Question | Answer |
First step in a transfusion reaction work-up | STOP THE TRANSFUSION |
Main indicator of survival of an acute HTR | amount of incompatible blood infused |
This protein binds to free HGB molecules, cleared by monocytes and macrophages in the RE system; Levels decrease sharply in hemolysis; Long turnaround time and acute phase reaction make for limited usefulness in acute setting | haptogobin |
Most common cause of Acute hemolytic transfusion reactions (AHTRs) | Clerical errors |
Rate of fatal hemolytic transfusion reaction per transfusion | 1 in 1.8 million transfusions |
Most common presenting symptom in a hemolytic transfusion reaction | Fever and chills > 80% |
RBC abnormality associated with Intravascular hemolysis | Schistocytes |
RBC abnormality associated with Extravascular hemolysis | Spherocytes |
Treatment of Acute hemolytic transfusion reactions (AHTRs) | Hydration/diuresis critical early components; Low-dose dopamine use is controversial; Consider DIC; (+/-) heparin; Consider early exchange transfusion,for high volume incompatible transfusion |
how can Acute hemolytic transfusion reactions be prevented? | 1) Training and careful attention to phlebotomy, labeling, issue, and administration 2) Two separate ABO/Rh types before transfusion 3) Advanced methods (RFID, bar codes, etc.) |
Pathophysiology of FNHTR | Increased pyrogenic substances, mostly from WBCs 1) Cytokines produced before transfusion 2) cytokines made after transfusion |
What can reduce risk of FNHTR? | leukoreduction |
Definition of FNHTR | Transient fever/chills (+/- rigors?) during or up to 2 hours after transfusion |
#1 infectious risk from transfusion | Transfusion-related sepsis (septic transfusion reaction) from platelets |
Most common bacterial infection from a RBC transfusion | Yersinia enterocolitica (most common historically) |
Most common bacterial infection from a platelet transfusion | Vast majority are gram-positive cocci (skin) |
#1 cause of transfusion-related fatality in the US | Transfusion-related acute lung injury (TRALI); TACO overtook TRALI in 2016 data |
Incidence of TRALI | Incidence varies: 1:1200 to 1:190,000 transfusions
1 in 5800 |
TRALI definition | New acute lung injury < 6 hours post transfusion |
Blood products implicated in TRALI cases | historically PLTs/plasma transfusions,
Now RBCs are most commonly implicated. |
List TRALI mitigation strategies | 1. Male-only or female never pregnant plasma has been shown to decrease the risk of TRALI (females have more anti-HLA and anti-neutrophil antibodies); 2. Female plasma/PLT donors with h/o pregnancy tested for antibodies |
Pathophysiology of allergic transfusion reactions | a) Type I (IgE-mediated) hypersensitivity to transfused plasma proteins b) Mast cell secretion of histamine and other mediators of allergic reactions |
Describe treatment and prevention optons for allergic transfusion reactions | Diphenhydramine IV 25-50 mg as treatment, oral form as prophylaxis; Washed products work too (not usually done); May restart transfusion after hives clear. |
What blood products are options in IgA deficient patients with h/o anaphylactic transfusion reaction? | Washed cellular products (RBCs, PLTs), or products from IgA-deficient donors; If possible, bank autologous units |
Drug classically associated with hypotensive transfusion reaction | angiotensin-converting enzyme inhibitors |
TRALI definition | New acute lung injury < 6 hours post transfusion;; Lack of other risk factors for pulmonary edema; No pre-existing acute lung injury; Usually fever, chills, transient hypertension then hypotension; Should have no JVD, widened pulse pressure |
In TRALI, an early CBC may show this finding | Transient neutropenia |
What strategies have been used for TRALI mitigation? | Male-only or female never pregnant plasma has been shown to decrease the risk of TRALI; |
Acute onset of congestive heart failure as a direct result of blood transfusion | Transfusion-associated circulatory overload (TACO) |
Outline differences between TACO and TRALI | Clinical (response to diuretics/positional changes in TACO, fever in TRALI); CXR: Less cardiac silhouette widening in TRALI; Lab: Elevated BNP favors TACO; Finding HLA/HNA antibodies establishes TRALI |
Results from an attack on recipient cells by viable T-lymphocytes in a transfused blood product | Transfusion-associated graft-vs-host disease (TAGVHD) |
Presentation of Transfusion-associated graft-vs-host disease | Fever 7-10 days post-transfusion Face/trunk rash that spreads to extremities; Mucositis, nausea/vomiting, watery diarrhea; Hepatitis; Pancytopenia and subsequent marrow aplasia; Most patients die from infections |
What can be done to prevent Transfusion-associated graft-vs-host disease? | irradiate blood products |
Radiation dose requirements for preventing Transfusion-associated graft-vs-host disease | 2500 cGy (“rad”) dose required targeted to center of bag, with at least 1500 cGy in all parts of the bag |
Condition with marked thrombocytopenia and increased risk of bleeding about ten days following transfusion (may be below 10,000/L) | Post-transfusion Purpura (PTP) |
Demographic group at risk for post-transfusion purpura | Multiparous females at risk (5:1 female-male ratio) |
Pathophysiology of post-transfusion purpura | Anti-HPA-1A (PLA1; 98% frequency) 75%; HPA-1A neg pts exposed via pregnancy/trnsfzn; HPA-1A-+ trnsfsd PLTs and HPA1a-negative pt PLTs both destroyed; Ab has autoab activity; Passive adsorption of Ag/Ab complexes or soluble PLT Ags suggested |