Emergency transfusion of patients with unknown blood type with blood group O Rhesus D positive red blood cell concentrates: a prospective, single-centre, observational study.

BACKGROUND: Emergency patients with unknown blood type usually receive O Rhesus D negative (RhD-) red blood cell concentrates until their blood group is determined to prevent RhD+ related adverse transfusion reactions. As 85% of individuals are RhD+, this consumption of O RhD- red blood cell concentrates contributes to shortages of O RhD- red blood cell concentrates, sometimes forcing transfusion of known RhD- patients with RhD+ red blood cell concentrates. Here we report the outcome of this transfusion policy transfusing all emergency patients with unknown blood type with O RhD+ red blood cell concentrates. METHODS: In this prospective single-centre observational study done between Jan 1, 2001, and Dec 31, 2015, we assessed all consecutive RhD- patients at the University Medicine Greifswald who received RhD+ red blood cell concentrates (emergency patients with unknown blood type; and RhD- patients receiving RhD+ red blood cell concentrates during RhD- red blood cell concentrate shortages). No patients were excluded. The primary endpoint was anti-D allo-immunisation at 2 months follow-up or later. Patients were followed up and tested for immunisation against red blood cell antigens using the direct antiglobulin test and an antibody screen every 3-5 days for 4 weeks or until death, or hospital discharge. Surviving patients were screened for development of anti-D antibodies for up to 12 months (at the predefined timepoints 2, 3, 6, and 12 months) after RhD+ red blood cell transfusion. FINDINGS: 437 emergency patients, of whom 85 (20%) were RhD-, received 2836 RhD+ red blood cell concentrates. The overall risk of inducing anti-D antibodies (in all 437 recipients) was 17 (4%, 95% CI 2·44-6·14) of 437 (assuming all patients lost to follow-up developed anti-D allo-immunisation). During this period, 110 known RhD- patients received RhD+ red blood cell concentrates during RhD- red blood cell concentrate shortages. Of these, 29 (26%; 95% CI 19·0-35·3) developed anti-D allo-immunisation (assuming all patients lost to follow-up developed anti-D), which was significantly higher than in the emergency patients with unknown blood type (p<0·0001). INTERPRETATION: Transfusing emergency patients with unknown blood type with O RhD+ red blood cell concentrates has a low risk of inducing anti-D antibodies (3-6%), but saves more than 10% of the total O RhD- red blood cell concentrate demand, thereby reducing shortage of O RhD- red blood cell concentrates, the need to transfuse known RhD-patients with RhD+ red blood cell concentrates, and thus the overall risk to induce anti-D allo-immunisation in the population. These findings should be considered for transfusion guidelines. FUNDING: University Medicine Greifswald.

Megakaryocyte impairment by eptifibatide-induced antibodies causes prolonged thrombocytopenia.

Glycoprotein (GP) IIbIIIa inhibitors are used in the treatment of acute coronary syndromes. Transient immune-mediated acute thrombocytopenia is a recognized side effect of GPIIbIIIa inhibitors. We provide evidence that GPIIbIIIa inhibitor-induced antibodies can affect megakaryocytes in the presence of eptifibatide. In a patient with acute coronary syndrome, acute thrombocytopenia occurred after a second exposure to eptifibatide 20 days after the initial treatment. Despite the short half-life of eptifibatide (t(1/2) = 2 hours), thrombocytopenia less than 5 x 10(9)/L and gastrointestinal and skin hemorrhage persisted for 4 days. Glycoprotein-specific enzyme-linked immunosorbent assay showed eptifibatide-dependent, GPIIbIIIa-specific antibodies. Bone marrow examination showed predominance of early megakaryocyte stages, and platelet transfusion resulted in an abrupt platelet count increase. Viability of cultured cord blood-derived megakaryocytes was reduced in the presence of eptifibatide and patient IgG fraction. These findings can be explained by impaired megakaryocytopoiesis complicating anti-GPIIbIIIa antibody-mediated immune thrombocytopenia. This mechanism may also apply to some patients with autoimmune thrombocytopenia.

Heparin-induced thrombocytopenia and cardiopulmonary bypass: perioperative argatroban use.

Heparin-induced thrombocytopenia (HIT), a serious complication of heparin therapy, mandates heparin cessation and alternative anticoagulation. We report a patient with a history of HIT who successfully underwent cardiopulmonary bypass (CPB) using short-term reexposure to heparin and perioperative therapy with argatroban. No bleeding complications or HIT-related problems occurred. The pharmacokinetics of argatroban, especially its hepatic rather than renal elimination, makes it the drug of choice for some HIT patients in whom other alternative anticoagulants (eg, danaparoid and hirudin) are less well suited. Because of interference with the international normalized ratio (INR), switching from argatroban to oral anticoagulants is not straightforward.