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Flashcards in Complications of Transfusion Deck (18):

Describe the process of surveillance and evaluation of transfusion reactions.

  • Patient status checks and vital signs:
    • pre-transfusion
    • at 15 min
    • hourly
    • post-transfusion
  • Key problems:
    • fever/chills
    • BP change
    • rash
    • respiratory complaints
  • Reaction evaluation:
    • stop unit
    • maintain IV line
    • notify blood bank
    • send labs for acute hemolysis—blood bank blood specimen
    • urinalysis
    • Exception: dermal-only allergic reaction—notify blood bank, but antihistamine Rx and unit restart with close observation may be feasible without lab testing for hemolysis


What are some common acute transfusion reactions? How is each one managed?

  • Allergic-- dermal: hives, itching, rash, facial swelling; airway: dyspnea, wheezing
    • Cause: IgE antibodies to allergens in donor plasma--more likely with plasma, platelets
    • Treat: antihistamines; if severe, epinephrine, corticosteroids
    • Prevent recurrence: pre-transfusion antihistamines; if persistent or severe, wash RBCs and wash or concentrate platelets
  • Febrile—chills, rigors, temperature rise >1°C
    • Causes: Recipient antibodies to donor WBCs, or cytokines in blood bag from donor WBCs
    • Treat: antipyretics
    • Prevent recurrence: pre-transfusion antipyretics; if persistent or severe, give leukoreduced RBCs and platelets—99.9% of WBCs removed
  • Transfusion-Related Circulatory Overload (TACO)—hypoxia, pulmonary edema, secondary cardiac injury
    • Cause: RBCs/plasma in blood product expands intravascular volume in susceptible patient
    • Treat: diuresis
    • Prevent: assess volume status pre-transfusion; concomitant diuresis if needed; slower infusion rate; transfuse units in divided parts


List the serious transfusion reactions.

  • Acute Hemolytic
  • Transfusion-Related Acute Lung Injury (TRALI)
  • Septic
  • Anaphylactic
  • Transfusion Associated Graft vs. Host Disease (GVHD)


What is the presentation, management, and prevention of acute hemolytic reactions to blood transfusions.

  • Acute Hemolytic—renal:
    • dark urine (hemoglobinuria)
    • renal insufficiency (acute tubular necrosis)
    • coagulopathy:
      • high prothrombin and partial thromboplastin times
      • bleeding (disseminated intravascular coagulation)
    • systemic:
      • fever/chills
      • hypotension
      • shock (cytokine storm)
  • Pathogenesis:
    • Antibody lyses RBCs
    • Lysed RBC membranes damage kidneys and activate clotting
    • RBC-antibody immune complexes activate inflammation
  • Causes: ABO-incompatible RBCs—incorrect blood bank specimen (another patient’s blood typing)
    • blood bank error (incorrect typing or wrong unit sent)
    • mistransfusion to wrong patient
    • non-ABO antibodies---missed in screening or specific to donor unit
  • Tests: Direct antiglobulin test, repeat blood typing, urinalysis
  • Treat: renal—diuresis; coagulopathy—plasma, platelets as needed for bleeding
    • systemic—blood pressure support, compatible RBCs if needed
  • Prevent: Follow procedures for blood bank specimen collection & blood transfusion [see RBC transfusion lecture]
    • blood bank checks of past blood typing and antibody records


What is the presentation, management, and prevention of Transfusion-Related Acute Lung Injury (TRALI)?

  • Transfusion-Related Acute Lung Injury (TRALI)
    • hypoxia
    • diffuse pulmonary edema
    • <6 hr after transfusion
  • Cause: Donor plasma in blood product contains antibodies against recipient WBCs
    • antibody-activated neutrophils damage pulmonary capillaries
    • highest risk of large volume of WBC antibodies is in platelet units from pregnancy-sensitized multiparous women
  • Treat: respiratory support, no TRALI-specific therapy
    • diuresis usually ineffective (unlike TACO)
  • Test: WBC antibodies (anti-HLA, anti-neutrophil) in plasma of involved donors
  • Prevent: Defer TRALI-causing donors
    • blood suppliers make plasma almost entirely from male donors
    • test plateletpheresis donors for WBC antibodies


What is the presentation, management, and prevention of septic responses to blood transfusions?

  • Septic
    • fever/chills/rigors
    • hypotension
    • shock
  • Cause: Bacteria in blood component bag from donor skin or blood
    • most often in platelets, stored at room temperature
  • Test: Culture patient and Gram-stain/culture blood bag content
  • Treat: Broad-spectrum antibiotics, with guidance from Gram stain/cultures
  • Prevent: donor history screening for infection; antiseptic blood collection
    • bacterial cultures of platelets by blood supplier


What is the presentation, management, and prevention of anaphylactic reactions to blood transfusions?

  • Anaphylactic
    • allergic reaction
    • plus hypotension
    • airway obstruction
    • shock
  • Cause: recipient antibodies to allergen in donor plasma
    • sometimes in IgA-deficient recipient with anti-IgA antibodies
  • Test: Patient plasma IgA level, anti-IgA antibodies
  • Treat: antihistamines, epinephrine, corticosteroids, BP support
  • Prevent: notify blood bank of IgA-deficient patients
    • washed RBCs/platelets after such reactions or in IgA-deficient patients
    • IgA-deficient plasma for patients with IgA reactions who need plasma


What is the presentation, management, and prevention of Transfusion-Associated Graft-Vs-Host Disease (GVHD)?

  • Transfusion-Associated Graft-Vs-Host Disease (GVHD)
    • rash
    • fever
    • diarrhea
    • pancytopenia
    • hepatic dysfunction
    • 3-30 days post-transfusion
    • cellular immune reaction of donor lymphocytes to recipient tissues
  • Causes: lack of normal rejection of transfused lymphocytes--severe recipient cellular immunosuppression, or donor closely HLA-matched to recipient (e.g., blood-relative directed donor)
  • Test: DNA chimerism studies of blood or tissue (sex chromosomes or “DNA fingerprinting”) to detect foreign donor WBCs
  • Treat: Immunosuppression of immune reaction
  • Prevent: gamma irradiation of RBCs/platelets for susceptible patients, to block donor WBC DNA division and proliferative cellular immune responses
    • patient risk groups:
      • hematopoietic stem cell transplants
      • leukemia
      • lymphoma
      • marrow failure
      • newborns
      • fetuses (maternal or intrauterine transfusions)
      • congenital cellular immunodeficiencies
      • fludarabine therapy
      • transfusions from blood relatives


List the types of alloimmunization.

  • RBC alloimmunization
  • Delayed Hemolytic Transfusion Reaction
  • HLA Alloimmunization


What is the cause, treatment, and prevention of RBC alloimmunization?

  • Cause: exposure to foreign RBC antigens
  • Treat: none
  • Prevent: extended antigen matching (Rh C,E; Kell K) in sickle-cell patients prone to antibodies


What is the cause, treatment, and prevention of Delayed Hemolytic Transfusion Reaction?

  • Cause: prior RBC alloimmunization, but circulating antibody not detected in current compatibility testing
  • Treat: Identify antibody by type & screen and direct antiglobulin test, and give compatible RBCs
  • Prevent: blood bank records of patient’s prior antibodies—give antigen-negative RBCs even if previous antibody is undetectable


What is the cause, treatment, and prevention of HLA Alloimmunization?

  • Problems from HLA antibodies:
    • febrile transfusion reactions
    • platelet refractoriness
    • organ and stem cell transplant rejection
  • Cause: donor WBCs in RBC/platelet units
  • Treat: complex immunomodulation protocols to reduce antibody in organ transplant patients
  • Prevent: leukoreduced RBCs/platelets in patients with febrile reactions; pre-or post-transplant; or (potential) need for prolonged platelet support (also see Cytomegalovirus below)


What are Transfusion-Transmitted Infections? What are the safety measures and major infections?

  • Layers of safety:
    • Donor self-deferral-- pre-donation reading material
    • Donor interview—risk history, vital signs
    • Testing—see table below
    • Donor deferral records—history, testing
    • Antiseptic collection and processing
    • Controlled storage and handling
    • Investigation of possible TTIs-- identify, defer infectious donors
  • Major infections tested for:
    • HIV
    • HCV
    • HBV
    • HTLV
    • West Nile
    • Chagas
    • Syphilis
    • Bacterial sepsis
    • Babesiosis
    • vCJD
    • Dengue


Who is at risk of getting cytomegalovirus and what are the methods of prevention?

  • Preventitive measures only in patients at risk
  • CMV biology: virus mainly in WBCs in donor RBCs, platelet units
  • Patients at risk: not previously CMV-infected (anti-CMV-negative) and immunosuppressed:
    • organ or stem cell transplant candidates or recipients (when donor also CMV-negative)
    • HIV infection
    • neonates
    • fetuses (intrauterine or maternal transfusions)
    • first-time infections are most severe
  • Prevent: give RBCs/platelets which are leukoreduced or from anti-CMV-negative donors
  • Residual risk: 1-3% of patients newly CMV-infected after course of leukoreduced/anti-CMV-negative units


What are the risks and benefits of directed donations from family/friends?

  • Not considered safer than volunteer community donors, who often have donated many times previously
  • First-time donors have higher deferral and test-marker rates
  • Blood relatives’ RBCs and platelets must be gamma-irradiated (GVHD above)
  • But a directed donor could donate multiple units, reducing donor exposures


What are the Chemical treatment options for pathogen inactivation of plasma or platelets?

  • Chemical treatment—solvent-detergent method for plasma​
    • Process: US product from plasma pools, treated and then aliquoted into 200-mL units
    • Approval: US FDA, 2013
    • Action: disrupts enveloped viruses (eg, HIV, HBV, HCV, HTLV, WNV)
    • Comments: reduced TRALI risk due to pooling and thus dilution of units with WBC antibodies; process does not kill non-enveloped viruses (hepatitis A, parvovirus) well--NAT of plasma pools is used to screen out these agents


What are the photochemical treatments for pathogen inactivation of plasma or platelets?

  • Process: chemicals added, then activated by UV or visible light
  • Approval: US FDA, December 2014
  • Actions: DNA or RNA damaged by free radicals or crosslinking
    • Blocks nucleic acid replication
  • Comments: individual units treated, not pools; platelet agents inactivate donor WBCs, preventing GVHD


What are the desadvantages of treatment for pathogens in plasma and platelets?

  • Chemicals (except riboflavin) potentially toxic, must be removed after treatment of component
  • Mild platelet damage—lower platelet count responses
  • No available inactivation yet for RBC units
    • Different chemicals neede---red Hgb blocks UV/light transmission for above photochemicals
    • First chemicals tried caused new antigens on RBCs, to which some recipients made antibodies