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Transfusion Medicine Fellowship > Transfusion reactions > Flashcards

Transfusion reactions Flashcards

1
Q

What is the rate of mistransfusion? How many result in AHTR? How many result in deaths?

A

Mistransfusion: 1 in 19,000
AHTR: 1 in 76,000
Death: 1 in 1,800,000

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2
Q

What risk factors predict hyperkalemic cardiac arrest in massive transfusion?

A

Acidosis, hypoglycemia, hypothermia, hypocalcemia.

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3
Q

What substances mediate shock in hemolytic transfusion reactions?

A

C3a and C5a (anaphylotoxins)
C3b (opsonin, mediates hemolysis)
Tissue factor (upregulated by complement and TNFa, IL-1)

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4
Q

What causes renal failure in AHTR?

A

Shock, mostly, with loss of renal perfusion, but also free hemoglobin, thrombi, and complex deposition.

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5
Q

How should AHTR be treated?

A

Stop transfusion. Preserve renal function with fluids and pressors. Monitor for pulmonary edema and hyperkalemic cardiac arrest. Dialyze for kidney failure, give products for DIC, and consider red cell exchange.

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6
Q

What are some transfusion-related causes of non-immune hemolysis?

A

Incomplete deglyerolization, storage lesion, use of a rapid infuser with a small needle. Overheating, hypotonic carrier solutions.

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7
Q

What is the key finding needed to diagnose transfusion-related sepsis?

A

Must culture the same organism from the bag as the patient.

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8
Q

What drives the pathophysiology of FNHTR and how can it be prevented?

A

Accumulated cytokines from passenger leukocytes but also anti-HLA antibodies play a role. Prevent with prestorage leukoreduction and sometimes plasma reduction (for platelet units?)

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9
Q

For what transfusion reaction is meperidine sometimes indicated?

A

FNHTR with extensive rigors.

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10
Q

How can allergic reactions be distinguished from the many other reactions that share similar features?

A

Allergic reactions generally occur within 4hrs of transfusion start. Urticaria and angioedema are very specific symptoms.

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11
Q

What are some causes of allergic transfusion reactions? Or anaphylactic reactions?

A

IgA deficiency, haptoglobin deficiency, complement deficiency

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12
Q

How can anaphylactic transfusion reactions be avoided?

A

Wash or use detergent-treated plasma, or use products from IgA-deficient donors.

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13
Q

What is the physiological “two-hit” model of TRALI pathogenesis?

A

There is generally a “priming” stressor that prepares neutrophils and endothelium, then an alloantibody or biological response modifier from transfusion.

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14
Q

What is the clinical presentation in TRALI?

A

Hypoxia, ARDS-like with an onset between 1-6 hours of transfusion. Hypotension, fever, tachycardia are common.

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15
Q

Who are most susceptible to TACO?

A

Infants and the elderly.

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16
Q

What are some helpful lab findings in TACO?

A

Non-specific overload features, but comparing BNP pre- and post is helpful (Post 1.5x pre, with >100ng/mL post).

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17
Q

What defines hypotensive transfusion reaction? What are some causes?

A

Adults: SBP drop of 30+ or post SBP of <80
Children: >25% SBP drop
Caused by bradykinin effect from ACEi, bypass, or recent prostatectomy. Associated with bedside LR filter use.

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18
Q

What are some possible consequences or complications of massive transfusion?

A 
Citrate toxicity
Potassium disturbances
Hypothermia
Acidosis
Coagulopathy
Air embolism
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19
Q

How is potassium metabolism affected in massive transfusion?

A

Children or renal failure patients may become hyperkalemic, but most patients become HYPOkalemic due to reaccumulation in donor cells, citrate effect, or effect of catecholamines & aldosterone.

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20
Q

When does coagulopathy of massive transfusion set in? How can it be predicted?

A

Starts after about 20-30 unit transfusions, and/or when platelet counts drop below 50k. Note that low fibrinogen levels are a better predictor than PT/PTT.

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21
Q

When can an air embolism be fatal? How should it be managed?

A

When the volume exceeds 100mL (or it is arterial). Lay patient on their left side with head down to dislodge it from the pulmonic valve.

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22
Q

What blood group systems are associated with DHTR? Can it occur with one transfusion?

A

KIDD, Duffy, Kell, MNS. Almost never results from one single exposure.

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23
Q

What are the requirements for TA-GVHD to occur?

A

The unit must have lymphs, which recognize host HLA as foreign, who is in turn immune-compromised.

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24
Q

How does TA-GVHD present?

A

Rashes, GI upset (enterocolitis), fever, liver abnormalities, and cytopenias. Nearly all patients die in 1-3 weeks.

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25
Q

How does PTP present?

A

Precipitous and unexpected massive thrombocytopenia usually about 2 weeks out from transfusion, usually in women and severe enough to cause death from ICH.

26
Q

How is PTP managed? What causes it?

A

Give IVIG, steroids, maybe TPE or even perform splenectomy. Washing and sometimes even matched units don’t always help? Caused by alloantibodies to usually HPA-1a.

27
Q

How much iron is in each RBC unit? After how many simple transfusions can iron overload occur?

A

200-250mg per red cell unit. Expect iron overload starting no sooner than 20 simple unit transfusions.

28
Q

Are allergic transfusion reactions caused by donor or recipient factors?

A

MOSTLY recipient factors (eg. Atopy, specific antibodies). However, donor factors can cause allergic symptoms, and allergic reactions have been described in autologous transfusion.

29
Q

What labs can be helpful in working up allergic reactions?

A

Serum tryptase and histamine levels can be measurably increased during and following allergic reactions.

30
Q

What groups of antigens can cause allergic reactions?

A

Endogenous donor proteins (eg. IgA), exogenous antigens from the donor (eg. Peanut antigens), donor IgE, and storage products (CCL5, C5a)

31
Q

How common is IgA deficiency? What is the diagnostic cutoff?

A

See in up to 1:600 caucasians. Defined as serum IgA <5 mg/dL, but severe deficiency is rarer and defined as <0.05 mg/dL.

32
Q

Haptoglobin deficiency

A

Seen mostly in asians, can cause severe ATRs

33
Q

What are the symptoms seen in allergic transfusion reactions?

A

Hypotension
Urticaria, angioedema
Can have GI upset due to degranulation in tract.
Severe: Respiratory / Cardiovascular collapse.

34
Q

What are the hemovigilance criteria for ATR?

A

Definitive: 2+ of hypotension, edema, rash, pruritus, respiratory distress, flushing

Probable: 1+ of above (except flushing or hypotension; too general)

35
Q

How are allergic reactions treated?

A

Antihistamines, bronchodilators, steroids, and epinephrine/O2/fluids for anaphylactic reactions.

36
Q

How can allergic reactions be prevented?

A

Give IgA-deficient units
Volume reduction, PAS, washing
Pre-treatment (not actually proven to reduce rate)

37
Q

What transfusion settings are especially high risk for TRALI?

A

Any transfusion from gravid mothers, and especially directed mother-child donations.

38
Q

What donor factors are thought to cause TRALI?

A

Anti-HLA > Anti-HNA (-3a) antibodies, most often seen in alloimmunized patients (classically gravid mothers).

39
Q

What is a “reverse TRALI”?

A

TRALI following transfusion of neutrophil-containing product into a patient who is heavily alloimmunized.

40
Q

What are the laboratory findings seen in TRALI?

A

There is a transient neutropenia that after ~6hrs converts to a neutrophilia. Post:Pre BNP levels should increase by only ~1.5x

41
Q

How is TRALI treated?

A

Just oxygen support. Diuretics and steroids are probably not helpful. Severe cases may require ECMO.

Experimental: TPE, IVIG

42
Q

How should TRALI reactions be reported and followed up on?

A

Lookback: Inform supplier, who screens donor sample for antibodies. If serology found, defer. Note that positive serology is not required to call the initial TRALI reaction.

43
Q

In what epidemiologic settings is TA-GVHD more likely to occur? Why aren’t HIV+ patients affected?

A

Populations with low HLA diversity (Japan); increases risk of one-way mismatches. HIV patients do not seem to manifest disease; perhaps the virus infects the donor lymphocytes.

44
Q

What special molecular test is required to definitely confirm TA-GVHD?

A

Recovery of donor DNA from recipient peripheral blood (T-lymphs).

45
Q

What types of units have been implicated in TA-GVHD?

A

Red cells more than whole blood more than platelets. Note only fresh (<14d) units have been implicated; whole blood probably higher risk than others.

46
Q

What methods can be used to reduce the risk of TA-GVHD?

A

Irradiation, leukoreduction, and pathogen reduction (INTERCEPT or Mirasol systems).

47
Q

What is the usual or main target antigen in passenger lymphocyte syndrome?

A

Recipient A/B/O.

48
Q

What is the system used to report transfusion-associated reactions or deaths in the US?

A

The NSHN, originally developed for hospital acquired infections. Nearly all hospitals already use this framework for other purposes, but many fewer use the hemovigilance module.

49
Q

What is the only existing tool in the US for tracking DONOR reactions?

A

Donor Hemovigilance Analysis and Reporting Tool (DonorHART)

50
Q

What is the current consensus list of definitions for transfusion reactions?

A

The 2014 AABB-ISBT Standard Definitions of complications related to blood donations.

51
Q

What is the role of Demerol in treating tranfusion reactions? Any special caveats about its use?

A

Meperidine can be used to relieve severe rigors, but it can cause respiratory depression–have Narcan around.

52
Q

What transfusion reaction may present with arrhythmia / cardiac arrest?

A

Many potentially can, but think about anaphylactic.

53
Q

What should be the immediate management following an AHTR?

A

Stop transfusion. FIND THE SWITCHED UNIT. Provide fluid and pressor support (D5W, NaHCO3, mannitol, dopamine)to maintain UOP of 1ml/kg/hr. Consider pulmonary artery catheterization?

54
Q

What are some patient factors or conditions that can confound a hemolytic reaction?

A

AIHA, Cold agglutinin disease, PCH, PNH, congenital and non-immune causes of hemolysis, mechanical valves, TMA, drugs effect, infection, G6PD deficiency…

55
Q

What are some clinical features of TACO?

A

Hypertension with widened pulse pressure
Fever (in 30% of cases)
Clinical features of volume overload otherwise
Older age (>70yo)

56
Q

What transfusion reaction are repeat donors more likely to cause?

A

Septic transfusion reaction; repeated phlebotomy causes scarring which can harbor skin bacteria.

57
Q

How should antibiotic treatment be guided in treatment of septic transfusion reactions?

A

Treat broadly, and cover for pseudomonas if the implicated unit was a pRBC.

58
Q

What is acute pain reaction?

A

A poorly understood and maybe incidental reaction that is somewhat associated with use of LR filters. May relate to cardiac demand ischemia?

59
Q

Can a DHTR be treated?

A

IVIG may have some benefit.

60
Q

What is transfusion-associated microchimerism?

A

A rare phenomenon usually seen in trauma settings where donor lymphocytes may engraft and proliferate at low levels. TA-GVHD-lite.

Transfusion Medicine Fellowship (34 decks)

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