Antiplatelet and anticoagulation medications and the surgical patient.

BACKGROUND: Acute coronary syndrome affects more than 750,000 Americans per year, and antiplatelet agents are the cornerstones of treatment. Atrial fibrillation affects 2.4 million patients in the United States, and venous thromboembolism occurs in 1 to 2 per 1,000 adults per year. Anticoagulants are commonly prescribed to affected patients. Surgeons are commonly called upon to care for patients taking medications that affect normal coagulation. It is important that the surgical community has a fundamental understanding of these agents' pharmacology, which may impact patients' clinical course. METHODS: A review of recent literature on pharmacologic agents that affect coagulation was performed. RESULTS: A number of medications that alter normal coagulation were reviewed in this article including their pharmacologic properties and reversal strategies. CONCLUSIONS: There are a variety of medications that affect a patient's coagulation ability, including many newer agents on the market. This review provides surgeons with the knowledge needed to assist in caring for individuals receiving these drugs.

Beta 2 microglobulin knockout mice are resistant to lethal intraabdominal sepsis.

beta 2 microglobulin knockout (beta2M-/-) mice lack CD8+ T and natural killer T cells. We hypothesized that beta 2M-/- mice are resistant to lethal intraabdominal sepsis. To test this hypothesis, mortality, cytokine production, and physiologic function were assessed in beta 2M-/- mice during sepsis caused by cecal ligation and puncture (CLP). beta 2M-/- mice survived significantly longer than wild-type mice after CLP but ultimately exhibited 100% mortality. Treatment of beta 2M-/- mice with anti-asialoGM1 to deplete natural killer cells conferred greater than 70% long-term survival. Compared with wild-type mice, beta 2M-/- mice treated with anti-asialoGM1 produced decreased amounts of proinflammatory cytokines and did not exhibit hypothermia or metabolic acidosis after CLP. Adoptive transfer of CD8+ T and natural killer cells into beta 2M-/- mice treated with anti-asialoGM1 re-established CLP-induced mortality. CD8 knockout mice treated with anti-asialoGM1, which are specifically deficient in CD8+ T and natural killer cells, exhibited 40% long-term survival after CLP. Furthermore, treatment of wild-type mice with antibodies to CD8 and asialoGM1 conferred a significant survival benefit compared with wild-type mice treated with nonspecific IgG. These findings demonstrate that beta 2M-/- mice treated with anti-asialoGM1 are resistant to CLP-induced mortality and that depletion of CD8+ T and natural killer cells largely accounts for the survival benefit observed in these mice.