Aird William C
Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass 02215, USA.
Mayo Clin Proc. 2003 Jul;78(7):869-81. doi: 10.4065/78.7.869.
Sepsis with acute organ dysfunction (severe sepsis) results from a systemic proinflammatory and procoagulant response to infection. Organ dysfunction in the patient with sepsis is associated with increased mortality. Although most organs have discrete anatomical boundaries and carry out unified functions, the hematologic system is poorly circumscribed and serves several unrelated functions. This review addresses the hematologic changes associated with sepsis and provides a framework for prompt diagnosis and rational drug therapy. Data sources used include published research and review articles in the English language related to hematologic alterations in animal models of sepsis and in critically ill patients. Hematologic changes are present in virtually every patient with severe sepsis. Leukocytosis, anemia, thrombocytopenia, and activation of the coagulation cascade are the most common abnormalities. Despite theoretical advantages of using granulocyte colony-stimulating factor to enhance leukocyte function and/or circulating numbers, large clinical trials with these growth factors are lacking. Recent studies support a reduction in the red blood cell transfusion threshold and the use of erythropoietin treatment to reduce transfusion requirements. Treatment of thrombocytopenia depends on the cause and clinical context but may include platelet transfusions and discontinuation of heparin or other inciting drugs. The use of activated protein C may provide a survival benefit in subsets of patients with severe sepsis. The hematologic system should not be overlooked when assessing a patient with severe sepsis. A thorough clinical evaluation and panel of laboratory tests that relate to this organ system should be as much a part of the work-up as taking the patient's blood pressure, monitoring renal function, or measuring liver enzymes.
伴有急性器官功能障碍的脓毒症（严重脓毒症）是由机体对感染的全身性促炎和促凝反应所致。脓毒症患者的器官功能障碍与死亡率增加相关。尽管大多数器官具有明确的解剖边界并执行统一的功能，但血液系统的界定并不清晰且具有多种不相关的功能。本综述探讨了与脓毒症相关的血液学变化，并为快速诊断和合理药物治疗提供了一个框架。所使用的数据来源包括以英文发表的有关脓毒症动物模型和重症患者血液学改变的研究及综述文章。几乎每位严重脓毒症患者都存在血液学变化。白细胞增多、贫血、血小板减少以及凝血级联反应激活是最常见的异常情况。尽管使用粒细胞集落刺激因子来增强白细胞功能和/或增加循环白细胞数量在理论上具有优势，但缺乏针对这些生长因子的大型临床试验。近期研究支持降低红细胞输血阈值以及使用促红细胞生成素治疗以减少输血需求。血小板减少症的治疗取决于病因和临床情况，但可能包括输注血小板以及停用肝素或其他诱发药物。对于部分严重脓毒症患者，使用活化蛋白C可能会带来生存获益。在评估严重脓毒症患者时，血液系统不应被忽视。全面的临床评估以及与该器官系统相关的一系列实验室检查应与测量患者血压、监测肾功能或检测肝酶一样，成为检查工作的一部分。
