Therapeutic plasma exchange and intravenous immune globulin in the treatment of heparin-induced thrombocytopenia: A systematic review.

Background: Immunomodulatory strategies in heparin-induced thrombocytopenia (HIT) include the use of intravenous immune globulin (IVIG) and therapeutic plasma exchange (TPE). The optimal application of these therapies is unknown and outcomes data are limited. We investigated treatment categories and laboratory and clinical outcomes of IVIG and/or TPE in HIT with a systematic literature review.

Alternatives to Transfusion.

Objectives: We discuss two main categories of blood substitutes: perfluorocarbons and hemoglobin-based oxygen carriers.

Methods: We provide a review of the notable products developed in both categories and include their attributes as well as their setbacks.

Results: We contribute a case report tothe growing literature of the successful use of Sanguinate.

Hemostasis testing and therapeutic plasma exchange: Results of a practice survey.

Introduction: Performing therapeutic plasma exchange (TPE) with albumin replacement decreases coagulation factor and platelet levels. No defined guidelines exist regarding laboratory testing to assess hemostasis in patients undergoing TPE.

Materials And Methods: A survey to evaluate hemostasis testing with TPE was distributed using online survey software.

Hemostasis management and therapeutic plasma exchange: Results of a practice survey.

Background: Patients undergoing therapeutic plasma exchange (TPE) may present with risks for hemorrhage or thrombosis. Use of replacement fluids devoid of coagulation factors will decrease factor levels and platelet levels. There are no established guidelines for hemostasis management in these situations.

Disseminated Intravascular Coagulation.

Objectives: To provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC).

Methods: A case scenario and a review of the literature related to the pertinent facts concerning DIC are provided.

Results: DIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation of coagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia.

How do I implement a more restrictive transfusion trigger of hemoglobin level of 7 g/dL at my hospital?

Background: The red blood cell (RBC) transfusion trigger is a major driver of transfusion practice and affects health care costs and in some instances patient outcomes. Reducing the transfusion threshold will decrease RBC utilization and hospital costs.

Study Design And Methods: The hospital transfusion committee, endorsed by the medical staff executive committee, developed an educational program for physicians, nurses, and blood bank staff focusing on the scientific basis for a transfusion trigger of hemoglobin (Hb) of 7 g/dL rather than 8 g/dL as well as a program to discourage the routine 2-unit RBC transfusion.

Consensus review of the treatment of cardiovascular disease in people with hemophilia A and B.

With advances in care, increasing numbers of people with hemophilia (PWH) achieve near-normal life expectancies and present with typical age-related cardiovascular conditions. Evidence-based guidelines for medical or surgical management of cardiovascular conditions in individuals with hemophilia are limited. Published recommendations exist for the management of some common cardiovascular conditions (eg, ischemic heart disease, atrial fibrillation), but identifying optimal strategies for anticoagulant or antithrombotic therapy constitutes the primary challenge of managing nonoperative cardiovascular disease (CVD) in PWH.

Comparison of outcomes of group O vs non-group O premature neonates receiving group O RBC transfusions.

Objectives: At some institutions all infants requiring RBC transfusions in neonatal intensive care units (NICUs) receive only group O RBCs. Although transfused group O plasma is minimized in packed RBCs, small amounts of residual anti-A, anti-B, and anti-A,B in group O packed RBCs may bind to the corresponding A and B antigens of non-group O RBCs, possibly hemolyzing their native RBCs and thereby releasing free hemoglobin, theoretically resulting in hypercoagulability and promoting bacterial growth from free iron.

Methods: Premature infants in the University of Kentucky Children's Hospital NICU database who were transfused (all received group O transfusions) were compared for a number of severity markers to determine if non-group O patients had worse outcomes than group O patients.