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非阻塞性肠系膜缺血

Authors
David A Tendler, MD
J Thomas Lamont, MD
Section Editors
John F Eidt, MD
Joseph L Mills, Sr, MD
Deputy Editor
Kathryn A Collins, MD, PhD, FACS
Translators
贾国葆, 副主任医师，副教授

引言

急性肠系膜缺血是指突然发生的肠灌注不足，可由动脉血流非阻塞性减少引起。非阻塞性动脉灌注不足，最常见由原发性内脏血管收缩导致。非阻塞性肠系膜缺血(nonocclusive mesenteric ischemia, NOMI)由Ende首次在心力衰竭患者中报道[1]。大多数病例涉及供应小肠和近端结肠的肠系膜上动脉(superior mesenteric artery, SMA)分支痉挛。早期诊断的依据是对具有危险因素的患者存在高度临床怀疑，但通常需要动脉造影来进行稳当的确诊。现如今NOMI比过去少见，在发生时采用逆转刺激因素来进行处理，包括停用血管收缩药物，纠正引起灌注不足的基础性原因(如果可能)，以及进行抗凝治疗以限制动脉血栓形成。对SMA选择性输注罂粟碱或其他血管扩张药是一种治疗选择，但现在很少进行。

本文将总结NOMI，累及小肠的急性和慢性肠系膜动脉阻塞，以及结肠缺血，将单独讨论。 (参见“急性肠系膜缺血”和“成人肠系膜静脉血栓形成”和“慢性肠系膜缺血”和“结肠缺血”)

小肠的血供

小肠的血循环主要来自于SMA和肠系膜下动脉(inferior mesenteric artery, IMA)(图 1和图 2)。静脉回流平行于动脉循环，并流入门静脉系统(图 3和图 4)。广泛的侧支循环(图 5)可保护肠段免受短暂的灌注不足之害[2,3]。

非阻塞性缺血性损伤

当细胞代谢所需的氧气和营养输送不足时，会发生肠缺血性损伤。发生肠缺血的可能性取决于全身灌注和侧支循环是否充足、受累肠系膜血管的数量和管径，以及缺血损伤的持续时间。肠系膜血流量急性减少约75%并且长达12小时的情况下，肠道尚可代偿而无严重损伤，部分原因是氧摄取增加[4]。

NOMI的发病机制与机体减少内脏和外周循环血流以维持心脏和脑部血流的稳态机制有关[5-7]。加压素和血管紧张素可能是这一现象的神经激素介质。痉挛也可能由血管活性药物和强心药物引起[5,8]。肠道的正常生理学和对缺血的反应将在别处作更详细的讨论。

                

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Literature review current through: 2017-06 . | This topic last updated: 2017-02-07.
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