Transfusion Medicine - Karafin Flashcards
- Minimum age to donate blood?
- Minimum interval for whole blood donation?
- How much blood is taken?
- 16 years old
- 8 weeks
- 500 +/-50 mL
What H&P findings are noted before a potential donor is allow to give blood?
- Vitals
- General appearance & that of venipuncture site
- Medical history
-
Hemoglobin level
- >12.5 (don’t need to know)
Name three blood products derived from donated whole blood.
- Red cell components
- Platelet components
- Plasma
Name four preservative compounds added to blood products to maintian the viability and function of cells, and what they do.
- Citrate
- Anticoagulant
- Phosphate
- Maintains 2,3-DPG levels
- Dextrose
- For cell metabolism
- Adenine
- For ADP/ATP production
- What happens to RBCs in storage over time?
- What causes these effects?
- How long do they last in storage before needing to be thrown out?
- Change in shape - membrane blebbing, spherocytosis
- Decrease in ATP, 2,3-DPG, & pH. Increased K+. Increased iron. Increased ROS.
- ~42 days
What are the three main components of processing/testing done on donated blood?
- Infectious disease testing
- ABO and Rh typing
- Antibody screening
What infectious agents are tested for in blood products?
What infection does a blood product recipient have the greatest risk of acquiring from the product?
- Hep B - greatest risk, currently at 1: 292,000 units
- Hep C
- HIV
- HTLV
- Syphilis
- West Nile
- Trypanosoma cruzi
All of the agents aside from Hep B have current risks less than 1: 1,000,000
[Yes, this was emphasized.]
Who discovered the ABO blood grouping system and when?
K. Landsteiner, circa 1900
In the ABO system, red cells and plasma follow (the same / opposite) rules of who can donate to whom. Therefore, the universal red cell donor is (Type O/Type AB), and the universal plasma donor is (Type O/Type AB).
Opposite.
The RBCs display the ABO antigens, while the plasma contains the antibodies.
Thus, Type O is the universal red cell donor (cells display no immunogenic antigens).
Type AB is the universal plasma donor (plasma contains no anti-A or anti-B Abs.)
When someone is said to be Rh+, what antigen in specifc is being referred to?
Rh Antigen D.
D is the most important antigen as it is highly immunogenic, with an 80% sensitization risk with exposure.
Its presence/absence determines if a person is Rh+/Rh-, respectively.
Name two ways in which an Rh- individual would develop Rh Abs, and the condition that could result in each of those circumstances.
- Pregnancy
- Hemolytic disease of the newborn - Abs cross the placental barrier
- Transfusion
- Hemolytic transfusion reaction
Name some other blood group systems.
How are they tested for?
[Likely not important to memorize.]
- KELL
- DUFFY
- KIDD
- MNSs
- Lewis
- Lutheran
Tested for via antibody screening.
- What is the purpose of an Indirect Antiglobulin Test (IAT)?
- How is the test done?
- The IAT is used for Compatibility Testing (also RBC testing, Ab detection & ID). For compatibility purposes, it detects antibody in the patient’s serum.
- Protocol (Compatibility):
- The recipient’s serum is combined with donor RBCs.
- If the serum contains anti-RBC Abs, they will bind the red cells.
- A anti-isotypic secondary Ab is added that will bind the serum antibodies, if present, as well as cause aggregation and precipitation of the RBCs if they are donor Ab-bound.
- A visible precipitate of RBCs is a positive test and indicates the donor’s plasma and recipient are incompatible.
- The recipient’s serum is combined with donor RBCs.
How can the IAT protocol be modified to act as an Ab screen, aka, detect antibodies within a patient’s serum?
- Test cells of a known phenotype (i.e., cells that express antigens for the suspected antibodies) with the patient’s serum.
- What is the purpose of a Direct Antiglobulin Test (DAT)?
- How is the test done?
- The DAT is useful for detecting **autoimmune-, drug-, or transfusion-induced hemolytic anemia **that is occuring in a paitent. It detects Ab attached to red cells in vivo.
- Protocol:
- Similar to the IAT, except here the “donor” Abs (which may indeed be from a mismatched donor, or could be autoimmune- or drug-induced) are already present on the patient’s red cells!
- Simply add an anti-isotypic secondary Ab to a sample of the patient’s blood. If anti-RBC Abs are present on the red cells, they will precipitate out of solution, producing a positive test result.
Name four causes of a positive DAT.
- Autoimmune hemolytic anemia
- Drug-induced hemolytic anemia
- Hemolytic transfusion reaction
- Hemolytic disease of the newborn
Describe the steps of pre-transfusion testing that should occur to ensure matched donor and recipient.
- Acquire Pt blood sample: ABO typing & Ab screen
- Ab screen neg: Select ABO compatible product
- Ab screen pos:
- Rub Ab ID panel
- Select ABO compatible, antigen-negative product
- Perform crossmatch
- Testing the **specific blood unit you chose **with the patients blood to double check for compatibility.
- Issue product
Whole Blood
- How much does a unit contain?
- How long does a unit last?
- In what conditions is it indicated?
- What is the expected outcome?
Whole Blood
- 500mL
- 35 days
- Hypovolemia with decreased O2 carrying capacity
- Raise Hb 1g/dl in an average adult
Red Blood Cells
- How much does a unit contain? What’s the Hct of the unit?
- How long does a unit last?
- In what conditions is it indicated?
- What is the expected outcome?
Red Blood Cells
- 300mL, Hct 55-60%
- 42 days
- Symptomatic anemia in normovolemic patient
- Raise Hb 1g/dl in an average adult
What do the results of the TRICC trial indicate regarding RBC transfusion in the critical care setting?
[Adapted from 2 Minute Medicine - http://tinyurl.com/mpetnvm]
- Using a restrictive [Hb kept at 7g/dl] transfusion strategy in critically ill patients did not significantly increase 30-day mortality when compared with a liberal [Hb kept at 10g/dl] transfusion strategy.
- Subgroup analyses demonstrated that a restrictive transfusion strategy was associated with significantly lower mortality in patients with APACHE II [ICU mortality risk calculator] score ≤20 and age <55 years.
Generally, at what Hb level is RBC transfusion useful (or necessary)?
- 8-10g/gl: avoid, consider a transfusion “trial”
- 6-8g/dl: give transfusion if necesssary
- <6g/dl: typically requires transfusion
Fresh Frozen Plasma (FFP)
- How much does a unit contain?
- How long does a unit last?
- In what conditions is it indicated?
- What is the expected outcome?
Plasma
- 200-250mL
- 1 year
- 10-15mL/kg raises all clotting factors by 20-30% in average adult
- Indications:
- Abnormal bleeding w/ documented coagulopathy
- Multiple factor deficiency
- DIC
- Surgical prophylaxis in pt w/ coagulopathy
- Therapeutic plasma exchange for TTP (?)
Name three treatments that FFP is not indicated for.
- Volume expansion
- Reversal of heparin
- Correction of minor PT prolongation
Cryoprecipitate
- What blood product is it derived from?
- How long does a unit last in storage?
- How much is in a unit?
- What does it contain? What’s considered most important?
- What is the expected outcome?
- FFP
- 1 year
- 15ml/unit
- Contents:
- Fibrinogen - most important.
- Factors VIII & XIII
- vWF
- Fibronectin
- 1 unit/10kg will raise fibrinogen by 50mg/dl in an average adult.
Cryoprecipitate
When is it indicated?
When is it not indicated?
- Indications:
- Hypofibrinogenemia / Dysfibrinogenemia
- DIC
- Severe liver disease
- Congenital
- Trauma w/ massive transfusion
- Hypofibrinogenemia / Dysfibrinogenemia
-
Not indicated:
- Hemophilia A
- VWD
What’s the goal level of fibrinogen in cryprecipitate therapy?
>150mg/dl
What are the two types of platelet transfusion products?
- Random Donor platelets
- Single Donor Apheresis platelets
- Concentrated platelets
What differentiates the “old” and “new” methods of obtaining concentrated platelets?
The apheresis technology allows for more effective harvesting of viable platelets from a single donor. One unit of apheresis platelets is equivalent to a “six-pack” of whole blood-derived platelets.
Platelets (any kind)
- How are the platelets seperated?
- How are they kept and for how long?
- What is the goal outcome?
- Centrifugation of whole blood or apheresis
- Room temperature with agitation. Shelf life is only 5 days!
- Raise PT count 30,000-60,000 in an average adult
Name four scenarios for which prophylactic PT transfusion is useful?
- Bone Marrow Failure (Aplastic Anemia)
- Surgery Prophylaxis
- Platelet inhibitory drugs (an overdose/overshoot, I assume)
- Congenital platelet dysfunction
At what PT level should you consider prophylactic PT transfusion in a marrow failure pt?
- 10-20K: Transfusion reasonable
- <10K: Transfusion indicated
An NEJM article showed that as long as PT levels are maintained over _______, the incidence of significant bleeding does not decrease with further PT administration.
6-10 x103/mm3
[Totally realistic clinical scenario…]
You’ve given your pt a PT infusion and are monitoring his PT count hourly. Worryingly, at no point over the next 24 hours does his platelet count seem to increase at all! What do you suspect?
An antibody-related response that is destroying the platelets
Name 5 possible immediate adverse effects of transfusion.
Which 2 are most common?
Which is the #1 cause of mortality in transfusions today?
- Hemolytic transfusion rxn
- (“Benign”) Febrile Non-hemolytic rxn - 2nd most common, ~28%
- Hives and other allergic rxns - most common, ~64%
- TACO (mortality also significant)
- TRALI - #1 cause of transfusion mortality
Name 4 possible **delayed **adverse effects of transfusion.
- Delayed hemolytic transfusion rxn
- Post-transfusion purpura
- Post-transfusion GvHD
- Iron overload
How common is TRALI? TACO?
- TRALI: 1 in 5,000
- TACO: 1 in 1,000
- Orders of magnitude more likely than an infected blood product
- What causes a febrile non-hemolytic transfusion reaction (FNHTR)?
- When does it occur relative to the transfusion?
- How common is it?
- Abs in recipient to the donor’s WBCs
- Activation of recipient’s macrophages, which produce endogenous BRMs (biological response modifiers - aka immune system activation)
- Plus BRMs that may be present from the donor WBCs
- At the end of transfusion, ~1-2 hours in
- **Common! **About 1:200 transfusions. 6-10% of the multitransfused population.
What are the signs and symptoms of FNHTR?
- Fevers (at least 1C elevation)
- Chills / Rigors
- HTN
- Tachycardia
- SOB
[KNOW THIS]
A hemolytic transfusion reaction results in RBC destruction in the recipient, as the name suggests.
- What causes acute hemolytic reactions?
- When does it occur relative to transfusion?
- Where does the hemolysis occur in acute reactions?
- What causes delayed hemolytic reactions?
- When does it occur relative to transfusion?
- Where does the hemolysis occur in delayed reactions?
-
Acute = ABO mismatch
- 1-2 hours after start of transfusion
- mainly Intravascular hemolysis
-
Delayed = Abs (not detected w/ Ab screen or cross match)
- 5-7 days after transfusion
- mainly Extravascular hemolysis
What are the signs and symptoms of acute hemolytic transfusion reactions?
- Fever
- Chills / Rigors
- Anxiety / Feeling of Doom
- “Trunk” pain (Chest, Abdomen, Flank, and/or Back)
- Nausea / Vomiting
- Dyspnea
- Hypo- & Hypertension
- Pain at infusion site
- Hemoglobinuria / Oliguria
Name signs and symptoms of an IgE-mediated transfusion reaction in the following systems [probably just have a general idea of these]:
- Skin
- Respiratory
- GI
- CV
- Skin
- Itching
- Hives
- Flushing
- Angioedema
- Respiratory
- Bronchospasm
- Wheezing / Stridor
- Check tightness / pain
- Dyspnea
- Cyanosis
- GI
- Nausea / vomiting
- Diarrhea
- Cramps
- CV
- Hypotension / Shock
- Tachycardia
- Arrhythmias / Arrest
- What does TRALI stand for?
- What is TRALI mediated by?
- Describe its pathogenesis?
- What is the “two-hit hypothesis” for TRALI?
- Transfusion-Induced Acute Lung Injury
- Donor Antibody-mediated
- HLA Abs
- anti-Neutrophil Abs
- (Wiki) Leukoagglutination [due to Ab binding] and pooling of granulocytes in the recipient’s lungs may occur, with release of the contents of leukocyte granules, and resulting injury to cellular membranes, endothelial surfaces, and potentially to lung parenchyma.
- In pts where neutrophils are already “primed” towards activation (first hit - surgery, sepsis, etc.), agglutination by the anti-neutrophil antibodies (second hit) will produce greater activation and more severe TRALI.
What are the signs and symptoms of TRALI?
- Pulmonary edema w/o heart failure
- ARDS
- Hypoxemia / Cyanosis
- Tachycardia / Hypotension
- Fever
- pO2 < 90mmHg with room air
When does TRALI occur relative to transfusion?
- Virtually always within 6 hours
- Usually within 2 hours
What causes Graft vs. Host Disease (GvHD?)
- Immunocompetent lymphocytes in donor blood (or other graft) recognize the recipient as foreign.
- Recipient’s immune system cannot recognize/react to the donor’s lymphocytes due to:
- HLA similarity (the relationship happens to work one way but not the other)
- Recipient is immunosuppressed
What are the signs and symptoms of transfusion-induced GvHD?
When do they occur relative to transfusion?
How lethal is it?
- Sxs:
- High fever, followed by diffuse rash for about 3 weeks post transfusion
- Nausea / vomiting / watery diarrhea
-
Pancytopenia
- Distinguishes transfusion-induced GvHD from BMT GvHD!
- >90% mortality!
Who is at highest risk of transfusion-induced GvHD?
The Immunosuppresed
- SCID
- BMT recipients
- Fetus or neonate
- High dose chemo ptr
