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Adverse Outcomes in Blood and Blood Component Therapy - page 12 / 19





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that the virus is present at various but generally high prevalences, not only in populations with parenteral risk exposure, such as intravenous drug users (6-40%) but also in apparently healthy individuals, such as blood donors (1-62%). High prevalences were first described in industrialized countries (Japan, and countries in Europe, North America, and South America) but also, recently, in rural African populations without any identified parenteral exposure (7-83%). Altogether, these findings suggest the existence of a nonparenteral route of virus transmission.44

The GB virus C (GBV-C), also called hepatitis G virus (HGV), has a worldwide occurrence, but its clinical significance is still unclear. It belongs to the family Flaviviridae, which also includes HCV. The virus has various prevalences in different blood donor populations, which range from 0.9% to 14.6%. Its possible role in fulminant hepatitis and aplastic anemia has been debated. It has been shown to replicate in peripheral blood mononuclear cells both in vivo and in vitro. Several studies suggest that it does not replicate in hepatocytes, but some investigators also have reported replication in liver cells.45 It is parenterally transmissible, and coinfections with HBV and HCV are common. The virus is more frequently transmitted to infants than HIV or HCV. Transmission of this agent is associated with high-titer viremia and mode of delivery. Sexual transmission has also been suggested, however, little is known about other modes of transmission that could explain the high prevalence and worldwide distribution of this virus. 45

Neither Creutzfeldt-Jakob disease (CJD) nor bovine spongiform encephalitis has ever been reported to be transfusion-transmitted, but current practice precludes donation from a person who has received human-derived growth hormone or a dura mater transplant or who has a family member with CJD. Solid evidence from experimentally infected animals and fragmentary evidence from naturally infected humans indicate that blood may contain low levels of the infectious agent of CJD, yet blood components have never been identified as a cause of CJD in humans.46 Epidemiologic evidence of the absence in humans of disease transmission from plasma components can probably be explained by the absence of significant plasma infectivity until the onset of symptomatic disease, and comparatively low levels of infectivity during the symptomatic stage of disease, the reduction of infectivity during plasma processing and 3 the need for at least five to seven times more infectious agent to transmit disease by the intravenous than intracerebral route. These and other factors probably also account for the absence of transmission after the administration of whole blood or blood components.46

Physically or Chemically Induced Transfusion Reaction Red cells may be damaged by the simultaneous administration or mixing of drugs or hypotonic or hypertonic solutions. The red cells may also sustain heat damage from warmers, or freezing damage in the absence of cryoprotective agents. Mechanical damage may result from cardiopulmonary bypass pumps or from roller pumps in the blood pump.2 These pose unique situations in that blood that is ABO, Rh and crossmatch compatible with patient is hemolyzed prior to it being transfused. Rapid transfusion of 10 or more units of citrated blood can increase plasma citrate levels and cause hypocalcemia. However, this is usually self-compensated with no need for calcium therapy.4 Other consequences of physically or chemically induced transfusion reactions include hypothermia, hyperkalemia, depletion or dilution of coagulation factors.2 The signs and symptoms may include facial numbness, chills, generalized numbness, muscle twitching, cardiac arrhythmias, nausea, vomiting, perioral tingling, altered respirations and anxiety.2   

Parasitic Contamination Malaria is transmitted easily through infected RBCs. Many donors are unaware that they have malaria, which may be latent and transmissible for 10 to 15 yr. Storage does not render blood safe. Prospective donors must be asked about malaria or whether they have been in a region where it is prevalent. Donors who have had a diagnosis of malaria or who are immigrants, refugees, or citizens from countries in which malaria is considered endemic are deferred for 3 yr; travelers to endemic countries are deferred for 1 yr. Babesia microti a protozoan of rodents which is transmitted through the bite of the Ixodes dammini tick has been responsible for a few cases of transfusion-transmitted disease.26 Babesiosis is characterized by fever malaise and hemolytic anemia and may be mistaken for malaria because of the similarity of symptoms.5

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