringer’s (LR) – calcium in the solution counteracts the
anticoagulant in the blood component permitting small clot
formation.
3. Foot IV/Access:
A foot IV should be used only as the last resort, when all other forms of access have
been attempted. The on-call resident pathologist may be consulted by clinical
colleagues regarding the need for transfusion using a foot IV.
Note: This is because there is a greater risk for venous stasis and phlebitis in a leg
vein.
4. A current type and screen (drawn within 3 days of the last RBC transfusion) is
needed for transfusion of all blood and/or blood components, except for
preadmission testing 2-3 weeks before when the patient has not been transfused or
pregnant in the previous three months. Exception: Plasma and platetets and
cryoprecipitate need only type and screen during that admission.
AUTOLOGOUS/DIRECTED DONATIONS:
Request for autologous and directed donations are handled through the American Red
Cross, Special Needs Coordinator (614/251-1450), Monday through Friday, 8:00am
through 5:00pm. Processing of each donation requires a minimum of 3-4 days (most often
5 days). All infectious disease testing is performed on each autologous and directed
donation collected at the American Red Cross. The Transfusion Service has available
prescription forms for autologous and directed donations. It is best to refer questions
concerning autologous and directed donations to a lead medical technologist.
Other Alternatives to Allogeneic Transfusion:
1. Intraoperative blood salvage.
2. Hemodilution.
3. Post operative blood salvage.
4. Pharmacological alternatives (e.g., vitamin K, Erythropoietin, iron).
5. Recombinant Growth Factor (e.g., erythropoietin, granulocyte-macrophage colonystimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF).
6. Fibrinolytic Inhibitors.
7. DDAVP.
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BLOOD WARMER:
The Transfusion Service has three blood warmers that are used in the following situations:
1. Patients with cold autoagglutinins requiring pre-warm techniques for resolution of
serological problems.
2. Neonatal exchange transfusion.
3. Patient requiring massive transfusion to prevent hypothermia.
4. OB/GYN procedures (see below).
The blood warmers are used for treating hypothermia and OB/GYN procedures
(amnioinfusion to supplement amniotic fluid or to cleanse meconium) only if available.
SICU and Labor and Delivery have their own blood warmers. Approval of the on-call
resident pathologist is required for the use of a blood warmer when not initiated by the
Transfusion Service.
Hypothermia:
Rapid infusion of larger volumes of cold blood can lower the temperature of the sinoatrial
node to below 30C, at which point, ventricular arrhythmia can occur. Hypothermia can
increase the toxicity of hypocalcemia or hyperkalemia and can result in serious lifethreatening ventricular arrhythmias or poor left ventricular performance. Treatment
consists of using warming blankets and lights, warmed intravenous solutions and the use
of a blood warmer.
POLICY ON CMV NEGATIVE AND/OR IRRADIATED BLOOD COMPONENTS:
Cytomegalovirus (CMV) can be a severe infectious complication in certain patients who
are sero-negative and severely immunocompromised.
CMV transmission can be
prevented by leukocyte-reduced blood components or CMV sero-negative. However, only
about 40% of the blood donors in Central Ohio are CMV sero-negative, limiting the supply
of CMV sero-negative blood components.
Therefore, CMV sero-negative blood
components must be restricted to certain patient populations. Leukocyte-reduced blood
can be used for these patients instead.
Irradiated blood components are indicated to prevent graft-versus-host disease in the
following situations:
1. BMT transplant.
2. Neonates and children
immunodeficiency status.
with
severe
or
known
congenital
or
acquired
3. IUT (intrauterine transfusion).
4. Recipients of cellular blood components from blood relatives (directed donation).
5. Patients with Hodgkin’s disease, lymphoma, AML (other malignancies less likely).
6. Neonates of weight less than 1500 grams.
7. HLA matched plateletpheresis components.
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CMV sero-negative blood components (red blood cells and platelets) are reserved for
the following patients:
1. Bone Marrow Transplant (BMT):
a. All allogeneic (related or unrelated donor) recipients who are CMV negative.
b. CMV sero-negative patients with acute bulemia who potentially are BMT
candidate.
2. Heart Transplant:
a. CMV sero-negative recipients and candidates.
3. CMV sero-negative (or unknown) pregnant women.
4. All neonatal infants and all fetuses.
Other patients including liver, kidney, and pancreas transplant patients, will receive CMV
untested leukocyte-reduced blood components.
HEMOTHERAPY
PATIENTS:
FOR
ALLOGENEIC
BONE
MARROW
TRANSPLANT
(BMT)
For allogeneic BMT, the patient will receive ABO identical and/or compatible blood
components, CMV negative (if the patient is CMV sero-negative), irradiated and leukocytedepleted. Exception: fresh frozen plasma and cryoprecipitate only need to be irradiated.
ABO and/or Rh(D) incompatibility between bone marrow transplant donor and recipient
does not adversely affect patient survival or development of graft-versus-host disease in
BMT patients. However, ABO and/or Rh(D) of the blood components transfused to these
patients must be carefully selected for both pre-BMT and post-BMT periods.
1. Rh(D) Incompatibility:
When the recipient is Rh(D) positive and the BMT donor is Rh(D) negative, all
packed red blood cells to be transfused starting from pre-operative regimen should
be Rh(D) negative. During the post-operative period, when the recipient red blood
cells are still demonstrable in the recipient’s circulation, Rh(D) positive
plateletpheresis may be given without resident pathologist approval. However,
once it is established that the recipient type red blood cells are no longer detectable
in the recipient’s circulation, all blood components including plateletpheresis should
be Rh(D) negative. The Reference Laboratory will be responsible for updating the
patient problem folder, computer system and Transfusion Service requisition(s) on
the basis of current serological testing.
When the recipient is Rh(D) negative and the BMT donor is Rh(D) positive, the
recipient should continue to receive Rh(D) negative packed red blood cells and
plateletpheresis.
After the Reference Laboratory has determined that the recipient has actually
received the bone marrow transplant from a Rh(D) positive donor, the Reference
Laboratory will update the patient problem folder, Transfusion Service requisition(s),
and the computer system that the patient can receive Rh(D) positive blood
components.
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2. ABO Incompatibility:
When there is major or minor ABO incompatibility between the donor and recipient,
the Reference Laboratory will make notations in the patient problem folder,
Transfusion Service requisition(s) and computer system according to the following
table:
ABO INCOMPATIBILITY
ABO OF BLOOD COMPONENTS
PACKED
FFP
PLATELETS
RED
CELLS
1st Choice 2nd Choice
O
A, AB
A,AB
B,O
O
B, AB
B,AB
A,O
O
AB
AB
A,B,O
DONOR
ABO
RECIPIENT
ABO
O
O
O
A
B
AB
A
A
A
B
O
AB
O
O
A
AB
A, AB
AB
AB
A,AB
AB
A,B
B
A,B
B
B
B
A
O
AB
O
O
B
AB
B, AB
AB
AB
B,AB
AB
A,B
A
A,B
AB
AB
AB
A
B
O
A
B
O
AB
AB
AB
AB
AB
AB
AB
AB
AB
3. Post-Engraftment:
The Reference Laboratory continues to receive specimens from BMT recipients
after discharge. They will continue to monitor the following on post-transplant
patients:

Disappearance of circulating ABO antibody to donor type red blood cells and
ABO titers if indicated.

Appearance and approximate percentage of donor type red blood cells.

Direct antiglobulin test.

Transfusion history.
4. Blood Type Change:
When a specimen is received more than three months from the last blood
component transfused and the Reference Laboratory determines:

All circulating red blood cells are of donor ABO type.
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
Recipient’s original ABO antibody directed against donor type red blood cells is
no longer demonstrable.

The patient has not been transfused in past three months.

The direct antiglobulin test is negative.
If all of the above criteria are met, the Reference Laboratory will send a general consult
to the Bone Marrow Transplant Unit, and change the patient’s blood type in the
computer system, patient problem folder and Transfusion Service requisition(s). From
this point forward, the recipient will receive donor type red blood cells and plasma
components.
THERAPEUTIC PHLEBOTOMY:
A request for a routine therapeutic phlebotomy could be arranged to be done by the
Apheresis Department, during hours of normal operation. Emergency therapeutic
phlebotomy is performed by members of the clinical unit, in which the patient is located.
For emergent therapeutic phlebotomy, a kit is available from the Transfusion Service.
NOTE: We do not perform re-infusion. Emergency phlebotomy is performed in
some severe cases of pulmonary edema or polycythemia rubra vera.
POLICY ON RH(D) NEGATIVE WOMEN OF CHILDBEARING AGE:
Whenever a request for a type and screen is received on an Rh(D) negative women of
childbearing age (usually but not exclusively  45 years old), it is the responsibility of
the Transfusion Service to determine if the patient could be pregnant. If the patient is
pregnant, appropriate measures should be taken to ensure Rh(D) immune globulin is
administered when indicated.
CORD BLOOD WORKUP:
Cord blood samples are routinely collected at delivery and sent to the Transfusion
Service. Cord blood testing is indicated in the following situations:
1. The mother is a Rh(D) immune globulin candidate (i.e., Rh(D) negative).
2. The mother has an antibody capable of causing hemolytic disease of the
newborn.
3. To determine if ABO incompatibility exists in jaundiced infants (upon physician
request).
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Special considerations when testing cord blood:
1. Previous intrauterine transfusions.
2. Blocked Rh(D). If the direct antiglobulin test is strongly positive and the mother
has anti-D, the cell’s antigen sites may be so completely coated with maternal
antibody that the Rh(D) appears negative with any anti-D reagent. If this occurs,
an eluate must be performed. The presence of anti-D in the eluate confirms that
the red cells are Rh(D) positive.
3. If the direct antiglobulin test is positive, the Rh(D) weak status on Rh(D) negative
infants cannot be determined. This can be resolved with chloroquine treatment
of the cord blood cells to remove attached antibody.
4. Family paternal/maternal antigen-antibody incompatibility.
RH(D) IMMUNE GLOBULIN:
Rh(D) Immune Globulin is prepared from a pool of human plasma containing high
tittered anti-D. The IM preparations are given as an IM injection and should never
be administered IV. An IV preparation of Rh(D) Immune Globulin (WINRhO) is
licensed and available. Although it can be used for Rh(D) negative mothers, it is
most often used for ITP. Each vial of Rh(D) Immune Globulin (IM) contains 300
gm of anti-globulin, which has been documented to cover 30 ml of whole blood or
15 ml of packed red blood cells in the circulation. Rh(D) Immune Globulin acts to
suppress the immune response of Rh(D) negative individuals exposed to the D
antigen. There is no evidence that Rh(D) Immune Globulin will benefit a patient
who is actively producing anti-D. The primary use of Rh(D) Immune Globulin is
prevention of immunization in female of childbearing age, thus preventing future
hemolytic disease of the newborn. Rh(D) Immune Globulin should be given less
than 72 hours post-delivery, abortion, miscarriage, amniocentesis; although if 72
hours has elapsed, the Rh(D) Immune Globulin should still be given. No more than
five vials of Rh(D) Immune Globulin per buttock at one time. Rh(D) Immune
Globulin can be given over a span of 72 hours after the event.
Indications:
1. Delivery of a Rh(D) or Rh(D) weak positive infant.

0.3% of deliveries have a 30 ml bleed.

1.0% have a 6 ml bleed.
2. Abortion or miscarriage (Fetal Blood Volume = 85 ml/kg).
3. Post amniocentesis.
4. Antepartum at 28 weeks.
5. Transplacental fetal-maternal hemorrhage, threatened abortion, external
cephalic version, antepartum bleeding, maternal abdominal hemorrhage, or
maternal trauma.
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6. Transfusion of Rh(D) positive blood and/or blood components to a Rh(D)
negative individual.

Random, single donor platelet concentrates generally contain <0.5 ml of
red blood cells; therefore, one vial of Rh(D) Immune Globulin will
suppress 30 or more Rh(D) positive random, single donor platelet
concentrates or 6 or more plateletpheresis.

Packed Red Blood Cells (RBC) Whole Blood (WB) Calculations:
(RBC volume X .65 (ADSOL))/15 = number of vials
(WB volume X .50)/15 = number of vials
7. Situations with greater than a 30 ml fetal maternal bleed:
Random 0.3%
Neonatal anemia: 26%
Perinatal death: 11%
Abrupto placenta: 7%
Manual removal of placenta:
Third trimester trauma:
Third trimester amnio:
Contraindications:
1. The mother has received Rh(D) Immune Globulin within 72 hours of the
delivery and her fetal blood screening test on the post delivery specimen is
negative. If the fetal blood screening test is positive, a stain for fetal
hemoglobin (Kleihauer-Betke) will need to be done to determine the fetal
bleed and the number of vials of Rh(D) Immune Globulin indicated.
2. The mother had an amniocentesis or an external cephalic version and
received one vial of Rh(D) Immune Globulin within the past 21 days and
there is a negative fetal screen. No additional Rh(D) Immune Globulin is
indicated.
When antepartum Rh(D) Immune Globulin has been administered, it is possible to
detect anti-D in the maternal serum at delivery in as many as 25-30% of women.
The infants of these women may occasionally have a positive direct antiglobulin test
due to anti-D. The presence of passive anti-D does not preclude administration
postpartum.
HEELSTICK SPECIMEN:
Serological workup on neonates can be done on a heelstick specimen. A neonate
is defined as less than four months old. Presence of blood group alloantibodies in
neonates is determined on the basis of the antibody screen done on the maternal
specimen, within 72 hours of delivery. If the maternal antibody screen was
negative, the infant can receive group O, Rh(D) compatible red blood cells without
crossmatch or repeated antibody screen for the entire admission. In the event the
mother has a significant antibody, a complete major crossmatch is performed
utilizing the maternal serum/plasma.
If the infant is four months of age or older, the infant must be treated as an adult
patient with a new specimen collected and crossmatches done every 3 days.
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Blood selection for simple transfusion:
1. Transfuse group O red blood cells, Rh(D) compatible.
2. Red blood cells should be less than 14 days old and must be CMV negative
and from a CPDA-1/CPD unit.
3. The red blood cells must be antigen negative for any corresponding maternal
antibodies.
Mother’s with anti-D due to Rh(D) Immune Globulin- the infant should receive Rh(D)
negative blood. A crossmatch is not needed.
Blood selection for exchange transfusion:
1. Transfuse group O red blood cells, Rh(D) compatible.
2. Red blood cells should be less than 7 days old, CMV negative, irradiated and
from a CPDA-1/CPD unit.
3. Reconstitute with AB fresh frozen plasma to a hematocrit of 50%.
To obtain a 50% hematocrit:

Weigh the red blood cells and subtract 40 gm for the weight of the
collection bag.

Multiple by 0.70 to determine the volume of red blood cells per ml.

Add 20 ml less of fresh frozen plasma than the volume of red blood cells.
4. Hemoglobin S negative blood will be provided at the physician’s request.
Non-red blood cell selection for transfusion:
1. Fresh Frozen Plasma: ABO compatible with the recipient’s red cells. The
FFP does not need to be CMV negative and/or irradiated.
2. Platelet: ABO/Rh(D) identical (preferred) or compatible with the recipient’s
red cells, as well as, CMV negative and irradiated.
BUFFY COAT FOR NEONATES:
A buffy coat is a granulocyte concentrate prepared from a single whole blood
donation. This component is indicated for neonates with extreme neutropenia plus
evidence of sepsis unresponsive to antibiotics. It may be prepared from freshly
drawn units of whole blood. The on-call resident pathologist must approve this
component. Procurement of the component can be done through the American Red
Cross by consultation with the Medical Director (Dr. M. Wissel) or the Chief
Executive Officer (Dr. A. Ng).
INTRAUTERINE TRANSFUSION:
Intrauterine transfusions are undertaken when the fetus is in critical condition due to
red blood cell destruction by maternal antibody as shown by a high Delta OD 450
and/or low hemoglobin value seen on cordocentesis. The primary objective is to
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correct anemia in the fetus, thus correcting heart failure, hydrops and
erythroblastosis. IUT’s are generally repeated on 2-3 week intervals.
Donor Red Cell Requirements:
1. Compatible with maternal serum.
2. Group O Rh(D) negative, unless the fetal cells have been typed Rh(D)
positive or mother has anti-c or anti-e.
3. Frozen/deglycerolized (especially if mother is a one-time directed donor).
4. CMV negative and irradiated.
5. Hemocrit should be 70% or greater.
Determination of IUT volume for transfusion:
gestational age – 20 X 10 = volume of donor red cells (ml)
KLEIHAUER-BETKE TEST (FETAL HEMOGLOBIN STAIN):
This test utilizes the fact that fetal hemoglobin is resistant to acid elution, whereas
adult hemoglobin is not. When a thin blood smear is exposed to an citrate
phosphate buffer, the adult red blood cells lose their hemoglobin into the buffer so
that only the stroma remains. Fetal red blood cells are unaffected and retain their
hemoglobin. The percentage of fetal cells in the maternal blood is used to calculate
the approximate volume of fetal maternal hemorrhage.
This test is performed after the D Rosette Test (Fetal Screen) as a quantitative test
for the amount of a fetal-maternal hemorrhage. This value assists in determining
the appropriate dose of Rh(D) Immune Globulin to be given to a Rh(D) negative
woman. It has also been used in cases of trauma; however, its correlation here is
very poor.
The Kleihauer-Betke test is performed routinely during dayshift. Between
3:30pm and 8am, the on-call resident pathologist must approve an order for a
Kleihauer-Betke. Fetal monitoring is better than Kleihauer-Betke result for
trauma (Transfusion 1999, 30:344-357).
A Kleihauer-Betke is not performed during the first trimester because the fetal blood
volume is <30ml.
NOTE: The Fetal Screen test will detect a 5cc red blood cell or 10cc whole blood
fetal maternal bleed.
NOTE: Results of Kleihauer-Betke are stated as a % of fetal cells seen.
Interpretation is based on the following table.
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FETAL MATERNAL HEMORRHAGE VOLUME (ML WHOLE BLOOD)
% Fetal Cells
Range*
Average
0.3-0.5
20
<50
0.6-0.8
35
15-80
0.9-1.1
50
22-110
1.2-1.4
65
30-140
1.5-2.0
88
37-200
2.1-2.6
115
52-250
Less than 0.3% fetal cells, give 1 vial of Rh Immune Globulin (IM)
Vials Of Rhig (I.M.
Preparation) To
Inject
2
2
3
3
4
5
*The
range provides for the poor accuracy and precision of the Kleihauer-Betke (acid
elution) test. These recommendations are based upon 1 vial of Rh Immune Globulin for
each 15 ml red blood cells or 30 ml whole blood.
Excessive values of fetal hemoglobin are seen in the following: aplastic anemia, sickle cell
anemia, erythremic myelosis, Hgb H disease, hereditary spherocytic anemia, hereditary
persistence of Hgb F, thalassemia major (40-90% HgbF) and thalassemia minor (5-10%
Hgb F).
DELTA OD 450 SCAN:
The examination of the amniotic fluid for bilirubin-like pigment is a method for evaluating
the degree of hemolysis occurring in the infant. The absorbance of the amniotic fluid is
measured and plotted on a modified Liley graph as a function of the wavelength. Amniotic
fluid from an affected pregnancy will show a characteristic “bulge” in the 450nm area. The
Delta OD 450 Scan is run Monday through Friday, 8:00am - 3:30 pm.
Interpretation and Recommendations:
1. Zone I:
Consistent with an unaffected or mildly affected fetus.
2. Zone IIa:
Consistent with a mildly affected fetus.
3. Zone IIb:
Consistent with a moderately affected fetus.
4. Zone III:
Consistent with a severely affected fetus. Hgb < 8.0 g/dl. Intrauterine
transfusion immediately if fetus is at least 20-22 weeks gestation. This
test has been almost wholly replaced by the middle cerebral artery peak
flow velocity.
HLA/PLATELET ANTIBODIES:
The chronic platelet user is usually a hematology or oncology patient. When platelet
therapy becomes warranted, usually following induction of chemotherapy protocols, the
first component used may be a pool of platelet concentrates. Exceptions may include
patients with aplastic anemia who, when needed, require platelet apheresis components
from the time of diagnosis onward, or other chronically transfused patients.
Platelet concentrates are readily available and are the component of choice for many
patients. Pre-storage leukocyte-reduction eliminates contaminating white blood cells for
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On-Call Manual
patients who will require components on a chronic, long-term basis. However, leukocytereduction does NOT entirely prevent sensitization.
Once a patient is expected to be a chronic platelet user, the patient should be HLA typed.
Fifty to seventy percent of these patients will develop HLA/lymphocytotoxic antibodies
during their clinical course. HLA antigens are present on platelet surfaces. As such,
HLA/lymphocytotoxic antibodies can be the cause of a poor response to platelet
transfusion. The HLA typing should be done as early as at the time of the patient’s
diagnosis. The patient’s own lymphocytes are used for this test.
Again, platelet concentrates can be used first. Apheresis platelets from family members
may be preferred by some clinicians. Lack of response to random donor plateletpheresis
or platelet concentrates should be documented before crossmatched plateletpheresis is
used. HLA-matched plateletpheresis may be effective in the refractory/unresponsive
patient.
Lack of efficacy is but one part of the indication for crossmatched platelet components. In
general, this is manifested by a poor response or lack of response to random platelets at
10 minutes to 1-hour post transfusion on two separate, usually consecutive occasions.
This is in the absence of clinical circumstances such as DIC, splenomegaly, sepsis, fever,
or hemorrhage.
A post transfusion increment, over the patient’s baseline, of less than 7,000 at 10 minutes
to 1-hour after transfusion raises the question of refractoriness, in the absence of bleeding
or other course for thrombocytopenia.
CROSSMATCHED PLATELETPHERESIS:
Once it is clear that the patient is refractory to platelet concentrates, a crossmatched
plateletpheresis should be considered. Another option is a plateletpheresis drawn from
siblings (since there is a 25% chance that a sibling will completely match the recipient).
This would purely be a case of transfusing the product and observe the response.
HLA-matched products can be considered if crossmatched platelets fail to demonstrate a
good response. A list of donors who share similar or cross-reacting HLA antigens is
generated on the basis of the patient’s HLA antigen profile determined earlier in the
patient’s clinical course.
HLA-matched plateletpheresis require the time-consuming process of finding an available,
matched donor from the recipient’s HLA list, procuring the component at the American Red
Cross, and testing that component for infectious diseases before release for transfusion.
Because of this, one needs to anticipate patient needs at least 24 hours in advance when
HLA-matched plateletpheresis are being used. Also, there is a need to anticipate patient
requirements for the weekend by at least the preceding Thursday in order to easily
guarantee a component or in the evaluation of suspected neonatal alloimmune
thrombocytopenia (NATP) or post-transfusion purpura (PTP).
PLATELET ANTIBODIES:
Platelet autoantibodies are associated with idiopathic thrombocytopenia purpura (ITP).
The autoantibody test is performed in Flow Cytometry (293-8326) to evaluate the patient’s
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own platelets for bound immunoglobulin. This is NOT an essential test in the diagnosis of
ITP (Blood 88:3-40, 1996). ITP is a CLINICAL diagnosis with other causes for
thrombocytopenia ruled out.
Platelet alloantibodies can occur (but rarely do so) after sensitization with antigen (i.e.,
previous transfusion or pregnancy). This test is performed by the American Red Cross or
other lab and is carried out by evaluation of the patient’s serum for platelet-specific
antibodies.
Heparin-induced thrombocytopenia is a syndrome in which a patient’s platelet count
decreases while on heparin. The test for heparin-induced thrombocytopenia is performed
in the Coagulation Laboratory (6-6501), Monday through Friday, 7:30am – 2:00pm.
Autoantibody tests are indicated for anyone who presents (de novo) with a low platelet
count. Heparin thrombocytopenia workup is indicated for anyone who has a low platelet
count and who has been treated with heparin. Platelet alloantibody is indicated for the rare
patient who does not respond to platelet transfusions despite crossmatched and HLAmatched plateletpheresis or in the evaluation of suspected neonatal immune
thrombocytopenia (NATP) or post-transfusion purpura (PTP).
AVAILABLE PLATELET COMPONENTS AT THE OSU MEDICAL CENTER
Product
Procurement
HLAmatched
Dose
Plt. Count
Platelet
Concentrate
From a unit of
whole blood
No
4
10 x 109 per unit
Random
plateletpheresis
Plateletpheresis
from a donor
No**
1 bag
At least
3 x 1011 per apheresis
200-350 ml per bag
Crossmatched
plateletpheresis
Plateletpheresis
from a donor
No**
1 bag
At least
3 x 1011 per apheresis
200-350 ml per bag
Volume
50-60 ml per unit
175-225 ml per
dose
At least
HLA-Matched
Plateletpheresis
Yes
1 bag 3 x 1011 per apheresis 200-350 per bag
plateletpheresis
from a donor
* All of the above donations are from volunteer donors. Resources are limited; therefore, a protocol for deciding
on the proper and indicated platelet components must be followed.
**Can be from random donors, family members, or platelet-crossmatch.
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APHERESIS ON-CALL PROCEDURE
The on-call pathology resident gets first call for therapeutic apheresis requests. The
following information is conveyed to the Transfusion Medicine attending on call:
1.
Name of patient
2.
Medical record number
3.
Diagnosis
4.
Location
5.
Physician contact name and pager
The attending may ask the resident to look at peripheral smear. Catheter is available at
Transfusion Service front desk.
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COAGULATION PARAMETERS
PROFILE OF HEMOSTATIC SCREENING TESTSa
Hemophilia
A, B or
Other
Intrinsic
System
Deficiency
or Inhibitor
Von
Severe
Willebrand
Heparin
Acute DIC
Disease
Warfarin
Final
Common
Factor VII
Pathway
Deficiency
Deficiency or Inhibitor
or Inhibitor
Hypofibrinogenemia or Chronic
DysfibroLiver
genemia
Disease
Plt Count
Normal
Normal
Low
Normal
Normal
Normal
Normal
Normal
Normal
Bleeding
time
Normal
Prolonged
Prolonged Normal
Normal
Normal
Normal
Normal
Normal
Fibrinogen
(Kinetic
Method)
Normal
Normal
Low
Normal
Normal
Normal
Low or
normal
Low or
normal
Thrombin
time
Normal
Normal
Prolonged Prolonged
Normal
Normal
Normal
Prolonged
Normal or
prolonged
Repilase
time
Normal
Normal
Prolonged Normal
Normal
Normal
Normal
Prolonged
Normal or
prolonged
PT
Normal
Normal
Prolonged
Normal or
Prolonged
Prolonged Prolonged
Prolonged
Prolonged
Prolonged
or normal
PTT
Prolonged
Prolonged
Prolonged Prolonged
Prolonged Prolonged
Normal
Prolonged
Prolonged
Normal
Adapted from Rossi EC, et al. Principles of Transfusion Medicine. Williams and Wilkens: Baltimore, MD:
2nd
Edition, 1996.
LABORATORY TESTS AND HEMOSTATIC DISORDERS
Bleeding
Time
PT
Platelet
Count
Possible Defects
aPTT
Fibrinogen
VIII, IX, XI, heparin
II, V, X, dysfibrinogenemia, heparin,
malnutrition, warfarin
Abnormal
Abnormal
Normal
Abnormal
Normal
Normal
Normal
Normal
Normal
Normal
von Willebrand’s disease
Afibrinogenemia, hyperfibrinolysis
Thrombocytopenia
Qualitative platelet disorder (aspirin,
other drugs, thrombopathy
Normal
Abnormal
Normal
Normal
Abnormal
Normal
Normal
Normal
Normal
Abnormal
Abnormal
Abnormal
Normal
Normal
Abnormal
Normal
Normal
Low
Normal
Normal
Factor XIII
DIC, severe liver disease
HMW Kininogen, prekalikrein, factor
XII, lupus anticoagulanta
Normal
Abnomral
Abnormal
Normal
Abnormal
Normal
Normal
Abnormal
Normal
Normal
Abnormal
Normal
Normal
Abnormal
Normal
aThe
appropriate sequence of screening tests differs for critically ill patients with acquired bleeding defects and for
patients who are seen for evaluation of possible mild congenital disorders. Late-stage defects with hypofibrinogenemia
and delayed fibrin polymerization from degradation components are common in critically ill patients, while intrinsic
system defects and platelet function abnormalities are common congenital disorders. Patients with absence of a 2plasma inhibitor or factor XIII will have excess bleeding despite normal screening tests. Clot solubility in 5 M urea is
abnormal in factor XIII deficiency, and patients with a2-plasmin inhibitor deficiency will have a short clot lysis time.
Adapted from Rossi EC, et al. Principles of Transfusion Medicine. Williams and Wilkens: Baltimore, MD: 2nd Edition,
1996.
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TYPICAL LABORATORY ABNORMALITIES IN THE BLEEDING SURGICAL PATIENTa
Basic Laboratory Screen
Normal
Ranges
Massive
transfusion
DIC
Drugs
Aspirin
Vitamin K
deficiency
Heparin
Uremia
Heparin
failure
CPB
Factor
deficiencies
Platelet
Count
250,000400,000/l
Bleeding
Time
<8-10
min

PT
aPTT
11-13 sec
25-35 sec






nl
nl
nl

Mild 
nl
Mild 
nl

nl
nl
nl/



nl/
nl/
Mild 
Mild 
>75,000


nl
Ancillary Laboratory Tests
Thrombin
Fibrinogen
FDP
Time
<12
25010 sec
g/ml
400 mg/dl
nl/

nl/
Repilase
Time
nl/
>40g/nl
nl/


nl
nl
nl/
nl/
nl/
nl
nl/
nl/
nl
nl
nl
nl
nl
Abbreviations and symbols: nl - normal; , significantly prolonged, CPB - cardiopulmonary bypass;  - significantly
decreased.
Adapted from Rossi EC, et al. Principles of Transfusion Medicine. Williams and Wilkens: Baltimore, MD,: 2nd Edition,
1996.
HEMOSTATIC DEFECTS IN PATIENTS WITH LIVER DISEASE
Screening Test Defect
aEtOH,
Potential Mechanism(s)
 Platelet Count
Folate deficiency
 Toxic effects of EtOHa
  Splenic pooling
 Viral suppression of production
 DIC (concomitant)
 Bleeding time (mild)



 Fribrinogen) degradation components
? Bilirubin
EtOH
 PT and PTT


 Vitamin K-dependent carboxylation
 Protein (factor) synthesis
 Fibrinogen


DIC (concomitant)
 Production (fulminant disease)
 Thrombin time


Dysfibrinogen ( sialic acid)
 Fibrin degradation components
Alcohol
Adapted from Rossi EC, Et al. Principles of Transfusion Medicine. Williams and Wilkens: Baltimore, MD; 2nd Edition,
1996.
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COAGULATION FACTOR REPLACEMENT
Deficient
factor
t1/2 in
vivo
I
3-4 d
Factor level
adequate for
hemostasis
100 mg/dL 1,
1, p
p 1033
Product name or
abbreviationa
Loading
dose
Maintenance
dose
Cryoprecipitate
1 bag/7 kg 4, p
1 bag/15 kg qd 8,
756; k
p 1108; k
FFP, cryopoor
plasma 3, p 24
10-20 mL/kg 4,
3 mL/kg q 24 h 1,
p 756; 1, p 841
p 841
Factor IX Complex
(Profilnine SD
[Alpha Therapeutic
Corp.])
FFP, cryopoor
plasma 3, p 24
20 IU/kg 6, m
5 IU/kg q 24 h 6, m
20 mL/kg 1, p
3-6 mL/kg q 12 h
843
1, p 843
FFP, cryopoor
plasma 3, p 24
10-20 mL/kg 4,
20 mL/kg q 4 h or
40 mL/kg q 8 h 14,
1033
II
2-5 d
20-40% 1, p
1, p
1033
1033
V
1536 h
25-30% 1, p
843
1, pp
843,
1033
VII
4-7 h
10-20% 1; pp
1, p
845, 1033
p 756; j
1033
VIII
9-18
h 1; pp
b
100%d
819,
1033
Factor VIIa
(Recombinant)
(NovoSeven [Novo
Nordisk])
Antihemophilic
Factor (Human)
(MONARC-M
[American Red
Cross]),
Antihemophilic
Factor
(Recombinant)
(Helixate FS
[Aventis Behring],
Recombinate
[Baxter])
Cryoprecipitate
15-30 mcg/kg
16
50 IU/kgc
50 IU/kg q 12 h,
or 50 IU/kg/12 h
by continuous
infusionc
0.5 bag/kg 3, pp
0.5 bag/kg q 12
he
50 IU FVIII:C/kg
q 12 h, or 50 IU
FVIII:C/kg/12 h
by continuous
infusionc
26-27
IX
2024 h
1; pp
819,
1033
100%d
Antihemophilic
Factor/von
Willebrand Factor
Complex (Human)
(Humate-P [Aventis
Behring GmbH])
Factor IX Complex,
Factor IX
(Recombinant)
(BeneFIX [Wyeth]),
Factor IX (Human)
(AlphaNine SD
[Alpha Therapeutic
Corp.])
Page 44
15-30 µg/kg q 46 h 16
50 IU
FVIII:C/kgc
100 IU/kgc
50 IU/kg q 12 hc
The Ohio State University Medical Center
Transfusion Service
On-Call Manual
Deficient
factor
t1/2 in
vivo
X
2042 h
Factor level
adequate for
hemostasis
10-40% 1, p
Product name or
abbreviationa
Loading
dose
Maintenance
dose
Factor IX Complex
(Profilnine SD
[Alpha Therapeutic
Corp.])
FFP, cryopoor
plasma 3, p 24
FFP, cryopoor
plasma 3, p 24
10-20 IU/kg 4,
8-10 IU/kg q 24 h
p 756; n
10, n
10-20 mL/kg 8,
3-6 mL/kg q 12 h
p 212
8, p 212
Not
applicable
Not applicable
Not applicable
Not applicable
1-5%g
Cryoprecipitate 1, p
1 unit/10-20
kgf
1 unit/10-20 kg q
3-4 wk 12
FFP
500 mL 8, p 1107
Antihemophilic
Factor/von
Willebrand Factor
Complex (Human)
(Humate-P [Aventis
Behring GmbH])
Antihemophilic
Factor (Human)
(Alphanate [Alpha
Therapeutic])
Cryoprecipitate
60-80 IU
VWF:RCo/kg
2-3 mL/kg q 4-6
wk 12, h
40-60 IU
VWF:RCo/kg q
8-12 h 1, p 833
848
1, p 848
XI
4080 h
15-25%
1, p
1033
10-20 mL/kg
4,
p 756
5 mL/kg q 12-24
h 12
1, p
1033
XII
4852 h
1, p
1033
XIII
12 d
1, p
238
1033
Von
Willebrand
Factor
(VWF)
3-5 h
25-50% 1, p
5, p 27
1033
1, p 833
60-70 IU
Factor
VIII:C/kgi
40-50 IU Factor
VIII:C/kg q 12 h 1,
1-2 bags/10
kg 1, p 832
0.7-1.4 bags/10
kg q 8-12 hi
p 832
Notes
a Product names are from references 17 and 18.
Abbreviation
Cryopoor plasma
Cryoprecipitate
FFP
Proper name 17, 18
Plasma, Cryoprecipitate Reduced
Cryoprecipitated AHF
Fresh Frozen Plasma
Pooled Plasma, Solvent/Detergent Treated, may be substituted for Fresh Frozen Plasma
(FFP).
b Other recommendations: 5 mL/kg q 6-24 h 12, 5 mL/kg q 6 h 15, 10-15 mL/kg q 3-4 d 11.
c For the most serious bleeding. See reference 1, p 819, for details.
d 100% for CNS, traumatic, surgical, or retroperitoneal bleeding; less for less severe
bleeding. See reference 1, p 819, for details.
e The maintenance dose is the same as the loading dose 1, p 819.
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f
The loading dose of Factor XIII concentrate recommended by Giangrande was about the
same as the maintenance dose he recommended. Thus, the loading dose of
Cryoprecipitated AHF has been set to be the same as the maintenance dose.
g 1-2% 1, p 238, 3-5% 12. But reference 12 recommends 25-50% following major trauma.
h An alternate recommendation of 500 mL q 2 d 8, p 1107 appears to be inconsistent with the
half-life of Factor XIII as well as with the recommendations of references 12 and 20.
i Based on the ratio of maintenance to loading doses for VWF:RCo 1, p 833.
j Assuming that the product contains 1 IU/mL 3, p 22.
k Each bag has about 250 mg of fibrinogen on average. 4, p 467
m Calculate volume of Profilnine SD using the estimate of 1.2 IU of factor II per IU of factor
IX. 19
n Calculate volume of Profilnine SD using the estimate of 0.6 IU of factor X per IU of factor
IX. 19
References
1.
Colman RW et al, eds. Hemostasis and thrombosis: basic principles and clinical
practice. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001. 1578 pp.
2.
Giangrande PLF. Factor XIII deficiency. Oxford Haemophilia Centre.
http://www.medicine.ox.ac.uk/ohc/xiii.htm, as seen on 12/21/01.
3.
American Association of Blood Banks, America's Blood Centers, American Red
Cross. Circular of information for the use of human blood and blood components.
http://www.aabb.org/All_About_Blood/COI/coiv2.pdf. 2000.
4.
Technical manual. 13th ed. Bethesda: American Association of Blood Banks,
1999. 798 pp.
5.
Blood transfusion therapy: a physician's handbook. 6th ed. Bethesda: American
Association of Blood Banks, 1999. 150 pp.
6.
Lechler E. Use of prothrombin complex concentrates for prophylaxis and treatment
of bleeding episodes in patients with hereditary deficiency of prothrombin, factor VII,
factor X, protein C, protein S, or protein Z. Thromb Res 1999;95:S39-S50.
7.
Practice guidelines for blood component therapy: a report by the American Society
of Anesthesiologists Task Force on Blood Component Therapy. Anesthesiology
1996;84:732-747.
8.
Colman RW et al, eds. Hemostasis and thrombosis: basic principles and clinical
practice. 3rd ed. Philadelphia: JB Lippincott Co, 1994. 1713 pp.
9.
Fresh-Frozen Plasma, Cryoprecipitate, and Platelets Administration Practice
Guidelines Development Task Force of the College of American Pathologists.
Practice parameter for the use of fresh-frozen plasma, cryoprecipitate, and
platelets. JAMA 1994;271:777-81.
10.
Larrain AC. Deficiencia congénita en factor X de la coagulación sanguínea.
Resultado exitoso del empleo de concentrados de complejo protrombinico en el
control de la tendencia hemorrágica en operación cesárea en 2 embarazos
[Congenital blood coagulation factor X deficiency. Successful result of the use of
prothrombin concentrated complex in the control of cesarean section hemorrhage in
2 pregnancies]. Rev Med Chil 1994;122:1178–83.
11.
Marder VJ, Shulman NR. Clinical aspects of congenital factor VII deficiency. Am J
Med 1964;37:182-94
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12.
13.
14.
15.
16.
17.
18.
19.
20.
Rodgers GM, Greenberg CS. Inherited coagulation disorders. In: Lee GR et al,
eds. Wintrobe's clinical hematology. 10th ed. Baltimore: Williams & Wilkins,
1999:1682-1732.
Horowitz MS, Pehta JC. SD Plasma in TTP and coagulation factor deficiencies for
which no concentrates are available. Vox Sang 1998;74 Suppl 1:231-5
Saint-Raymond S, Greffe B, Carré J, et al. Attitude pratique en cas d'intervention
chirurgicale chez un sujet atteint d'un déficit congénital en facteur VII [Practical
approaches for surgical procedures in congenital factor VII deficiency]. Ann Fr
Anesth Réanim 1989;8:518-521
Caldwell DC et al. Clinics in Obstetrics and Gynecology 1985;28(1):53-72. Cited
in: Fadel HE, Krauss JS. Factor VII deficiency and pregnancy. Obstet Gynecol
1989;73(3 Pt 2):453-454
Scharrer I. Recombinant factor VIIa for patients with inhibitors to factor VIII or IX or
factor VII deficiency. Haemophilia 1999; 5:253-259
USP DI. Drug information for the health care provider. Rockville, MD: United States
Pharmacopeial Convention, 2002.
Code of Federal Regulations, Title 21--Food and Drugs, Part 640--Additional
standards for human blood and blood products.
Gross, John, RN, MS; Director, Professional Services; Alpha Therapeutic Corp. Email to Barry Siegfried, MD; 5/10/02.
Board PG et al. Factor XIII: inherited and acquired deficiency. Blood Rev
1993;7:229-242.
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BLOOD COMPONENTS AND PLASMA DERIVATIVES
Component/Product
Whole Blood
Composition
RBCs (approx. Hct 40%); plasma
WBCs; PLTS
Volume
500 mL
Indications
Increase both red cell mass and plasma volume
(WBCs and PLTS not functional; plasma
deficient in labile clotting Factors V and VIII)
Red Blood Cells
RBC (approx. Hct 75%);
Reduced plasma, WBCs, and PLTS
250 mL
Increase red cell mass in symptomatic anemia
(WBCs and PLTS not functional)
Red Blood Cells,
Adenine-Saline Added
RBC (approx. Hct 60%);
Reduced plasma, WBCs and PLTS;
100 mL of additive solution
>85% original volume of RBC;
<5 x 106 WBCs; few PLTS; minimal
plasma
330 mL
Increase red cell mass in symptomatic anemia
(WBCs and PLTS not functional)
225 mL
Increase red cell mass; <5 x 106 WBCs to
decrease the likelihood of febrile reactions,
immunization to leukocytes (HLA antigens) or
CMV transmission
RBCs Washed
RBCs (approx. Hct 75%);
<5 x 108 WBCs; no plasma
180 mL
Increase red cell mass; reduce risk of allergic
reactions to plasma proteins
RBCs Frozen; RBCs
Deglycerolized
RBC (approx. Hct 75%);
<5 x 108 WBCs; no PLTS; no plasma
180 mL
Increase red cell mass; minimize febrile or
allergic transfusion reactions; use for prolonged
RBC blood storage
Granulocytes Pheresis
Granulocytes (>1.0 x 1010 PMN/unit;
lymphocytes; PLTS (>2.0 x 1011/unit);
some RBCs
PLTS (>5.5 x 1010/unit); RBC; WBCs;
plasma
220 mL
Provide granulocytes for selected patients with
sepsis and severe neutropenia (<500 PMN/L)
50 mL
Bleeding due to thrombocytopenia or
thrombocytopathy
PLTS (>3 x 1011/unit; RBCs; WBCs;
plasma
PLTS (as above); <5 x 106 WBCs per
final dose of pooled PLTS
300 mL
Plasma; all coagulation factors;
complement (no PLTS)
Fibrinogen; Factors VIII and XIII; von
Willebrand factor
220 mL
Same as PLTS; sometimes HLA matched or
platelet crossmatched
Same as PLTS; <5 x 106 WBCs to decrease the
likelihood of febrile reactions, allo-immunization
to leukocytes (HLA antigens) or CMV
transmission
Treatment of some coagulation disorders
Factor VIII
(concentrates,
recombinant human
Factor VIII)
Factor IX
(concentrates,
recombinant human
Factor IX)
Albumin/PPF
Factor VIII; trace amount of other
plasma proteins (products vary in
purity)
25mL
Factor IX; trace amount of other
plasma proteins (products vary in
purity)
25 mL
Hemophilia B (Factor IX deficiency)
Albumin, some -, globulins
Volume expansion
Immune Globulin
IgG antibodies; preparations for IV
and/or IM use
(5%);
(25%)
varies
Rh Immune Globulin
IgG anti-D; preparations for IV and/or
IM use
RBCs Leukocytes
Reduced (prepared by
filtration)
Platelet
Platelets Pheresis
Platelets Leukocytes
Reduced
FFP; DR-P; SD-P
Cryoprecipitated AHF
300 mL
15 mL
varies
Deficiency of fibrinogen; Factor XIII; second
choice in treatment of Hemophilia A, von
Willebrand disease
Hemophilia A (Factor VIII deficiency); von
Willebrand’s disease (off-label use for selected
products only)
Treatment of hypo- or agammaglobulenemia;
disease prophylaxis; autoimmune
thrombocytopenia (IV only)
Prevention of hemolytic disease of the newborn
due to D antigen; treatment of autoimmune
thrombocytopenia; Transfusion Accidents
RBCs = red blood cells; Hct = hematocrit; WBCs = white blood cells; PLTS = platelets; CMV = cytomegalovirus; PMN =
polymorphonuclear cells; FFP = fresh frozen plasma; PPF = plasma protein fraction; IV = intravenous; IM = Intramuscular;
DR-P = donor rested plasma; SD-P = solvent/detergent-treated plasma
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BLOOD TRANSFUSION THERAPY DATA-CARD®
ADMINISTRATION OF BLOOD COMPONENTS
A. Positive identification of the recipient to be transfused and the designated blood unit to
be used is essential.
B. Compatibility of red blood cells with IV solutions:
1. Use 0.9% Sodium Chloride for injection, USP.
2. DO NOT use 5% Dextrose solutions (may induce hemolysis).
3. DO NOT use Lactated Ringer’s (contains Ca++ which may induce clot formation in
the blood bag and/or administration set).
4. Add NO medications to blood.
5. Plasma (type compatible) or Albumin (5%) is acceptable in special circumstances.
C. Blood Warming: Use only a temperature-monitored blood warmer to avoid hemolysis.
Indications for blood warming:
1. Adults receiving blood over 50ml/kg/hour.
2. Children receiving blood over 15ml/kg/hour.
3. Patients with clinically active cold agglutinins.
4. Rapid infusion of blood through central lines (cold blood may induce arrhythmias).
D. Blood Filters. ALL BLOOD COMPONENTS MUST BE INFUSED THROUGH A
FILTER.
1. Use a standard blood filter (170-260 microns screen) for all blood components.
2. Leukocyte-reduction filters are used to:
a. Decrease febrile transfusion reactions.
b. Decrease risk of alloimmunization to leukocyte or HLA antigens.
c. Reduce CMV transmission (proper technique is critical).
E. Time Limit for infusion. Components should be infused within 4 hours. Note: the blood
bank can divide components into aliquots as needed.
F. Irradiation of Blood and Cellular Components. A minimum of 25 Gy should be used to
reduce the risk of TA-GVHD in susceptible patients such as: selected immunoincompetent or immuno-compromised recipients (i.e., hematopoietic progenitor
transplant, congenital immune deficiency, etc.), a fetus receiving intrauterine
transfusions, recipients of donor units from blood relatives, recipients of HLA-matched
platelets.
Darrell J. Triulzi, MD(ed) Copyright © 1981, 1993, 1996, 1999
American Assocation of Blood Banks, 8101 Glenbrook Road, Bethesda, MD 20814
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RED BLOOD CELLS (RBC)
Red blood cells remaining after separating plasma from human blood by centrifugal or
gravitational force.
Volume: CPD:
CPDA-1:
Volume
Hct
250-300 ml
80%
250-300 ml
80%
AS-1:
350-400 ml
55-65%
Action:
1. Increases oxygen-carrying capacity.
2. Increases RBC/mass for volume replacement.
Indications:
1. Improve Hgb/Hct to increase oxygen-carrying capacity.
2. Replacement of blood loss (i.e., trauma, surgical procedures, hemorrhage).
3. Clinical use: anemia, cardiac patients, liver and kidney disease.
Contraindications:
1. Do not use when anemia can be corrected with specific medications.
2. Do not use for correcting coagulation deficiencies.
Side Effects & Hazards:
1. Hemolytic transfusion reaction
2. Infectious disease transmission
3. Graft versus Host response
4. Alloimmunization
5. Febrile reactions
6. Circulatory overload
7. Iron overload
8. Allergic reactions
9. Bacterial contamination
10. Microaggregates
11. Air embolism
12. Metabolic complications
13. Coagulation proteins and platelet depletion (if a massive transfusion)
Dosage:
Depends on clinical condition. Should raise patient’s hematocrit 3% or 1 gm/dl/unit.
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Rate of Infusion:
Depends on clinical condition. No slower than four hours per unit.
Storage: 1-6C
Shelf life:
CPD:
21 days
CPDA-1: 35 days
AS-1:
42 days
Administration:
1. Must be ABO and Rh(D) compatible (crossmatch required).
2. Y-type tubing with blood filters; 0.9 NaCl prn. (50-100 ml).
3. If clinically indicated, blood may be warmed (not to exceed 42C).
For additional information refer to Circular of Information for the Use of Human Blood and
Blood Components.
CPD QUADS AND BABY SPECIALS (FILTERED)
Baby specials and quads are CMV negative O positive or O negative red blood cells
intended for neonatal transfusions. The baby special is a CPD packed cell that has 4
satellite bags attached.
Volume: CPD packed cell:
Hct:
Action:
250-300 ml
60-75%
Same as for Red Blood Cells
Indications:
1. Improve Hgb/Hct to increase oxygen-carrying capacity.
2. Exchange transfusion.
Side Effects and Hazards:
1. Similar to those indicated for Red Blood Cells.
Dosage:
2. Depends upon clinical conditions. 5-10 ml/kg or 1 unit/35 kg.
Rate of Infusion:
1. No slower than 4 hours per aliquot.
Storage:
1-6C
Shelf life:
1. CPD: 21 days. These red blood cells will be <14 days old.
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Administration:
1. Must be ABO and Rh(D) compatible.
2. Y-type tubing with blood filters; 0.9 NaCl prn.
3. If clinically indicated, blood may be warmed (not to exceed 42C).
RED BLOOD CELLS, FILTERED
The high efficiency leukocyte removal (3rd generation leukocyte-depletion filter) traps a
large number of leukocytes and allows for excellent red cell recovery.
Volume: <4.0 x 105 WBC remaining (ARC)
93% RBC recovery (ARC)
55% Hct (plasma similar to PRC)
Action:
Same as for Red Blood Cells.
Indications:
1. Febrile transfusion reactions
2. Delay of leukocyte alloimmunization
3. Chronic dialysis patients who are transplant candidates
4. Aplastic anemia, patients anticipating bone marrow transplantation
5. Patients with PNH (actually preferred over deglyc’ed/washed RBC’s).
6. To prevent transfusion-induced immunosuppression and potentially prevent
transfusion-induced CMV infection
7. All patients?
Contraindications: Same as for Red Blood Cells.
Side Effects and Hazards: Similar to those indicated for Red Blood Cells.
Dosage:
Depends on clinical condition.
Rate of Infusion:
Storage:
No slower than four hours per unit.
1-6C
Shelf life:
Original outdate if filtered in-line prestorage.
Administration:
1. Must be ABO and Rh(D) compatible.
2. Y-type blood recipient set; 0.9 NaCl prn.
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3. If clinically indicated, blood may be warmed (not to exceed 42C).
For additional information, refer to Circular of Information for the Use of Human Blood and
Blood Components.
RED BLOOD CELLS DEGLYCEROLIZED
These are red cells primarily frozen with glycerol (storage over 10 years). They are usually
of rare antigen phenotype.
Volume: 80% RBC recovery.
Action:
Same as for Red Blood Cells.
Indications:
1. Patients with high frequency antibodies requiring rare blood.
2. Patients with multiple antibodies requiring rare blood.
3. Patient with severe febrile reactions unresponsive to filtered/leuko-depleted blood.
4. Patients exhibiting excessive reactions to plasma (PNH, IgA sensitization and IgA
deficiency [although washed RBC’s are less expensive and have a faster turnaround time]).
5. Autologous predeposit of red cells, rarely.
6. Intrauterine transfusion.
Contraindication:
Same as for Red Blood Cells.
Side Effects and Hazards: Similar to those indicated for Red Blood Cells.
Dosage: Depends on clinical condition.
Rate of Infusion: No slower than four hours per unit.
Storage: 1-6C
Shelf life: 24 hours after thawing.
Administration:
1. Must be ABO and Rh(D) compatible.
2. Y-type blood recipient set; 0.9 NaCl prn.
a. Two units of deglycerolized cells, requiring no special antigen typing, can be
completed and available from the American Red Cross in approximately 1½
hours. This is an approximate time, which is dependent on the American Red
Cross workload.
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b. Two units of deglycerolized cells, requiring special antigen typing, can be
completed and available from American Red Cross in approximately 4 hours.
This does not include Reference Laboratory consultation, if needed. This time is
an approximate time dependent on the American Red Cross workload.
For additional information, refer to Circulation of Information for the Use of Human Blood
and Blood Components.
PLATELETS
Platelets collected from one unit whole blood donation and suspended in a specific volume
of original plasma.
Volume: 45-65 ml plasma containing a minimum 5.5 x 10 10 platelets (AABB Standards).
The Central Ohio American Red Cross 1996, average 9-10 x 1010.
Action:
Corrects hemostatic deficit. Used most to treat hemorrhage, but also (in
practice) to elevate the platelet count prophylactically:
1. Patients with thrombocytopenia or an abnormality of platelet function or both
who have significant bleeding should receive platelets if the platelet disorder
is likely to be causing or contributing to the bleeding.
2. Prophylaxis for patient with severe thrombocytopenia (<10 to 20,000/l).
3. Patients given massive transfusions in which dilutional thrombocytopenia
results.
4. Uremia with bleeding or invasive procedure (after DDAVP or dialysis or
cryoprecipitate), cardiopulmonary bypass.
5. Medications decreasing platelet function.
6. Prior to an invasive procedure or surgery when platelet count is <50,000.
Contraindications:
1. Do not use if bleeding is unrelated to thrombocytopenia or abnormality functioning
platelets.
2. Rapid platelet destruction: ITP (except in acute hemorrhage).
3. Contraindicated in TTP, except in acute hemorrhage or surgery.
Side Effects and Hazards:
1. Infectious disease transmission
2. Bacterial contamination
3. Allergic reactions
4. Febrile reactions
5. Circulatory overload
6. Air embolism
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7. Graft versus Host response
8. Alloimmunization
9. Hypotension reactions, cytokine associated
Dosage:
1. Depends on clinical situations.
2. One unit of platelet concentrate usually increases the platelet count by 10,00015,000/l in a 70-kg adult and 20,000 or more in an 18-kg child.
3. The usual dose in a patient with bleeding symptoms of a platelet count below 20,000
l is 4 units.
4. Pooled platelet concentrates, 4 platelets concentrates (200 ml).
5. Pediatrics: 5-10cc/kg or dose of 1 x 1011/kg.
Rate of Infusion: approximately 60 minutes per pool.
Storage: 20-24C with continuous gentle agitation.
Shelf life: 5 days
Administration:
1. Platelet ABO incompatible with the recipient’s plasma may be used if not grossly
contaminated with red blood cells (crossmatching not required if less than 2ml of
RBC), although ABO identical strongly encouraged.
2. Blood component infusion set.
3. 0.9 NaCl prn.
NOTE:
The container and filter may be flushed with normal saline to maximize the
number of platelets administered.
NOTE:
Less than 2,500 platelet count increase per unit transfused equates to a
refractory state.
Alloimmunization should be considered with a corrected count increment
(CCI) less than 7,500, drawn 10 minutes to 1 hour post-transfusion.
CCI = platelet increment X body surface area divided by the number of
platelets (X 1011)
One platelet concentrate is equal to at least 0.55 X 10 11 platelets. (Central
Ohio American Red Cross average .9-1 x 1011)
For additional information, refer to Circular of Information for the Use of Human Blood
and Blood components.
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PLATELETPHERESIS
The separation and retention of platelets
Plateletpheresis Guidelines
1. CMV-negative irradiated single-donor platelet: (with or without HLA-matching or
platelet crossmatching)
For bone marrow transplantation program patients (excluding CMV positive
autologous BMT) at OSU as decided by the BMT team.
2. Crossmatched or HLA-matched single donor platelet:
Reserved for thrombocytopenic patients who have demonstrated evidence of alloimmunization to platelets and have become refractory to random-donor platelet
concentrates.
The following sequential steps should be followed by the physician attempting to
optimize platelet support for needy patients.
a. Thrombocytopenia and prophylactic platelet transfusion:
i. Platelet count <10,000 in stable patients.
ii. Platelet count <20,000 in high risk patients
iii. Platelet count <50,000 in patients with invasive procedure or clinical
bleeding.
b. Alloimmunization:
i. Evidence is established when a 10 minute to 1 hour corrected count
increment is less than 7,500.
ii. HLA-antibody or platelet antibody screening is positive and may indicate
alloimmunization (see iv).
iii. Without other clinical factors of platelet destruction, namely, DIC, sepsis,
fever, splenomegaly, brisk hemorrhage, or drug-induced antibody; then
platelet-crossmatched or HLA-matched products can be tried when (i) and (ii)
are satisfied.
iv. If there are clinical factors of platelet destruction, then a 10-minute posttransfusion C.C.I. should be done subsequent to the next random-donor
platelet transfusion. If this is <7.500, then platelet-crossmatched or HLAmatched platelet support is a reasonable and productive means of managing
the patient.
v. A 1-hour post-transfusion C.C.I.* is an essential means of monitoring the
outcome of the transfusion and will help in the selection of best donors.
c. Availability of Components:
i. Due to the donor’s need for advance notice, we strongly recommend all
orders be written 24 hours in advance. Every attempt will be made to fill
orders.
ii. Emergencies will be expedited as much as possible.
*C.C.I.
= Platelet Increment x Body Surface Area (sq.m.)
number of platelets transfused (1011)
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Platelet Increment is Pre-transfusion Platelet Count – Post-Transfusion Platelet Count
The post-transfusion count should be done at 10 minutes to 1 hour and 24 hours*
Number of platelets transfused (1011) = 0.9 x number of platelet concentrate (assuming 1
platelet concentrate = 0.9 x 1011 platelets); 3.0 for apheresis platelet
Volume:
200-300 ml
3-4 x 1011 platelets (1996, ARC)
Storage: Store at room temperature (22C) using gentle agitation.
Shelf life: 5-day storage.
Administration:
1. Usually will be ABO and Rh(D) compatible.
2. Y-type blood component recipient set and 0.9 NaCl prn.
3. Infuse as quickly as possible.
Plateletpheresis – Single Donor – 5-day Expiration:
1. For split platelet compoents, contents from the two bags should be pooled into the
labeled bag before transfusion and must be transfused within 24 hours after pooling
(or sooner if the 5-day period elapses before then).
2. Store at 20C-24C with agitation. Preferably use a rotator, which operates at 70
strokes per minute with the length of the stroke being 1½ inches.
3. Compatibility testing is not required for administration of product, unless pheresis
contains >2 ml red blood cells.
4. Administer over 60 minutes through component recipient set.
For additional information, refer to Circular of Information For the Use of Human Blood and
Blood Components.
FRESH FROZEN PLASMA (FFP)
Single donor plasma frozen within 8 hours of collection and stored at –18C or colder.
Volume:
greater than 150 ml (ARC)
200 units Factor VIII/unit
400 mg Fibrinogen/unit
~200 units of all coagulation factors
Action:
1. Provides coagulation factors, anti-thrombotic factors, other plasma proteins and
enzymes (i.e., C1-esterase inhibitor).
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Indications:
1. Patients with coagulation protein deficiency for which specific factor concentrates
are unavailable or undesirable (II, V, VII, X and XI).
2. Dcumented coagulation defects during or after massive transfusion.
3. Reversal of warfarin effect in patients who are bleeding or who will be undergoing
an invasive procedure (holding dose on vitamin K preferred).
4. Multiple coagulation defects as in liver disease.
5. Therapeutic plasma exchange for thrombotic thrombocytopenic purpura (second
line).
Contraindication:
1. Do not use when coagulopathy can be corrected with specific therapy (i.e., Vitamin
K and waiting 24 hours for an effect).
2. FFP should not be used as a volume expander nor as a nutritional source since
safer and more appropriate therapies exist.
Hazards:
1. Allergic reactions + anaphylaxis)
2. Febrile reactions/TRALI
3. Circulatory overload
4. Citrate toxicity, hypothermia and other metabolic problems with large volume.
5. Infectious disease transmission
Dosage:
1. Depends on the clinical situation and may be determined by serial laboratory
assays of coagulation function (PT, PTT).
1 FFP may increase all coagulation factors 6-8%.
2. Bleeding: 13-15 ml/kg (i.e., 2-4 FFP in one dose)
Neonatal children: 13-15 ml/kg.
3. 15-20mg/dl increase in fibrinogen per unit.
Rate of Infusion: Approximately 5-10ml per minute.
Storage:
1. –18C or colder (1 year); STORE FLAT.
2. 1-6C AFTER THAWING.
Shelf Life:
1. 1 year in frozen state.
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2. 24 hours after thawing.
3. 5 days as thawed plasma.
Administration:
Patient type
Can Receive FFP of Type
O
A, B, AB, O
A
A, AB
B
B, AB
AB
AB
1. Must be ABO compatible, Rh(D) type need not be a consideration.
2. Thaw product between 30-37C with gentle agitation.
3. Use Y-type or straight line set with component filter.
For additional information, refer to Circular of Information for the Use of Human Blood and
Blood Components.
Emergency Replacement Therapy with Plasma for
Miscellaneous Specific Coagulation Deficiencies
Disease
Hemophilia A (factor VIII
deficiency)
Loading Dose
Not required
Maintenance Dose
15 ml/kg every 8 hours for 12 days and every 12 hours
thereafter
Hemophilia Ba (factor IX
deficiency)
60 ml/kg
7 ml/kg every 12 hours
von Willebrand’s diseasea
Not required
10 ml/kg daily
Prothrombin deficiency
15 ml/kg
5-10 ml/kg daily
Factor V deficiency
20 ml/kg
10 ml/kg every 12 hours
Factor VII deficiency
10 ml/kg
5 ml/kg every 6-24 hours
Factor X deficiency
15 ml/kg
10 ml/kg daily
Factor XI deficiency
10 ml/kg
5 ml/kg daily
Factor XIII deficiency
5 ml/kg every 1-2 weeks Not Required
aSpecific
factor concentrates are available and more effective and convenient than plasma in most
situations.
(From Wintrobe MM. Therapy of The Hereditary Coagulation Disorders. In: Clinical Hematology.
Philadelphia: Lea & Febiger, 1979:1190).
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CRYO POOR PLASMA/CRYO SUPERNATANT LIQUID PLASMA
Fresh frozen plasma is thawed at 4C and the cryoprecipitate forms. The liquid supernatant
plasma is separated from the cryoprecipitate and then refrozen.
Volume: 200-250 ml
Indications:
1. Infusion of cryosupernatant is used for the treatment of patients with thrombotic
thrombocytopenia purpura. This disease is characterized by the development of
fever, thrombocytopenia, hemolytic anemia, renal failure and CNS disturbance.
Many patients with TTP respond satisfactorily to fresh frozen plasma given as an
infusion or as plasma replacement with plasmapheresis. However, patients with
TTP have been reported to respond to treatment of cryosupernatant.
The pathophysiology of TTP is a matter of ongoing research. However, evidence
indicates that platelets and large multimeric forms of VWF are consumed in
association with intravascular platelet aggregation. Therefore, it is postulated that
plasma depleted of large multimers of VWF would be preferable in the treatment of
TTP. Cryopoor plasma can be used either as first-line therapy or after failure of
FFP for TTP.
Precautions:
1. Cryosupernatant will have reduced amounts of FVIII:C, FVIII:VWF, fibrinogen, FXIII
and fibronectin and should not be used for patient who require therapeutic doses of
these factors.
Dose:
1. Dependent on the clinical response of the patient.
Storage:
1. –18C (1 year); store flat
2. 1-6C after thawing (24 hours)
Side Effects and Hazards:
1. Similar to those indicated for fresh frozen plasma.
Administration:
1. Must be ABO compatible, Rh(D) type need not be a consideration.
2. Thaw product between 30-37C with gentle agitation.
3. Use Y-type tubing with component filter or straight line set with component filter.
For additional information, refer to Circular of Information for the Use of Human Blood and
Blood Components.
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CRYOPRECIPITATE AHF
A concentrated source of fibrinogen, FVIII:C, VWF and FXIII obtained from a single unit of
fresh frozen plasma.
Volume: 10-15 ml/unit (ARC)
Minimum Factor VIII Activity: 80 units/bag.
ARC Factor VIII activity average: 135 units/bag.
Also contains: Factor VIII, Factor XIII, Fibrinogen, Fibronectin and von
Willebrand’s factor.
Fibrinogen: 250 mg/bag.
Action:
Provides a source of coagulation Factor VIII, XIII, fibrinogen, VWF and
Fibronectin.
Indications:
1. Hypofibrinogenia or fibrinogen abnormality (dysfibrinogenemia).
2. Hemophilia A-Factor VIII deficiency (when factor concentrates are not available).
3. von Willebrand’s disease (second line of therapy behind DDAVP and/or Humate P).
4. Factor XIII deficiency.
5. Massive trauma.
6. DIC.
7. To prepare “fibrin glue”.
Contraindications:
1. Do not use unless results of laboratory tests indicate specific coagulation defect for
which this product would be beneficial.
Cryoprecipitate should not be used to treat patients with deficiencies of factors other
than Factor VIII, fibrinogen, von Willebrand’s Factor or Factor XIII.
Side Effects & Hazards:
1. Infectious disease transmission
2. Air embolism
3. Febrile reactions
4. Allergic reactions
5. Hyperfibrinogenemia
6. Bacterial contamination
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Dosage:
1. Hemophilia A: USUALLY NOT USED ANYMORE BECAUSE OF FACTOR
CONCENTRATES. Varies on patient and clinical situation. If given, dosage can be
calculated using the following formula:
a. 40 ml/kg X Body Weight (kg) = PV (ml)
b. Desired Factor VIII level (%) X Plasma Volume (ml) =
100 X 80 (minimum units Factor VIII per unit/bag)
= number of bags of Cryoprecipitate AHF needed (Quick and Dirty: 0.5 bags/kg
for Hemophilia A). To maintain hemostatic levels, repeat Factor VIII
transfusions need to be given at 8-12 hour intervals; due to the 12-hour halflife of Factor VIII activity.
c. 1 pool of CRYO will increase fibrinogen at least 30 mg/dl (except for local ARC
pool at least 50mg/dl).
d. neonate/children: 1 ml/kg or one single, random donor cryoprecipitate AHF/10
kg.
2. von Willebrand’s:
a. Smaller amounts of Cryoprecipitated AHF will usually correct this deficiency, if
DDAVP and Humate P are ineffective. (Type III-Humate P, Type I/IIa-DDAVP).
b. Calculate Cryoprecipitated AHF dosage as for Factor VIII deficiency (roughly 1
bag/10 kg).
3. Fibrinogen >50<100 1 cryo pool.
Fibrinogen <50 1 cryo pool, then re-evaluate.
4. Congenital Afibrinogenemia/Hypofibrinogenemia
4 bags/10 kg @ first.
2 bags/10 kg 24 hours later.
Rate of Infusion: As quickly as possible (about 10 ml of diluted component per minute).
Storage:
1. –18C or colder (1 year).
2. 20-24C (room temperature) after thawing.
Shelf life:
1. 1 year in frozen state.
2. 4 hours after thawing or 4 hours after pooling.
Administration:
1. Does not require ABO compatibility. If transfusing more than 350 ml per day, give
ABO identical (crossmatch not required).
2. Thaw rapidly at 30-37C (up to 15 minutes).
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3. Maintain at room temperature until transfused; because, refrigeration may
encourage reprecipitation of the concentrated Factor VIII.
4. Administer within 4 hours of thawing or 4 hours of pooling (whichever is shorter!!).
5. Do not refreeze after thawing.
6. Use blood component infusion set and syringe for IV push or blood component
recipient set for IV drip (pooled).
7. 0.9 NaCl prn.
CRYOPRECIPITATE, POOLED
Volume: Approx. 100-140 ml (6 units per pool)
Factor VIII activity: 480 units/pool
Fibrinogen: >900mg (Supplier provides 1500mg/pool)
Storage:
1. –18C or colder (1 year).
2. 20-24C (room temperature) after thawing.
Shelf life:
1. 1 year in frozen state.
2. 4 hours after thawing.
Rate of Infusion: IV drip as quickly as possible.
Administration:
1. Does not require ABO compatibility unless transfusing more than 350 ml per day,
then give ABO identical (crossmatch not required).
2. Thaw rapidly at 30-37C (up to 15 minutes).
3. Maintain at room temperature until transfused; because refrigeration may
encourage reprecipitation of the concentrated Factor VIII.
4. Cryoprecipitated AHF, pooled, should be administered as soon as possible, but no
longer than 4 hours after thawing.
5. Do not refreeze after thawing.
6. Y-type blood component recipient set for IV drip.
7. 0.9 NaCl prn.
For additional information, refer to Circular of Information for the Use of Human Blood
and Blood Components.
GRANULOCYTES
Medical approval is needed when ordering granulocytes.
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Volume: 50 ml
3.2 X 109 WBC/bag
Action:
Fight infection.
Need to monitor clinical response.
Indications:
The indications for the use of granulocyte transfusions are the presence of neutropenia
and evidence of bacterial infection.
1. Absolute neutropenia (<500 PMN’s/l).
2. Documented sepsis, unresponsive to appropriate antibiotic therapy for 48 hours.
The evidence of bacterial infection includes:
1. Positive culture from any internal body fluid.
2. Positive CIEP (Counter Immunoelectropheresis) or latex agglutination for bacterial
antigens from body fluids.
3. Positive gram-stain from CSF or pleural fluid plus a clinical diagnosis of sepsis.
Dosage:
The efficacy of granulocyte transfusions has been correlated with the dosage given. It has
been suggested that the ideal dosage would be equivalent to the total neutrophil pool. In
the neonate, the total neutrophil pool is estimated to be 0.7-0.8 108 cells/kg. It seems
reasonable that this should be taken as the minimal goal in neonatal granulocyte
transfusion dosage.
Adult:
1 pheresis product/day for 5-7 days
Pediatric: 15 ml/kg body weight prepared as buffy coat from unit of whole blood.
Storage: 20-24C
Shelf life: 24 hours
Administration:
Blood component/recipient set.
Depth-type microaggegate filter is prohibited.
Leukodepletion filter is prohibited.
Crossmatch required
Prevention of Adverse Reactions:
1. Volume overload: This is prevented limiting the transfusion volume to 15 ml/kg and
the transfusion rate to greater than 45 minutes.
2. GVHD: This is prevented by irradiating the products before transfusion.
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3. CMV Infection: This is prevented by procuring products from CMV-antibody
negative donors when the infant is < 1500 g birth weight and has a seronegative
mother.
4. Chills and fever, severe allergic reactions are common.
diphenhydramine, steroids and or non-aspirin antipyretics.
Premedicate with
5. Respiratory reactions with SOB, “white-out” on chest x-ray can occur.
For additional information, refer to Circular of Information for the Use of Human Blood
and Blood Components.
ANTIHEMOPHILIC FACTOR (HUMAN) (Method M. Monoclonal Purified)
Volume: Lyophilized
Quantity of Factor VIII activity is stated on the bottle
Action:
Anti-Hemophilic Factor (human) is a plasma protein, which corrects the coagulation defect
in patients with severe congenital Factor VIII deficiency (Hemophilia A).
Indications:
1. Patients with moderate to severe congenital Factor VIII deficiency (Hemophilia A).
2. PATIENTS WITH LOW TITER FACTOR VIII INHIBITORS.
3. When used in patients with acquired Factor VIII inhibitors, the level of inhibitors
should not increase >10 Bethesda units/ml. In these cases, the dosage should be
controlled by frequent laboratory determinations of circulating AHF.
CAUTIONS:
1. IDENTIFICATION OF THE CLOTTING DEFECT AS FACTOR VIII DEFICIENCY IS
ESSENTIAL.
2. Do not use for treatment of von Willebrand’s disease (except Humate P).
3. Development of a positive direct antiglobulin test or hemolysis is possible due to the
presence of anti-A or anti-B alloagglutinins in the concentrates.
4. Patient may form antibodies to mouse protein, inhibitors to clotting factors.
5. Patients may develop signs and/or symptoms of certain viral infections.
6. With high doses, marked elevations in fibrinogen.
7. Allergic reactions.
8. Venous thrombosis.
Dose:
1. Units required = body weight (kg) X 0.4 units/kg X desired AHF increase (% of
normal).
Example: 70 kg x 0.4 units/kg X 50% = 1400 units
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Expected AHF increase (% of normal) =
Units administered
Body weight (kg) X 0.4 units/kg
Example:
1400 units
70 kg X 0.4 units/kg
= 50%
Half-life is 10-12 hours.
2. One unit of Factor VIII concentrate/kg will equate to a two percent increase in
Factor VIII.
Storage:
1. Recommended storage at 2-8C until reconstituted.
2. Bring to room temperature (22C) for reconstitution and administer within one hour.
Do not refrigerate after reconstitution.
3. Do not freeze.
Shelf life:
1. See expiration date on product.
2. Reconstituted Antihemophilic Factor (Human) should be used within one hour of
reconstitution.
Administration:
1. Intravenously.
2. See manufacturer’s instruction for reconstitution.
Dispense through pharmacy.
SERUM ALBUMIN, 5% SOLUTION
Volume: 250 ml – 5% albumin
500 ml – 5% albumin
Indications:
1. Plasmapheresis (Therapeutic Plasma Exchange)
2. Nephrotic syndrome: short-term use with diuretic treatment; acute severe peripheral
or pulmonary edema.
3. Liver and pancreas transplantation: serum albumin <2.5g/dl, pulmonary wedge
pressure <12mm Hg, Hct >30%.
4. Third line:
a. Parocentesis
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b.
c.
d.
e.
f.
g.
h.
i.
j.
k.
Hepatorenal syndrome
Veno-occlusive disease (BMT)
Hemorrhagic shock
Non-hemorrhagic shock
Burns
Cerebral ischemia
Hepatic resection
Neonatal hypoalbuminemia
Cardiac or vascular surgery
Hemodialysis
Contraindications:
1. In patients susceptible to fluid overload, albumin should be used with caution.
2. Albumin will not correct hypoproteinemia.
3. Should not be used for long-term therapy.
Dosage: Depends upon clinical condition of patient, see package insert.
Rate of Infusion: May be infused rapidly if necessary.
Storage: Store at room temperature (22C).
Shelf life: See expiration date on product.
Administration:
1. Crossmatch is not required.
2. Blood component recipient set or may have administration set included.
3. Filter is recommended.
Dispensed through pharmacy. For additional information, refer to The Ohio State
University Medical Center, Clinical Practice Guidelines: Criteria for Use of Human
Albumin on the intranet.
IMMUNE SERUM GLOBULIN (ISG)
Volume: 2 ml
10 ml
Indications:
1. Provides passive prophylaxis of measles and Hepatitis A.
2. Replacement of gamma globulin in patients with hypo-agammaglobulinemia.
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Contraindications:
Individuals with a history of IgA deficiency or severe anaphylactic reactions to plasma
should not be given ISG.
Dosage: See manufacturer’s instructions.
Storage: Recommended storage is at 2-8C.
Shelf life: See expiration date on product.
Administration:
1. See manufacturer’s instructions.
2. Intramuscular.
3. Divided doses may be given.
Dispensed through pharmacy.
IMMUNE GLOBULIN INTRAVENOUS (IGIV)
Volume: Lyophilized
Quantity stated on vial
Indications:
1. Primary immunodeficiency states.
2. Prevention of bacterial infections associated with B-cell
Chronic Lymphocytic Leukemia.
3. ITP.
4. Kawasaki Syndrome.
5. Primary agammaglobulinemia or secondary hypogammaglobulinemia.
6. Chronic inflammatory demyelinating polyneuropathy and other neurologic conditions
such as GBS and myasthenia gravis.
Dosage and Administration: See Manufacture’s instructions (IV administration only).
Storage:
1. Store at a temperature not to exceed 25C.
2. Protect from freezing.
Systemic reactions:
1. Urticaria, pruritus
2. Chills, fever, tremor
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3. Headache, flushing, malaise
4. Nausea, vomiting
5. Backpain, joint pains
6. Dyspnea, bronchospasm
7. Hypotension
Dispensed through pharmacy.
HEPATITIS B IMMUNE GLOBULIN (HBIG)
Volume: 5 ml
Action:
1. Hepatitis B Immune Globulin provides passive immunization for individuals exposed
to Hepatitis B virus (HBV).
Indications:
1. Persons who have had contact with Hepatitis B through needlestick, serum (blood)
aspiration, oral, sexual, neonatal route.
Contraindications:
1. Should be given with caution to patients with a history of prior systemic allergic
reactions following administration of ISG.
Dosage:
Recommended dose is 0.06 ml per kilogram of body weight; the usual adult dose is 3 to 5
ml.
Storage: Refrigerate at 2-8C.
Shelf life: See expiration date on product.
Administration:
1. Administer as soon as possible after exposure (preferable within 7 days.
2. Administer vaccine shortly after (same day or next day).
Complete immunization schedule.
3. Administer intramuscularly.
Dispense through pharmacy.
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VARICELLA ZOSTER IMMUNE GLOBULIN (VZIG)
Volume: Contains 125 units of antibody to varicella-zoster virus in a volume of 2.5 ml or
less.
Indication:
1. Provides passive immunization against varicella in immunosuppressed children who
have been exposed.
2. Also used for prophylaxis in exposed (susceptible) pregnant women and organ
transplant recipients.
Contraindications:
1. Should not be administered to individuals having a history of severe reactions
following administration of ISG.
Dosage: Based on body weight.
Kilograms
Pounds
Units
# of Vials
0-10
0 -22
125
1
10.1 - 20
22.1 - 44
250
2
20.1 - 30
44.1 - 66
375
3
30.1 – 40
66.1 -88
500
4
over 40***
over 88
625
5
***There
is a single vial of 625 units for patients over 40 kilograms
Storage: Refrigerate at 2-8C.
Shelf life: See expiration date on product.
Administration:
1. Administer the product by deep intramucular injection in the gluteal muscle.
2. Dispensed through Transfusion Service, requires Transfusion Medicine approval.
PLASMA AND PLASMA DERIVATIVES AND THE TREATMENT OF DISEASE
PPF (PLASMA PROTEIN FRACTION) (PLASMANATE = TRADE NAME)
1. Provides volume expansion and colloid replacement without the risk of
hepatitis/HIV.
2. Used interchangeably with 5% albumin.
3. Dispensed from pharmacy.
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4. Cannot be infused rapidly (may cause hypotension).
PROTHROMBIN COMPLEX
1. Contains the vitamin K dependent factors (II, VII, IX, X).
2. Used in cases of Hemophilia A with inhibitors and hemorrhage or invasive
procedure.
3. Can be used for the rapid reversal of warfarin toxicity with or without bleeding.
Much more potent and much less volume than FFP.
4. Dispensed by pharmacy.
5. Risk of thrombosis in liver disease.
FACTOR IX CONCENTRATES
1. Used for replacement in Hemophilia B.
2. Monoclonal preparations contain no other factors except Factor IX.
3. During surgery, desired levels of Factor IX should be >50-75 U/dL.
4. Half of the initial dose in 12-24 hours.
Two units of Factor IX concentrate/kg will equate to a one percent increase in
Factor IX.
5. Dispensed by pharmacy.
6. Cannot be used for Factor VIII inhibitor patients since these only contain Factor IX
as opposed to activated Prothrombin complexes, which contain enough vitamin K
dependent factors to bypass Factor VIII’s step in coagulation cascade (especially in
Hemophilia A patients with Factor VIII inhibitors.
C1-ESTERASE INHIBITOR DEFICIENCY
1. Can cause angioneurotic edema.
2. Plasma (FFP) is a source of C1 esterase inhibitor.
3. New concentrates exist and are in the testing phase for both prophylactic and
symptomatic use.
ANTITHROMBIN III CONCENTRATES
1. Dispensed by pharmacy.
2. Approved for use in Antithrombin III deficiency (hereditary).
3. Not yet approved for acquired deficiency states (DIC, etc).
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Procedures not listed either require no blood or are rarely performed.
Service.Surgical/ Procedure
I.
DENTAL
1. All Procedures
0.0
II. EAR/NOSE/THROAT
2. Acoustic Tumor Excision
T/S
3. Composite Resection
4
4. Esophagoscopy, Inj. Of Varices
T/S
5. Ethmoidectomy, Complete
T/S
6. Exploration of Maxilla
T/S
7. G. Jugular/Skull Base Tumor Exc.
2
8. Glossectomy
2
9. Laryngectomy
2
10. Closure
2
11. Mandibulectomy
2
12. Maxillary Osteotomy
T/S
13. Maxillectomy
4
14. Neck Dissection
2
15. Osteotomy
T/S
16. Parotidectomy
T/S
17. Radical Neck
1
III. GENERAL SURGERY
18. Abdominal Perineal Resect
1
19. Adrenalectomy
T/S
20. Anterior Resection
1
21. Antrectomy
T/S
22. Axillary Dissection
T/S
23. Biliary Duct Exploration
T/S
24. Bone Marrow Aspiration
T/S
25. Chole Cutaneous Fistula Rep.
T/S
26. Colon Resection
T/S
27. Colostomy/Ileocolostomy
T/S
28. Colostomy Closure
T/S
29. Common Duct Exploration
T/S
30. Debridement
Choice
31. Dialysis AV Fistula/Shunt Rev.
T/S
32. Duodenectomy
T/S
33. Enteroenterostomy
T/S
34. Flank Exploration
Choice
35. Fundoplication
T/S
36. Gastrectomy/Antrectomy
T/S
37. Gastrojejunostomy
T/S
38. Gastroplasty
T/S
39. Gastrostomy
T/S
40. Groin Exploration
T/S
41. Hepatic Resection
4
42. Hepatico-Jejunostomy
2
43. Hernia, Hiatal Diaphragmatic
T/S
44. Hernia, Repair Paraesophageal
T/S
45. Hip Disarticulation
2
46. Ileostomy Closure
T/S
47. Jejunostomy
T/S
48. Jejunal Bypass/Take Down
T/S
Service.Surgical/ Procedure
49. Laparotomy Exploratory
50. Large Bowel Resection
51. Liver Transplant
52. Mastectomy
53. Pancreatectomy
54. Pancreatic Exploration
55. Pancreatic Pseudocyst
56. Protocolectomy
57. Rectal Bridge, Division
58. Rectal Carcinoma Excision
59. Rectal Prolapse Repair
60. Recto-Vaginal Fistula Repair
61. Renal/Pancreas TX Recipient
62. Renal Transplant Donor
63. Rib Resection
64. Sigmoid Colectomy
65. Sigmoid Resection
66. Skin Graft
67. Small Bowel Resection
68. Spincterotomy
69. Splenectomy
70. Staging Laparotomy
71. Stump Closure
72. Subhepatic Abscess Drain
73. Sympathectomy Abscess Drain
74. Thrombectomy
75. Thyroidectomy
76. Vagectomy/Vagotomy
77. Whipple
IV. NEUROSURGERY
78. Aneurysm, Evaculation of Cran
79. Aneurysm, Clipping
80. Anterior Cervical Disc
81. AV Malformation
82. Brain Biopsy
83. Burr Holes
84. Carotid Ligation with Clamp
85. Cervical Disectomy
86. Cervical Rib Excision
87. Cordotomy
88. Cranioplasty
89. Crainiotomy
90. Crainiotomy, Tumor > 4 cm
91. Disc Cervical and Fusion
92. Disc Lumbar and Fusion
93. Excision Disc
94. Foraminotomy
95. Hypophysectomy
96. Laminectomy
97. Lumbar Decompression
98. Lumbar Peritoneal Shunt
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Service.Surgical/ Procedure
99. Micro Dissection
100.
Neuroma, Acoustic
101.
Occipital Neurectomy
102.
Pituitary Tumor
103.
Shunts
104.
Spinal Instrumentation
105. Subdural Hematoma
106. Supraclavicular Symphathecto
107. Transphenoidal Hypophysecto
108. Untether Spinal Cord
V. OB/GYN
109. Abortion, Therapeutic
110. A/P Repair
111. C-Section
112. Cone Biopsy
113. Comual Reimplantation
114. Cystectomy
115. D&C
116. DS/Pre-Op Previa
117. Hysterectomy, Abd. Vag, TAH
118. Hysterectomy, Radical
119. Lymphadenectomy
120. Laparotomy/Cyst
121. Metroplasty
122. Mini-Lap Tubal
123. Myomectomy
124. Oophorectomy
125. Ovarian Cystectomy
126. Pelvic Exenteration
127. Rectocele
128. Rectovaginal Fistula
129. Salpingostomy
130. Tubal Reanastomosis
131. Tuboplasty
132. Uterine Myomectomy
133. Vaginoplasty
134. Vesicocele
135. Vulvectomy
VI. ORTHOPEDIC
136. Anterior Spinal Release
137. Bankhart Procedure
138. Bil Grice Procedure
139. Bil Hip Abductor Rel Post Fus
140. Block Nail Tibia or Femur
141. Bone Graft
142. Closed Craig Needle Biopsy
143. Compression Screw, Hip
144. Corpectomy, Cervical
145. Costal Cartilage, Resection
146. Deltoid to Triceps Trans Bil
147. Dwyer Anterior Release
148. Enders Nail, Hip
149. Forage Procedure
150. Gaint Cell Tumor Excision
T/S
2
T/S
2
T/S
4
1
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2
1
T/S
T/S
T/S
T/S
T/S
T/S
T/S
2
T/S
1
1
T/S
2
T/S
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2
T/S
T/S
T/S
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2
T/S
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4
1
1
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2
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2
2
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4
Service.Surgical/ Procedure
151. Girdlestone Procedure, Hip
152. Harrington Rod, Scoliosis
153. Harrington Rod, Fracture
154. Harrington Rod, Removal
155. Hip Arthroplasty
156. Hip Pinning
157. Hip, Replacement Pin Screws
158. Hip, Removal of Prosthesis
159. Hip Rev Long Stem Comp
160. Hockstad Rod, Insert
161. Hoffman Procedure, Other
162. IM Nail Femur with Circlage
163. IM Nail Tibia
164. Jewett Nail
165. Interspinous Wiring/Fusion
166. Kempf, Locke Nail, Tibia
167. K Nail
168. Knowles Pinning
169. Lugue Rods
170. Magnusen Repair Shoulder
171. Moore Prosthesis for Hip
172. Olecranon Fracture
173. Omega Hip Screw
174. Open Reduction, Arm, Leg
175. Open Reduction, Hip Anter.
176. Open Reduction, Hip Poster.
177. Open Reduction, Internal Fix
178. Osteotomy Hip, Pelvic, Femur
179. Osteotomy, Lumbar Spine
180. Osteotomy, Elbow, Knee
181. Osteotomy, Salter Innominate
182. Osteotomy, Tibia, Fibula
183. Pelvis, Internal Fix Sacroileac
184. Plate/Screws Femur, Insert
185. Post Fusion Harrington/LaRue
186. Resection
187. Removal Hardware, Other
188. Richards Compression
189. Richards Hip, Plate, Screw
190. Shoulder Reconstruction
191. Spinal Decompression
192. Spinal Fusion
193. Tendonesis, Bilateral
194. Total Elbow Relocating
195. Total Elbow Revision
196. Total Hip, Bilateral
197. Total Knee
198. Total Knee, Bilateral
199. Total Shoulder
200. Turco Procedure
201. Zickle Nail
VII. PLASTIC
202. Abdomen Attenuation, Repair
203. Abdominoplasty
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Service.Surgical/ Procedure
204. Cleft Palate
205. Debridement
206. Decubitus/Ulcer
207. Flap
208. Lipectomy, Abdominal
209. Palatal Fistual Closure
210. Reduction Mammoplasty
211. Skin Graft
VIII. THORACIC
212. Aortic Valve
213. AV Fistula
214. CABG
215. Closure ASD
216. Commisurotomy
217. Decortication
218. Epicardial Lead Pacing Wire
219. Esophagogastrectomy
220. Esophago-Myotomy
221. Fundoplication
222. Heart Transplant
223. Injection Varices
224. Insertion Implantable Defib.
225. Lobectomy
226. Mediastinal Exploration
227. Mediastinoscopy
228. Mediastinotomy, Parasternal
229. Mitral Valve
230. Open Lung Biopsy
231. Open Pleural Biopsy
232. Open Rib Biopsy
233. Pectus Excavaturn
234. Pericardectomy
235. Pericardial Cyst. Exc.
236. Pericardial Window
237. Pharyngo-Esophageal Divert
238. Pleurectomy
239. Pnuemonectomy
12. Maxillary Osteotomy
240. Pulmonary Resection
241. Rib Resection
14. Neck Dissection
242. Scelerosing of Varcies
243. Sinus Venous Defect
244. Sternal Wiring
245. Sternotomy
246. Thoracotomy
247. Thoracoplasty
248. Thymectomy
249. Valvulotomy Pulmonic
IX. UROLOGY
250. Adrenalectomy
251. Closure of Evisceration
252. Closure Vesico-Vaginal Fist.
255. Cyst Exploration
T/S
Choice
Choice
Choice
1
T/S
T/S
T/S
6
T/S
6
4
4
T/S
1
4
T/S
T/S
6
T/S
T/S
2
2
T/S
2
6
T/S
T/S
1
T/S
4
2
T/S
T/S
T/S
2
T/S
2
T/S
2
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4
2
2
2
T/S
4
4
Service.Surgical/ Procedure
256. Cystocele
257. Cystolithotomy
258. Diverticulectomy
259. Exploratory Celiotomy
260. Ileo Loop, Creat, Div, Rev.
261. Nephrectomy, Rad, Simple
262. Orchiectomy, Radical, Explor
263. Pelvic Lymph Node
264. Penectomy
265. Prostatectomy (TURP)
266. Prostatectomy, Open, Rad.
267. Retroperitoneal Lymph Node
268. Renal Artery Thrombectomy
269. Sphincter
270. Stricture
271. Suprapublic Cystotomy
272. TUR-BT
273. Ureteral Implant
274. Ureterectomy
275. Ureterolysis
276. Urethral Fistula Repair
277. Urethral Suspen, Tapering
278. Urethropexy/plasty
279. Vesicopexy, Anterior, Needle
280. Vesicostomy
X. VASCULAR
281. Amputation A/K
282. Aneurysm, Femoral
283. Aneurysm, Popliteal, Brachial
284. Aneurysm, Thor/Abdominal
285. Aorto Bifemoral Bypass
286. Carotid Bypass
287. Embolectomy
288. Endarterectomy, Renal Artery
289. Endarterectomy, Carotid
290. Endarterectomy, Aortic Ileac
291. Fem-Fem Graft
292. Femoral-Popriteal Graft
293. Femoral-Popriteal Thrombect.
294. Fem-Tib Bypass Graft
295. Popliteal Aneurysm
296. Portacaval Shunt
297. Renal Artery Reconst/Bypass
298. Spleno-Renal Shunt
299. Subclavian Bypass
300. Vena Cava Umbrella Replace
XI. OTHER
301. Specify On Order
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
TRANSFUSION GUIDELINES
TRANSFUSIONS IN ADULTS
Definitions of Recommendation Levels
(The quality of evidence determines the strength of the guideline.)
Quality of Evidence
Level of Evidence
Definition
I
Good
Evidence obtained from at least one properly randomized controlled trial or from
well-designed cohort or case-control analytic studies, preferably from more than
one center or research group, or national consensus panel recommendations
based on controlled, randomized studies.
II
Fair
Evidence obtained from multiple time series with or without intervention, or
national consensus panel recommendations based on uncontrolled studies with
positive outcomes or based on studies showing dramatic effects of an
intervention.
III
Poor
Opinions of respected authorities, based on clinical experience, descriptive
studies, or reports of expert committees.
Strength
Strength of Recommendation
Definition
A
It is advised that this
be done. . .
in a periodic health examination, or a diagnostic maneuver should be
done, or treatment of a medical problem should be given. There is
good evidence (level I) to support the recommendation.
B
This may be done . . .
in a periodic health examination, or a diagnostic maneuver may be
done, or treatment of a medical problem may be given.
B1
It should be done in
most cases.
There is fair evidence (level II) to support the recommendation.
B2
It should NOT be done
in most cases.
There is poor evidence (level III) regarding the recommendation, which
may be made on other grounds.
C
It is advised that this
NOT be done . . .
in a periodic health examination, or a diagnostic maneuver should not
be done, or treatment of a medical problem should not be given.
There is good evidence (level I) to support the recommendation that
this not be done.
Note: Practice guidelines are not standards that are meant to be applied rigidly and
followed in virtually all cases. Patient choice and physician judgment must remain
central to the selection of diagnostic tests and therapy. Practice guidelines should be
helpful to physicians and patients alike in making their decisions. At the Ohio State
University Medical Center, clinical practice guidelines are reviewed annually to
incorporate new evidence.
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OBJECTIVE
To define the appropriate use of blood components for transfusion therapy.
GUIDELINE STATEMENT
(“B1” Recommendation: This should be done in most cases.
There is fair evidence [Level II] to support the recommendation.)
Patients should be evaluated for blood component therapy by clinical and laboratory
assessment. The appropriate blood component is selected and given in the appropriate
dose.
KEY WORDS
blood, blood products, transfusion
BACKGROUND
RED BLOOD CELLS
The main purpose of red blood cell transfusion is to increase oxygen-carrying capacity.
However, the critical hemoglobin level requiring transfusion is unclear. Animal data
indicate that hemoglobin levels of 3-5 g/dl are critical; below those levels,
decompensation for the anemia occurs. For healthy humans, the hemoglobin level for
decompensation is similar at something less than 5 g/dl. One study deliberately bled
patients and volunteers to hemoglobin levels < 5.0 g/dl without clinical sequelae. 1
Several randomized clinical trials have shown no differences in outcome whether the
transfusion triggers were high or low. One recent large random controlled trial (RCT)
showed that mortality was less for those critically ill patients who received red blood
cells for hemoglobin levels < 7.0 g/dl than for those transfused to maintain the
hemoglobin > 10 g/dl.2 Patients with cardiac disease showed no differences in outcomes
in this study.
Another study of elderly patients > 60 years of age showed that transfusion had no
effect on mortality as long as the hemoglobin level was > 8 g/dl.3 Two studies of
Jehovah’s Witnesses showed that mortality did not increase for hemoglobin < 5 g/dl,
even for cardiovascular patients.4, 5 One patient with postoperative hemoglobin of 2.7
g./dl survived.
Recent published guidelines have cautioned against a uniform hemoglobin level as an
indication for red blood cell transfusion. The American Society of Anesthesiologists
Task Force on Blood Component Therapy6 as well as the Red Blood Cell Administration
Practice Guideline Development Task Force of the College of American Pathologists 7
recommend that transfusion is rarely indicated when the hemoglobin level is > 10 g/dl,
and almost always indicated when the
hemoglobin level is < 6 g/dl. If the hemoglobin level is between 6 and 10 g/dl,
transfusions should be “based on the patient’s risk for complication of inadequate
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oxygenation.” 6, 7 In acute hemorrhage, the hemoglobin level may not reflect the
severity of hemorrhage nor the true amount of blood loss.
Other considerations to limit or avoid transfusions include careful surgical hemostasis,
limiting blood loss for laboratory assays, use of specific pharmacological agents in
chronic anemia (e.g., vitamins, erythropoietin), reducing risk of hemorrhage caused by
many types of drugs (e.g., aspirin, warfarin, heparin, low molecular weight heparin), and
correcting any existing coagulopathy.
PLATELETS
The purpose of platelet transfusion is to treat clinically significant thrombocytopenia and
treat hemorrhage caused by thrombocytopenia or platelet functional disorders. In the
absence of clinically significant hemorrhage, the customary platelet count triggering
platelet transfusion has been 20,000/μl. However, several authors have evidence for a
lower transfusion trigger, such as 5,000/μl or 10,000/μl in stable patients. 8,9,10,11
Patients with concomitant conditions, such as sepsis, antibiotic therapy, and other
abnormalities of hemostasis, may require higher transfusion triggers. For hemorrhage
or invasive procedures, the recommended level is 50,000/μl.12,13
Two platelet preparations are available: platelet concentrates prepared from whole
blood, and platelets collected by apheresis. For most blood suppliers, 4-6 units (bags)
of platelet concentrates are equal to one plateletpheresis. Platelet donors may be
selected for their CMV status, HLA type, or platelet crossmatch compatibility, as well as
ABO and Rh types.
Patients who have poor posttransfusion platelet recovery and survival present
challenges for platelet therapy.14,15 Sepsis, hypersplenism, fever, DIC, amphotericin,
hemorrhage, ABO mismatch, and alloimmunization affect platelet recovery and survival.
The cause of poor platelet recovery and survival in most patients is nonimmune. A trial
of ABO matched and fresh (less than 3 days old) platelet products for transfusion can
be worthwhile. For alloimmunized patients, antibodies may be HLA and/or platelet
specific. HLA matching requires HLA typing for the patient and donor, and collection,
processing, and delivery of the plateletpheresis product. On the other hand, platelet
crossmatching can be performed on platelet products in inventory. Because of this,
platelet crossmatched products are more readily available.
FRESH FROZEN PLASMA
Fresh frozen plasma (FFP) is transfused to correct hemostatic abnormalities.
Generally, hemostasis is adequate when coagulation factors are at least 20-30% of
normal and fibrinogen is greater than 75 mg/dl. Bleeding is generally associated with
PT and/or PTT values greater than 1.5 to 1.8 times normal during surgery or massive
transfusion.16,17 However, abnormal PT and PTT values up to 2.0 times normal are
poor predictors of bleeding associated with minor invasive procedures such as
paracentesis, thoracentesis, percutaneous liver biopsy, and central venous
catheterizations.18,19,20
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In addition, expert opinion does not support the use of FFP to reverse warfarin effect
associated with bleeding or before invasive procedures if the INR is < 1.8. 21,22 For
surgery, expert opinion supports holding one or more doses of warfarin or administering
low-dose vitamin K (2-4 mg orally) and using postoperative prophylaxis with low
molecular weight heparin and warfarin.23
Generally, massive transfusion is not accompanied by excessive bleeding until more
than one blood volume is replaced. Correcting thrombocytopenia has been shown to be
of greater importance in excessive microvascular bleeding than correcting PT and PTT
prolongation.24
For patients receiving heparin, protamine sulfate, rather than FFP, should be used to
correct prolonged PTT.
CRYOPRECIPITATE-POOR PLASMA
Cryoprecipitate-poor plasma (also called cryo-poor plasma) is the supernatant
remaining after separation of cryoprecipitate.
The high-molecular-weight von
Willebrand factor is removed in this process. As high-molecular-weight von Willebrand
factor is present in hemolytic uremic syndrome and thrombotic thrombocytopenia
purpura, cryo-poor plasma and solvent detergent (SD)-treated plasma (see below) are
preferred for therapy of these diseases.25 Cryoprecipitate-poor plasma may be used as
a direct infusion in patients with TTP/HUS or as the replacement fluid during therapeutic
plasma exchange (plasmapheresis.)
SOLVENT-DETERGENT (SD)-TREATED PLASMA
Solvent-detergent-treated plasma is prepared from large pools of fresh frozen plasma,
cleared of the solvent and detergent, filtered, and transferred in 200 ml aliquots to bags,
which are again frozen. The solvent-detergent treatment is effective against lipid
enveloped viruses such as HIV and hepatitis B and C in the donor plasma.
Disadvantages are the smaller volume compared to FFP (200 ml vs. 250-300 ml),
possible decreased hemostatic effectiveness, and the higher cost per bag.
CRYOPRECIPITATE
Cryoprecipitate is rich in factor VIII, fibrinogen, von Willebrand factor, and factor XIII.
However, factor concentrates, treated to be virally safe, are available for treatment of
factor VIII deficiency and von Willebrand disease. Factor XIII is a rare deficiency.
Therefore, cryoprecipitate is used to treat hypofibrinogenemia and as a source for fibrin
glue. There is little scientific evidence about the effectiveness of cryoprecipitate in the
treatment of hypofibrinogenemia; however, expert opinion agrees that cryoprecipitate is
likely to be effective when used to correct fibrinogen levels < 80 mg/dl.6
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SPECIAL PRODUCTS
Leukocyte-Reduced Red Blood Cells and Platelets
Leukocyte-reduced blood is used to prevent febrile non-hemolytic transfusion reactions
in patients with repeated or severe febrile reactions. Several studies have shown that
leukocyte reduction with fourth-generation filters (those in use currently) are effective in
reducing transmission of cytomegalovirus (CMV) by transfusion in premature neonates
and patients with bone marrow or solid organ transplants. 26,27,28 Leukocyte depletion of
platelet transfusions has been shown to reduce the incidence of human leukocyte
antigen (HLA) alloimmunization in patients who are anticipated to receive repeated
platelet transfusions. Similarly, leukocyte depletion of red blood cells may reduce HLA
alloimmunization in patients waiting for organ transplantation.
Many studies have examined the effect of transfusion on cancer recurrence, metastasis,
and mortality. A pooled analysis of 20 studies showed that if an adverse effect exists, it
has to be small.29 Posttransfusion infections have been studied, with rates of infection
about 20-30% with allogeneic transfusion versus about 0-10% with autologous
transfusion.30 A large prospective trial did not show a reduction in length of stay for
cardiac surgery patients receiving leukocyte-reduced blood. Another concern has been
new variant Creutzfeldt-Jacob disease (nvCJD). Prions have been found in human
lymphocytes, granulocytes, platelets, and plasma. However, no evidence has been
found that CJD has been transmitted by blood transfusion.
Cytomegalovirus (CMV) Seronegative Red Blood Cells and Platelets
Donor CMV status is important for premature infants, seronegative recipients of solid
organ and autologous bone marrow transplants, and all allogeneic bone marrow
transplant recipients. CMV disease in these patients can be severe and life threatening.
Only about 40% of the donor population in this area is CMV seronegative. Therefore,
CMV seronegative RBC and platelets are in short supply. Leukocyte-reduced blood
products are equally effective as seronegative blood products in preventing CMV
transmission.
Gamma Irradiation
Transfusions-associated graft-versus-host disease (TA-GVHD) is caused by donor
lymphocytes proliferating in the recipient. The risk of the disease is increased for
patients who are immunosuppressed (bone marrow transplant, Hodgkin’s disease) and
those with immature immune systems (low birth weight neonates). However TA-GVHD
has also been reported in immunocompetent patients, especially those receiving fresh
blood or blood from blood relatives. TA-GVHD can be prevented by gamma irradiation
of cellular blood products.
ADVERSE REACTIONS
The most common adverse transfusion reactions are febrile reactions, urticarial
reactions, and volume overload. Febrile reactions can be treated and prevented by
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antipyretics such as acetaminophen; urticarial reactions respond to diphenhydramine.
Rarer are the hemolytic reactions. The most common symptom of hemolytic transfusion
reaction is fever; therefore, fever in a patient receiving RBC transfusion should be
investigated to rule out a hemolytic reaction.
Another rare, but serious, reaction is transfusion-related acute lung injury (TRALI),
caused by aggregation of leukocytes in the pulmonary vasculature. Treatment is
respiratory support. Most cases resolve in a few days.
Many diseases can be transmitted by blood; however, transmission is generally rare.
The estimated risk of transmission of HIV is < 1:600,000.
RECOMMENDATIONS
Red Blood Cell Transfusion
Hemoglobin
Recommendation
Level of
Rec.
> 10 g/dL
6.0-10.0 g/dL
< 6.0 g/dL
Acute blood loss > 20% B.V.
RBC transfusion rarely needed
RBC needed only for symptomatic patients
RBC transfusion generally needed
Fluid resuscitation; RBC transfusion
B1
B1
B1
B1
Platelets
Acute Hemorrhage or Invasive Procedure
Level of
Rec.
Platelet count < 50,000/ul
Platelet dysfunction unresponsive to other modalities (e.g., DDAVP, dialysis)
B1
B1
Prophylaxis
Level of
Rec.
Platelet count < 10,000/μl
Platelet count < 20,000/μl
Platelet count < 20,000/μl in next 24 hours
Stable patient
High-risk patient
Decreasing platelet count
B1
B1
B1
Fresh Frozen Plasma (FFP)
Active Bleeding or Invasive Procedure
Level of
Rec.
INR > 1.8 (PT > 18 sec.)
APTT > 60 sec. (Use protamine sulfate to correct PTT prolongation due to heparin.)
Coagulation factor assay < 25%
Urgent reversal of warfarin (INR > 1.8) (hold dose or low-dose vitamin K preferred)
Multiple coagulation factor deficiency (severe liver disease, DIC, vitamin K depletion)
B1
B1
B1
B2
B1
Other
Level of
Rec.
Plasma exchange for TTP/HUS (second line)
B1
RECOMMENDATIONS (CONTINUED)
Cryoprecipitate-Poor Plasma
Plasma exchange for TTP/HUS
Level of
Rec.
B1
Cryoprecipitate
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Fibrinogen
Condition
Level of
Rec.
< 50 mg/dL
< 100 mg/dL
Stable patient
Acute hemorrhage or invasive procedure
B1
B1
von Willebrand’s disease (second line)
Fibrin surgical adhesive
B1
B1
Leukocyte-Reduced Red Blood Cells and Platelets
Leukocyte-reduced blood transfusion is recommended for:
 Patients with severe or repeated febrile non-hemolytic transfusion reactions.
 Patients for whom CMV seronegative red blood cells and platelets are indicated.
 Patients who are anticipated to receive repeated platelet transfusions (to reduce HLA
alloimmunization).
Cytomegalovirus (CMV) Seronegative Red Blood Cells and Platelets
CMV seronegative red blood cells and platelets are recommended for:
 Premature infants, seronegative recipients of solid organ and autologous bone
marrow transplants, and all allogeneic bone marrow transplant recipients
Gamma Irradiation
Gamma irradiation of cellular blood products is recommended for prevention of
transfusion-associated graft versus host disease in:
 Patients who are immunosuppressed (bone marrow transplant, Hodgkin’s disease)
 Patients with immature immune systems (low birth weight neonates)
 Some immunocompetent patients, especially those receiving fresh blood or blood
from blood relatives
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
RECOMMENDATIONS (CONTINUED)
Adverse Reactions




Febrile reactions to transfusion
- can be treated and prevented by antipyretics such as
acetaminophen
Urticarial reactions
- can be treated with diphenhydramine
Fever in a patient receiving RBC transfusion
- should be investigated to rule out hemolytic reaction
Transfusion-related acute lung injury (TRALI)
- treated with respiratory support
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
ADAPTED BY
Melanie Kennedy, MD; Department of Pathology; Division of Transfusion Medicine.
APPROVED BY


The Clinical Practice Guideline Policy Group, June 21, 2000.
The Leadership Council for Clinical Value Enhancement, ____________________.
COPYRIGHT
© 2000. The Ohio State University. No part of this publication may be reproduced in
any form without permission in writing from The Ohio State University.
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Transfusion Service
On-Call Manual
REFERENCES - TRANSFUSION GUIDELINES
1. Weiskopf RB, Viele MK, Feiner J, et al. Human Cardiovascular and Metabolic Response to Acute,
Severe Isovolemic Anemia. JAMA 279:3:217-221, 1998.
2. Hebert PC, Wells G, Blajchman MA, et al. A Multicenter, Randomized, Controlled Clinical Trial of
Transfusion Requirements in Critical Care. N Engl J Med 340:6:409-417, 1999.
3. Carson JL, Duff A, Berlin JA, et al. Perioperative Blood Transfusion and Postoperative Mortality.
JAMA 279:3:199-205, 1998.
4. Spence RK, Alexander JB, DelRossi AJ, et al. Transfusion Guidelines for Cardiovascular Surgery:
Lessons Learned from Operations in Jehovah’s Witness. J Vasc Surg 16:825-31, 1992.
5. Viele MK, Weiskopf RB. What can we learn about the need for transfusion from the patients who
refuse blood? The experience with Jehovah’s Witnesses. Transfusion 34:396-401, 1994.
6. American Society of Anesthesiologists Task Force on Blood Component Therapy.
guidelines for blood component therapy. Anesthesiology 84:732-747, 1996.
Practice
7. Simon TL, Alverson DC, AuBuchon J, et al. Practice Parameter for the Use of Red Blood Cell
Transfusions. Arch Pathol Lab Med Vol. 122:130-138, 1998.
8. Rebulla P, Finazzi G, Marangoni F, et al. The Threshold for Prophylactic Platelet Transfusions in
Adults with Acute Myeloid Leukemia. N Engl J Med 337:26:1871-1875, 1997.
9. Heckman KD, Weiner GJ, Davis CS, et al. Randomized Study of Prophylactic Platelet Transfusion
Threshold During Induction Therapy for Adult Acute Leukemia: 10,000/L Versus 20,000/L. Am J
Clin Oncol 15:3:1143-1149, 1997.
10. Sagmeister M, Oec L, Gmür J. A Restrictive Platelet Transfusion Policy Allowing Long-Term Support
of Outpatients with Severe Aplastic Anemia. Blood 93:9:3124-3126, 1999.
11. Wandt H, Markus F, Ehninger G, et al. Safety and Cost-Effectiveness of a 10 x 109/L Trigger for
Prophylactic Platelet Transfusions Compared with the Traditional 20 x 10 9/L Trigger: A Prospective
Comparative Trial in 105 Patients with Acute Myeloid Leukemia. Blood 91;10:3601-3606, 1998.
12. Royal College of Physicians of Edinburgh. Consensus Conference on Platelet Transfusion. British J
Cancer 78(3):290-291, 1998.
13. Office of Medical Applications of Research. Platelet Transfusion Therapy. JAMA 257:13:1777-1780,
April 1987.
14. McFarland JG, Anderson AJ, Slichter SJ. Factors Influencing the Transfusion Response to HLASelected Apheresis Donor Platelets in Patients Refractory to Random Platelet Concentrates. British J
Haematol 73:380-386, 1989.
15. Slichter SJ. Algorithm for Managing the Platelet Refractory Patient. J Clin Apheresis 12:4-9, 1997.
16. Domen RE, Kennedy MS, Jones LL, Senhauser DA. Hemostatic Imbalances Produced by Plasma
Exchange. Transfusion 24:336-339, 1984.
17. Murray DJ, Pennell BJ, Weinstein SL, Olson JD. Packed Red Cells in Acute Blood Loss: Dilutional
Coagulopathy as a Cause of Surgical Bleeding. Anes Analg 80:336-342, 1995.
18. McVay PA, Toy PTCY. Lack of Increased Bleeding After Paracentesis and Thoracentesis in Patients
with Mild Coagulation Abnormalities. Transfusion 31:164-171, 1991.
(
19. Ewe K. Bleeding After Liver Biopsy Does Not Correlate with Indices of Peripheral Coagulation. Dig
Dis Sci 26:5:388-393, 1981.
20. Foster PF, Moore LR, Sankary HN, et al.
Coagulopathy. Arch Surg 127:273-275, 1992.
Central Venous Catheterization in Patients with
(Continued on next page)
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The Ohio State University Medical Center
Transfusion Service
On-Call Manual
REFERENCES - TRANSFUSION GUIDELINES (CONTINUED)
21. Practice Parameter – College of American Pathologists. Practice Parameter for the Use of FreshFrozen Plasma, Cryoprecipitate, and Platelets. JAMA 271:10:777-781, 1994.
22. Plasma – Consensus Conference. Fresh-Frozen Plasma. JAMA 253:4:551-553, Jan 1985.
23. Hirsh J, Dalen JE, Anderson DR, et al. Oral anticoagulants: mechanism of action, clinical
effectiveness and optimal therapeutic range. Chest 114;445S-469S, 1998.
24. Counts RB, Haisch C, Simon TL, et al. Hemostasis in massively transfused trauma patients. Ann
Surg 190:91-99, 1979.
25. Owens MR, Sweeney JD, Tahhan RH, Fortkolt P. Influence of type of Exchange Fluid on Survival in
Therapeutic Apheresis for Thrombotic Thrombocytopenic Purpura. J Clin Apheresis 10:178-182,
1995.
26. Bowden RA, Slichter SJ, Sayers M, et al. A Comparison of Filtered Leukocyte-Reduced and
Cytomegalovirus (CMV) Seronegative Blood Products for the Prevention of Transfusion-Associated
CMV Infection after Marrow Transplant. Blood 86:3598-3603, 1995.
27. De Graan-Hentzen YCE, Gratama JW, Mudde GC, Verdonck LF.
Prevention of Primary
Cytomegalovirus Infection in Patients with Hematologic Malignancies by Intensive White Cell
Depletion of Blood Products. Transfusion 29:757-760, 1989.
28. Van Prooijen HC, Visser JJ, Van Oostendorp WR, et al. Prevention of Primary TransfusionAssociated Cytomegalovirus Infection in Bone Marrow Transplant Recipients by the Removal of
White Cells from Blood Components with High-Affinity Filters. British J Haematology 87:144-47,
1994.
29. Vamvakas E, Moore SB. Perioperative Blood Transfusion and Colorectal Cancer Occurrence: A
Qualitative Statistical Overview and Meta-analysis. Transfusion 33:9:754-765, 1993.
30. Blumberg N, Triulzi DJ, Heal JM.
Transfusion-Induced Immunomodulation and Its Clinical
Consequences. Transfusion Med Rev IV:4 (Suppl 1):24-35, 1990.
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Transfusion Service
On-Call Manual
REFERENCES – ON CALL MANUAL
1. Klein HG. Standards for Blood Bank and Transfusion Services. 17th ed. Bethesda, MD: American
Assocation of Blood Banks, 1996.
2. National Archives and Records Administration. Code of Federal Regulations (Food and Drugs Title
21. Washington, DC: Office of the Federal Register National Archives and Record Administration,
Parts 211, 600, 610, 640, 1994.
3. Walker RH. Technical Manual. 11th ed. Bethesda, MD: American Association of Blood Banks, 1993.
4. Vengelen-Tyler, V. Technical Manual. 12th ed. Bethesda, MD: American Association of Blood Banks,
1996.
5. Jones FS. Accreditation Requirements Manual. 5th ed. Bethesda, MD: American Association of
Blood Banks, 1994.
6. Circular of Information for the Use of Human Blood and Blood Components. The American Red
Cross, Council of Community Blood Centers and American Association of Blood Banks, 1996.
7. General Laboratory Procedure Manual.
Service, 1996.
The Ohio State University Medical Center, Transfusion
8. Reference/Prenatal Procedure Manual.
Service, 1996.
The Ohio State University Medical Center, Transfusion
9. Hospital Manual. The American Red Cross, Central Ohio Region Blood Services, 1995.
10. Henry JB. Clinical Diagnosis and Management by Laboratory Methods, 19th ed. W.B. Saunders –
Philadelphia 1996.
11. Rossi EC, et al. Principles of Transfusion Medicine. Williams and Wilkins: Baltimore, MD: 2nd ed,
1996.
12. Winthrobe MN. Therapy of the Hereditary Coagulation Disorders.
Philadelphia: Lea and Febiger 1190, 1979.
13. Westphal RG, et al.
Arlington, VA, 1992.
In: Clinical Hematology,
Transfusion Management of Some Common Heritable Disorders.
AABB,
14. Chamberland M, Khnnaz R. Emergency Issues in Blood Safety, Inf Dis Clin NAM 12(1):217-29,
1998.
15. Petz LD. Drug-induced Hemolytic Anemia. Transfusion Med Rev 7(4):242-54, 1993.
16. Jefferies LC. Transfusion Therapy in Drug-Induced Hemolytic Anemia. Hen OncClin NAM 8(6):1087194.
17. Physicians’ Desk Reference, 52nd Edition. Medical Economics – New Jersey, 1998.
The authors wish to acknowledge the other individuals who contributed to this
manual: Mary E. Wissel, M.D., Richard Morgan, M.D., Randy Sosolik, M.D., Gina
Fino, M.D., Aamir Ehsan, M.D., Carmen Julius, M.D., Larry Lasky, M.D., and Frank
Counts, MLT(ASCP)SBB.
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