Case Studies from the Transfusion Service

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1 Case Studies from the Transfusion Service Andrea McGonigle, M.D. Associate Medical Director, Transfusion Medicine UCLA Health System 2 3 McGonigle, Andrea 1

2 4 Case 1: Transfusion issues in an IgA deficient patient 5 Case Background 10:15 am: Anesthesiologist call 69 yo M with interstitial lung disease Patient undergoing single lung transplant today Concern for risk of IgA anaphylaxis Pre-op assessment revealed history of IgA deficiency IgA <7 mg/dl(reference range: ) No known testing for anti-iga antibodies 6 McGonigle, Andrea 2

3 Case Background Pre-op Hgb 17.4 g/dl Anticipated needs for surgery: Likely no RBCs needed No platelets, plasma needs anticipated 7 What would you do next? 8 Our Initial Response Recommended use of autologous blood Perioperative salvage (Cell saver), Acute Normovolemic Hemodilution (ANH) Recommended against plasma containing products Prepared washed RBCs immediately Asked for pre-op samples from patient for: Anti-IgA antibody testing Confirmation of IgA quantification 9 McGonigle, Andrea 3

4 10 Role of IgA Most abundant type of antibody in the body Majority of IgA is present in mucosal secretions 2 nd most common antibody in plasma circulation Normal function Neutralizes pathogens in respiratory system, gut, and genitourinary tracts Assists in clearance of pathogens from circulation Reduces allergenicity of food antigens by binding them 11 Defining IgA Deficiency Absolute deficiency <0.05 mg/dl Requires sensitive test (typically only reference laboratories) Relative IgA deficiency Below reference range, generally <5-7 mg/dl Can be determined by less sensitive tests (available at most university hospitals) NOTE: Values in older literature differ greatly Definition of IgA deficiency ranges from 1-10 mg/dl Sandler SG Transfusion 2006:10-12 McGonigle, Andrea 4

5 13 IgA Anaphylaxis Anaphylaxis following transfusion of blood component In context of absolute IgA deficiency & anti-iga antibodies Mechanism Anti-IgA antibody activates mast cells Mast cells release histamine Results in itching, hives, mouth/airway swelling, respiratory distress Sandler SG Transfusion 2006:10-12 IgA Anaphylaxis: Risk Factors Absolute IgA deficiency Patients can form anti-iga Patients with anti-iga are at risk of IgA anaphylaxis Relative IgA deficiency or normal IgA level Patients may form antibodies to subclasses of IgA (IgA1 and IgA2) Rare, unconfirmed reports of mild allergic transfusion reactions Sandler SG Transfusion 2006:10-12 McGonigle, Andrea 5

6 IgA Anaphylaxis: Risk Factor Controversy Absolute IgA deficiency Patients can form anti-iga Patients with anti-iga are at risk of IgA anaphylaxis However, conventional anti-iga assay is nonspecific 1:1200-1:1560 healthy blood donors are IgA deficient with anti-iga Incidence of anaphylactic transfusion reactions is 1:20,000-1:50,000 Sandler SG Transfusion 2006:10-12 Palmer DS Transfusion 2010: IgA Anaphylaxis: Risk Factor Controversy Testing may overestimate number of persons at risk Healthy donors with absolute IgA deficiency & anti-iga far exceeds incidence of anaphylactic transfusion reactions in patients No way currently to tell which of those who test positive for anti-iga will be like the healthy donors or like the IgA deficient patients who have experienced anaphylaxis Sandler SG Blood 1994: IgA Anaphylaxis: Risk Factor Controversy Antibodies still more common in IgA deficient patients with history of anaphylaxis than asymptomatic blood donors 76% of IgA deficient patients who experienced anaphylaxis had antibodies 22% of IgA deficient donors who had NO history of anaphylaxis had antibodies Thus, still concern for formation of anti-iga in patients with absolute IgA deficiency And still concern for risk of anaphylaxis in patients with anti- IgA antibody Sandler SG Blood 1994: McGonigle, Andrea 6

7 19 Management of IgA Deficient Patient *Ask for pre-transfusion sample to confirm history, if not done previously If history confirmation demonstrates presence of any IgA Risk of anti-iga anaphylaxis practically excluded Transfuse with regular products, no antibody testing needed 20 Management of IgA Deficient Patient *Ask for pre-transfusion sample to confirm history, if not done previously **Tested following most recent transfusion OR no risk of antibody formation (e.g patient given IgA deficient units following last test) 21 McGonigle, Andrea 7

8 Case 1 Patient Results Successful single lung transplant Estimated blood loss <100cc All shed blood collected by Cell Saver and returned to patient 500cc of whole blood collected prior to cardiopulmonary bypass Returned after patient weaned off bypass No significant postoperative bleeding IgA antibodies resulted as negative No sample ever collected for repeat IgA quantification Case 2: Is it hyperhemolysis syndrome? 24 McGonigle, Andrea 8

9 Case Background 43 yom with sickle cell disease, multiple alloantibodies, warm & cold autoantibodies, admitted for pain crisis, anemia 24 hour rise in total bilirubin 2.6 to 4.5 (Reference range: mg/dl) Increasing absolute reticulocyte count 0.08 to 0.13 x 10 6 /ul (Reference range: ) Hemoglobin decreased from baseline 3.3 g/dl(reference range: g/dl) Baseline g/dl Clinical Question Is it hyperhemolysissyndrome? 25 Additional Background ESRD, generally transfused about 1x/month Recent transfusion history Transfusion ~1 month ago, 2 RBCs Hgb3.6 to 6.2 g/dl No signs of transfusion reaction No signs of hemolysis up to discharge (2 weeks following transfusion) Day of consult, received 2 RBCs Hgb3.3 to 5.0 g/dl 125 mg solumedrol pre-treatment for history of allergic transfusion reaction 26 Additional Background RBCs for transfusion fully phenotype matched No plasma or platelet transfusions Leg hematoma present at discharge 1 month prior still visible Clinical team planned imaging to determine if stable in size Admitted with pain consistent with his sickle cell pain No reported history of infection, afebrile Blood cultures negative WBC:18.24 to x 10 3 /ul (Reference range: ) 27 McGonigle, Andrea 9

10 So is it hyperhemolysis? 28 Our immediate answer Hyperhemolysis not likely Post transfusion hemoglobin > pre transfusion Dose of Solumedrol pre-treatment not high enough to prevent hyperhemolysis Results point toward infection and/or sickle crisis McGonigle, Andrea 10

11 Defining Hyperhemolysis Syndrome (HS) Transfusion reaction Occurs days following transfusion Also called Hyperhemolytic transfusion reaction (HHTR) Delayed hemolytic transfusion reaction/hyperhemolysis (DHTR/H) Seen predominantly in hemoglobinopathy patients Very rare Danaee et al. review found 9 cases in 1,000 patients Danaee A, Transfusion Medicine Reviews 2015 Defining Hyperhemolysis Syndrome (HS) Worsening anemia after transfusion Post transfusion Hgb lower than pre Anemia further exacerbated by additional transfusion(s) Reticulocytopenia Lab evidence of hemolysis Increased bilirubin (indirect and direct), LDH Hemoglobinuria 32 Versus delayed hemolytic transfusion reaction HS Signs of hemolysis Elevated bilirubin, LDH 2-19 days post transfusion Severe hemolysis Hb drops below pre-tx value ReticulocytOPENIA +/- New RBC alloantibodies +/- positive DAT Worsens with further RBC transfusions DHTR Signs of hemolysis Elevated bilirubin, LDH 1-28 days post transfusion Less severe hemolysis Hbdrop back to pre-tx level ReticulocytOSIS New RBC alloantibodies Usually positive DAT DanaeeA, Transfusion Medicine Reviews 2015 McGonigle, Andrea 11

12 34 Pathophysiology Incompletely understood why allogeneic and autologous RBCs undergo destruction Proposed mechanisms include: Bystander hemolysis Immune mediated hemolysis of autologous cells Cells lack antigen for which antibody directed Macrophage activation Win N. Transfusion 2008: DanaeeA Transfusion Medicine Reviews 2015 Pathophysiology: Bystander Hemolysis Proposed causes Enhanced complement activation Caused by cross reactivity between RBC alloantibody and autologous RBC OR caused by non-rbc alloantibodies (e.g. HLA antibodies) Enhanced complement sensitivity Sickle RBCs may have faulty complement regulatory processes Complement lysis can therefore occur independent of antibody Win N. Transfusion 2008: McGonigle, Andrea 12

13 Pathophysiology: Macrophage Activation Sickle RBCs adhere to macrophages more avidly than normal RBCs Macrophage activity thought to be increased in HS Activated macrophages remove autologous RBCs and reticulocytes May also explain removal of allogeneic RBCs By HLA antibody-antigen recognition Win N. Transfusion 2008: DanaeeA Transfusion Medicine Reviews Transfusion Medicine Reviews 2010 McGonigle, Andrea 13

14 DanaeeA Transfusion Medicine Reviews 2015 Hyperhemolysis Treatment Most important features are: High suspicion Early treatment Prevention Give 1 dose IVIG and/or steroids with future transfusions 41 Case 2 Patient Results Chronic left thigh hematoma Imaging completed 3 days after consult Revealed increase in size Gas concerning for infection IR procedure demonstrated frank pus Fluid grew Propionibacterium acnes 42 McGonigle, Andrea 14

15 Case 2 Patient Results Admission pain consistent with his sickle cell pain Pain predominantly located in area of infected hematoma Infected hematoma was treated with drain, antibiotics Hematoma decreased in size Infection resolved Patient returned to baseline hemoglobin Transfusion needs returned to baseline Case 3: Jehovah s Witness patients do we have a role? 45 McGonigle, Andrea 15

16 Case Background 42 yof Jehovah s Witness with HIV, Burkitt'slymphoma, transfer from OSH Bleeding uterine fibroids x 3 days Drop in Hgb 8.0 g/dl(11/18/2015) to 5.2 (11/21/2015) Clinically stable, but concern for further Hb drop Clinical question, can we obtain Hb-based oxygen carriers (HBOCs)? 46 Additional Background Patient refuses cellular blood products (RBC, PLT) Patient accepts acellularproducts (FFP, cryo, factor concentrates) Baseline hemoglobin 8.0 g/dl Hormone therapy started to target bleeding fibroids McGonigle, Andrea 16

17 Transfusion Transfusion 2014 Transfusion 2014 McGonigle, Andrea 17

18 52 Transfusion refusal is personal Using a Jehovah s Witness as an example Bible commands abstinence from blood, blood represents life, refusal of blood in obedience to bible and respect for God as Giver of life The decision to use certain products is explicitly personal Use of intraoperative salvage and Hgb alternatives is personal Individuals may not conform with generalized guidelines McGonigle, Andrea 18

19 55 Transfusion Medicine Role Ask clinician to clarify products patient is willing to accept Require detailed refusal to be placed in patient s chart Help honor patient s wishes Refusal comment in patient s blood bank record 56 Point Clinicians in the Right Direction Understand risk of mortality peaks when Hgb<5.0 g/dl If Hgb <5 g/dl, consider Hgb alternative Medications can increase endogenous RBC production (EPO, Iron, Vitamin C, Folate, Vitamin B12) Optimize patient Avoid hemodilution, control bleeding Reduce oxygen consumption (control fever, work of breathing) Supplemental oxygen to maintain sao2>95% 57 McGonigle, Andrea 19

20 Transfusion 2014 Case 3 Patient Results Refusal form reviewed with patient; actually refused RBC, platelets, plasma and cryoprecipitate Would accept Albumin, clotting factor concentrates Patient also refused hemoglobin alternatives Fibroid bleeding stopped the day of consultation Nadir Hgb 4.8g/dL 59 Questions 60 McGonigle, Andrea 20

21 McGonigle, Andrea 21

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