Postpartum obstetric red cell transfusion practice: A retrospective study in a tertiary obstetric centre.

BACKGROUND: Traditional management of anaemia due to postpartum haemorrhage (PPH) has relied upon salvage therapy with red cell transfusion. Recently published guidance recommends a change in approach toward holistic patient blood management. AIMS: To determine whether postpartum red cell transfusion practices are consistent with best practice and to identify opportunities for improvement. MATERIALS AND METHODS: A retrospective audit of postpartum red cell transfusions was conducted at a tertiary level obstetrics unit. Relevant clinical and laboratory data were collected for all cases of postpartum red cell transfusions and PPH. Clinical decision making and appropriateness of transfusions were evaluated. RESULTS: Among the 3235 women who delivered in 2013, 110 (3.4%) received a postpartum red cell transfusion. About 101 of the transfusions were associated with primary PPH. Overall PPH complicated 460 (14.2%) deliveries. Antenatal anaemia was identified as a major correctable risk factor for transfusion in women who experienced PPH (odds ratio 6.55, 95% CI: 3.17-13.6). Volume of blood loss and the aetiology of PPH were additional risk factors for transfusion. Transfusion was associated with lower birth weight and increased maternal length of stay. Transfusion triggers were more likely to be appropriate when transfusion took place in the operating theatre, within 12 h of delivery and when prescribed by anaesthetists. Post-transfusion Hb levels were uniformly above target for all women transfused. CONCLUSIONS: A significant number of red cell transfusions were outside the recommendations of the new guidelines. Maximising red cell mass during pregnancy and improving transfusion practices were identified as opportunities for future improvement.

Integrative Genomics Identifies the Molecular Basis of Resistance to Azacitidine Therapy in Myelodysplastic Syndromes.

Myelodysplastic syndromes and chronic myelomonocytic leukemia are blood disorders characterized by ineffective hematopoiesis and progressive marrow failure that can transform into acute leukemia. The DNA methyltransferase inhibitor 5-azacytidine (AZA) is the most effective pharmacological option, but only ∼50% of patients respond. A response only manifests after many months of treatment and is transient. The reasons underlying AZA resistance are unknown, and few alternatives exist for non-responders. Here, we show that AZA responders have more hematopoietic progenitor cells (HPCs) in the cell cycle. Non-responder HPC quiescence is mediated by integrin α5 (ITGA5) signaling and their hematopoietic potential improved by combining AZA with an ITGA5 inhibitor. AZA response is associated with the induction of an inflammatory response in HPCs in vivo. By molecular bar coding and tracking individual clones, we found that, although AZA alters the sub-clonal contribution to different lineages, founder clones are not eliminated and continue to drive hematopoiesis even in complete responders.