Suspected TRALI
Acute onset within 6 h of blood transfusion
PaO2/FiO2 < 300 mmHg, or worsening of P to F ratio
Bilateral infiltrative changes on chest radiograph
No sign of hydrostatic pulmonary edema (pulmonary arterial occlusion pressure ≤ 18 mmHg or central venous pressure ≤ 15 mmHg
No other risk factor for acute lung injury
Possible TRALI
Same as for suspected TRALI but another risk factor present for acute lung injury
Delayed TRALI
Same as for (possible) TRALI and onset within 6–72 h of blood transfusion
b.
Occurs in 1 in 5000 PRBC transfusions and 1 in 2000 units of plasma-containing products:
i.
The exact mechanism of injury is unknown. However, it is proposed that due to underlying host factors, neutrophils adhere to the pulmonary epithelium. The neutrophils and endothelial cells are then activated by mediators in the blood product which results in capillary leak and pulmonary edema.
ii.
Due to nonspecific symptoms and absence of specific disease markers and diagnostic tests, the incidence is likely to be higher.
iii.
Incidence is higher in ICU patients than in the general hospital population.
c.
Clinical presentation:
i.
Dyspnea, tachypnea, and hypoxia
ii.
Possibly fevers + / − rigors
iii.
Tachycardia
iv.
Hypotension
d.
Overall mortality of 5–10 % making it the leading cause of transfusion-associated deaths in the United States
e.
Proposed risk factors:
i.
Presence of mechanical ventilation
ii.
Emergency cardiac surgery
iii.
Hematologic malignancy
iv.
Positive fluid balance
v.
Sepsis/shock
f.
Differential diagnoses:
i.
Transfusion-associated circulatory overload
ii.
Anaphylaxis
iii.
Sepsis
iv.
Acute hemolytic transfusion reaction
g.
Treatment:
i.
Supportive measures:
Supplemental O2
Mechanical ventilation with low tidal volumes
Maintain euvolemic status
No evidence for use of corticosteroids
ii.
If reaction occurs during product infusion, the product should be returned to the blood bank for culture and rechecking of ABO compatibility
iii.
Symptoms typically resolve within 96 h of onset
12.2 Peri-HSCT Considerations
1.
Major ABO incompatibility:
a.
This circumstance exists when the recipient’s plasma has anti-donor RBC antibodies (i.e., recipient is blood group O (absence of A, B substances), donor is blood group A or B or AB)
b.
Complications of major ABO incompatible HSCT
i.
Acute hemolytic reaction during infusion of the HSCT product
ii.
Delayed RBC engraftment
iii.
Pure red cell aplasia
c.
Recommend HSC product hematocrit be kept to < 2 % to minimize exposure to incompatible RBC volume; however, there are no regulations regarding the volume of RBCs allowed in an HSC product
d.
To reduce the complications associated with infusion of ABO-incompatible HSC marrow products:
i.
Red cell depletion by:
Hetastarch separation
Mononuclear cell separation by machine centrifugation
Chemical separation via density gradient separation
ii.
Reduce the titer of incompatible recipient isohemagglutinin:
Plasma exchange
Immunoadsorption columns
In vivo reduction by infusion of pre-HSCT donor-type secretor plasma
Slow infusion of donor-type RBCs
Despite aggressive hydration and premedication with antihistamines, serious transfusion reaction may occur resulting in fever/rigors, hematuria, and/or hemolysis
e.
Manipulation of the marrow HSC product may result in decreased overall CD34 + cell count of the product
2.
Minor ABO incompatibility:
a.
This circumstance exists when the donor’s plasma is incompatible with the recipient’s RBCs
i.
Group AB recipient/ group non-AB donor
ii.
Group A recipient/ group B or O donor
iii.
Group B recipient/ group A or O donor
b.
Marrow HSC products may require plasma reduction if donor anti-recipient titer is high:
i
To decrease risk, many centers will plasma-deplete all minor ABO-incompatible products
ii.
Peripheral blood HSC products are already plasma- and RBC-reduced but are easily further plasma-depleted.
iii.
There is always concern for minor RBC antibodies not detectable by crossmatch:
In the case of a reaction, the HSC infusion should be stopped immediately and donor/recipient identity, crossmatch, and antibody screens reviewed.
If no error is identified, an immediate density gradient, mononuclear cell separation is required.
3.
Major–minor ABO incompatibility:
a.
Mononuclear cell concentration or density gradient mononuclear separation is required
b.
Consider pre-HSCT infusion of donor-type plasma
4.
Due to major and minor ABO incompatibility between donors and recipients, guidelines for transfusion of blood products have been established to decrease the risk of complications (see Table 12.2).
Table 12.2
Guidelines for selecting ABO group for erythrocyte and platelet-containing components for patients undergoing HSCT.
Recipient ABO group | Donor ABO group | Transfuse RBCs | Transfuse platelets/plasma productsa |
|---|---|---|---|
A | B | O | AB |
A | O | O | A |
A | AB | O | AB |
B | A | O | AB |
B | O | O | B |
B | AB | O | AB |
O | A | O | A |
O | B | O | B |
O | AB | O | AB |
AB
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