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Managing a platelet blood product inventory in a hospital-based transfusion service (TS) is challenging. Thus, to optimize platelet inventory availability and to prevent excess outdating, most tertiary care center-based TSs do not require ABO-identical platelet (PLT) transfusions. To mitigate the risk of hemolysis associated with the transfusion of high titer ABO antibody-containing PLT, our institutional policy allows the transfusion of PLT containing ABO-incompatible plasma only if PLT is re-suspended in platelet additive solution (PAS). Despite the steps taken to reduce the risk of hemolytic transfusion reactions to PLT transfusions at our institution, our center has observed hemolytic reactions to PLT in PAS. The current case study highlights the importance of recognizing a hemolytic reaction (HTR) from ABO-incompatible PLT transfusions and discusses the current strategies and recommendations to mitigate this risk.

Establishing transfusion guidelines during trauma resuscitation is challenging. Our objective was to evaluate indications for transfusion in trauma patients who emergently received ≤2 units of red blood cells (RBC) during the first hour of resuscitation.A single center retrospective study included non-massively bleeding trauma patients stratified into 2 groups: 1) with a clinical indication for transfusion and 2) with no indication for transfusion. Admission vital signs (VS), injury severity score (ISS), shock index, and laboratory values were compared between the two groups using the Wilcoxon rank-sum test.Among 111 non-massively bleeding trauma patients, 40 presented no indication for transfusion. All patients presented similar ISS and VS. The 71 patients presenting with an indication for transfusion had higher bicarbonate (22.6 vs 20.8) and lower lactate levels (4.7 v 6.6) (Lactate and bicarbonate blood levels may be potential indicators for RBC transfusion need during trauma resuscitation in non-massively bleeding patients.

Hemoglobinuria was observed after packed red blood cell transfusion in a series of patients at our pediatric treatment center. Laboratory testing was suggestive of intravascular hemolysis with no support for an immunohematologic process.We investigated these adverse events to define a quality improvement plan and to prevent future hemolytic adverse events. Multiple factors were investigated, and the only change identified was the implementation of a new infusion pump (Pump A) that replaced a previous model (Pump B).In vitro pump analyses, a retrospective review of urinalyses, and prospective urinalysis and nursing surveillances were also performed.In in vitro analysis of the pumps, irradiated units with higher hematocrit at a low flow rate through Pump A had a greater than thirty-fold increase in free hemoglobin from baseline compared to minimal free hemoglobin changes seen with Pump B. Irradiated units with a lower hematocrit had a minimal change in free hemoglobin from baseline with both Pumps A and B at either low or high flow rate. Subsequently, only units with lower hematocrits were issued for transfusion of pediatric patients, and Pump A was replaced by Pump B in the outpatient unit. Retrospective and prospective surveillances found no additional unexplained cases of gross hemoglobinuria associated with transfusion.The investigation determined that infusion of higher hematocrit units using a specific commercial pump was associated with mechanical hemolysis. The change to units with lower hematocrit through an alternative pump has been an effective corrective action to date.

Biomaterial encapsulation of islets has been proposed to improve the long-term success of islet transplantation by recreating a suitable microenvironment and enhancing cell-matrix interactions that affect cellular function. Protein polymer hydrogels previously showed promise as a biocompatible scaffold by maintaining high cell viability. Here, enzymatically-crosslinked protein polymers were used to investigate the effects of varying scaffold properties and of introducing ECM proteins on the viability and function of encapsulated MIN6 β-cells. Chemical and mechanical properties of the hydrogel were modified by altering the protein concentrations while collagen IV, fibronectin, and laminin were incorporated to reestablish cell-matrix interactions lost during cell isolation. Rheology indicated all hydrogels formed quickly, resulting in robust, elastic hydrogels with Young's moduli similar to soft tissue. All hydrogels tested supported both high MIN6 β-cell viability and function and have the potential to serve as an encapsulation platform for islet cell delivery in vivo.

This study assessed the active role of the portal vein endothelium in the functional loss of pancreatic islet (PI) grafts, considered in the context of PI transplantation for treatment of type I diabetes mellitus. We hypothesized that PI engraftment may be jeopardized by portal vein endothelial cell-induced activation of host T cells. We designed an in vitro system using portal vein endothelial cells (PVEC) from Lewis (Lew) rats and PI from Brown-Norway (BN) and Lew rats. PI were co-cultured with Lew PVEC for three days. The PI were removed and trypsinized PVEC were divided into three groups: (A) PVEC not exposed to PI; (B) PVEC exposed to syngeneic PI; and (C) PVEC exposed to allogeneic PI. The groups were analyzed by flow cytometry for ICAM-1 and MHC Class I and Class II molecules. Functional assays of lymphocytes (ie, lymphocyte proliferation assay, 51Cr release assay, and cytokine release assay) were also performed. We observed MHC Class I and ICAM-1 upregulation on PVEC after PI contact. MHC Class II molecule was not upregulated on PVEC after PI exposure. IL-6 production was increased non-specifically following PI coculture with PVEC. TNF-a was increased only after allogeneic PI-PVEC coculture. PVEC exposed to either allogeneic or syngeneic PI could not stimulate naïve splenocyte proliferation or cytotoxicity. We conclude that PVEC allo-PI interaction results in increased ICAM-1 and MHC Class I expression on the PVEC. Neither lymphocyte proliferation nor cytotoxicity could be enhanced in response to enhanced MHC Class I and ICAM-1 expression, which was associated instead with non-specific inflammatory cytokine release.