Hematology
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Injuries are common and account for almost 15% of all blood use in the U. S. The historic view that the coagulopathy associated with severe injury was largely dilutional is being replaced by epidemiologic and molecular evidence for a distinct syndrome of trauma-associated coagulopathy. ⋯ Preventing the coagulopathy of trauma is best accomplished by preventing injury and hypothermia. Treating the coagulopathy of trauma requires its early recognition, prompt control of hemorrhage with local and systemic treatments, including in some patients the use of plasma instead of crystalloid solutions, and the prompt treatment of acidosis and hypothermia. The planned early use of allogenic plasma to treat many tens of thousands of massively transfused patients each year creates new demands for the immediate availability and improved safety of plasma products.
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Pain is the insignia of sickle cell disease and the acute painful crisis is the number-one cause of hospital admissions. Tissue damage due to vaso-occlusion releases numerous inflammatory mediators that initiate the transmission of painful stimuli and the perception of pain. The acute sickle cell painful crisis evolves along four distinct phases coupled with changes in certain markers of the disease. ⋯ Failure to treat acute pain aggressively may lead to chronic pain syndrome. Management of sickle pain is primarily pharmacologic in nature, and opioids are the analgesics used most often. Cellular and molecular mechanisms of opioids explain individual differences among patients and justify the use of individualized treatment plans.
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There continues to be a general but unfounded enthusiasm for fresh frozen plasma (FFP) or frozen plasma (FP) usage across a range of clinical specialties in hospital practice. Plasma for transfusion is most often used where there are abnormal coagulation screening tests, either therapeutically in the face of bleeding, or prophylactically in nonbleeding patients prior to invasive procedures or surgery. Little evidence exists to inform best therapeutic transfusion practice, and most studies describe plasma use in a prophylactic setting. ⋯ There is a need to undertake new trials evaluating the efficacy and adverse effects of plasma, both in bleeding and non-bleeding patients, to understand whether the presumed benefits outweigh the real risks. In addition, new hemostatic tests that better define the risk of bleeding and monitor the effectiveness of the use of FFP should be validated. Last, there is an opportunity to develop effective educational strategies aimed at addressing understanding and compliance with recommendations in guidelines.
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The clinical management of individuals with hereditary hypercoaguable disorders has evolved from initial broad recommendations of lifelong anticoagulation after first event of venous thromboembolism to a more intricate individualized risk-benefit analysis as studies have begun to delineate the complexity of interactions of acquired and hereditary factors which determine the predilection to thrombosis. The contribution of thrombophilic disorders to risk of thrombotic complications of pregnancy, organ transplantation, central venous catheter and dialysis access placement have been increasingly recognized. The risk of thrombosis must be weighed against risk of long-term anticoagulation in patients with venous thromboembolism. Thrombophilia screening in select populations may enhance outcome.
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Transfusion-associated acute lung injury (TRALI) has emerged as a leading cause of transfusion-related morbidity and mortality. TRALI is characterized by acute non-cardiogenic pulmonary edema and respiratory compromise in the setting of transfusion. The study of TRALI has been hampered by inadequate case definitions and an incomplete understanding of the pathologic mechanisms. ⋯ A subsequent second event such as exposure to lipids, cytokines or antibodies in a blood component would then cause activation of adherent neutrophils and a release of bioreactive molecules leading to lung injury. There are limited clinical and animal studies to support the "two hit" model. These proposed mechanisms are not mutually exclusive in that donor leukocyte antibody can be pathogenic in both models and have implications for new strategies to prevent TRALI.