Transfusion

Question 1

acute transfusion reaction

Answer 1

description

benign to life-threatening reactions.

nonspecific symptoms such as fever or chills.

types

TRALI

TACO

acute haemolysis

anaphylaxis

sepsis

febrile nonhaemolytic reaction - FNHTR is a diagnosis of exclusion; the possibility of other febrile transfusion reactions must be eliminated, including AHTR, sepsis, and TRALI. The most common cause of FNHTR is release of cytokines from white blood cells (WBCs) in a product that has not been leukoreduced.

Assessment

●Time the transfusion was initiated

●Time symptoms began

●Time the transfusion was stopped

●Patient symptoms including fever, chills/rigors, respiratory distress, chest pain, back pain, pain/burning at the intravenous site, and hematuria

●Patient vital signs

●A clerical check of the component container, label, paperwork, and initial patient sample used for typing and crossmatching

●Repeat ABO testing on the post-transfusion patient sample

●A visual check of both pre-and post-transfusion patient samples for evidence of hemolysis

●A direct antiglobulin (Coombs) test (DAT) on the post-transfusion patient sample

management

Acute haemolysis - Hydration with normal saline should be used to maintain renal output of >1 mL/kg/hour; an intravenous diuretic such as furosemide is often used.

●Repeat ABO compatibility testing

●Additional antibody studies if ABO incompatibility is excluded

●Repeat crossmatch with pre-and post-transfusion specimens using an indirect antiglobulin (IAT) method

●Direct antiglobulin (Coombs) testing (DAT)

●Observation of the serum for pink color and analysis for free hemoglobin

●Serum haptoglobin, lactate dehydrogenase (LDH), and unconjugated bilirubin levels to document hemolysis

●Coagulation testing for DIC if the patient has increased bleeding, including prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen level, and D-dimer

●Observation of the urine for pink color and analysis for free hemoglobin

●Serial hemoglobin levels to determine the severity of hemolytic anemia and possible need for additional red blood cell (RBC) transfusions

anaphylaxis

hypotension, wheezing, angioedema) should receive epinephrine (0.2 to 0.5 mL of a 1:1000 solution) intramuscularly or subcutaneously;

Intravenous fluids (saline) and an H1-antihistamine (eg, loratadine or cetirizine, 10 mg orally, or diphenhydramine, 25 or 50 mg orally or intravenously, for itch or angioedema)

inhaled bronchodilators, continuous positive airway pressure (CPAP), and an H2-antihistamine (eg, famotidine), may be appropriate in some patients with severe bronchospasm

Laboratory testing for an anaphylactic reaction should include quantitative immunoglobulin A (IgA) levels, which will be absent (level, <7 mg/dL) in individuals with IgA deficiency, as well as the presence of antibodies to immunoglobulin A (anti-IgA)

sepsis

(CBC, WBC, culture

broad spec antis

non-haemolytic rxn

●Stopping of the transfusion.

●Administration of antipyretics if the fever is bothersome to the patient.

●Evaluation for other causes of fever, which include more serious (and potentially life-threatening) transfusion reactions as well as non-transfusion-related infection or fever.

●Hospital admission (if the transfusion is administered in an out-patient setting) for presumptive treatment of infection, if this is considered to have high enough likelihood (eg, in a patient with functional asplenia from sickle cell disease).

●Administration of other medications, if needed, such as meperidine (25 to 50 mg) for severe chills or rigors, which may characterize any FNHTR but are most often precipitated by a granulocyte transfusion

urticaria

Question 2

delayed transfusion reaction

Answer 2

●Delayed hemolysis

●Thrombocytopenia

●Graft-versus-host disease

Question 3

Transfusion associated GVHD

Answer 3

Description:

• rare and usually fatal complication of blood transfusion
• lymphocytes from the transfused blood component attack the recipient’s tissues, especially the skin, bone marrow, and gastrointestinal tract.
• leads to bone marrow aplasia and profound pancytopenia, which is typically the cause of death
• There are no highly effective treatments, so prevention is essential.

Pathogenesis:

• viable T-lymphocytes from the transfused blood component are able to engraft, proliferate, and attack HLA-expressing tissues in the host (transfusion recipient) as foreign. Mostly HLA-II are involved. Target host cells inc HSCs, Gi epithelium, skin, BM
• Immune attack is mediated by the transfusion donor’s T cells, either through direct destruction of host cells or via inflammatory cytokines that activate other immune cells including natural killer (NK) cells, macrophages, and other lymphocytes
• normally, an immunocompetent host is able to destroy recipient T lymphocytes prior to mounting a response. In this case, the recipient’s immune system does not recognise the donor lymphocytes as foreign, or is unable to mount an effective immune response.

Implicated blood products:

any blood product containing viable T-lymphocytes

●Whole blood

●Packed red blood cells (pRBCs)

●Platelets

●Plasma that has not been frozen

●Granulocytes

Risk fx:

• immunodeficiency: primary (e.g. SCID), haematological (e.g. CLL, AML, ALL), immunosuppressant therapy (fludarabine), Allo-HCT (these patients require multiple transfusions)

Presentation:

Symptoms usually commence 1-2 weeks post-transfusion, which inc:

• GI: diarrhea, abdominal pain
• skin: generalized erythroderma that can progress to desquamation
• fever
• BM: profound pancytopenia from bone marrow aplasia
• Liver: Hepatomegaly and abnormal LFTs

Treatment:

• There is no effective treatment for ta-GVHD other than hematopoietic cell transplantation (HCT), and HCT is rarely a viable option because there is usually insufficient time to identify an appropriate donor, test them for suitability to donate, and obtain sufficient hematopoietic stem cells (HSCs) for transplant. In some cases, immunosuppressive therapy has been effective in attenuating the course of the disease.

Prevention:

• treatment of the blood component to inactivate viable lymphocytes prior to transfusion.
• irradiating (or otherwise inactivating) lymphocytes in any blood components transfused to at-risk recipients
• Leukodepletion may provide some protection but it is not sufficient to eliminate all viable lymphocytes.
• bone marrow aplasia cannot be rescued by autologous or allogeneic HSCs due to lack of immediate availability of these HSC sources.

Indications for irradiated RBCs:

• Intrauterine transfusions
• Neonatal transfusions, particularly low birth weight premature neonates, and those with any immune deficiency*
• Individuals with congenital cell-mediated immunodeficiencies (thymic hypoplasia [DiGeorge syndrome], Wiskott-Aldrich syndrome, Leiner disease, 5’ nucleotidase deficiency)
• Individuals treated with purine analogs (eg, fludarabine, cladribine, deoxycoformycin, bendamustine, clofarabine)
• Individuals treated with ATG or alemtuzumab, including patients with aplastic anemia or solid organ transplant recipients
• Individuals with Hodgkin lymphoma (any stage)
• Hematopoietic stem cell donors, during the week prior to hematopoietic cell harvesting (donation)
• Recipients of hematopoietic stem cell transplantation (allogeneic or autologous)¶
• Individuals with hematologic disorders expected to undergo hematopoietic stem cell transplantation imminently
• Recipients of directed donations from biologic relatives
• Recipients of donations from HLA-matched donors