Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5565_Библиотеки_им_академика_М_И_Перельмана.pdf
ADVERSE EFFECTS OF TRANSFUSION 67
Question 2: Which statement is true about the events that occur during a transfusion
reaction workup?
A. The posttransfusion venous sample should be in an EDTA-containing (purple
top) tube to prevent a false-negative DAT result.
B. If the posttransfusion urine is dipstick-positive for blood in the absence of intact
red cells seen microscopically, then this is highly suggestive of a hemolytic
transfusion reaction.
C. The suspected unit should be returned to the blood bank without any tubing.
D. If a hemolytic transfusion reaction is suspected, the unit should undergo ABO
typing, antibody screening, and repeat crossmatch using the recipient’s pre-
transfusion red cells.
E. In addition to DAT, the posttransfusion venous sample should be examined for
evidence of autoantibodies.
B. Free hemoglobin in the absence of intact red cells is highly indicative of a hemo-
lytic transfusion reaction. The presence of intact red cells could indicate bladder
infection, cancer, renal calculi, etc.
________________________________ ________________________________
夝
Question 3: Which statement about acute hemolytic transfusion reactions is NOT
true?
A. By definition, the reaction must occur within 4 hours of the transfusion.
B. The reaction is caused by preformed antibodies and complement.
C. Red cells undergo intravascular hemolysis.
D. Signs/symptoms include fever, flank pain or infusion site pain, and hyperten-
sion.
E. Signs/symptoms include red urine, red plasma, rash, chest tightness.
D. Hypotension may occur, hypertension in this situation is exceptionally rare.
The signs/symptoms to look for and/or ask the patient about include:
- Fever - Red plasma/urine(hemoglobinemia\uria)
- Hypotension - Bilirubinemia (several hours after transfusion)
- Severe flank pain - Pain at the infusion site
- Urticaria - Flushing
- Chest tightness - Oozing from IV sites (DIC)
________________________________ ________________________________
夝
Question 4: Which of the following statements about delayed hemolytic transfusion
reactions is not true?
68 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
A. The reaction typically occurs 15 to 30 days after the transfusion.
B. The reaction is caused by preformed antibodies and complement.
C. Red cells undergo extravascular hemolysis.
D. Recipients are often asymptomatic; it is usually discovered when the recipient
has an unexplained drop in hematocrit or increase in bilirubin.
E. The DAT is always positive at the time of workup.
B. Delayed hemolytic transfusion reactions are due to anamnestic antibody produc-
tion by previously sensitized lymphocytes. Antibodies are produced and coat the
donor red cells; then the coated cells are removed by the reticuloendothelial system
(extravascular hemolysis).
________________________________ _______________________________
夝
Question 5: Which of the following is NOT a sign/symptom of a febrile nonhemo-
lytic transfusion reaction (FNHTR)?
A. Hypotension.
B. Fever (temp above 38 C) or temperature increase of more than 1 C.
C. Shaking chills (rigors).
D. Hypertension.
E. Tachycardia and/or palpitations.
A. Hypotension (or shock) is not typically seen with FNHTRs.
________________________________ _______________________________
夝
Question 6: Which statement about FNHTRs is true?
A. FNHTRs are only rarely caused by preformed recipient antibodies directed
against leukocytes or platelets.
B. Unlike some anaphylactoid and urticarial reactions, mast cells are usually
involved in the pathogenesis of FNHTRs.
C. FNHTRs may be caused by cytokines released during storage of cellular blood
components, particularly platelets.
D. Studies have shown that leukocyte reduction eliminates the risk of FNHTRs.
E. FNHTRs tend to recur during subsequent transfusions.
C. Leukocyte reduction is most effective when it is performed immediately after (or dur-
ing) collection, probably because cytokines are released during storage. However, even
with prestorage leukocyte reduction the risk of FNHTR is not eliminated completely.
ADVERSE EFFECTS OF TRANSFUSION 69
________________________________ ________________________________
夝
Question 7: Which statement regarding anaphylactoid/anaphylactic transfusion
reactions is true?
A. Both anaphylactoid/anaphylactic reactions are IgE-mediated.
B. Anaphylactic reactions may occur even the first time a plasma-containing com-
ponent is transfused to an IgA-deficient recipient.
C. Both anaphylactoid and anaphylactic transfusion reactions require prior “sensi-
tization” for the immune response to occur.
D. Anaphylactic transfusion reactions can occur if the donor had been taking anti-
biotics before the transfusion.
E. Anaphylactoid and anaphylactic transfusion reactions cannot be treated the
same way.
D. Strictly speaking, an anaphylactic reaction is IgE-mediated. Anaphylactoid reac-
tions appear clinically similar but may not be IgE-mediated. A common example is
the IgA-mediated reaction that can occur with IgA-deficient patients. A pre-existing
anti-IgA in the patient is directed against an epitope in donor plasma. Anaphylactic
reactions (IgE-mediated) most commonly require previous exposure to an inciting
agent, such as a medication (eg, penicillin).
________________________________ ________________________________
夝
Question 8: Which statement about transfusion-related acute lung injury (TRALI) is
true?
A. TRALI is believed to be caused by either lipid activators of neutrophils or anti-
bodies directed against neutrophil or HLA antigens.
B. No laboratory tests are available to help support the diagnosis of TRALI.
C. The clinical picture is similar to ARDS with acute onset of dyspnea and hypox-
emia, but ARDS has a better prognosis.
D. A TRALI diagnosis may include transfusion-associated circulatory overload
(TACO).
E. Pooled plasma derivatives (ie, albumin, IVIG, RhIG, etc) are associated with
TRALI.
A. There are several theories about the cause of TRALI but most agree that the pro-
cess involves activation of recipient neutrophils and subsequent noncardiogenic
pulmonary edema. Clinically, patients with TRALI appear to have ARDS but the dis-
tinction from ARDS should be made because for the most part TRALI has a more
favorable outcome. TRALI should also be distinguished from other causes of pulmo-
nary edema, including volume overload (TACO). There are some data to indicate
that B-type natriuretic peptide (BNP) may be more commonly elevated in TACO
than in TRALI, helping to make the distinction between the two clinically similar
70 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
entities. There has been some concern that TRALI is under-recognized and many
studies are showing this to be the case. Vigilance is encouraged. Although any com-
ponent containing plasma can cause TRALI, it is very rare for it to be associated with
plasma derivatives.
________________________________ _______________________________
夝
Question 9: Which statement about transfusion-associated graft-vs-host disease (TA-
GVHD) is true?
A. The fatality rate is the same as that for transplant-related GVHD.
B. Patients receiving blood components from close relatives are not at increased
risk of TA-GVHD.
C. Leukocyte reduction reliably prevents TA-GVHD.
D. Irradiation shortens the lifespan of RBC units to 14 days from the date of irradi-
ation.
E. Signs/symptoms of TA-GVHD include diffuse rash, severe diarrhea, abnormal
liver function tests, and pancytopenia.
E. Transfusion-associated graft-vs-host disease is caused by the engraftment of donor
lymphocytes into most commonly an immunocompromised patient. Given the
exceptionally high mortality of TA-GVHD it is said that there are two treatments for
the condition – prevention and death. Prevention can occur with irradiation (and
subsequent inactivation of lymphocytes) in blood components destined for immuno-
compromised patients. Irradiation can potentially shorten the life span of RBC units.
Irradiated units should be held for only 28 days or until the original outdate of the
unit, whichever comes first.
________________________________ _______________________________
夝
Question 10: Which statement about bacterial contamination of blood components
is true?
A. RBC units are more likely to be contaminated with gram-positive organisms.
B. Platelets are more likely to be contaminated with gram-negative organisms.
C. RBC-associated sepsis occurs more frequently than platelet-associated sepsis.
D. There is a much lower risk of sepsis with autologous transfusions compared to
allogeneic transfusions.
E. In the event of a possible septic transfusion reaction, Gram’s stain and culture
of the unit should always be performed, along with recipient blood culture(s).
E. The answers for A and B are reversed. Gram-positive skin flora is more likely to
grow as a contaminant at room temperature, where platelets are stored. The major-
ity of cases of sepsis from contaminated blood components is due to contaminated
platelets. However, due to endotoxin production by gram-negative organisms, sep-
ADVERSE EFFECTS OF TRANSFUSION 71
sis due to transfusion with contaminated RBC units is associated with a higher mor-
tality rate (though the number of fatalities due to platelet contamination is higher
due to an overall high rate of contamination).
________________________________ ________________________________
夝
Question 11: About a week after receiving a RBC (or platelet) transfusion, the recip-
ient notices several rashes on his body. His test results reveal only a decreased plate-
let count and no other abnormalities. What is the most likely explanation?
A. The recipient has been previously sensitized and is exhibiting an anaphylactic
or anaphylactoid reaction.
B. The recipient has been previously sensitized and is exhibiting an anamnestic
response to a high-frequency platelet antigen.
C. The recipient’s own platelets are protected from this destructive process.
D. The recipient has a disease process that cannot be treated.
E. If the recipient requires another RBC transfusion in the future, washing the unit
will be of no value in preventing recurrence.
B. This is posttransfusion purpura. It is believed to be caused by an anamnestic
response in which the immune system makes antibodies directed against HPA-1a
antigen on the surface of the donated platelets. The recipient’s own platelets are not
spared (bystander effect), suggesting that the antigen is soluble and can bind to the
surface of the patient’s platelets, causing their destruction as well. IVIG followed by
transfusion of antigen-negative platelets may be helpful in severely symptomatic
patients.
________________________________ ________________________________
夝
Question 12: Which of the following statements about viral hepatitis infections is
true?
A. Hepatitis A may be transmitted by blood components, and may cause chronic
hepatitis.
B. Hepatitis before the age of 11 excludes a person from donating blood.
C. About one-third of patients with hepatitis B virus infection are asymptomatic
and without long-term sequelae.
D. Donors are screened for HBV infection by testing for HBsAg and/or anti-HBc.
E. HBV is not effectively inactivated by solvent/detergent (SD) treatment.
D. Hepatitis A is not primarily spread as a blood-borne agent (though it can be), but
rather in a fecal-oral manner. In addition, hepatitis A does not cause chronic hepati-
tis, whereas HBV and HCV can. Hepatitis A is more common than HBV or HCV in
children. Hence, viral hepatitis before age 11 is not an absolute exclusion from
blood donation as viral hepatitis after age 11 is. Up to two-thirds of patients with
72 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
HBV are asymptomatic. Due to the low levels of virus that may be present, serologic
tests are more effective than nucleic acid testing for detecting chronic carriers.
________________________________ _______________________________
夝
Question 13: Which of the following statements about hepatitis C infections is true?
A. HCV is less likely to lead to chronic hepatitis and hepatocellular carcinoma
than HBV.
B. HCV is the second most common reason for liver transplantation in the United
States today.
C. The only effective way to detect HCV infection is by either detecting the viral
DNA in the serum or by detecting HCV antigens in the serum.
D. There is no effective method currently available to immunize against HCV.
E. A combination of interleukin-2 and riboflavin may be effective therapy for
chronic HCV patients.
D. A significant portion of individuals infected with HCV will develop chronic dis-
ease (>80%). Viral hepatitis is the most common reason for liver transplantation in
the United States. Treatment of chronic HCV usually involves interferon with or
without ribavirin.
________________________________ _______________________________
夝
Question 14: Which of the following statements about HIV infection is NOT true?
A. The HIV p24 antigen can be detected as early as 16 days following infection.
B. HIV can be detected by reverse transcriptase PCR as early as 10 days following
infection.
C. HIV antibody takes at least 3 weeks to reach detectable levels following infec-
tion.
D. With current testing regimens, the risk of being infected with HIV due to a
transfusion is about 1:100,000.
E. Among the donor population, less than 20% of people who screen positive for
HIV on enzyme immunoassay end up confirming positive on Western blot.
D. The risk is much lower. According to a recent large study of blood donation
screening from the American Red Cross, the residual risk for contracting HIV from
donated blood is 1:1,467,000. For HCV the risk is similar, 1:1,149,000. (Zou et al,
Transfusion 2010;50:1495-504.)
ADVERSE EFFECTS OF TRANSFUSION 73
________________________________ ________________________________
夝
Question 15: Which of the following statements about HTLV-I is true?
A. It is the etiologic agent of adult T-cell leukemia/lymphoma.
B. It is the etiologic agent of filariasis.
C. It is transmitted by sexual contact only.
D. Influenza immunization within the preceding months can cause false-negative
test results.
E. Donors are screened for this virus using Western blot or recombinant immuno-
precipitation assay (RIPA).
A. HTLV-I is implicated as the causative agent of both adult T-cell leukemia/lym-
phoma and tropical spastic paraparesis (also known as HTLV-associated myelopa-
thy). HTLV can be spread by sexual contact in addition to exposure to contaminated
blood and vertical transmission via breast milk. Screening for donors in the United
States is with an enzyme immunosorbent assay (EIA); the confirmatory assay is
Western blot or recombinant immunoprecipitation assay (RIPA).
________________________________ ________________________________
夝
Question 16: Which of the following statements about CMV is true?
A. CMV is thought to be transmitted as intact, infectious virion particles.
B. A CMV-reduced-risk unit is almost as effective as a CMV-seronegative unit in
preventing infection. Both significantly reduce risk of transmission
C. Newborns, HIV-positive patients, and transplant recipients frequently develop
CMV infections, but they are most often asymptomatic.
D. The primary CMV-related concern for marrow transplant recipients is CMV
encephalitis.
E. HIV-infected patients are particularly at risk for CMV pneumonitis.
B. A meta-analysis of controlled trials concluded that CMV-seronegative cellular
components are more efficacious than leukocyte-reduced components at preventing
CMV infection, although considerable controversy still exists. In Canada and Swit-
zerland, CMV-seronegative components are considered to be the standard for CMV
safety and that leukocyte-reduced units are not yet considered equivalent. HIV-
infected patients are at a higher risk for CMV retinitis, encephalitis, or enteritis than
transplant patients, who are at the highest risk for CMV pneumonitis.
74 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
________________________________ _______________________________
夝
Question 17: Which statement about Creutzfeldt-Jakob disease is NOT true?
A. There has never been a report of blood-borne transmission of classic CJD.
B. Variant CJD occurs in younger patients and tends to have a faster clinical
course leading to death than classic CJD.
C. The prion protein has never been isolated in lymphoid tissue in either classic or
variant CJD; therefore, it is not possible for these diseases to be transmitted by
blood.
D. Histologically, CJD is characterized by spongiform degeneration with neuronal
loss in the absence of inflammation.
E. The causative agent in CJD is an abnormally folded protein, called a prion.
C. Prions have been detected in lymphoid tissues of variant CJD patients. That is
why there is so much concern about the possibility of transmission by blood compo-
nents, and that is one of the reasons Canada and Great Britain have mandated the
universal use of leukocyte-reduced blood components. There is still controversy in
the literature as to whether actual cases exist of vCJD that have been transmitted
solely through transfusion.
________________________________ _______________________________
夝
SUGGESTED READING
General
Carson TH, ed. Standards for blood banks and transfusion services. 27th ed.
Bethesda, MD: AABB, 2011.
Davenport RD, for the Scientific Section Coordinating Committee. Guidelines for
the laboratory evaluation of transfusion reactions. Bethesda, MD: AABB, 2003.
Goodnough LT, Brecher ME, Kanter MH, AuBuchon JP. Transfusion medicine: First
of two parts—blood transfusion. N Engl J Med 1999;340:438-47.
Honig CL, Bove JR. Transfusion-associated fatalities: A review of Bureau of Biologics
reports 1976-1978. Transfusion 1980;20:653-61.
Kleinman S, Chan P, Robillard P. Risks associated with transfusion of cellular blood
components in Canada. Transfus Med Rev 2003;17(2):120-62.
Popovsky MA, ed. Transfusion reactions. 4th ed. Bethesda, MD: AABB Press, 2012
(in press).
Roback JD, Grossman BJ, Harris T, Hillyer CD, eds. Technical manual. 17th ed.
Bethesda, MD: AABB, 2011.
ADVERSE EFFECTS OF TRANSFUSION 75
Sazama K. Reports of 355 transfusion-associated deaths: 1976 through 1985. Trans-
fusion 1990;30:583-90.
Serious Hazards of Transfusion Steering Group. The 2010 Annual SHOT Report.
Manchester, England: SHOT Office, 2011.
Snyder EL. Treatment of blood transfusion reactions: A user’s guide. Transfus Med
Topic Update 1991;4:3-15.
Hemolytic Reactions
Moore SB, Taswell HF, Pineda AA, Sonnenberg CL. Delayed hemolytic transfusion
reactions: Evidence of the need for an improved pretransfusion compatibility test.
Am J Clin Pathol 1980;74:94-7.
Ness PM, Shirey RS, Thoman SK, Buck SA. The differentiation of delayed serologic
and delayed hemolytic transfusion reactions: Incidence, long-term serologic find-
ings, and clinical significance. Transfusion 1990;30:688-93.
Pineda AA, Brzica SM Jr, Taswell HF. Hemolytic transfusion reaction: Recent experi-
ence in a large blood bank. Mayo Clin Proc 1978;53:378-90.
Pineda AA, Taswell HF, Brzica SM Jr. Delayed hemolytic transfusion reaction: An
immunologic hazard of blood transfusion. Transfusion 1978;18:1-7.
vonSabern I, Ehlers M, Grunwald U, et al. Release of mediators of systemic inflam-
matory response syndrome in the course of a severe delayed hemolytic transfusion
reaction caused by anti-D. Transfusion 1998;38:459-68.
Febrile Nonhemolytic Reactions
Heddle NM. Webert K. Febrile nonhemolytic transfusion reactions. In: Popovsky
MA, ed. Transfusion reactions. 4th ed. Bethesda, MD: AABB Press, 2012 (in press).
Heddle NM, Klama LB, Singer J, et al. The role of the plasma from platelet concen-
trates in transfusion reactions. N Engl J Med 1994;331:625-8.
Muir JC, Herschel L, Pickard C, AuBuchon JP. Pre-storage leukocyte reduction
decreases the risk of febrile reactions in sensitized platelet recipients (abstract).
Transfusion 1995;35(Suppl):S45S.
Anaphylactic Reactions
Sandler SG. How I manage patients suspected of having an IgA anaphylactic trans-
fusion reaction. Transfusion 2006;46:10-13.
Sandler SG, Mallory D, Malamut D, Eckrich R. IgA anaphylactic reactions. Transfus
Med Rev 1995;9:1-8.
76 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
TRALI
Bux J, Becker F, Seeger W, et al. Transfusion-related acute lung injury due to HLA-
A2-specific antibodies in donor blood. Br J Haematol 1996;93:707-13.
Cooling L. Transfusion-related acute lung injury (letter). JAMA 2002;288:315-16.
Dry SM, Bechard KM, Milford EL, et al. The pathology of transfusion related acute
lung injury. Am J Clin Pathol 1999;112:216-21.
Goldman M, Webert KE, Arnold DM, et al. Proceedings of a Consensus Conference:
Towards an understanding of TRALI. Transfus Med Rev 2005;19:2-31.
Kao GS, Wood IG, Dorfman DM, et al. Investigations into the role of anti-HLA class
II antibodies in TRALI. Transfusion 2003;43:185-91.
Kleinman S, Caulfield T, Chan P, et al. Towards an understanding of transfusion-
related acute lung injury: Statement of a consensus panel. Transfusion 2004;44:
1774-89.
Kopko PM, Marshall CS, MacKenzie MR, et al. Transfusion-related acute lung
injury: Report of a clinical look-back investigation. JAMA 2002;287:1968-71.
Kopko PM, Popovsky MA, MacKenzie MR, et al. HLA Class II antibodies in transfu-
sion-related acute lung injury. Transfusion 2001;41:1244-8.
Lenahan SE, Domen RE, Silliman CC, et al. Transfusion-related acute lung injury
secondary to biologically active mediators. Arch Pathol Lab Med 2001;125:523-6.
Popovsky MA, for the Scientific Section Coordinating Committee. Guidelines for the
management of transfusion-related acute lung injury. Bethesda, MD: AABB, 2003.
Popovsky MA, Chaplin HC, Moore SB. Transfusion-related acute lung injury: A
neglected, serious complication of hemotherapy. Transfusion 1992;36:589-92.
Popovsky MA, Moore SB. Diagnostic and pathogenetic considerations in transfu-
sion-related acute lung injury. Transfusion 1985;25:573-7.
Silliman CC, Paterson AJ, Dickey WO, et al. The association of biologically active
lipids with the development of transfusion-related acute lung injury: A retrospective
study. Transfusion 1997;37:719-26.
Toy P, Popovsky MA, Abraham E, et al. Transfusion-related acute lung injury: Defi-
nition and review. Crit Care Med 2005;33:721-6.
Webert KE, Blajchman MA. Transfusion-related acute lung injury. Transfus Med Rev
2003;17(4):252-62.
Zhou L, Giacherio D, Cooling L, Davenport RD. Use of B-natriuretic peptide as a
diagnostic marker in the differential diagnosis of transfusion-associated circulatory
overload. Transfusion 2005;45:1056-63.