Transfusion Medicine
TRANSFUSION-RELATED ACUTE LUNG INJURY
Once thought a rare complication, transfusion-related acute lung injury (TRALI) is increasingly being recognized, with an incidence of approximately 1:5000 patients; it is now the most frequent cause of transfusion-related death.24,25 TRALI is noncardiac pulmonary edema and typically manifests clinically with hypoxemia, fever, bilateral infiltrates, and hypotension 2 to 6 hours after blood is given. Ventilatory support is often required. Recovery is usually rapid (24–48 hours) and complete. The etiology is complex. In many cases, transfused anti-HLA antibodies react with the recipient’s white cells leading to pulmonary damage. Another theory is that transfusion of preformed cytokines leads to pulmonary damage. Because plasma products from multiparous women are most often associated with anti-HLA antibodies, the restricted use of blood products from women has decreased the incidence of TRALI over the past few years.26
TRANSFUSION-ASSOCIATED CIRCULATORY OVERLOAD
Increasingly it being recognized that volume overload resulting from transfusions can lead to significant morbidity.27 Patients with heart or renal disease or patients who already have compromised fluid status are at risk for transfusion-associated circulatory overload (TACO). Another risk factor is transfusion of multiple blood products. Patients with TACO develop dyspnea within 6 hours of transfusion, but do not have fever or rash with the dyspnea. The diagnosis is made by demonstrating circulatory overload (eg, high venous pressure, B-type natriuretic peptide). Treatment is aggressive diuresis. Strategies to prevent TACO include judicious use of blood products, especially in patients at risk for TACO, and the use of prophylactic diuretics, especially with red cell or plasma transfusions.28
TRANSFUSION-RELATED GRAFT-VERSUS-HOST DISEASE
TGVHD is a rare reaction, but one that is most often fatal.29 TGVHD occurs when donor lymphocytes attack the blood recipient’s organs—skin, liver, intestines, and marrow. This is very rare in the normal blood recipient unless the donor and recipient share some HLA haplotypes.30 In immunosuppressed patients, TGVHD can occur with lesser degrees of HLA similarity, with cases reported in blood recipients who are mainly patients with Hodgkin disease or acute leukemia undergoing chemotherapy, and in patients receiving purine analogs. TGVHD had not been reported in AIDS patients despite profound immunosuppression, perhaps because the milieu of the patient does not allow lymphocyte expansion. Symptoms of TGVHD are an erythematous rash that may progress to epidermal toxic necrolysis, liver dysfunction, diarrhea, and pancytopenia. TGVHD is prevented by irradiating blood products given to at-risk patients with 2500 to 3500 rads. Directed blood donation from all blood relatives should also be irradiated. TGVHD cannot be prevented by leukopoor blood because the minute amount of lymphocytes that are not filtered still can lead to these complications.
POST-TRANSFUSION PURPURA
Patients with post-transfusion purpura (PTP) develop severe thrombocytopenia (< 10 × 103/µL) with often severe bleeding 1 to 2 weeks after receiving any type of blood product.31 Patients who develop PTP most often lack platelet antigen PLA1 or other platelet antigens. For unknown reasons, exposure to the antigens from the transfusion leads to rapid destruction of the patient’s own platelets. The diagnostic clue is thrombocytopenia in a patient, typically female, who has received a red cell or platelet blood product in the past 7 to 10 days. Treatment consists of intravenous immunoglobulin32 and plasmapheresis to remove the offending antibody. If patients with a history of PTP require further transfusions, only PLA1-negative platelets should be given.
IRON OVERLOAD
Every transfusion of red cells delivers approximately 250 mg of iron to the recipient. Since there is no natural way of ridding the body of iron, heavily transfused patients are at risk of iron overload. This is most often seen in children heavily transfused for thalassemia. Starting in the second decade of life, these individuals will develop endocrinopathies due to iron overload, liver problems, and often fatal cardiomyopathies. Studies have shown that chelation of iron with deferoxamine can be effective in preventing this fatal complication.33 Oral iron chelators such as deferasirox and deferiprone are also effective. The risk of iron overload in heavily transfused patients with myelodysplasia or other transfusion-dependent anemias is unclear, and uncertainty exists about the need for chelation.34
