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Blood Transfusion
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
If the recipient develops antibodies to antigens present on the donor cells during or after the transfusion, a reaction can occur even if apparently compatible blood is transfused. This is caused by very low levels of antibody in the recipient which are not detectable in the cross-match procedure. Following the transfusion, there is a secondary response with a rapid rise of IgG antibodies. The antibodies most frequently involved are against antigens of Kidd (Jk), Duffy (Fy), Rhesus (Rh), Kell (K) and S blood group systems; these may have been acquired by previous exposure to the antigens during pregnancy or previous blood transfusions. White cell reactions: Febrile reactions occur in approximately 2% of all transfusions and are caused by donor white cells reacting with alloantibodies induced by previous transfusions or pregnancy.Graft-versus-host reactions: Graft-versus-host disease – a rare complication of blood transfusion – is characterized by the deposition of donor lymphocytes in the recipient's skin, liver or gastrointestinal tract, leading to a rash, hepatitis or diarrhoea.Post-transfusion purpura: This is a consumptive thrombocytopenia occurring 7–10 days after transfusion of a blood product and is usually self-limiting, lasting for 2–6 weeks.Anaphylaxis to plasma proteins: Life-threatening anaphylaxis during blood transfusion usually occurs in IgA-deficient patients whose sera contain anti-IgA antibodies. Urticaria may also occur in patients when recipient antibodies react to antigens in donor plasma, especially IgA.Transfusion-related acute lung injury (TRALI): TRALI is one of the most common causes of morbidity of blood transfusion. The clinical features of TRALI are acute respiratory, non-cardiogenic oedema occurring within a few hours after a blood component transfusion and severe hypoxaemia. The pathological findings include pulmonary oedema with capillary leukostasis and extravasation of neutrophils. The pathogenesis of TRALI remains controversial. It is now considered that it is caused by leucocyte antibodies present in fresh frozen plasma and platelet concentrates, especially from multiparous donors, and the priming of neutrophils and endothelium by the patient's comorbidity. Supportive ventilation is required and the symptoms usually resolve in 24–48 hours.
Adverse transfusion reactions and what we can do
Published in Expert Review of Hematology, 2022
Yajie Wang, Quan Rao, Xiaofei Li
Post-transfusion purpura (PTP) is a rare syndrome caused by alloimmunization of human platelet-specific antigens (mostly HPA-1a), resulting in severe thrombocytopenia and bleeding within 2–14 days after blood transfusion [144]. PLT alloantibodies in the patient are preformed due to previous pregnancy or blood transfusion, and PLT alloimmunization can lead to the PLT refractoriness associated with the clinical symptoms. The incidence is about 1:50,000–100,000 transfusions and multiparous women are most often to be affected [145]. The diagnosis of PTP may be challenging, because these patients are usually post-surgery or critically ill, and there are alternative understandings for thrombocytopenia, such as drugs, infections, etc. Generally, it can be confirmed by detecting the platelet-specific alloantibodies in the serum [146]. Patients may experience purpura, petechial, or mucosal bleeds, since antibodycoated PLTs are severe destroyed by macrophages (<10 × 109/L). Fortunately, the majority of patients are self-limited and the PLT count will recover within 3 weeks. However, it has a mortality rate of 10–20% for cases with a secondary high bleeding risk [147]. Intravenous immunoglobulins (IVIGs) are the primary treatment, which has a rapid onset of action and response rate of 75–95%. Alternatively, corticosteroids may be managed together with IVIG, although the reaction seems unpredictable. Plasmapheresis is occasionally regarded as a second-line treatment [10,144]. PLT transfusions, especially with units lacking the antigen, may be useful for individuals with severe bleeding.
Post-cardiac surgery thrombotic thrombocytopenic purpura: presence of anti-ADAMTS13 autoantibodies at preoperative baseline
Published in Platelets, 2022
Bryan Tordon, Theodore E. Warkentin, Jane C. Moore, Donald M. Arnold
Postoperative immune-mediated complications, such as HIT, drug-induced immune thrombocytopenia (e.g., vancomycin), and post-transfusion purpura, typically begin approximately one week post-surgery [26–28]. In our patient, given the rapid development of TTP so soon after surgery, we examined the patient’s preoperative plasma for ADAMTS13 activity, as well as for presence of anti-ADAMTS13 antibodies. Indeed, despite absence of anemia or thrombocytopenia prior to cardiac surgery, we found absent ADAMTS13 activity in the preoperative plasma sample, as well as presence of inhibitory anti-ADAMTS13 antibodies. This is consistent with a “two-HIT” hypothesis for TTP, in which anti-ADAMTS13 antibodies alone does not necessarily lead to TTP, but where other factors are needed [29]. After cardiac surgery, postoperative blood samples typically show greatly increased levels of VWF, along with parallel decrease in ADAMTS13 activity (although postoperative ADAMTS13 activity levels are not usually <50%) [30]. However, if a patient (such as ours) had preoperative presence of inhibitory anti-ADAMTS13 antibodies, these post-cardiac surgery changes could plausibly precipitate an episode of acute TTP.
Clinical challenges and promising therapies for chemotherapy-induced thrombocytopenia
Published in Expert Review of Hematology, 2021
Hanny Al‐Samkari, Gerald A. Soff
While diagnosis of CIT is often straightforward, a number of other etiologies must be considered in the differential diagnosis of thrombocytopenia in the cancer patient [1,2]. Tumor metastases to the bone marrow are common in breast, prostate, lung cancer, and lymphoma [15], and should be considered in patients with slow declines over time in the baseline platelet count that appear unrelated to treatment-related fluctuations. Patients with cancer frequently develop infectious complications due to immunosuppression, compromise of tissue planes by invading tumor, and iatrogenic etiologies such as indwelling catheters and procedures. Infections may result in thrombocytopenia via a number of mechanisms, including consumptive coagulopathy, the action of bacterial neuraminidase on platelets resulting in their clearance by the Ashwell-Morell receptor in the liver, and bone marrow suppression [16,17]. Medications aside from cancer chemotherapy – such as heparin agents and antibiotics – may result in thrombocytopenia, as can blood product transfusions via precipitation of post-transfusion purpura [17]. Finally, other tumor and treatment-related etiologies, including radiotherapy-induced thrombocytopenia (in particular, when the pelvis has been irradiated), immune thrombocytopenia, and thrombotic microangiopathy must be considered.