BLOOD_DS RBC I & II

One 4-6 unit Apheresis Platelet Unit would be expected to increase the platelet count of a 70 kg adult by 25,000 to ___________.

50,000/ uL

Delayed Febrile Reactions (>24 hours from transfusion)

Delayed Hemolytic Transfusion associated graft versus host disease

Discuss prevention of the Hemolytic Disease of the Newborn

Determine Rh status of mother by a blood test (ABO and Rh) & test for atypical antibodies as well At present, Rh D incompatibility is the only cause of HDN for which screening is routine 17% of Caucasians are Rh D negative If mother is not sensitized, reduce the risk of future sensitization To find out whether a pregnant Rh D negative mother has been sensitized to the Rh D antigen, an indirect Coombs test is performed. If anti-D is not found in the mother's serum, it is likely that she has not been sensitized to the Rh D antigen. Risk of future sensitization can be greatly reduced by giving all unsensitized mothers anti-D Ig which "mops up" any fetal RBCs that may have leaked into the maternal circulation, reducing risk of first time exposure to the D antigen Injections given at 28 weeks, 34 weeks, and a few weeks before labor begins This prophylaxis regime against Rh D sensitization is effective. However, currently, there is no routine prophylaxis for HDN caused by incompatibility of other blood group antigens. If the mother is sensitized, determine whether the fetus is at risk and monitor accordingly. Determine risk of fetus by confirming the Rh status of the fetus. If the father is homozygous for the D allele (D/D) the fetus will be D positive. If the father is hetero (D/d) there is a 50/50 chance that the fetus is D positive and the only way to know for sure is to take a test of fetal blood cells. If fetus is Rh D positive, the pregnancy is carefully monitored for signs of HDN. Monitoring includes regular US scans of fetus and monitoring of the amount of anti-D in the mother;s serum. Active hemolysis is indicated by a rise in anti-D. If a fetal blood test confirms fetal anemia, depending upon its severity a blood transfusion can be done in utero to replace the lysed fetal blood cells. Blood transfusions may also be needed to correct anemia in the newborn period. During this period there may also be a sharp rise in level of bilirubin in the neonate, which can be lowered by phototherapy and exchange transfusions.

Direct Coombs Test

Diagnoses HDN Detects maternal anti-D antibodies that have already been bound to fetal RBCs First a sample of fetal RBCs is washed to remove any unbound antibody (Ig). When the test antibodies (anti-Ig) are added, they agglutinate any fetal RBCs to which maternal antibodies are already bound. This is called the direct Coombs test because the anti-Ig binds "directly" to the maternal anti-D Ig that coats fetal RBCs in the HDN

Hypotensive

Drop in systolic BP > 30 mmHg to below 80 mmHg that occurs during start of transfusion and stops quickly after transfusion is stopped. Activation of the contact pathway (prekallikrein converting to kallikrein) induced in plasma by the negatively charged surface of some leukoreduction filters. Syndrome more severe in patients on ACE inhibitors. Marked Thrombocytopenia

Signs of Transfusion related acute lung injury

Dyspnea, hypoxemia, fever, hypotension

Transfusion-associated circulatory overload (TACO)

Dyspnea, hypoxia during or after transfusion, sudden onset dyspnea, jugular venous distension, congestive heart failure. Cardiopulmonary disease with too rapid blood infusion; very old and very young most at risk. Distinguishing characteristics: absence of hemoglobinuria and hemoglobinemia and absence of positive posttransfusion DAT result distinguish the reaction from one caused by immune hemolysis. Likewise, the absence of fever, chills, or urticaria should help distinguish TACO from the febrile or allergic types of reactions. Reaction <24 hours from transfusion

Signs of a hypervolemic reaction

Dyspnea, tachycardia, hypertension, HA, JVD

Undefined febrile/afebrile

Electrolyte Toxicity Hypotensive Delayed serologic Transfusion-associated dyspnea Transfusion-transmitted infection

TRUE/FALSE: Fever is a symptom specific for hemolytic transfusion reactions

FALSE

Red cell transfusion threshold should be based solely on laboratory findings.

False

Describe the Formation of Anti-Rh

Formation of Anti-Rh Agglutinins When RBCs containing Rh factor are injected into a person whose blood does not contain the Rh factor (that is an Rh negative person) anti-Rh develops slowly, reaching max concentrations of agglutinins 2-4 months later. This immune response occurs to a much greater extent in some people than others. With multiple exposures to the Rh factor, an Rh negative person eventually becomes "synthesized"

Signs of a Febrile reaction

fever, chills, rigors

What is a common cause of transfusion related GVHD?

Transfusion from a relative

What is the expected increase in a patient's hemoglobin after a single unit RBC transfusion?

1 g/dL

Each unit of RBCs (separated) or Whole Blood (not used very much) contains enough hemoglobin to increase the hemoglobin concentration in an average-sized adult by approximately....

1 g/dL and increases hematocrit by 3%

Delayed Hemolytic Transfusion Reaction

>24 hours from transfusion Fever, anemia 3-10 days after transfusion, hemoglobinuria, hemoglobinemia Anamnestic response to reexposure to red blood cell antigen previously known to the patient's immune system through transfusion, pregnancy, or stem cell transplant. (+) DAT with an elute showing a new RBC alloantibody ↓Hematocrit

Which blood types is possible in a child whose parents are blood type B and AB?

A, B, AB

An A positive patient needs an RBC transfusion. Which blood type would probably cause a serious hemolytic transfusion reaction?

AB negative

How does Acute Intravascular Hemolytic Transfusion Reaction work?

ABO Abs are spontaneously occurring immunoglobulin (Ig) M and IgG antibodies to foreign A and B blood group antigens. IgM antibodies efficiently fix complement after binding to ABO incompatible RBCs and are responsible for initiating the hemolytic and inflammatory cascades that cause significant acute intravascular hemolytic transfusion reactions. Process: In IgM mediated ABO incompatible transfusion reactions, activation of the complement cascade generates anaphylatoxin C3a and C5a, which leads to capillary leak, hypotension, and phagocyte and mast cell activation. Also the deposition of C3b on the RBC membrane in extravascular hemolysis Excessive complement action results in C5-9 membrane attack complexes overwhelming complement regulatory factors on the RBC membrane leading to osmotic lysis. Plasma heme also induces renal vasoconstriction through nitric oxide scavenging. Cytokines also play role

Describe the genetic determination of agglutinogens

ABO blood group genetic locus has three alleles (means three different forms of the same gene). The three alleles IA, IB, and IO determine the blood types. I stands for immunoglobulin Type O → functionless or almost functionless so causes no significant agglutinogen → recessive Type A and B → can cause strong agglutinogens → codominance Since each person only has two sets of chromosomes, only one of these alleles is present on each chromosome. However, the presence of three different alleles means that there are six possible combination of alleles: OO, OA, OB, AA, BB, AB. These combinations are known as genotypes and each person is one of six genotypes. Ex. OO produces no agglutinogens so blood type is O Ex. OB produces B agglutinogens so blood type is B Relative Frequencies of the Different Blood Types O and A genes occur frequently, whereas the B gene occurs infrequently.

Acute Febrile Reactions (during or <24 hours from transfusion)

Acute Hemolytic Febrile nonhemolytic Bacterial Contamination Transfusion related acute lung injury (TRALI)

Air emboli transfusion reaction

Acute cardiopulmonary insufficiency - air lodges in right ventricle preventing blood from entering the pulmonary circulation - causing cyanosis, pain, cough, shock, arrhythmia Since the replacement of evacuated glass bottles by plastic bags, the risk for air embolism from phlebotomy or transfusion has virtually disappeared however air still may be infused into patients by roller pumps contained in various transfusion devices especially apheresis machines and intraoperative salvage machines Reaction <24 hours from transfusion

Transfusion related acute lung injury (TRALI)

Acute lung injury <6 hours after transfusion. Bilateral CXR infiltrates, hypoxemia, no cardiac dysfunction, tachypnea, dyspnea, diffuse pulmonary edema. HLA/granulocyte specific antibodies (usually of donor origin) reacting with recipient leukocytes or directly with endothelium. Lysophosphatidylcholines that accumulate during component storage can activate neutrophils in an antibody independent manner. Chest XR, blood gas, blood HLA or antineutrophil antibodies Reaction < 24 hours from transfusion

A 28 year-old G1P0 is blood type O negative. Prenatal screening includes an indirect Coombs test, that shows no evidence of anti-D antibody. What is the most appropriate method to minimize future risk of Rh-associated hemolytic disease of the newborn?

Administer anti-D Ig (Rhogam or other brand) at appropriate dosage and intervals

Origin of Agglutinins in the Plasma

Agglutinins are gamma globulins, almost all are antibodies and they are produced by the same bone marrow and lymph gland cells that produce antibodies to any other antigen. Most of them are IgM and IgG immunoglobulin molecules. But, why are these agglutinins produced in people who do not have the respective agglutinogens in their RBCs? Small amounts of Type A and B antigens enter the body in food, bacteria, etc. and these substances initiate the development of the anti-A and anti-B agglutinins

Acute NON Febrile Reactions (during or <24 hrs from transfusion)

Allergic Transfusion-associated circulatory overload (TACO) Hypothermia Air Emboli

An A positive patient would be expected to make which naturally occurring antibodies?

Anti-B

What are the lab tests used in diagnosing Hemolytic Disease of the Newborn?

Background: To detect HDN, presence of maternal anti-Rh IgG must be identified. In vivo, these antibodies destroy RhD positive fetal RBCs In vitro, these do not lyse cells or even cause agglutination Direct Coombs Test Indirect Coombs Test

Post Tranfusion Purpura

Bleeding 5-10 days after transfusion. Patients often have hx of sensitization with prior transfusions or pregnancies. Thrombocytopenia present. Recipient antibody versus absent platelet antigen (HPA-1a). A delayed adverse reaction to a blood transfusion or platelet transfusion that occurs when the body has produced alloantibodies to the allogeneic transfused platelets' antigens. Delayed Afebrile reactions > 24 hours from transfusion

Storage of Plasma

Can be fresh frozen at -18C within 8 hours of collection and stored for over 1 year. Must be thawed to room temp before transfusion. FFP = Fresh Frozen Plasma

Febrile Nonhemolytic transfusion reaction

Fever chills only, negative workup. Rigors, chills. Accumulated cytokines (IL-6, TNF); HLA antibodies Post transfusion DAT should yield negative findings, b/c FNHTRs do not involve RBC alloantibodies Reaction < 24 hours from transfusion

Signs of Sepsis

Fever, chills, hypotension, tachycardia, vomitting

Signs of Acute Hemolytic reaction

Fevers, chills, dyspnea, vomitting, HTN, tachycardia, infusion site pain, back pain, hemoglobinuria, DIC

Acute Hemolytic Reaction

Fevers/ chills, back/flank pain, HGBemia/uria, bleeding, DIC ACO incompatible red cells given to patient (rarely from incompatible plasma hemolyzing patient's RBCs) Reaction less than 24 hours from transfusion

Which factors are present in cryoprecipitated antihemophilic factor?

Fibrinogen VIII XIII vWF Fibronectin

Lab tests for acute extravascular hemolytic transfusion reaction

Findings Positive DAT caused by recipient RBC alloantibodies binding to the incompatible circulating donor RBCs Increase in indirect bilirubin Increase in LDH Decrease in hematocrit Confirmatory Tests DAT with an eluate Eluate identifies the antibody coating the RBCs Positive DAT results reflexes the patient's antibody (or antibodies) coating the incompatible donor RBCs. B/c this is not an autoantibody the patient's own RBCs are not involved in the reaction

Clinical presentation of acute intravascular hemolytic transfusion reaction

First sign = fever; therefore transfusion must be stopped when transfusion develops >/= 1 C Cardinal signs = fever, hemoglobinemia (presence of red plasma) and hemoglobinuria (dark urine) Additional symptoms: Fever, chells, SOB, CP, back pain, anxiety, renal failure

What is the purpose of cryoprecipitated antihemophilic factor (AHF)?

Made by thawing a unit of FFP (fresh frozen plasma) which contains clotting factors (VIII, C, vWF, fibrinogen, and factor XIII) It is used in patients who are in low fibrinogen states and have been unresponsive to other measures of coagulation.

What causes TRALI?

HLA/ Neutrophil antibodies of donor origin

Describe the characteristic of an Rh tranfusion reaction

If an Rh negative person has never before been exposed to Rh positive blood, transfusion of Rh positive blood into that person will likely cause no immediate reaction. However, anti-Rh antibodies can develop in sufficient quantities during the next 2-4 weeks to cause agglutination of the transfused cells that are still circulating in the blood. These cells are then hemolyzed by the tissue macrophage system. Thus, a delayed transfusion reaction occurs, although it is usually mild. Upon subsequent transfusion of Rh positive blood into the same person, who is now already immunized against Rh factor, the transfusion reaction is greatly enhanced and can be immediate and as severe as a transfusion reaction caused by mismatched type A or B blood.

Severe, potentially fatal allergic reactions to transfusions are most likely in patients with..

IgA deficiency

What antibody mediates a delayed hemolytic transfusion reaction?

IgG

Which antibody type typically mediates hemolytic disease of the fetus and newborn?

IgG

What antibody mediates an ABO incompatible acute hemolytic transfusion reaction?

IgM

Describe the quantity of agglutinins at different ages

Immediately after birth, quantity of agglutinins in plasma is zero. You are not born with agglutinins. Peak # of agglutinins produced is around age 8-10 and declines for the rest of life.

Describe Rh Blood Types

In the OAB system, the plasma agglutinins responsible for causing transfusion reactions develop spontaneously, whereas in the Rh system, spontaneous agglutinins almost never occur. Instead, the person must first be massively exposed to an Rh antigen, such as by transfusion of blood containing the Rh antigen, before enough agglutinins can cause a significant transfusion reaction to develop.

How does an acute extravascular hemolytic transfusion reaction work?

In this reaction, complement is either not fixed at all or only to C3b. In both, complement action with fixation of the C5b-9 complex does not occur. The presence of IgG bound to the RBCs or C3b fixation results in an extravascular reaction because the antibody coated cells are cleared by IgG receptors in the spleen or C3b receptors in the liver. In these circumstances, RBC lysis does not occur in the intravascular space. B/c of lack of gen of C3a or C5a an extravascular hemolytic transfusion reaction does not usually present as a clinical emergency.

Transfusion associated graft versus host disease

LEAST COMMON & >24 hours from transfusion Fever, diarrhea, skin rash, n/v, anorexia, fever, diarrhea, liver dysfunction, Fatal in 90% of cases Cellular immune response by transfused T lymphocytes versus host. Occurs when immunologically competent lymphocytes are introduced into a host who cannot destroy the donor lymphocytes. The immunocompetent donor lymphocytes engraft host HLA antigen is presented to donor lymphocytes and the activated lymphocytes attack host tissues. t-GVHD occurs after transfusion of non irradiated cellular blood donor and recipient share HLA antigens.

Lab tests in Acute Intravascular Hemolytic Transfusion Reactions

Lab findings → hemoglobinuria, hemoglobinemia, and a haptoglobin level that is low to undetectable, bilirubin increases modestly, lactate dehydrogenase rises Direct Antiglobulin Test becomes positive in an immune hemolytic reaction (if tested before all the incompatible RBCs are destroyed) Antibody eluate is a procedure that chemically separates the bound antibody from the RBCs and concentrates it so it can be identified (looking for IgG antibody)

How does acute hemolysis occur during some transfusion reactions?

Leads to immediate hemolysis of RBCs due to the Abs causing lysis of the RBCs by activating the complement system, which releases proteolytic enzymes (lytic complex) that rupture cell membranes. Immediate intravascular hemolysis is far less common than agglutination followed by delayed hemolysis, b/c it requires there to be a high titer of Abs for lysis to occur and also a different type of Ab seems to be required (mainly IgM antibodies; these antibodies are called hemolysins)

Iron Overload

Liver, pancreas, cardiac dysfunction Iron deposition from multiple transfusions. Delayed afebrile reaction > 24 hours form transfusion

Allergic Transfusion Reaction

Localized or diffuse hives/ redness, angioedema, pruritus, hypotension, abdominal pain, emesis, poss anaphylaxis IgE mediated hypersensitivity to transfused protein. Mast cells are primary allergic effector cell for immediate hypersensitivity reactions. MOST COMMON Reaction <24 hours from transfusion

Clinical presentation of acute extravascular hemolytic transfusion reaction

Low grade fever, renal failure, shock and hemostatic abnormalities are rarely seen

Describe the morphology of hemolytic disease of the newborn

Mild = small increases in the rate of hemolysis is tolerated by fetus, at birth child experiences mild anemia and jaundice both of which may resolve without treatment Moderate = level of bilirubin low during pregnancy due to mothers ability to circulate blood but after birth immature liver is unable to keep up with demands Severe = Organs increase production of RBCs to compensate for loss, drive to produce RBCs causes liver and spleen to increase in size, ultimately fatal. Condition is fatal either in utero or soon after birth

Electrolyte toxicity

Mild circumoral paresthesias to frank tetany. Usually mild and self limiting. Citrate = component of the preservative solution used in blood storage, functions as an anticoagulant. Rapid transfusion of citrated blood is associated with a drop in ionized calcium levels. Risk mainly in patients with abnormal liver function.

An AB negative patient would be expected to make which naturally occurring antibodies?

NONE

Define Hemolytic Disease of the Newborn

Newborn's RBCs are being attacked by Ab from the mother. The attack begins while the baby is in the womb and is caused by an incompatibility between the mother's and baby's blood.

A donor implicated in a severe TRALI case may _____________________________.

Not donate any blood in the future

A trauma patient with severe bleeding presents to the ER. His type and screen reveals O negative blood type with no unexpected antibodies. What blood type would you ideally transfuse?

O negative

A trauma patient with severe bleeding presents to the ER. His type and screen reveals O negative blood type with no unexpected antibodies. What blood type would you ideally transfuse if all of the O negative was used up?

O positive

Why is ABO incompatibility not as bad as Rh?

One reason is the fetal RBCs express less of the ABO blood group antigens compared with adult levels. Additionally, in contrast to the Rh antigens, ABO blood group antigens are expressed by a variety of fetal (and adult) tissues, reducing the chances of anti-A and anti-B binding their target antigens on the fetal RBCs.

Which blood product is most likely to be associated with bacterial contamination?

Platelets

Delayed Afebrile Reactions (>24 hours from transfusion)

Post Transfusion purpura Iron Overload

After a whole blood donation, the blood is separated in to which three parts?

RBCs (packed cells) Platelets Plasma **Antibodies will still be present in the plasma

Describe Blood Typing

RBCs are first separated from the plasma and diluted with saline solution. One portion is mixed with anti-A agglutinin and another portion with anti-B agglutinin. After several minutes, the mixtures are observed under a microscope. If the RBCs have become clumped - one knows that an antibody-antigen reaction occurred

Bacterial Contamination or Transfusion Transmitted Reaction

Rapid high fever, rigors, shock, GI symptoms, DIC, renal failure, cardiac arrest. Bacteria in donor's blood or through collection site. Platelet concentrates stored at room temperature have the highest risk of contamination (usually pseudomonas). It is extremely difficult to tell by visual inspection if a unit is contaminated. *** Septic transfusions differ from acute hemolytic reactions by lack of characteristic hemoglobinuria and hemoglobinemia. Gram stain Reaction <24 hours from transfusion

What is true for TRALI?

Risk is reduced using male donors only

What is the genetic explanation of Rh blood types?

Six common types of Rh antigens (called Rh factor) C, D, E, c, d, and e A person who has a C antigen does not have the c antigen, but the person missing the C antigen always has the c antigen. The same is true for the rest of the combinations. Also, each person has one of each pair of antigens. Type D antigen is widely prevalent - and considered most antigenic - anyone who has this antigen is said to be Rh positive, whereas a person who does not have the type D antigen is said to be Rh negative 85% of white people = Rh positive 95% of "american blacks" = Rh positive 100% of "african blacks" = Rh positive

Storage of RBCs

Stored at 1 - 6C for up to 35 days using CPDA-1

Storage of Platelets

Stored at room temperature - up to 5 days with gentle agitation.

Hypothermia transfusion reaction

Subnormal body temperatures, ventricular fibrillation, coagulopathy Can occur with rapid infusion of large quantities of refrigerated blood. reaction <24 hours post transfusion

Discuss the pathogenesis of Hemolytic Disease of the Newborn

The first step is sensitization which normally occurs during the mother's first pregnancy (most likely in the circumstance of an Rh+ father and Rh- mother that is carrying an Rh+ child). Sensitization can occur near the end of pregnancy or during the birth of the child. If the child's blood ABO type is incompatible with the mothers, risk of sensitization decreases because the blood cells will be destroyed prior to any development of antibodies to the Rh+ part of the blood. When the mother's blood is exposed to Rh+ blood, it begins to develop antibodies. Initially, maternal and anti-D that is formed at the time of sensitization is of IgM which can not cross placenta. In subsequent pregnancies, a repeat encounter with the Rh D antigen stimulates the rapid production of type IgG anti-D which can be transported across the placenta and enter the fetal circulation. Once in the fetal circulation, anti-D attaches to the RhD antigens found on the fetal RBCs marking them to be destroyed.

Platelet Dosage:

The therapeutic adult dose is 1 unit of Apheresis Platelets or 4 to 6 units of whole blood-derived platelets, either of which usually contain ≥3.0 × 1011 platelets.

Describe platelet donation

They can be generated as part of a single whole blood unit (random donor) or as pheresis units from a single donor (comparable to 5-6 random donor units)

Which pregnancies are most at risk for Hemolytic Disease of the Newborn?

Those in which an Rh D - negative mother becomes prego with an RHD positive child; mothers response to the fetal D antigen is to form antibodies against it (anti-D). These Ab are usually of the IgG type, the type that is transported across the placenta and hence delivered to the fetal circulation. HDN can also be caused by an incompatibility of the ABO blood group → this occurs when a mother with blood type O becomes pregnant with a fetus with a different blood type (A or B or AB). Mother's serum contains naturally occurring anti-A or anti-B which tend to be of the IgG class and can cross the placenta and hemolyse fetal RBCs.

Signs of an allergic reaction

Urticaria, pruritis, flushing, angioedema

What is the most common transfusion reaction?

Urticarial

Indirect Coombs Test

Used in Prevention of HDN Finds anti-D antibodies in the mother's serum. If these were to come into contact with fetal RBCs they would hemolyse them and hence cause HDN. By finding maternal anti-D before fetal RBCs have been attacked, treatment can be given to prevent or limit the severity of HDN. For this test, mother's serum is incubated with Rh D-positive RBCs. If any anti-D is present in the mother's serum they will bind to the cells. The cells are then washed to remove all free antibodies. When anti-Ig antibodies are added, they will agglutinate any RBCs to which maternal antibodies are bound. This is called indirect Coombs test b/c the anti-Ig finds "indirect" evidence of harmful maternal antibodies - requiring addition of fetal RBCs to show capacity of maternal anti-D to bind to fetal RBCs.

Hemolytic Disease of the Newborn What happens? Why is it important? What's the downside?

What happens? During pregnancy, some of the mother's antibodies are transported across the placenta and enter fetal circulation. Why is this important? It is necessary b/c by the time of birth, newborns have only a primitive immune system and the continuing presence of maternal antibodies helps to ensure that they survive while their immune system matures. What's the downside? The mother's antibodies may target fetal RBCs causing HDN. Downside = by targeting fetal RBCs, maternal Ab can also cause HDN

Describe the Agglutination Process in Transfusion Reactions

When bloods are mismatched (anti-A or anti-B plasma agglutinins are mixed with RBCs that contain A or B agglutinogens, respectively) RBCs agglutinate as a result of the agg attaching themselves to the RBCs/ B/c the agg have 2 binding sites (IgG type) or 10 binding sites (IgM type) a single agglutinin can attach to two or more RBCs at the same time thereby causing the cells to be bound together by the agglutinin. Agglutination → process by which cells are bound and clump together due to the attaching of agglutinins to RBCs Following this process, physical distortion of the cells or attack by phagocytic WBCs destroys the membranes of the agglutinated cells, releasing hemoglobin into the plasma which is called hemolysis of RBCs.

Describe the development of agglutinins

When type A agglutinogen is not present in a person's RBCs, antibodies known as anti-A agglutinins develop in the plasma. Also, when type B agglutinogen is not present in the RBCs, antibodies known as anti-B agglutinins develop in the plasma.

Agglutinin

an antibody, lectin, or other substance that causes agglutination.

Agglutinogen

an antigen that stimulates the production of a particular agglutinin, such as an antibody.

Major Cause of HDN

incompatibility of the Rh blood group between the mother and fetus. Most commonly, hemolytic disease is triggered by the D antigen, although other Rh antigens such as c, C, E, and e can also cause problems.

Define Acute Extravascular Hemolytic Transfusion Reaction

type of transfusion reaction in which the donor's RBCs are recognized and bound to IgG antibodies; this presentation is usually associated with Rh antibodies but can be seen with any number non-ABO antigen antibody complexes.

Define Acute Intravascular Hemolytic Transfusion Reaction

type of transfusion reaction that occurs during or immediately after incompatible RBcs are transfused into a patient who already possesses the corresponding antibody. Ex. ABO incompatible RBC transfusion

Each unit of cryoprecipitated AHF should contain ...

≥80 IU Factor VIII and ≥150 mg of fibrinogen in approximately 5 to 20 mL of plasma