Transfusion Reactions

define adverse transfusion reaction

an undesirable response or effect in a pt following a blood/blood product transfusion

what are the top causes of transfusion-associated fatalities

1. TRALI (transfusion related lung injury)

2. TACO (transfusion associated circulatory overload)

3. non-ABO hemolytic transfusion reaction

4. microbial infections

5. ABO hemolytic transfusion

6. anaphylactic reactions

the majority of transfusion-associated fatalities are due to

TRALI (transfusion related lung injury)

what are some clinical features that may be present in pts who are having an adverse transfusion reaction?

• fever increase > 1 deg C or a fever > 38 deg C

• chills & rigors

• signs of respiratory distress (wheezing, coughing, cyanosis, dyspnea)

• HTN or hypotension

• pain (abd, chest, flank or back, at the infusion site)

• rash, flushing, edema, urticaria

• jaundice or hemoglobinuria

• N/V

• abnormal bleeding

• oliguria or anuria

• decreased H&H with spherocytes

which of the following is NOT a sign of an adverse transfusion reaction?

• fever > 101 deg F

• wheezing

• excessive urination

• vomiting

excessive urination (you would start peeing less)

what is the etiology of an acute transfusion reaction

happens immediately and upon first exposure to incompatible units

what are the most common symptoms of an acute HTR

fever with or without chills

hemoglobinuria

what is the incidence of AHTR

1:50K transfusions

what is the progression of AHTR

1. pt antibody binds to donor RBCs in vivo

2. complement activated → direct lysis and anaphylatoxin release (IgM mediated) causes intravascular hemolysis and HYPOtension

3. activation of phagocytes that release cytokines (IgG mediated) causes extravascular hemolysis and fever

4. RBC lysis and release of free Hgb causes a decrease in haptoglobin

5. coagulation cascade activated causes DIC

6. shock and renal failure

the most common signs of AHTR are

fever & hemoglobinuria

what is the etiology of a delayed hemolytic transfusion reaction

pt antibodies directed to donor RBC antigens bind to donor RBC membrane

• typically complement is NOT activated or not activated COMPLETELY

• pts will present days to weeks after transfusion

• other symptoms include jaundice, leukocytosis, hemoglobinuria

• often seen in multiply transfused pts (sickle cell, thalassemia)

what is the progression of DHTR

1. antibody and complement binds to RBC in vivo

2. activation of phagocytes that release cytokines (IgG mediated) → extravascular hemolysis

3. reduction in H&H and haptoglobin. Spherocyte formation and hemoglobinuria

when does DHTR typically occur

when a preformed antibody is NOT initially present at significant titer and has an anamnestic response

OR

patient makes a new antibody fast enough to bind to transfused RBC

what is the incidence of DHTR

1:10K transfusions (more common)

H&H is reduced in DHTR because

antibody/complement bound RBCs are removed by the body

what are 3 common causes of non-immune RBC destruction

1. pt has an underlying hemolytic disorder

2. inadequate deglycerolization after freezing

3. physical damage to donor RBC’s

what are some examples of physical damage to donor RBCs that can occur

• overheating

• incompatible fluids being infused at the same time

• excessive pressure/infusion rate

• bacterial contamination

which of the following is NOT a cause of non-immune RBC destruction

• physical damage to RBCs

• underlying hemolytic disorder

• inadequate deglycerolization

• frostbite

frostbite

what are some key differences between AHTR and febrile non-hemolytic transfusion reaction (FNHTR)

no hemolysis

negative DAT

(there is an increase in temp. but you must rule out AHTR)

what is FNHTR caused by

• transfused cytokines

• cytokine released from recipient in response to transfused WBC

• antibodies targeted at transfused WBC

how is FNHTR prevented

using leukoreduced units

which of the following is symptoms of FNHTR

• temperature increase

• positive DAT

• hemolysis

• positive IAT

temperature increase

what causes transfusion-associated allergic reactions

factors present in donor PLASMA

what are the 2 forms of transfusion-associated allergic reactions

1. urticarial - IgE mediated hypersensitivity to an allergen in the donor plasma (mast cells)

2. anaphylactic - non IgE mediated mast cell degranulation (typically caused by IgA)

what are some clinical manifestations of urticarial allergic transfusion reactions

urticaria (hives) & pruritus (itching)

what usually causes anaphylactic allergic transfusion reactions

pts who are IgA deficient in plasma have anti-IgA that binds to donor IgA

what are some clinical manifestations of anaphylactic allergic transfusion reactions

start out with GI issues followed by urticaria, angioedema, hypotension, and eventually shock

how are anaphylactic allergic transfusion reactions treated

immediately with epinephrine & maintaining the airway/appropriate blood pressure

anaphylactic transfusion-associated allergic reaction is

typically caused by IgA

TRALI is typically caused by

incompatible FFP (but it can happen with any PLASMA containing component)

what is the running theory of how TRALI occurs

1. HLA antibodies activate neutrophils in pulmonary circulation

2. activated neutrophils cause damage to pulmonary epithelial cells

3. pulmonary edema forms

AABB standard requires plasma donors to be:

• male

• have never been pregnant OR have been pregnant without HLA antibodies in their plasma

what are some signs and symptoms of TRALI

• symptoms onset ~6 hrs after transfusion

• hypoxemia ( <90% on room air)

• no evidence of L atrial hypertension

• bilateral infiltrates on chest radiograph

what is transfusion associated circulatory overload (TACO)

large volume of blood is too much for patient to handle/process

what are some symptoms of TACO (at least 3 of them need to be present within 6 hrs of transfusion)

• acute respiratory distress

• elevated BNP

• elevated central venous pressure

• evidence of L heart failure

• evidence of (+) fluid balance

• radiographic evidence of pulmonary edema

how do you prevent TACO

use pRBC units only and slower rate & lesser volume aliquots

what is the main difference between TACO and TRALI

fever commonly occurs in TRALI

what is not an indicator of TACO

• acute respiratory distress

• left heart failure

• pulmonary edema

• fluid on the brain

fluid on the brain