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Flashcards in Transfusion complications Deck (27)
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Transfusion reaction workup

If reaction is mild allergic or mild circulatory overload, transfusion can be restarted and reaction need not be reported to the lab


  1. Clerical checks
  2. Inspection for hemolysis
    • Visually check patient serum/plasma for hemolysis
    • Check urine with hemoglobin dipstick
      • if positive, examine urine microscopically for hematuria
      • in an intravascular HTR there is hgb-uria without hematuria
      • myoglobin can cause FP
    • Blood drawn >8 hours after may be negative visually for hemolysis, but may be icteric so a serum bilirubin should be done up to 36 hours following event
    • free serum myoglobin may give false positive visual inspection (should be h/o trauma in this case)
  3. Recheck ABO on post-transfusion sample
  4. DAT
    • positive in HTR usually
    • may be negative if hemolysis was very severe
  5. If reaction deemed nonhemolytic then additional transfusions can be administered
  6. If there is hemolysis, additional workup including ABO and Rh typing and antibody panel should be done to determine the antibody
  7. Notification
    • transfusion fatality or serious morbidity must be reported within 24 hours to the FDA by telephone and within 7 days in writing
    • when fatality/morbidity appears to be caused by a single donor, the collecting facility must be notified immediately, followed by notification in writing
    • when a transfusion related infection is confirmed or cannot be excluded, then the identity of the donor units must be conveyed to the collecting facility, any other recipients of the blood components from the donor, and each recipient's physician
  8. Written report should be in the chart


Febrile nonhemolytic transfusion reaction

- incidence

- definition

- mechanism

- treatment

  • most common type of TR
  • 1/200 transfusions
  • defined as increase in temperature of 1 degree C or 2 degrees F 
    • no other explanation for TR
  • mediated by cytokines released by WBCs in stored unit of blood
    • incidence can be reduced by prestorage leukoreduction
  • treatment: antipyretics and/or transfusion with leukocyte reduced products


Allergic transfusion reactions

- relative incidence and incidence

- symptoms

- mechanism

- lab findings

- treatment


  • 2nd most common TR
  • mild (urticaria/pruritis) to severe (anaphylaxis)
  • 1/300 transfusions
  • mediated by allergic (IgE mediated) reaction to plasma proteins
    • IgA deficient recipient may have a reaction to IgA in donor plasma
    • IgA deficiency affects 1 in 700 recipients, but severe reactions in a minority
  • there are no findings on the transfusion reaction workup
  • Treatment
    • for mild reactions: symptomatic 
    • if recurrent, can pretreat with antihistamines
    • for anaphylaxis, give parenteral epinephrine 
    • IgA deficient patients with anaphylaxis should receive IgA deficient units or washed units


Acute hemolytic transfusion reactions



Clinical presentation

Lab findings


  • 1/6000 to 1/30000
  • Intravascular or extravascular 
    • Intravascular: related to ABO incompatiblity and most often result from clerical error
      • rarely non-ABO antibodies (e.g., Kidd) may be responsible
    • Extravascular: usually non-ABO
  • non-immune causes
    1. prolonged storage
    2. improper storage
    3. malfunction of mechanical infusion devices or blood warmers
    4. needles of too small caliber
    5. addition of anything other than normal saline to infusion
    6. bacterial contamination (e.g., clostridia)
    7. donor may have intrisic red cell defect 
  • Clinical presentation of intravascular hemolysis:
    • abrupt onset of fever, chills, back pain, pain at infusion site, hypotension, DIC
  • Clinical presentation of extravascular hemolysis
    • often asymptomatic
    • may present with pallor, hyperbilirubinemia, or anemia
  • Lab findings
    • positive DAT
    • Intravascular hemolysis
      • pink serum 
      • hemoglobinuria
      • coagulation abnormalities
      • schistocytes
    • Extravascular hemolysis
      • hyperbilirubinemia
      • spherocytes
  • Treatment
    • leave line open with saline infusion
    • hemodynamic support


DHTR and delayed serologic transfusion reaction

- define DHTR

- define DSTR


- Lab findings

- most common antigens

- symptoms

- treatment


  • DHTR refers to hemolysis of transfused blood occurring days to weeks after transfusion (typically 5-14 days)
  • DSTR is a newly detectable alloantibody following transfusion without hemolysis
  • DSTR: DHTR = 3:1
  • Lab findings:
    • positive DAT (often mixed field)
    • hyperbilirubinemia
    • microspherocytes
    • new antibody screen/panel will identify causative antibody
  • Most common antigens
    1. Kidd (severe intravascular hemolysis)
    2. E
    3. c
    4. Kell
    5. Duffy
  • May have symptoms or not
  • No treatment needed


Bacterial contamination (transfusion transmitted sepsis)

- mortality rates for platelet and red cell transmitted sepsis

- incidence of contaminated units

- incidence of transfusion transmitted sepsis

- source

- organisms associated with platelets and red cells

- clinical presentation

- treatment

- lab evaluation

- prevention

  • mortality rate 25% with platelet transmitted sepsis and 70% with red cell transmitted sepsis
  • most common transfusion transmitted infection
  • incidence of contaminated units between 1/1000 and 1/4000
  • incidence of transfusion transmitted sepsis is 1/25,000 platelet transfusions and 1/250,000 red cell transfusions
  • bacteria originate from donor skin and less commonly donor blood
  • in platelets, staph are frequently implicated
  • in red cells:
    1. yersinia enterocolitica (#1)
    2. serratia liquifaciens
    3. citrobacter
    4. pseudomonas
  • Clinical presentation
    • high fever and shock (also consider hemolytic reaction in this setting)
    • blood product may be visibily discolored, hemolyzed or contain clots
    • recipient serum and urine often contain free hemoglobin, but DAT is negative
  • Treatment: stop transfusion; broad Abx
  • Evaluation
    • perform gram stain on unit of blood
    • culture both unit and recipient blood
    • notify blood supplier
  • Prevention
    • proper screening and aseptic technique at time of donation
    • discarding first 15-30 cc of blood drawn into a diversion pouch
    • AABB required methods to detect bacterial contamination in platelets


Transfusion associated GVHD

- fatality rate

- mechanism

- presentation

- prevention

- treatment

  • Highly (>90%) fatal complication of transfusion of cellular blood products
  • mechanism
    • immunocompetent T cells from donor engraft in immunocompromised recipient and mount reaction to recipient tissue
    • can affect immunocompetent recipient if donor is HLA similar
  • present with tetrad:
    • dermatits (periauricular, palmar and plantar erythroderma)
    • enterocolitis (watery diarrhea)
    • hepatitis (aminotransferase elevation)
    • bone marrow suppression (pancytopenia)
  • prevention
    • irradiation of blood products
  • no effective treatment; most cases are fatal


Transfusion associated acute lung injury (TRALI)

- incidence and mortalty

- clinical setting

 - tests

- mechanism

- criteria

- risk factors

  • most common cause of transfusion related fatality (15% of fatal transfusion reactions, with 5-10% mortality overall)
    • Incidence: 1/5000 transfusions
  • noncardiac pulmonary edema following transfusion of plasma containing blood products
  • No readily available test that confirms TRALI
    • can be confirmed by finding antigranulocyte, anti HLA class I or anti HLA class II antibodies in donor plasma
  • Criteria
    • acute onset during or within 6 hours of transfusion
    • hypoxemia (e.g, PaO2: FiO2 <300 or O2 saturation <90% on room air)
    • bilateral pulmonary infiltrates on CXR
    • no preexisting acute lung injury
    • no competing risk factors for acute lung injury
    • no evidence of circulatory overload (e.g., elevated pulmonary arterial wedge pressure)
  • Mechanism
    • donor antigranulocyte and/or anti HLA antibodies target recipient granulocytes, producing microaggregates in pulmonary circulation
  • Risk factors
    • recipient risk factors
      • induction chemo for hematologic malignancy
      • cardiac bypass surgery
    • donor risk factors
      • multiparity
    • plasma containing blood components (platelets and plasma) pose greatest risk


Clinical presentation of TRALI

  • tachypnea
  • cyanosis
  • dyspnea
  • fever
  • hypoxemia
  • diffuse bilateral fluffy infiltrates on CXR (resembles pulmonary edema)
  • within 6 hours of transfusion


TRALI differential diagnosis

  1. Volume overload (transfusion associated circulatory overload - TACO)
    • usually responds rapidly to diuresis
    • elevated BNP
    • elevated pulmonary capillary wedge pressure
  2. anaphylaxis
    • wheezing and upper airway edema
    • usually responds to epi
    • usually lack infiltrates
  3. Bacterial contamination
    • culture positive
    • hemodynamic features predominate over respiratory
  4. Hemolytic transfusion reaction
    • positive DAT and hemolysis
  5. Acute respiratory distress syndrome
    1. difficult to distinguish
    2. temporal features most important


TRALI treatment and prevention

  • Treatment
    • stop transfusion
    • supportive
    • surviving patients recover within 72 hours
  • Prevention
    • risk of second episode is very low
    • exclude implicated donors from future transfusion
    • exclude plasma products from women or at least from multiparous women


Posttransfusion purpura

  • profound thrombocytopenia 2-14 days following red cell or platelet transfusion
  • affected recipients are almost always multiparous women
  • Mechanism
    • platelet alloantibodies, most commonly anti HPA-1a
    • these cause destruction of both donor and recipient platelets
  • 2% of population is HPA-1a negative and capable of producing antibodies
  • PTP is usually self-limited process that resolves within 3 weeks
  • treat with IV gamma globulin results in more rapid recovery wihtin 3-5 days


Platelet refractoriness

- what is it

- occurs in

- mechanism

- risk factors

- diagnosis

- prevention

  • Progressive diminution in quantity of platelet increase following platelet transfusion
  • arises in patients who require repeated platelet transfusions
  • Mechanism
    • secondary platelet refractoriness is most commonly caused by
      • infection
      • splenomegaly
      • drugs (amphotericin)
      • DIC
    • primary platelet refractoriness is caused by HLA alloimmunization
  • Risk for all types related to multiple factors, particulary the status of the spleen
    • splenectomized patients have lowest risk, patients with palpable spleen the highest
  • Diagnosis
    • lower than expected posttransfusion platelet increment in 2 consecutive occasions
    • 4 pack of single donor platelets has expected increment of 20,000/uL
    • a 6 pack or pheresis pack has expected increment of 30,000 /uL
    • platelet count increment calculation:
      • CCI= (Platelet countpost – Platelet countpre) x BSA(m2) / Number of platelets transfused(1011

      • normal is >= 7500

    • timing of posttransfusion count: within 10-60 minutes after transfusion (and then again?)

  • Prevention

    • minimize transfusions
    • minimize donor exposure (use pheresis products)
    • leukoreduction filtration


Testing for Hepatitic C

  • highly transmissible by transfusion
  • screened for by history and lab testing
    • test for anti HCV
    • positive anti HCV confirmed by RIBA
    • PCR for HCV RNA (HCV NAT)


Testing for hepatitis B virus

  • highly transmissible by transfusion
  • screened for by history and lab testing
    • anti HBc
    • HBsAg
    • HBV NAT is optional
  • hepatitis D virus screened for with HBV screen



transfusion transmission is rare


HTLV and HIV screening

  • screened with history and labs
  • HIV
    • test for HIV1/2 antibodies
    • HIV RNA (NAT)
    • p24 antigen no longer required
    • readily transmissible by transfusion
    • endemic in Japan and Caribbean
    • causes late sequelae (adult T cell leukemia/lymphoma and HTLV associated myelopathy (tropical spastic parapersis)
    • screened for by testing for HTLV I/II antibodies



- transmission

- who needs CMV negative products?

- alternative to CMV negative? 

  • transmitted by mononuclear WBCs
  • important to reduce transmission of CMV in CMV negative transplant candidates/recipients and low birth weight neonates
  • if CMV negative not available, give leukoreduced


West Nile virus testing

  • most infections with WNV are asymptomatic or mild
  • severe infection occurs in 1/150 cases (1/1000 is fatal)
  • viremia precedes symptoms by several weeks
  • prevention: NAT testing recommended during outbreaks; donors deferred if symptomatic



Can be transmitted by transfusion

Screened for only by history



  • Treponema pallidum is transmitted by transfusion only very rarely
  • no new transfusion transmitted cases have been reported in decades


Chagas disease

  • can be transmitted by transfusion
  • prevalent in Central America and South America 
  • In Mexico, nearly 1/100 donors are positive 



  • never been documented to be transmitted by transfusion
  • variant CJD has been documented to be transmitted by transfusion
  • Excluded from donating:
    • in the US people at risk for vCJD by history (those who have traveled to or lived in BSE endemic areas)
    • dural transplant recipients
    • patients getting pituitary derived growth hormone
    • patients getting bovine insulin
    • relative of patients with CJD are deferred


Changes in electrolytes due to transfusion

  • Hypocalcemia (due to citrate)
  • HyperK
    • stored cellular blood products usually have excess extracellular potassium
    • risk highest for neonates and those with impaired renal function
  • HypoK
    • transfusion of cells that are intracellularly potassium depleted, leading to transcellular shifts of serum potassium



  • With large volumes of unwarmed products, core body temperature can be reduced
  • exacerbates the effects of hypocalcemia and hyperkalemia
  • prewarming recommended for massive transfusion; AABB requires that temperature not exceed 42 degrees


Iron overload

  • Each unit contains 200 mg of iron
  • when whole body iron burden reaches 500 mg/kg clinical iron overload can develop affecting heart and liver
  • iron chelation with parenteral deferoxamine or oral deferasirox can be given


Transfusion related immunomodulation

transfusion of cellular blood products causes immunosuppression