Page 2025 - Hematology_ Basic Principles and Practice ( PDFDrive )
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1796   Part XI  Transfusion Medicine


                                                              ranitidine,  respectively.  Corticosteroids,  provided  in  advance  of  a
         Management and Prevention of Allergic Transfusion Reaction
                                                              transfusion,  also  may  be  useful  in  patients  with  serious  recurrent
          A  34-year-old  man  with  thrombotic  thrombocytopenic  purpura  has   reactions.
          been receiving daily 60 mg prednisone and daily plasmapheresis for   Most  anaphylactic  transfusion  reactions  are  idiopathic.  Case
          8 days without complication. Halfway through the ninth procedure, the   reports describe moderate or severe anaphylactic reactions in patients
          patient rapidly develops severe angioedema of the face and tongue,   who  are  severely  IgA  deficient  (<0.05 mg/dL)  and  have  anti-IgA
          stridor,  wheezing,  and  diffuse  flushing  and  urticaria.  Tachycardia   antibodies. The generalizability of this mechanism is low. Most cases
          develops with stable blood pressure. A code is called and the patient   of  fatal  anaphylaxis  are  not  related  to  IgA  deficiency,  and  most
          is administered oxygen, 0.5 mg epinephrine intramuscularly, albuterol   severely IgA-deficient people tolerate transfusions well. Thus, patients
          nebulizer,  diphenhydramine,  ranitidine,  and  methylprednisolone.   with incidental IgA deficiency may receive routine blood components,
          Symptoms resolve over the next 12 hours without the need for esca-  and IgA/anti-IgA testing should be reserved for patients with anaphy-
          lated  respiratory  support.  The  patient  receives  another  3  weeks  of
          plasma  exchanges  with  two  sporadic  minor  allergic  reactions  (focal   lactic reactions. Quantitative haptoglobin can also be considered as
          urticaria and pruritus only).                       a screening test, as rare cases of haptoglobin deficiency are associated
           Among chronically transfused patients, most will have none or only   with anaphylactic reactions.
          one allergic transfusion reaction. Even among the minority of patients
          with  recurrent  reactions,  most  transfusions  will  not  result  in  another
          reaction, including anaphylactic reactions. Most cases of anaphylaxis   HYPOTENSIVE TRANSFUSION REACTION
          are idiosyncratic to a specific unit and do not recur, as in this case.
          Nevertheless, when platelet and red blood cell components are sub-  A  less  recognized,  but  severe  acute  transfusion  reaction  is  isolated
          sequently needed, plasma reduction is prudent because anaphylaxis   hypotension during or immediately following a blood product infu-
          can recur in a minority of patients. Screening for IgA deficiency can
          identify the rare cases of anaphylactic reactions caused by severe defi-  sion.  For  adults,  the  definition  includes  a  drop  in  systolic  blood
          ciency. Severe haptoglobin deficiency can occur in Asian populations.   pressure greater than 30 mmHg to below 80 mmHg, and it is most
          Nevertheless, even among fatal anaphylactic reactions, IgA deficiency   likely when hypotension occurs within minutes of the start of the
          is not present in most cases.                       transfusion and resolves quickly after the transfusion is stopped. This
           The medications used in the previous case are effective at treating   type of transfusion reaction was initially reported after transfusion of
          allergic reactions, but not preventing them, according to randomized   platelets administered through some types of bedside leukoreduction
          controlled trial and observational evidence. Because most transfusions   filters. Later it was also reported in other types of blood products
          do not result in an allergic transfusion reaction, clinicians sometimes   including  plasma  and  RBCs.  The  pathogenesis  of  this  syndrome
          have the confounded belief that adding premedications after a reaction   appears to be related to the activation of the contact pathway (prekal-
          prevented subsequent reactions, when no additional reaction was to
          occur,  anyway.  Histamine  H1  and  H2  receptor  blockers  are  readily   likrein converting to kallikrein) induced in plasma by the negatively
          accessible in nearly all transfusion settings and can readily be admin-  charged surface of some leukoreduction filters. Kallikrein activation
          istered  if  allergic  symptoms  develop.  Patients  often  do  not  like  the   stimulates  the  conversion  of  high-molecular-weight  kininogen  to
          wide array of side effects associated with premedication, particularly   bradykinin. Notably these reactions have also been reported in cases
          diphenhydramine. As in the earlier case, the small subset of patients   where leukoreduction filters were used before storage, indicating that
          with severe or highly recurrent reactions, premedication is reasonable   bradykinin generation may occur via pathways other than via bedside
          to consider on subsequent transfusions to mitigate symptoms that are   filtration.  The  syndrome  is  often  more  severe  in  patients  already
          more likely to occur than with unselected patients.  taking  angiotensin-converting  enzyme  (ACE)  inhibitors.  ACE  is
                                                              identical to kininase II, which is responsible for degrading bradykinin.
                                                              Blockage of the kininase II degradation of bradykinin by ACE inhibi-
        activating factor, a potent arachidonic acid derivative that mediates   tors results in a prolonged bradykinin half-life and a reaction that can
        anaphylactic shock, is produced rapidly, along with a variety of other   be very severe. Two surgical settings that may pose increased risk of
        eicosanoids, for example, leukotrienes.               hypotensive reactions include (1) procedures involving the prostate,
           Over 90% of allergic transfusion reactions occur during infusion.   because another kallikrein gene family member, hK2, can generate
        When allergic symptoms develop, transfusion should be stopped and   bradykinin, and (2) cardiac bypass surgery because the pulmonary
        the  patient  given  25–50 mg  of  diphenhydramine. The  transfusion   vasculature is an important site for kinin metabolism.
        may resume, but only if the symptoms resolve and the patient feels
        well. A mild allergic reaction (urticaria and pruritus) during a blood
        transfusion usually does not progress to a more severe anaphylactic   INFECTIOUS COMPLICATIONS OF TRANSFUSION
        reaction after infusion of additional blood from the same unit. The
        severity  of  allergic  transfusion  reactions  is  not  directly  related  to   Transfusion-transmitted  diseases are discussed  in  detail in Chapter
        volume infused or infusion rate.                      120. A focus on the clinical presentation of acute reactions is pre-
           Most  patients  never  experience  an  allergic  transfusion  reaction,   sented here.
        and for those who have one, it is usually isolated. Even among the   Bacterial contamination of stored blood can pose grave risks to
        minority of patients with recurrent reactions, most transfusions are   the  recipient.  Bacteria  can  enter  the  blood  collection  bag  during
        tolerated well. Patients who have had more than one mild allergic   venipuncture  as  a  result  of  inadequate  skin  preparation,  during
        reaction  may  continue  to  receive  routine  units.  Washed  RBCs  or   component preparation, or through the collection of blood from a
        plasma-reduced  platelets  can  be  used  to  prevent  severe,  recurrent   donor with an occult infection or asymptomatic bacteremia. Platelet
        reactions; however, washing cellular products compromises compo-  concentrates, stored at room temperature, have the highest risk of
        nent quality. Washing RBCs leads to accelerated in vitro hemolysis.   bacterial contamination. Many reports describe fatal septic transfu-
        Washing platelets increases platelet activation and lowers posttransfu-  sion reactions caused by platelet components containing a variety of
        sion platelet count increments. Platelets collected in platelet additive   species, including Pseudomonas, Salmonella, and Staphylococcus. Bac-
        solution  and  pooled,  solvent  detergent  plasma  are  relatively  new   teria that grow well at refrigerated blood bank temperatures (1°C to
        products that have been shown to reduce the incidence of allergic   6°C), including Pseudomonas, Yersinia, Enterobacter, and Flavobacte-
        transfusion reactions. Leukocyte depletion or microaggregate filters   rium, are organisms commonly associated with a contaminated unit
        are of no value.                                      of RBCs. Units of blood that are contaminated need not be obviously
           There is no evidence that antihistamine premedication prevents   discolored, malodorous, or clotted; it is extremely difficult to deter-
        allergic  transfusion  reactions,  although  antihistamines  do  mitigate   mine by simple visual inspection whether a unit is contaminated.
        symptoms when they occur. Studies in healthy volunteers support a   Patients who receive a unit of contaminated blood may develop
        synergistic role for treating histamine-mediated reactions with both   fever, rigors, skin flushing, abdominal cramps, myalgias, DIC, renal
        H1 and H2 receptor antagonists, for example, diphenhydramine and   failure,  hypotension,  and  cardiac  arrest.  These  reactions  may  be
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