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Flashcards in Complications of Transfusion Deck (18):
1

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

2

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

3

List the serious transfusion reactions.

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

4

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

5

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

6

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

7

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

8

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

9

List the types of alloimmunization.

  • RBC alloimmunization
  • Delayed Hemolytic Transfusion Reaction
  • HLA Alloimmunization

10

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

11

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

12

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)

13

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

14

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

15

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

16

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

17

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

18

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