BB II Unit #3

An ATHR is most often caused by what type of incompatibility?

ABO and as little as 10mL

Sequence of events in AHTR

Ab binds to RBC, activation of complement forming MAC, activation of phagocytosis and cytokines, activation of coagulation, shock/renal faliure

Intravascular Hemolysis

Complement fixed by IgM, Schistocytes, Marked hemoglobinuria, and acute onset

Extravascular Hemolysis

Macrophages in liver/spleen, IgG. Spherocytes, Minimal, Acute or delayed

Common preventable cause of ABO-incompatible AHTR

wrong draw, mislabeled tube, issuing wrong unit. Strict bedisde labeling and patient id safeguard prevent this

Why is a DAT neg duirng AHTR

Donor cells were rapidly destroyed and cleared

Define FNTHR criteria

Greater than 1C rise in temperature. Occurs by transfused leukocyte stimulating cytokine or pyrogenic cytokine in plasma of stored components

Leukoreduction

removes leukocytes responsible for triggering cytokine release and HLA Ab rxn that causes FNTHR

FNHTR PLT

storage requires constant agitation that activates and releases cytokine

Why must FNTHR be a diagnosis of exclusion

It must be separated from AHTR, TRALI, and septic rxns b/c they all present with fever

What type of hypersensitivity underlies allergic transfusion rxn?

Type I with IgE binding to mast cells and basophil releasing histamine

Mild (Urticarial) Reaction

Pruritis, rash, hives. Within minutes of transfusion, Only clerical check needed. Antihistamine with or without steroid to treat

Severe/Anaphylactic Reaction

Uticaria and angioedema, respiratory distress, cardiac distress. Typically early within transfusion. Needs full workup. Antihistamine, steroid, epinephrine to treat.

Explain the traditional IgA deficiency to severe anaphylactic reaction?

It was attributed to IgA deficient patients who formed Anti-IgA and then received a plasma component with IgA

A patient has confirmed history of anaphylatic transfuiosn reactions what blood modifications should be made?

Washed cellular components or IgA decreased plasma/cryopercipitate

What are the two leading causes of transfusion associated death in the US?

TACO and TRALI

TRALI - immune response

During transfusion or within six hours, present, hypotension, normal BNP, no improvement with diuretics, Bat wing chest X-ray, Donor anti-HLA activate neutrophil

TACO - Transfusion circulatory overlaod

During transfusion or within twelve hours, absent, hypertension, elevated, Improves with diurectics, Enlarged herat. Volume overload

What donor-eligibiilty requirements reduce the risk of TRALI

Blood products from donor who has never been pregnant (or have tested neg for anti-HLA since pregnancy)

Which blood component is most frequently implicated in bacterial infections

PLT b/c they store at RT

Describe the findings that correlate with bacftieral contamination

Visually inspect unit for clots, cloudiness, or disocloration. Gram stain and culture the unit

What two donor practices help prevent bacterial contamination of blood products?

Disinfection of donor skin prior to venipuncture and diversion of first 10mL away from final blood component.

PLT must undergo mandatory bacterial detection

List four nonimmune causes of red cell hemolysis

exposure to extreme temps, mechanical destruction, wrong IV, improper deglycoerolization of frozen RBC, intrinsic RBC defects

Does a DAT rule out a hemolytic transfusion rxn?

No, sensitized cells may have already been destroyed so nothing is left to detect

AHTR

less than 24 hours onset. ABO incompatibility. IgM. Intravascular. severe or fatal. DAT pos (may be neg if cells destroyed)

DHTR

greater than 24 hours onset. Response after alloimmunization (Rh, Kidd, Duffy, Kell, MNS). IgG. extravascular (kidd=intravascular). less severe. newly positive DAT

DHTR

hemolytic reaction days-weeks after immune response, previously sensitized

DSTR

new serologic finding of alloantibody with no hemolysis

Which blood group systems are most commonly implicated in DHTR/DSTR

Rh, Kidd, Duffy, MNS

Why are Kidd Ab especially tricky?

Ab titers fall quick and often become undetectable and can cause both intra and extravascular hemolysis

What are clinical signs of DHTR?

fever, fatigue, jaundice. No rise in hemoglobin. Sphereocytes in PB

Why is a DAT typically positive in a mf patient?

agglutination of sensitized donor cells mixed with non-reactive autologous cells

A DAT is pos, why is an elution preformed?

Eluate concentrates the Ab that may reveal specificity not detectable on plasma

DHTR Lab Workup

clerical check, DAT, repeat Ab screen/panel, elution on pos DAT, Ag typing, repeat testing on segments

What type of RBC product should be selected for future transfusions in a patient who experienced DHTR/DSTR?

Red cells that are neg for Ag corresponding to identified Ab. Keep records to prevent future problems (eventually Ab will become undetectable again)

Define bystander hemolysis

Destruction of patients own Antigen neg RBC. Ab screen/DAT can be neg making it easy to miss. Symptoms mimic vaso-occlusive pain crisis.

Explain pathophisiology of TA-GVHD

Immunocompetent donor lymph are transferred into immunologically incompetent recipient or close HLA match. Recipient cant mount immune response. Donor cells proliferate and kill patient tissues (bone marrow failure)

Describe the clinical presentation of TA-GVHD

Highly lethal (90%). Symptoms after 2days to 6weeks. Rash starts on trunk. Fever, diarrhea, pancytopenia, and increased liver enzymes

Why is a recipent who is HLA similar to the donor at risk for TA-GVHD

When donor is HLA similar the recipient immune system does not recognize them as foreign but the donor lymphs do

How does irradiation prevent TA-GVHD?

inactivates donor lymphs with minimum of 25gy to central container and 15gy elsewhere

Are leukocyte-reduced components sufficient to prevent TA-GVHD?

No. reduction does not remove all lymph and does not inactive their ability to engraft

What blood component does not need to be irradiated and why?

Fresh frozen plasma/Frozen plasma. The freeze-thaw inactivates lymps

Why do fresh cellular components carry higher risk of TA-GVHD?

Over time cells undergo apoptosis. In a fresh sample less cells have undergone apoptosis.

Define hemosideroisis and three pt population at risk

iron overload from chronic transfusions. Thalassemia, myelodysplastic syndrome, sickle cell

Why does chronic transfuions lead to iron overload?

Each RBC unit contains 200-250mg of iron. While the body can only excrete 1-2mg a day. Humans lack a mechanism to excrete excess iron so it deposits in tissues

Which organs are damaged by transfuional iron overload, and which complication is a leading cause of death?

Liver, heart, and endocrine glands. Iron-overload cardiomyopathy

What is the role of iron chelatin therapy?

Chelator bind excess iron so it can be excreted in stool/urine. Preventing organ damage from iron toxicity

Name two chelatin agents

Deferoxamoine and deferiprone

Besides chelatin, what transfusion strategy can reduce the net iron burden?

exchange transfusion

How does hemosiderosis differ from an AHTR?

it is chronic and develops over many transfuions taking months to years. No immune response is present

Define PTP and describe the typical timing and presentation?

sudden servere drop in PLT within 2 weeks. Generalized purpura and increased bleed risk

Explain the mechanism of PTP

High incidence PLT-Ag HPA-1A in an HPA-1A neg patient. Classically women sensitized during pregnancy. Destroys BOTH donor and autologous PLT

What is the recommended management of PTP?

IVIG, pasmaphresis, or exchange transfusion

Why does PLT transfusion not work with PTP?

All PLT are being destroyed. Adding more does not do anything

What is the National Hemovigilance Model (NHSN)?

confidential, voluntary surveillance system with cooperation of AABB and CDC which track transfusion rxn.

NHSN Type

Reaction category

NHSN Severity

Grade of severity from non-severe to fatal

NHSN Imputability

Likelihood product caused rxn and not from other factor

What must a transfusion service do with the records of a patient who has experienced adverse transfusion rxn?

Retain them indefinitely

A suspected transfuion reaction death occurs. According to FDA what must the facility do?

Report to FDA within 7 days and file investigational report

What additional reporting responsibilities exist beyond FDA? (Joint Comission)

Cases of transfusion related disease or bacterial contamination

Which type of transfusion complication poses a greater risk to patients today? Infectious or non-infectous.

noninfectious (TACO, TRALI, hemolysis)

What two types of donor testing are performed on every donation for HIV, HBV, and HCV?

Serologic and Nucleic Acid Testing (NAAT)

Define the window period

interval between donor infection and detectable identification of the infection. Donors can slip through and pass tests

What is the purpose of a donor questionnaire?

It acts as a safeguard for those who may be in the undetectable window period

Name other infectous agents or conditions for which donor screening may be performed in addition to HIV, HBV, and HCV

West Nile, Zika, Trypsomona cruzi, syphillis, HTLV, bacterial detection on PLTs

Describe the look-back process?

It is triggered when a donor's subsequent donation tests reactive for a transfusion-transmissible infectious marker. The collecting facility reviews the donor's prior donations, notifies the transfusion services that received components from those donations, and (per protocol) recommends notification and testing of the recipients of the earlier, potentially infectious units.

What is the transfusion services role when they receive a lookback notification?

Review test results on the donor blood for infectious disease markers or test the patient sample as suggested by clinical symptoms; report positive/reactive results to the physician, the blood supplier, and the appropriate regulatory agency; and perform the look-back procedure per facility SOP

Define emergency release of blood

the release of blood components before pretransfusion compatibility testing is complete. The physican determines the risk of delaying transfusion is greater than the risk of mismatched blood

Three clinical situations that could require emergency release of blood

Life-threatening hemorrhage

Recipient testing is incomplete

Incompatible crossmatch with no time to resolve

Why are Group O Dneg units reserved for females of childbearing age and children in emergencies?

Alloimmunization to the D antigen can cause HDFN in future pregnancies. Males and postmenopausal females have no future pregnancy risk

Why must a T/S sample still be collected from a patient receiving emergency-released units?

It must be collected before the transfusion begins. This allows the blood bank to transition the patient to crossmatch-compatible units as soon as possible

What are the two criteria that determine a MTP?

replacement of a patients total blood volume within 24 hours (roughly >10 RBC units)

Or 4 units transfused within 4 hours (hemorrhaging patient)

Volume Overload

From sheer volume of fluid and blood components infused rapidly

Hypocalcemia

Citrate anticoagulant chelates ionized calcium as its rapidly infused. Impaired citrate metaboilsm worsens it. Depresses cardiac function and worsens hypocoagulable state

Hypothermia

From rapid transfusion of cold components. Use blood warmers to prevent cardiac arrythmia

Acidosis

Related to citrate metabolism. Increases the risk of hyperkalemia as H+ enters cells and K+/Na+ shift into plasma

Hyperkalemia

From rapid transfusion of RBC units nearing their outdate (leaked intracellular potassium).

Dilutional Coagulopathy

PLT and coagulation factors are diluted as large volumes of RBC are transfused. This is why plasma and PLT are also transfused during MTP

Hemoglobin S-negative (sickle neg) units

Patients with sickle cell disease, they are not given donor red cells that are themselves functionally compromised

CMV-neg untis

CMV-seronegative pregnant patients, intrauterine/neonatal transfusion, and certain immunocompromised or transplant patients

Irradiated Units

Patients at risk of TA-GVHD

Washed Units

Patients with history of severe allergic/anaphylactic transfusion reactions (IgA deficent patients)

Why might more RBC units be needed during an MTP than expected to restore a patients O2 carrying capacity?

Stored RBC have low 2,3-BPG, so more units may be needed than a simple calculation suggests

Which blood component is the primary concentrated source of fibrinogen?

Cryoprecipitate

What is the MTP target goal of cryopercipitate?

Greater than 100

Do plasma, PLT, and cryopercipitate typically require a XM before transfusion?

No. They contain little to no red cell. Pooled PLT and granulocyte concentrates require a XM if the unit contains more than 2mL of red cell

Red Blood Cells (RBC)

Restores oxygen carrying-capacity, the core component replaced in significant hemorrhage

Plasma

Contains coagulation factors. ABO compatibility is based on antibody content

Platelets

Primary hemostasis (clot formation), can be pooled or single donor/aphresis

Cryopercipitate

Concentrated source of fibrinogen, factor VIII, von Willerbrand factor, and factor XIII

Recombinant Factor VIIa

Adjunct hemostatic agent from pharmacy used when bleeding isnt controlled by replacement alone