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Chapter 119  Transfusion Reactions to Blood and Cell Therapy Products  1799


            splenectomy  may  also  be  useful.  Patients  with  acute  bleeding  and   supernatant of an RBC unit can reach 7 mEq at the end of storage.
            needing platelet support should receive platelets without the platelet-  Neonates and children can receive transfusions of up to 20 mL/kg
            specific  antigen,  if  possible.  If  random  donor  platelets  are  given,   RBC for routine transfusions over 3–4 hours without concern for
            patients  can  develop  severe  reactions,  including  allergic  reactions.   hyperkalemia.  For  large  volume  transfusions  or  transfusion  in  the
            Recurrence of PTP is rare.                            setting of hyperkalemia, fresher or washed RBC components can be
                                                                  requested. As there is increased potassium leakage from RBCs after
                                                                  exposure to 25 Gy of radiation to prevent posttransfusion GVHD, a
            Hypothermia                                           maximum 28-day shelf life from the day of irradiation is imposed on
                                                                  this blood component.
            Hypothermia  can  occur  with  rapid  infusion  of  large  quantities  of
            refrigerated  (1–6°C)  blood,  such  as  in  cases  of  rapid  and  massive
            transfusions. Rapid infusion of blood (1 unit every 5 minutes) may   Iron Overload
            lower the temperature of the sinoatrial node to less than 30°C, at
            which  point  ventricular  fibrillation  may  occur.  Hypothermia  also   Iron loading from RBC transfusion is not categorized as a transfusion
            induces  coagulopathy,  possibly  attributed  to  inefficient  enzymatic   reaction, but it is a common adverse consequence of chronic RBC
            activity below physiologic temperatures. Use of warming devices may   transfusion. One milliliter of RBCs at a hematocrit of a typical RBC
            reduce the incidence of coagulopathies associated with major trauma   unit contains approximately 0.75 mg of iron. A unit of blood with
            and also help to overcome cardiac complications. Most transfusions   300 mL of RBCs thus contains approximately 225 mg of iron, and
            need not be given this rapidly. For routine transfusion, blood does   4 units of blood contain ~1 g of iron, roughly the amount stored in
            not have to be warmed. Indeed, overwarming a unit of blood can   the  bone  marrow.  Men  and  nonmenstruating  women  lose  only
            cause RBC thermal injury and produce hemolysis, DIC, or shock.  approximately 1 mg of iron each day. Continued use of transfusion
              If blood is to be warmed, the temperature must be monitored and   therapy in individuals with a hemolytic anemia, such as those with
            kept below a level that could cause hemolysis. Usually, this is less than   thalassemia or sickle cell disease, in which iron is not lost from the
            42°C. Heating blood under running hot tap water or heating in a   body but is recycled, can thus result in the accumulation of excessive
            microwave device is unacceptable.                     tissue  stores  of  iron.  Over  long  periods,  the  iron  that  is  stored  in
                                                                  parenchymal cells results in oxidative injury and organ failure, par-
                                                                  ticularly  in  the  heart,  liver,  and  endocrine  organs.  Iron  chelation
            Electrolyte Toxicity                                  therapy is now widely used to mitigate positive iron balance. The
                                                                  availability of oral iron chelators such as deferasirox and deferiprone
            Citrate,  a  component  of  the  preservative  solution  used  in  blood   provides expanded access to iron chelation therapy.
            storage,  functions  as  an  anticoagulant  by  chelating  calcium  and
            interfering with the coagulation cascade. Rapid transfusion of citrated
            blood  is  associated  with  a  drop  in  ionized  calcium  levels.  Citrate-  Air Emboli
            containing blood products, however, are routinely infused without
            any problem because the citrate is rapidly metabolized to bicarbonate.   Since the replacement of evacuated glass bottles by plastic blood bags,
            In patients with normal liver function, citrate infusion is unlikely to   the risk for air embolism from phlebotomy or transfusion has virtually
            produce reactions. Mild to severe citrate toxicity can be seen, however,   disappeared  from  transfusion  practice.  Air,  however,  still  may  be
            in  individuals  undergoing  therapeutic  apheresis  when  citrate  is   infused into patients by the roller pumps contained in various transfu-
            infused to anticoagulate blood flowing through the instrument and   sion devices, especially apheresis machines and intraoperative salvage
            large  volumes  of  citrated  RBCs  or  plasma  are  simultaneously   machines. All such devices currently manufactured, however, contain
            reinfused.                                            air-in-line sensors. However, any operators using this equipment must
              The effects of hypocalcemia range from mild circumoral paresthe-  be well trained and remain alert to the potential risk for air emboliza-
            sias to frank tetany. However, severe citrate toxicity, even with massive   tion at all times while the patient is being treated. Patients who receive
            transfusion, is rare. More commonly, the reaction is mild and self-  air intravenously experience acute cardiopulmonary insufficiency. The
            limiting and can be treated by merely slowing the rate of reinfusion.   air tends to lodge in the right ventricle, preventing blood from enter-
            If prolonged QT intervals or signs of tetany are seen, calcium can be   ing the pulmonary circulation. Acute cyanosis, pain, cough, shock,
            administered.  Calcium  need  not  be  infused  routinely,  even  after   and arrhythmia may occur, and death may result unless immediate
            large-volume blood transfusions. However, it is prudent to monitor   action is taken. The patient should be placed head-down on the left
            calcium status in patients undergoing massive transfusion and patients   side; this may displace the air bubble from the pulmonary valve. Use
            at risk for hypocalcemia arising from citrate toxicity. Under no cir-  and removal of central lines may also pose a risk for air embolism.
            cumstances should calcium be added to a unit of blood or a line used
            for blood infusion because it would recalcify the unit and cause clots
            to form. In addition to the effects on calcium, the metabolism of   Complications Associated With Massive Transfusion
            citrate also can result in a metabolic alkalosis because of the genera-
            tion of large amounts of bicarbonate.                 Massive transfusion is variably defined as the transfusion of one whole
              Citrate also chelates magnesium, so correction of the hypocalcemia   blood  volume  within  24  hours,  4  units  of  RBCs  in  1  hour  with
            may require infusion of magnesium, as well. Actual clinical complica-  anticipation of more blood needed, or transfusion of 50% of total
            tions  of  transfusion-induced  hypomagnesemia,  however,  have  not   blood volume in 3 hours. Common problems associated with massive
            been well documented other than in cases of apheresis.  transfusion  include  coagulopathy,  hypothermia,  and  metabolic
              Hyperkalemia caused by infusion of stored blood is a rare occur-  abnormalities.
            rence. Although hyperkalemia is often thought to be a problem in   Coagulopathy  of  massive  transfusion  is  multifactorial  and  can
            massive  transfusion,  development  of  hypokalemia  is  of  greater   have devastating consequences. Classically the coagulopathy associ-
            concern.  With  storage,  leakage  of  potassium  from  RBCs  to  the   ated with massive transfusion was thought to be attributable solely
            extracellular fluid occurs. However, after infusion the RBCs reverse   to  consumption  of  factors  owing  to  ongoing  hemorrhage  and/or
            the biochemical storage lesion by restoring the Na-K ATP membrane   dilution  owing  to  the  large  volume  of  fluids  and  RBCs  typically
            pump, and intracellular potassium levels are restored. As the citrate   infused. However, the understanding of hemostasis in massive trans-
            is metabolized to bicarbonate, the blood becomes alkalotic, contrib-  fusion now includes a form of coagulopathy that occurs before coagu-
            uting to hypokalemia. In massive transfusion, it is not uncommon   lation  factors  and  platelets  are  consumed.  Early  coagulopathy,
            for  this  to  result  in  the  need  for  administration  of  potassium.   described  primarily  in  the  setting  of  trauma,  is  driven  by  tissue
            Depending  on  the  storage  solution,  the  potassium  content  in  the   hypoperfusion and increased fibrinolysis. Early coagulopathy is not
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