Landow L, Andersen L W
Department of Anaesthesia, University of Massachusetts Medical Center, Worcester.
Acta Anaesthesiol Scand. 1994 Oct;38(7):626-39. doi: 10.1111/j.1399-6576.1994.tb03969.x.
Multiple organ failure remains the leading cause of death in the intensive care unit. Increasing numbers of investigators have focused their attention on the role of gastrointestinal tract in the pathogenesis of this syndrome. Their data indicate that inadequate gut perfusion leads to a measurable imbalance between oxygen delivery and the needs of the tissues, i.e., ischaemia. Gut ischaemia of sufficient duration impairs gastrointestinal tract barrier function, facilitating the passage of enteric bacterial endotoxin into the circulation. It has been hypothesized that production of tumor necrosis factor alpha, and other biologic mediators by endotoxin-stimulated macrophages, triggers a generalized and uncontrolled inflammatory response that ultimately leads to multiple organ failure. Preliminary evidence suggests that survival can be improved significantly if gut ischaemia is promptly identified and aggressively treated by administration of fluids and inotropic drugs, using gastric intramucosal pH as the therapeutic endpoint. Future studies are needed to determine whether additional treatment modalities can improve outcome once the inflammatory response has fully developed.
多器官功能衰竭仍然是重症监护病房患者死亡的主要原因。越来越多的研究人员将注意力集中在胃肠道在该综合征发病机制中的作用上。他们的数据表明,肠道灌注不足会导致氧输送与组织需求之间出现可测量的失衡,即缺血。持续时间足够长的肠道缺血会损害胃肠道屏障功能,促使肠道细菌内毒素进入循环系统。据推测,内毒素刺激的巨噬细胞产生肿瘤坏死因子α和其他生物介质,引发全身性失控的炎症反应,最终导致多器官功能衰竭。初步证据表明,如果能通过胃黏膜内pH值作为治疗终点,及时识别并积极给予液体和血管活性药物治疗肠道缺血,患者生存率可显著提高。一旦炎症反应充分发展,是否有其他治疗方式能够改善预后,还需要未来的研究来确定。