LL: One in four CA-3 residents correctly chose cryoprecipitate as the most appropriate of given choices to reverse the effects of urokinase in a hemorrhaging patient requiring urgent surgery.
Urokinase is an enzyme produced in the kidney and found in the urine. Urokinase for injection is a thrombolytic agent produced from kidney cells by tissue culture techniques. Urokinase acts on the fibrinolytic system, converting plasminogen to plasmin. Plasmin degrades clot, obviously increasing the amount of fibrin degradation products.,
There are three indications for urokinase therapy
1. pulmonary embolism,
2. coronary artery thrombosis,
3. intravenous catheter clearance.
Urokinase has an established role in the treatment of acute massive pulmonary embolus obstructing blood flow to a lobe or multiple segments. The diagnosis should be confirmed by pulmonary angiography. Urokinase has been reported to lyse acute thrombi obstructing coronary arteries and clotted blood in central venous catheters.
Urokinase is contraindicated in
the setting of
1. active internal bleeding,
2. a history of CVA,
3. recent intracranial surgery,
4. trauma, and
5. known bleeding diathesis.
According to the PDR, reversal of urokinase can be achieved with
1. whole blood (preferably fresh whole
2. packed red blood cells and
3. cryoprecipitate. or
4. fresh frozen plasma
Workup of the bleeding problem
1. Chronic blood loss is manifested as?
2. Acute blood loss is manifested as
1. chronic- hypochromic, microcytic anemia
2. acute blood loss- normochromic, normocytic anemia
FA and -B12 deficiency result in hypochromic, macrocytic anemia.
- Decreased retic count implies inability to ?
- Increased retic count implies ?
-consumption of formed RBC's.
PT/PTT: Evaluate the intrinsic and extrinsic pathways from the standpoint of both the amount and function of procoagulants.
Prolonged PTT is associated with ?
von Willebrand's disease.
Both PT and PTT are generally prolonged following
Chronic severe liver disease.
Platelet count: Generally, platelet count should be > 50,000-100,000.
Thrombocytopenia: (A useful mnemonic: "The platelets HID")
1. Hypersplenism: cirrhosis, lymphoma
2. Idiopathic thrombocytopenic purpura (ITP): 90% recover.
3. Drugs: e.g. quinidine
Inhibited platelet function
1. Aspirin: Irreversibly acetylates the cyclooxygenase enzyme
3. Von Willebrand's disease
1. If one blood volume has been transfused, about ?? of platelets will be lost.
2. If two blood volumes are transfused, about ?? are lost.
There are three components to coagulation:
1. a vascular component-
2. a platelet component (count and function)
3. a pro coagulant component.
2. Platelets: Procoagulants and platelets are responsible for forming clot. Platelet survival is about ?? days.
Two features with respect to platelets are important, their number and their function.
1) Number: Platelet count should be > 100,000, with the minimum required for surgery about ?
50,000. In a nonsurgical situation, a much lower number is acceptable-about 20,000.
The intrinsic and extrinsic pathways probably share activation and amplification routes via factors Xlla, IXa, and Vila. These are shown by the arrows.
1. Extrinsic (PT 12-14 seconds)
2. Intrinsic (PTT 25-35 seconds): Hemophilia A, Hemophilia B, and von Willebrand's Disease all affect the intrinsic system.
All procoagulants are synthesized in the liver except factor VIII which is synthesized in the reticuloendothelial system.
Factors 2, 7, 9,10 are vitamin K dependent
Vitamin K is responsible for the production of gamma carboxyglutamic acid, which is essential for the proper function of factors.
Summary of common problems with procoagulants:
Summary of common problems with procoagulants: ?problem
1. Hemophilia A:
2. Hemophilia B:
3. von Willebrands disease: lack of protein important for the function of factor VIII as well as platelet function.
1. Factor VIII deficiency
2. Factor IX deficiency
3. lack of protein important for the function of factor VIII as well as platelet function.
The gene for hemophilia A is found on the ??1
Hemophilia A Is manifested by
There must be at least ??3 normal factor VIII for clotting to occur.
Factor VIII deficiency resulting in hemophilia A can be replaced with ??4
1. X chromosome (sex linked).
2. prolonged PTT and normal PT
4. factor VIII concentrate.
Factor IX deficiency causing hemophilia B also occurs in ??1
Like hemophilia A, hemophilia B results in ??2
The treatment of choice for hemophilia B is ??3
1. males only.
2. prolonged PTT and normal PT.
3. human purified and recombinant factor IX as well as FFP (as a second choice).:;
von Willebrand disease is ??and effects both sexes.
The hallmark of von Willebrand disease is
prolonged bleeding time.
von Willebrand disease is caused by
decreased concentration of factor VIII, leading to prolonged PTT, and lack of a protein moiety important for both factor VIII and platelet function,
The best treatment is for Von WIllebrand dz is
1. Humate P (F-VIII concentrate) or
2. DDAVP (desmopressin acetate), depending upon the responsiveness of the patient to DDAVP.
3. Cryoprecipitate can also be administered (40 units/kg), but is less efficient.
-Monoclonal antibody purified factor VIII alone will not compensate for the defect, because of the missing platelet factor.
-Platelet transfusion is also ineffective, (past exams)
-Caution must be exercised regarding regional anesthesia or IM premeds unless the level of factors is clearly ??
DDAVP (desmopressin acetate)
DDAVP temporarily increases various moieties of the factor VIII:vWF complex by causing their release from endothelial cells.
DDAVP can be efficacious in the preoperative preparation and treatment of vW disease.
Humate-P and the finer points of treatment (which we are responsible for): Cryoprecipitate, DDAVP, and FFP can all be used in the setting of emergency surgery and vW disease. However, the most favored product is purified Factor VIII concentrate which is virus deactivated, e.g. Humate P. This is a derivative of plasma and has von Willebrand's factor.
what is the problem?
The problem is that many hospitals do not have it. If that is the case, since most type 1 von Willebrands patients are DDAVP responsive one would administer DDAVP.
If the patient has a history of poor responsiveness to DDAVP, however, and virus deactivated, purified concentrate is not available, cryoprecipitate or FFP should be administered.
Vitamin K is synthesized in the _____ with the help of intestinal flora and then absorbed with the help of ______.
Lack of production of vitamin K can be caused by ______ or _____induced elimination of intestinal flora.
Lack of absorption of vitamin K can be caused by____ . The lack of bile acids in this situation results in actual failure of absorption.
Vitamin K is necessary in the liver for the production of ________which is necessary for the biologic function of several factors.
gamma carboxyglutamic acid
Treatment for vit. K def is
Parenteral K requires 3-6 hours to work and is not therefore appropriate to treat vitamin K deficiency in the emergency situation.
FFP administration is necessary in this setting.
How does Heparin act? know this
Heparin acts indirectly by means of a cofactor, anti-thrombin III, which neutralizes several coagulants
(IX, X, XI) and inactivates thrombin—preventing its action on fibrinogen.
Heparin is inactivated in
both the liver and the kidneys so hepatorenal syndrome prolongs heparin's effect.
Heparin is a strong acid and protamine is a strong base. Acid-base neutralization is the reason protamine antagonizes heparin, (past exam) The appropriate dose is
1 mg protamine/100 units of heparin administered.
If too much protamine is administered, bleeding can worsen because it can act as an anticoagulant.
There are three types of reactions to protamine:
Type 1 describes hypotension related to rapid drug administration;
Type 2 describes anaphylactoid responses;
Type 3 describes catastrophic pulmonary hypertension.
Does Protamine have a direct myocardial depressant effect?
It does, however, have the capability to dramatically decrease systemic vascular resistance and to dramatically increase pulmonary vascular resistance. Flushing, edema, and bronchospasm are frequent symptoms of a protamine reaction.
Increased central venous pressure can certainly occur if pulmonary hypertension is pronounced enough to cause right heart failure.
The best initial treatment for a severe protamine reaction is
epinephrine, followed by fluids as hemodynamics dictate.
What increases with coumadin, PT or PTT and how do you reverse it?
Both PT and PTT are prolonged following the administration of Coumadin.
-Reverse Coumadin with FFP or vitamin K.
-recall that the antidote for heparin is protamine while the antidote for Coumadin is Vitamin K.
The fibrinolytic system.
Plasminogen is a protein normally in the blood. It is degraded into plasmin, a process which actually begins with the activation of the coagulation cascade. Plasmin acts upon fibrin to break down or degrade clot-forming fibrin split products.
The fibrinolytic system. Three separate drugs have been tested relative to this system in the past several years
urokinase- eats clot
Factor XII —► Plasminogen -►Plasmin -►Fibrin —►Fibrin split products
Urokinase is an enzyme produced in ___
the kidney and found in the urine.
Urokinase for injection is a thrombolytic agent produced from kidney cells by tissue culture techniques. Urokinase acts on the fibrinolytic system, converting plasminogen to plasmin. Plasmin degrades clot, obviously increasing the amount of fibrin degradation products.
Tranexamic acid and aminocaproic acid do what?
a. Tranexamic acid is a competitive inhibitor of plasminogen activation, inhibiting the breakdown of clot. Similar in action to aminocaproic acid, it is ten times more potent.
a trypsin inhibitor which inhibits plasmin's fibrinolytic activity and has
been shown to reduce perioperative blood loss,
Type and screen versus type and crossmatch:
1 Type and screen determines?
2.Type and crossmatch determines?
1. T/S: determines ABO and Rh status and the presence of the most commonly encountered antibodies. Type and screen does not protect against reactions to lower incidence antigens. The risk of adverse reaction is about 1:1,000. takes about 5 min. to perform
2. T/C determines- ABO and Rh status as well as adverse reaction to even low incidence antigens. The risk of reaction is 1:10,000. Type and crossmatch involves actually mixing donor blood and recipient blood to determine possible incompatibility.
takes about 45 min
Routine tests include those for
HBAg, Syphilis, HIV, and ALT, a marker for the presence of hepatitis non A, non B.
Normal red cell lifetime is 120 days.
In a blood bank, survival is measured on the basis of 70% RBC survival 24 hours after transfusion.
On this basis, there is a _____ half-life of blood stored in CPD-A.
For ACD stored blood, the half-life is ____.
35 day- CPD
21 days- ACD
RBC's are the component of choice to restore or maintain O2 carrying capacity but it should be remembered that they provide only minimal expansion of blood volume.
What should guide platelet transfusion?
The platelet count in the setting of trauma should exceed 100,000. In the elective situation, as low as 20,000 is acceptable.
under what instances should platelets from a Rh+ donor be
given to a Rh- recipient.
Only in life threatening instances
Is ABO compatibility crucial in platelet transfusion?
How about Rh status?
ABO compatible platelets are no better than ABO incompatible platelets in terms of hemostasis but they probably last longer and should be used if possible. Therefore, the ABO status of platelets is not as crucial as the Rh status,
(recall that FFP and cryoprecipitate can generally be given without regard to Rh status because they don't contain red cells.)
One unit of platelets increases platelet count by
An eight pack is needed to measurably increase platelet count.
The normal blood macrofilter is about ____ microns. Microfilters are _____ microns.
Banked blood contains microaggregates and these can act as microemboli but there doesn't seem to be a difference in outcome with respect to which type of filter is used. Macrofilters adequately eliminate microaggregates and therefore, the added expense of microfilters is probably unjustified
There are several different types of blood transfusion reactions:
1. Urticarial-Pruritic reaction
2. Febrile non-hemolytic reaction
3. Febrile Hemolytic transfusion rxn
4. Anaphylactic reaction
most common blood transfusion reactions. If urticaria and pruritis are the only signs, it is usually not necessary to stop the transfusion.
Febrile non-hemolytic reaction:
If temperature rises one degree centigrade or more with the transfusion, a febrile non-hemolytic reaction; must be suspected . The cause of fever in the setting of blood;transfusion must be, explored. Administer antipyretics and diphenhydramine.
Leukocytes have been implicated in the reaction and one treatment is washed red blood cells, which greatly diminishes leukocyte exposure (multiple past exams (see below).
Febrile Hemolytic transfusion reaction
Febrile hemolytic transfusion reactions may occur following infusion of only a few cc's of blood, with exhaustion of haptoglobin binding capacity and lysis of cells. Associated signs and symptoms include high temp, hypotension, hemoglobinuria, and DIC.
Anaphylactic reactions are usually associated with wheezing and hypotension. Hemolysis can also occur.
An anaphylactic reaction in a patient who has been previously transfused is most often due to an IgA deficiency (see below).
With the exception of urticarial-pruritic reactions, each of these complications of blood administration should be considered potentially life threatening. In this setting, what should be done?
1. Stop the transfusion and
2. support oxygenation, ventilation, and circulation.
3. Maintain urine output.
4. Send blood samples to the lab to detect free hemoglobin and for recrossmatch.
If blood is desperately needed during the interim the universal donor, O negative, should be administered.
Send blood for PT, PTT, platelets, and fibrinogen. ,
More than 50% of CA-3 residents did not know that recipient IgA deficiency is the most likely cause of an anaphylactic transfusion reaction in a patient who has previously been transfused
Memorize as fact
Leukocyte Reduced RBCS; Indications:
a. The washing process removes most plasma proteins, microaggregates, platelets, and leukocytes. The use of washed RBCs reduces the incidence of febrile, urticarial, and certain types of anaphylactic reactions.
b. Washed RBCs may be beneficial in IgA-deficient patients who can have anaphylactic reactions when transfused with blood containing IgA.
c. The washing process does not affect the survival of cells which are eventually transfused. Washed RBCs are prepared in an open system and must be administered within 6 hours if stored at 20 degrees C and within 24 hours if stored at 1-6 degrees C.
Order of transfusion in "emergency" situations where full crossmatch is not possible:
a. Type specific partial crossmatch
b. Type specific uncrossmatched
c. Type O, Rh - (can give whenever emergency blood is needed)
Should PRBC's be diluted with lactated ringers solution?
No, only normal saline is recommended by the American Association of Blood Banks. Lactated ringers contains calcium which when combined with blood can form microdots. Microdots form because calcium is binding citrate, which is the anticoagulant for the blood.
Citrate intoxication can also cause a
hypocalcemia with its associated problems of seizures, tetany, and Iaryngospasm.
Indications for FFP
a. Replacement of isolated factor deficiencies or replacement of antithrombin III deficiency.
b. Documented deficiency of factors V or VIII (less than 25%) or where such deficiencies are thought to exist based upon massive blood loss in the setting of clinical bleeding.
c. Thrombotic thrombocytopenic purpura
If a patient is bleeding at the end of a surgery in which many units of blood have been transfused, and there exists a coagulopathy based upon laboratory values one should administer
FFP and/or platelets
Hemolytic transfusion reactions under anesthesia:
- The incidence of acute hemolytic transfusion is 1: 4,000-6,000. The incidence of fatal reaction is 1:100,000. Classic signs and symptoms include
fever, fever with chills, nausea, flushing, dyspnea, and chest and flank pain.
These are generally masked under general anesthesia.
-bleeding diathesis occur and are usually more apparent.
A severe reaction can occur with as little as 50 cc of blood, the amount that typically exceeds the haptoglobin binding capacity.
Tests to detect hemolytic transfusion rxn?
-plasma free hemoglobin,
-Antiglobulin (detects presence of antibody on the RBC)
1. Stop the transfusion
2. Obtain blood and urine samples
3. Support the CV system with fluids-drugs (epinephrine) and maintain UOP.
a) Fluids, mannitol, lasix, NaHC03
4. Send blood back to the lab for recrossmatching
DIC is consumptive coagulopathy, presenting as excessive bleeding or intravascular thrombosis.
-Factors, with V and VIII most frequently exhausted
Suggestive of DIC?
1. PT >15 sec
2. Fibronogen < 150mg% (nl 150-200mg%), in pregnant pt should be 300mg%
3. Platelet count <150,000
Causes of DIC: (another SAT)
-Sepsis (especially gram neg)
-Amniotic fluid embolism
Cryoprecipitate is used to replace
von Willebrand's factor.
Cryo and FFP can be given without regard to ___ status. _____compatibility should be maintained.
Massive blood transfusibn-Problems: remember PATCH
P: Platelets (thrombocytopenia), potassium (hyperkalemia)
A: ARDS - Acid-base changes: Major tendency is to acidosis based upon volume
T: Temp decrease-hypothermia
C: Citrate intoxication leading to hypocalcemia (prolonged QT and hypotension)
H: Hepatitis-other forms of infection such as syphilis and AIDS..
Citrate intoxication with blood administration
a. Citrate intoxication is not caused by citrate ion per se but because citrate binds calcium.
b. Signs of citrate intoxicaton are those of ?
-narrow pulse pressure,
-prolonged QT intervals on EKG, and -elevated end diastolic pressure and --central venous pressure.
Cardiovascular changes of citrate toxicity don't occur unless
ACD blood is given at one unit/ 5 minutes (average adult size). Newer preservatives have less citrate and therefore intoxication is less likely.
Re: citrate tox,
In a bleeding patient, "emphasis should be placed upon correcting the underlying disorder (hypovolemia) and calcium administration is rarely necessary."
Serum calcium often returns to normal rapidly after blood transfusion because [citrate is metabolized by the liver and calcium is mobilized from endogenous sources.
Re: massive transfusions
When coagulation factor levels drop to less than 75%, such as can occur following massive transfusion, PT/PTT are generally only slightly prolonged. Therefore, one can see an abnormality of PT/PTT without being at high risk for spontaneous hemorrhage. Spontaneous bleeding generally occurs when?
Spontaneous bleeding generally occurs in the 10-20% factor range and oozing from the surgical wound in the 20-30% factor range.
ACT is not as sensitive an indicator of coagulation status as PT/PTT.
Aspirin: impairs platelet aggregation in two major ways
-First, it inhibits cyclooxygenase, an enzyme which converts arachadonic acid to prostaglandin (PGG2).
-Second, it prevents the formation of thromboxane, a potent platelet aggregator.
Platelets normally aggregate to one another and adhere to nonplatelet surfaces. The most potent aggregating agent is ?
The platelet occlusive plug is subsequently stabilized by fibrin formation.
Besides increasing 2,3-DPG,
the major advantage of preoperative transfusion is
increased oxygen carrying capacity.
What causes intraoperative coagulopathies- unexplained bleeding:
2. Dilutional thrombocytopenia
3. Low factors
4. Hemolytic transfusion reaction
In order to treat DIC the diagnosis must be made and the cause determined, for example sepsis, shock, tissue injury from trauma, or abruptio placenta? Along with treatment of the cause, treat with
2. Dilutional thrombocytopenia
After replacement of one entire blood volume, only 40% of platelets remain. In the setting of clinical bleeding and a platelet count in the range of 50-75,000, what should be done?
platelets should be administered. One unit of platelets increases platelet count by about 10,000 (recent exam).
3. Low factors
1) PTT screens for levels of V and VIII. If PTT > than 1.5 times control,
FFP should be administered.
4. Hemolytic transfusion reaction should be suspected in the presence of hypotension, hemoglobinuria, or DIC.
Diagnosis is confirmed by ?
-presence of free hemoglobin in spun plasma with a direct Coombs test.
Whenever the need for blood is immediate, administer type O Rh- blood. Neither A or B antigens exist in the O neg; blood and therefore reactions with anti-A or anti-B antibodies do not occur!
After transfusion of four or more units of uncrossmatched blood, one should continue to use uncrossmatched blood or incompatibilities with the newly transfused blood can become manifest.
Autologous blood transfusion
-Patients can give how much?
Patients can,give one Uinit per week for 4 weeks.
Blood can be frozen indefinitely:
What determines the infusion rate of blood, the speed at which it can be administered?
a. Directly proportional to the radius of the catheter and the pressure difference.
b. Inversely proportional to the viscosity of the blood and the length of the tubing.
How does blood change as it sits on the shelf: (recent examinations)
a. PaCQ2 increases, leading to acidemia
b. 2,3-DPG decreases
c. Platelets decrease
d. Factors deteriorate, especially V and VIII
e. Potassium increases from hemolysis
Cigarette smokers can have an effective anemia because of
binding of hemoglobin by carbon monoxide to create carboxyhemoglobin.
What is the minimum safe level of Hb?
a. The 10 gram hemoglobin rule is unnecessarily restrictive.
b. Oxygen delivery varies little between hematocrits of 20-50%.
c. Assuming normal intravascular volume, a healthy patient can tolerate a hematocrit of 20%. A patient with poor LV function or ischemic heart disease probably should have a
higher hematocrit of about 30%, since this optimizes oxygen delivery and does not predispose to compensatory cardiovascular changes such as tachycardia, which increase myocardial oxygen consumption.
What about the paitient who refused blood transfusion? There are alternatives.
a. Autologous blood: Such patients generally accept autologous blood.
b. Cell saver: Some will accept salvage techniques such as the cell-saver.
c. Acute normovolemic hemodilution:
d. Fluosol-DA: In combination with 100% oxygen, fluosol (20 mg/kg) increases oxygen content and improves mixed venous oxygen saturation.
- Fluosol has a very short half life and may predispose to coagulopathies.
Cell savers are used in situations of high volume usage, including mediastinal, CABG, orthopedic, neurosurgical, plastic, obstetric (i.e. ruptured ectopic pregnancy with uncontrolled bleeding) major vascular and trauma surgery when ____ of blood is likely to be lost, (past exam)
Another use has been in the setting of difficult cross-match problems where availability of enough blood to meet expected surgical losses is in doubt.
b. If the risk of contaminated blood (infection, gut perforation, malignancy) is high, cell savers should not be used.
c. The problem with cell savers for tumor surgery: is the risk of systemic spread.
d. During AAA surgery, the cell saver is often used but if gut perforation is suspected, it should be avoided. If the AAA has ruptured, the cell saver should not be used to salvage blood which has clotted in the abdomen.
e. The cell saver has found special use in surgery involving Jehovah's Witnesses, as they will often accept a return of their own blood but not cross-matched blood.
Blood salvaged in a cell saver essentially consists of salvaged what?
-red blood cells and
Coagulation factors, platelets, and even calcium are not
what is Acute normovolemic hemodilution (ANH)
(ANH) is a technique in which blood is collected prior to operative blood loss with simultaneous replacement of cell-free solutions to maintain intravascular volume.
ANH may reduce the need for and potential risks associated with allogenic blood. At the same time, it provides a source of fresh whole autologous blood for transfusion
ANH results in ?
-decrease in blood viscosity
( which results in increased tissue perfusion as well as reduced intraoperative red blood cell loss).
-also results in decreased arterial oxygen content.
(The compensatory mechanism is increased heart rate and increased cardiac output).
Both lead to increased myocardial oxygen consumption. The most significant potential complication from ANH is myocardial ischemia.
Patient selection for ANH is based upon several factors, including
-expected blood loss,
-preoperative hemoglobin level
-absence of significant cardiac, pulmonary, renal, and hepatic disease.
*The patient should be free of infection and have normal clotting function
what is a simplified formula recommended by the ASA is: to determine the amount of blood to be withdrawn?
Vol to be removed= EBV X (Ho-Hf/Ha)
Ho= Initial hemoglobin
Hf= Final hemoglobin
Ha= Average of initial and final hemoglobin
Blood can be withdrawn from central or peripheral veins or arteries and collected in standard blood bags. Blood may be stored at room temperature up to eight hours or at
1-6 degrees centigrade for 24 hours.
Crystalloid or colloid are infused during blood withdrawal, crystalloid in amount 3 times the volume of blood withdrawn and colloid in amount equal to the blood volume withdrawn.
How should the blood be infused?
in reverse order of removal. (bld removed last should be given first)
The first unit of collected blood has the highest Hct, platelets, and clotting factors and is preferably re- transfused last. (ASA, Questions and Answers about Transfusion Practices)
Blood following trauma:
-If a traumatized patient is hypotensive and has evidence of massive hemorrhage, such as a positive abdominal tap, what type of blood should be given?
type specific uncrossmatched or partially cross-matched blood should be administered. If the blood bank runs out, type O Rh neg blood should be administered.
**Fresh whole blood is for all practical purposes never indicated
(It is usually not available anyway because of the critical need for components on the part of blood banks. Many regard whole blood transfusion as inefficient use of a scarce product.)
why is definitive intravenous access especially imperative in the setting of massive abdominal hemorrhage?
Once the abdomen is opened, the tamponade effect is lost and bleeding can be massive.
Massive on-going blood loss is an indication for a cell saver.
LL: More than 50% of CA-3 residents did not know that: Hepatitis B is now more often transmitted in blood transfusions than Hepatitis C,
Memorize as fact.
Forward group interpretation:
A. Specific antigens are on specific cell membranes and they react with specific antibodies.
-What antigen is on the cell membrane?
A antigen reacts with A antibody
B antigen reacts with B antibody
AB antigen reacts with both an'ti-A and anti-B antibodies
O has no antigen. Does not react with either anti-A or anti-B antibodies.
Reverse group interpretation:
(Serum: Factors not present; Plasma: Factors present.)
-In a patient's serum, there are naturally occurring antibodies directed at the missing antigen.
Grp A PRBC has A ag & ?serum
Grp B has B ag & ? in serum
Grp AB has A and B ag & ? s
Grp O has no ag & ? serum
A - An antibody to B antigen is present in group A serum.
B - An antibody to A antigen is present in group B serum.
AB - No antibodies to either A or B antigens are present in group AB serum.
O - Antibodies to both A and B antigens are present in O serum.
If Donor PRBC's Are
what can the plasma of the recipient can be?
The Plasma of the Recipient Can be:
Two questions u should ask?
-what ab is in pt's serum
-what ag does donor have
S-anti B| anti A| no ab| anti A & anti B
Rbc- A ag| B ag | A ag B ag| no ag
If donor PRBC's are O, the plasma of the recipient can be:
1. O: Antibodies to both A and B antigen are present in O serum. There are no A or B antigens on O so
O serum is acceptable.
2. A: Antibodies to B antigen are present in A serum. There are no B antigens on O cells. A serum is
3. B: Antibodies to A antigen are present in B serum. There are no A antigens on O cells. B serum is
4. AB There are no antibodies to A or B antigens in AB serum. There are neither on O cells. AB serum is
If donor PRBC's are A, the plasma of the recipient can be:
1. A: Antibodies to B antigen are present in A serum. With donor A cells, we don't fear B antibodies. A
serum is acceptable in the setting of A donor PRBC's.
2. AB There are no antibodies to A or B antigens in AB serum. Therefore, donor PRBC's with A antigen
will not present a problem to AB serum recipient.
3. O: There are A and B antibodies in O serum. The antibodies to A will cause lysis.
4. B: There are A antibodies in B serum. The A antibodies will react with A antigen on A cells to cause
If donor PRBC's are B, the plasma of the recipient can be:
1. B: Antibodies to A antigens are present in B serum. With donor B cells, A antibodies are not a
2. AB No antibodies to A or B antigens are in AB serum. Donor PRBC's with B antigen will not present
3. O: There are A and B antibodies in O serum. The antibodies to B will cause lysis.
4. A: There are B antibodies in A serum. These will bind B antigens on B cells and cause lysis.
If donor PRBC's are AB, the plasma of the recipient can be:
1. AB There are no antibodies in AB serum to react with A and B antigens. AB is acceptable.
2. O: There are both A and B antibodies in O serum. These will bind A and B antigens on AB cells and
3. A: There are B antibodies in A serum. These will bind B antigens on AB cells and cause lysis.
4. B: There are A antibodies in B serum. These will bind A antigens on AB cells and cause lysis.
The majority of the calibration group did not know that an A positive patient who has received
10 units of O negative RBCs can still safely receive both A negative and A positive RBCs.
According to the ASA (Questions and Answers About Transfusion Practices): "How should emergency transfusion needs be met before crossmatched blood is available? ... If the patient has cardiac disease, pulmonary disease or cerebrovascular disease, and acute anemia will pose increased risk, or if there is not time to wait because the patient is in extremis, then either type specific or type O Rh-negative red .cells can be administered while awaiting a formal crossmatch . Type O Rh-positive Red Blood Cells for males or postmenopausal females can be transfused in this setting as well. Administration of uncrossmatched blood has been shown relatively safe, in part related to the low incidence of unexpected antibodies observed during crossmatch in patients with (1%) or without (0.1%) a previous history of transfusion."
What concept has led to the recommendation that one should not switch back to the patient's blood type after administration of two units of Group O Whole Blood?
The ASA further states: "Administration of Group O Rh negative blood may lead to hemolysis if multiple units of Group O Whole Blood (containing anti-A and anti-B antibodies) have been transfused to patients with Group A or B blood;
The patient can be switched back to his or her inherent type-specific blood after subsequent testing by the blood bank indicates it is safe to do so. The passively transfused anti-A and anti-B antibodies are seldom a problem after Group O Red Blood Cells are transfused."
LL: More than 50% of PG3 residents did not know that an AB negative patient cannot safely receive O-negative plasma.
an AB negative patient cannot safely receive O negative plasma. An AB patient has antigens which react with both anti-A and, anti-B antibodies. O serum or plasma contains both anti-A and anti-B antibodies.; Specifically, if a patient is AB negative only AB plasma is acceptable because there are no antibodies in AB serum to react with A and/or B antigens. However, again, O plasma or serum contains both A and B
antibodies which will react with A and B antigens and lyse red blood cells.