Transfusions + Blood bank - POM/DA Exam 1

Why transfusion

-RBC improve O2 carrying capacity to organs and tissues

-stop or prevent bleeding

-blood can be used as replacement fluid in therapeutic apheresis tx

Avoid transfusions

-specific coagulation factor concentrate vs plasma

-treatment of underlying condition may be sufficient

-patient may not have any symptoms

-transfusion rxns are always possible

Blood Products

-packed RBCs

-platelets

-plasma

-cryoprecipitate

-whole blood

-others - often not routinely available (granulocytes)

Packed Red Blood Cells

-Dose: 1 unit = adult dose, 10-15 mL/kg = pedi

-multiple units for RBC exchanges or massive transfusion protocols

-adult effect: increases Hb 1g/dL and hct 3%

-ped effect: increases Hb 2-3 g/dL and HCt by 6-9%

Packed RBC - Indications

-Active bleeding

-symptomatic severe anemia

-transfuse a hemodynamically stable, adult inpatient when Hb <7.0 g/dl, a higher threshold nay be clinically indicated

Packed RBC - Contraindications

-someone who refuses blood

-rare blood types or chronic anemias (eval by hematologist/transfusion med specialist)

-do not give when better treatment available

-look at the patient

Platelets Dose and Effect

-Adult Dosing: 1 unit apheresis PLTs = 5-6 pooled whole blood derived PLTs

-Ped dosing: 10-15 mL/kg

-Effect: 1 dose increases PLTs by 25-50 x 10^3/uL

Platelets Indications

-stable, non-bleeding inpatient, give PLTs when PLT count <10x10^3/uL

Otherwise:

-central line placement (PLTs <20x10^3 uL)

-LP, surgery, deep biopsies (PLTs <50x10^3/uL)

-Neurosurgery, ophthalmic procedures (PLT <100 X 10^3/uL)

-platelet dysfunction

-massive transfusion protocl

Platelets CI

-treat underlying condition

-thrombotic thrombocytopenic purpura (more thrombi caused)

-immune thrombocytopenic purpura (only if actively bleeding give PLTs)

-heparin induced thrombocytopenia (more thrombi caused)

Plasma Dose and Effect

-Dose: 10-15 mL/kg

-Effect: 1 dose increases coag factors by 30%, most units are frozen, thawed, then transfused

Plasma Indications

-large volume blood loss

-used in some therapeutic apheresis procedures

-limited role in non-dilutional coagulopathies (DIC when bleeding, coag factor deficiency when no factor concentrate available)

Plasma CI

-repeat, severe allergic/anaphylaxis to plasma transfusion

-Anti-IgA antibodies w/ IgA deficiency (need IgA deficient plasma)

Plasma Alternatives

-factor concentrates --> factor deficiency

-cryoprecipitate (fibrinogen deficiency)

-intraoperative topical products --> fibrinogen glue

-alternative meds --> antifibrinolytics

Cryoprecipitate

-derived from fresh frozen plasma (fibrinogen, factor VIII, and other clotting factors)

-standard dosing: 10 pooled units (2 packs, adult)

Cryoprecipitate Indications

-fibrinogen deficiency in bleeding patients

-rarely used in uremic patients or rare factor deficiency patients

Cryoprecipitate CI

-do not use if factor concentrate is present

-limited role in bleeding patients without fibrinogen deficiency

Pre-transfusion Typing

-ABO type

-Rh type

Pre-transfusion Screening

-RBC antibody screen, rule out antibodies to minor RBC antigens

-if positive --> antibody identification

Pre-transfusion Cross-match

-virtual vs full

-incompatible transfusions can be fatal

Forward ABO type

-what's on patient's RBCs

-Reagent Anti-A and Anti-B are used

-positive rxns = type of RBCs patient has

Reverse ABO type

-what's in the patient's plasma

-reagent A cells and B cells are used

-positive Rxn = opposite to type of RBCs the patient has

Universal Donors

-packed RBCs from group O donors can be transfused to any ABO type

-Group O has NO ABO antigens to cause incompatibility

ABO type

plasma and platelets from group AB donors can be transfused to any ___________-

AB donors

-group AB has no ABO antigens to cause incompatibility

-plasma has no Rh antigens/antibodies, Rh match not needed

-platelets have few RBCs, Rh matching may be necessary

Rh Testing

-determine if patient has D antigen

-Rh negative patients at risk of forming Anti-D when exposed to Rh positive RBCs

-can cause severe hemolytic dz of fetus and newborn and delayed transfusion rxns

Rh Significance

-anti-D --> hemolytic disease of fetus and newborn

-R neg mothers w/ Rh pos babies can form anti-d

-once anti-d forms, subsequent pregnancies may develop HDFN

-prevented by Rh-immunoglobulin

Hemolytic Dz of Fetus and Newborn

-may result in fetal death, still birth

-will impact newborn - anemia, jaundice, risk for kernicterus

Antibody Screen

-patient plasma mixed w/ a screen set of reagent type O RBCs

-expected result is a negative rxn

-positive rxns require antibody identification panel workups

-Coomb's reagent

Indirect Coombs Test

Used to detect circulating antibodies against RBCs

-type AND screen

Antibody identification

-patient plasma mixed with a panel of group O RBCs

-pattern of pos vs neg rxns is key

-blood bankers "rule out" possible antibodies by finding negative rxns and looking for antigens

Negative Antibody rxn

-antibody is not specific to ay of the present antigens

Antibody Panel

extended version of an antibody screen

Direct Coombs Test

Causes of pos results:

-HDFN in baby if cord blood DAT positive

-transfusion rxn w/ hemolysis or antibody

-autoimmune dz

-drug rxn

-infxn

Direct Coombs Test

is done on infant blood to determine the presence of antibody-coated RBCs, Bilirubin levels of the infant blood indicate the extent of RBC destruction

Antibody titer

-pregnant patients

-patient has Rh antibodies titered

-high or increasing = high risk for HDFN

CrossMatch test

-after all antibodies identified, blood that is negative for the corresponding antigens is allocated

-segments from the units of blood are mixed w/ patient's plasma called a "full crossmatch"

-as long as crossmatch is neg = compatible

Positive Crossmatch

-when the patient's plasma still reacts w/ antigen neg units

-may be d/t rare antibodies, select a new unit

-may represent a flaw with your workup

-may be unavoidable

Acute Transfusion Rxn

<24 hr after transfusions

-FNHTR

-Allergic/anaphylactic

-AHTR

-TACO

-TRALI

-TAD

-Septic

-hypotensive

-non-immune hemolysis

-air embolism

Delayed transfusion rxn

>24 hr after transfusion

-TTI

-DHTR

-DSTR

-PTP

-TA-GVHD

Transfusion Monitoring

-pt must be closely monitored

-vital signs - including O2 sat

-pre-existing symptoms

-slow initiation of blood transfusion

-frequent checks and confirmation from pt about any changes

Transfusion rxn S/S (first)

-fever

-itching

-pain

-dyspnea

STOP Transfusion

-any new symptom

-any previous symptom worsens

-any noticeable changes in vitals

-THEN: keep IV open w/ saline infusion, take patient's vitals

Investigation Transfusion Rxn

-STOP transfusion

-assess all new or changed symptoms

-draw blood sample

-get urine sample

-send blood bag(s), tubing, IV bags to blood bank

Febrile Non-hemolytic transfusion rxn

-fever or chills/rigors w/in 4 hr of transfusion

-cytokines in the unit cause an elevation in body temp, can further body to respond with shivering

-all other more serious rxns must be ruled out

-tx is for symptoms, using anti-pyretics

Allergic tranfusion rxn

-hypersensitivity rxn: vasodilation, edema, bronchoconstriction

-severity ranges from mild to life-threatening

-can lead to shock and even be fatal

-Tx: antihistamine, steroids and H2 receptor antagonists if more severe, epi if life-threatening

IgA Deficiency

-congenital deficiency that results in immune suppression with increased respiratory and GI infxns

-can develop anti-IgA after exposure

-a minority of IgA def patients have anti-IgA --> fatal anaphylaxis

Haptoglobin Deficiency

-still would require prior exposure

-after exposure, may have strong immunity against these proteins

-severe allergic rxn

IgA deficiency rxn prophylaxis

-must have antibodies AGAINST IgA to cause rxn

-plasma products donated by IgA deficient donors

Washed RBCs or platelets

-washing removes plasma and allergens

-significant reduction in allergic rxns, but comes at a cost --> less cells and less function

idiosyncratic

the majority of anaphylactic transfusion rxns are ____________ and rarely occur again w/ future transfusions

Acute Hemolytic transfusion rxn

-cause: antibodies in patient's plasma or antibodies in transfusion bind to RBCs, which fix complement and lyses RBCs

-intravascular hemolysis, only requires 5-10 mL of incompatible blood

-Sx: Fever, chills, rigors, back/flank pain, chest pain, hypotension, shock, feeling of impending doom

AHTR Tx

-keep iv line open and infuse saline

-flushes kidneys free of hemoglobin and improves hypotension

Intravascular hemolysis

-common pathogenesis of acute hemolytic transfusion rxns

-usually IgM that fixes complement

-causes lysis of RBCs and inflammation

-Sx: fever, tachycardia, hypotension, vascular collapse, DIC, and shock

AHTR Labs

-red discoloration of plasma from hemolysis

-increased free Hb in blood and urine

-increased intracellular components in blood (K+ and LDH)

-positive DAT

-urine dipstick positive for blood (d/t Hb)

AHTR managment

-shock: may require vasopressors with fluids, ICU transfer for aggressive management

-DIC: plasma products, platelets, hematology consult

Transfusion Associated Circulatory Overload

-cause: transfusion --> increased blood volume --> increased pre-load on the heart

-heart failure, fluid backs up into pulmonary circulature

-left atrial enlargement

-pulmonary vascular congestion and edema

-RF: older age, smaller size, pre-existing CVD, current fluid overload

TACO symptoms

-dyspnea

-oxygen saturation

-HTN

-chest pain

-HA

TACO Testing

-imaging --> CXR --> pulmonary edema and/or vascular congestion, possible cardiomegaly

-EKG --> left atrial enlargement

-Labs --? B type natriuretic peptide (BNP)

TACO Tx

-LASIX --> remove pulmonary edema

-slow transfusion rate, split units

Transfusion Related Acute Lung Injury

-antibodies against human leukocyte antigens or human neutrophil antigens bind to neutrophils in recipient lungs

-diffuse pulmonary edema (primary to lungs)

-acute respiratory failure

-fever, hypotension

-supportive care ONLY

TRALI

what is the second most common cause of fatal transfusion rxns?

Delayed Hemolytic Transfusion Rxns

-RBC antigen in transfusion not present in patient

-Patient's immune system forms new antibody

-new antibody causes hemolysis (extravascular)

-may have recurrent symptomatic anemia

-potential need for another transfusion

Extravascular Hemolysis

-usually IgG, no complement involved

-RBCs covered in IgG are "opsonized"

-Rbcs are phagocytized in spleen and liver by macrophages

-broken down into LDH, unconj bilirubin

-jaundice and anemia develop

Transfusion Associated graft vs Host disease

-lymphocytes are present in transfusions

-immunosuppression prevents destruction of these lymphocytes

-donor lymphocytes attack patient

-bone marrow fails, skin lesions, GI lesions, lung lesions

-die from bone marrow failure and pancytopenia

irradiation

what is the treatment for TA-GVHD?

Transfusion transmitted infection

-viral transmission and bacterial septic transfusion rxns most common

-presence indicates contamination of blood supply

Donor Testing

-ABO/Rh testing

-Red cell antibody screening

-infectious disease testing (serologic, NAT)

Abo Testing

-test donor RBCs for antigens A and B

-test donor plasma for antibodies to A and B

-donor should have antigens that are opposite to their antibodies

O blood

lacks A or B antigens but has both Anti-A and Anti-B

Ab blood

has both A and B antigens but lacks Anti-A and Anti-b

Rh Testing

-tests donor RBCs for D antigen

-Rh negative --> additional testing to rule out D variants

-D variants may be missed

-patient may form anti-D

RBC antibody screen

-test donor plasma for any antibodies to other RBC antigens

-use reagent O RBCs to remove interference from Anti-A or Anti-B

-donors must not have antibodies to other RBC antigens

-only antibody screen NEG blood is accepted

ID Testing

-Hep B virus

-Hep C virus

-HIV

-Human T-cell leukemia virus

-Syphilis

-West Nile Virus