修回日期: 2016-05-23
接受日期: 2016-05-31
在线出版日期: 2016-09-18
急性肠缺血发病急, 病死率高, 临床表现无特异性, 诊断困难. 64层以上多层CT由于快速、亚毫米薄层扫描和精细的三维重建, 可清楚显示肠系膜血管有无狭窄和闭塞, 评估肠壁及肠系膜形态和血流灌注异常, 快速准确诊断急性肠缺血、肠梗死及其病因, 而成为临床怀疑肠缺血最有价值的一线检查方法. 急性肠缺血病因病理、缺血程度和发病部位不同, 以及有无肠壁出血或感染, 其CT表现复杂多样. 本文就各种原因的急性肠缺血不同阶段的多层CT表现和诊断价值进行系统阐述.
核心提要: 急性肠缺血(acute mesenteric ischemia, AMI)多层CT诊断应以CT血管造影肠系膜血管狭窄、闭塞为主要依据, 结合肠壁、肠系膜的形态和强化改变做出诊断; 提高对AMI的认识和警惕, 注意早期CT征象, 可早期诊断AMI; 根据肠壁强化消失或肠壁、肠系膜静脉积气诊断肠梗死, 并根据肠系膜血管形态和病史诊断出病因, 指导临床治疗.
引文著录: 任小军. 急性肠缺血的多层CT诊断. 世界华人消化杂志 2016; 24(26): 3772-3778
Revised: May 23, 2016
Accepted: May 31, 2016
Published online: September 18, 2016
Acute mesenteric ischemia (AMI) has an acute onset and a high mortality rate with nonspecific clinical presentation and is difficult to diagnose. In recent years, due to fast submillimeter scanning and subtle three-dimensional reconstruction, 64-row multi-slice CT can distinctly demonstrate the stenosis and occlusion of the mesenteric vessels, assess the alteration of morphology and blood perfusion of the intestinal wall and mesentery, and promptly and accurately diagnose AMI, intestinal infarction and its etiology. Therefore, CT has become the most valuable and first-line diagnostic modality for evaluating patients with suspected AMI. AMI has different and complicated CT findings due to different etiology, pathology, extent, position, as well as with or without mural hemorrhage or infection. In this article, we systematically review the multi-slice CT manifestations of AMI and its diagnostic value in various causes of AMI in different stages.
- Citation: Ren XJ. Multi-slice CT for diagnosis of acute mesenteric ischemia. Shijie Huaren Xiaohua Zazhi 2016; 24(26): 3772-3778
- URL: https://www.wjgnet.com/1009-3079/full/v24/i26/3772.htm
- DOI: https://dx.doi.org/10.11569/wcjd.v24.i26.3772
急性肠缺血(acute mesenteric ischemia, AMI)是血流灌注急剧减少引起的肠及肠系膜急性缺血或梗死, 分别占急腹症入院和CT检查的1%和4%, 死亡率达59%-93%[1-3]. 近年随着心血管疾病发病率的增高, 其发病逐渐增多, 临床表现和实验室检查无特异性, 常被误诊, 早期肠系膜血管重建和手术切除坏死肠管可将死亡率从72%降到14%[4-7], 因此, 早期诊断和针对病因的正确治疗对患者的预后极为重要. 腹部平片诊断价值有限, 超声和磁共振成像对AMI的诊断进行了积极的探索[8-11], 但临床应用少, 准确性较低. 64层以上多层CT和双源CT快速、亚毫米薄层扫描和精细的三维重建, 通过平扫和增强评估肠管有无形态和血流灌注异常, 通过CT血管造影(CT angiography, CTA)清楚显示肠系膜血管及其分支有无狭窄和闭塞, 可快速准确诊断AMI、肠梗死及其病因, 诊断敏感度和特异度可分别达到93.3%-100%、95.9%-100%[12-14], 可指导临床及时准确的治疗. 因此, 多层CT检查, 已成为临床怀疑AMI最有价值的一线检查方法[13]. 本文, 即对AMI的多层CT表现及其诊断价值做一综述.
AMI分类不统一, 根据病因可分为原发性和继发性. 原发性AMI由于肠系膜血管病变引起, 可分为肠系膜动脉阻塞(包括肠系膜动脉栓塞和血栓形成, 分别占40%-50%和20%-30%)、肠系膜静脉阻塞(血栓形成, 占5%-15%)和非阻塞性AMI(占5%-15%).
AMI 肠系膜动脉栓塞多为肠系膜上动脉(superior mesenteric artery, SMA)栓塞, 栓子多来源于伴有房颤的左心房、风心病的瓣膜和动脉粥样硬化的斑块. 急性肠系膜动脉血栓常常在动脉粥样硬化的基础上发生. 肠系膜动脉阻塞也可以由主动脉或SMA夹层, 主动脉术后引起[15-17]. 其他原因还有自身免疫性疾病引起的血管炎, 如系统性红斑狼疮, Wegener肉芽肿, 类风湿性血管炎等[18-20]. 静脉阻塞的原因为肠系膜静脉血栓形成, 由门静脉高压、高凝状态、恶性肿瘤、血管炎、腹腔和肠道炎症等[21-25]引起. 非阻塞性AMI为心力衰竭、休克等[26]原因引起心输出量降低所致.
AMI病理分为三个阶段[34]. 第一阶段为可逆性肠缺血, 以肠壁黏膜局灶性坏死、溃疡和出血为特征, 未累及肌层, 损伤可以完全愈合. 肠管反射性收缩、痉挛, 肠腔萎陷, 形成痉挛性肠梗阻. 第二阶段, 肠缺血累及黏膜下及肌层, 愈合后引起肠管纤维性狭窄; 此时, 肠壁肌肉和神经丛缺血或坏死, 肠管张力降低, 蠕动减弱, 肠腔扩张、积气, 形成低张性肠梗阻. 在动脉阻塞和非阻塞性AMI, 因静脉引流通畅, 肠壁血液和组织液减少, 颜色苍白, 菲薄如纸. 这个阶段, 需要尽早手术切除坏死肠段和恢复肠系膜血流通道. 第三阶段, 全层肠壁缺血坏死、穿孔, 形成腹膜炎, 肠系膜水肿, 腹腔积液, 肠蠕动消失, 肠腔扩张、积气, 形成麻痹性肠梗阻, 肠腔气体进入破损的黏膜、黏膜下层及肠系膜静脉和门静脉, 肠壁细菌感染, 炎症细胞浸润, 产生自由基和毒素, 引起全身多脏器损害和功能衰竭. 此时, 即使切除坏死肠段, 仍可能并发多脏器功能衰竭而死亡. 动脉阻塞性AMI血管再通或侧枝循环形成后, 发生再灌注损伤, 肠壁渗出、水肿、增厚, 甚至出血性肠梗死, 损伤加重[35]. 静脉阻塞性AMI, 肠壁及肠系膜淤血、水肿、出血, 肠壁颜色暗红, 肠壁增厚较动脉阻塞性AMI更加显著.
AMI的临床表现无特异性, 其病因不同, 临床表现不一致. 最常见的症状为腹痛, 最典型的表现为剧烈腹痛与腹部轻压痛的体征不成比例, 其他症状有恶心、呕吐、腹泻、肠鸣音亢进的胃肠排空表现. 肠系膜动脉栓塞, 起病突然, 腹痛剧烈, 而肠系膜动脉和静脉血栓形成者, 腹痛发展相对较慢. 当发展成透壁性肠梗死时, 出现持续的弥漫性腹痛、腹胀和腹肌紧张、全腹压痛、肠鸣音消失, 甚至休克、败血症和全身脏器损害表现.
机器多应用64层或以上螺旋CT, 或者双源CT. 由于为急腹症, 可不口服胃肠道对比剂, 直接行平扫和增强扫描. 增强扫描动脉期延迟30-35 s, 静脉期延迟60-70 s. 扫描层厚≤1 mm, 间隔1 mm. 对比剂注射速率为3.0-3.5 mL/s. 扫描范围从膈顶至耻骨上缘. 扫描后行冠状面和矢状面多平面重组(multiplanar reformation, MPR)、最大密度投影、容积重建后处理, 以全面准确观察肠系膜动脉、静脉有无狭窄或闭塞及其范围, 以及肠管走行形态和强化程度.
AMI的特异性CT表现为肠系膜动脉或静脉狭窄、闭塞, 肠壁强化降低或消失, 相对特异性表现为肠壁、肠系膜静脉和门静脉积气. 非特异性CT表现为肠系膜水肿、渗出, 肠管收缩或扩张, 肠壁变薄或增厚, 腹腔积液. 肠壁强化降低或消失与患者正常肠壁比较而言, 不同的CT扫描条件、延迟时间、静脉注射对比剂速率和心脏功能, 肠壁的CT强化值不同. Chen等[36]测量69例病理证实的AMI的CT增强前后肠壁密度, 发现缺血肠段显著低于正常肠段, 在动脉期缺血肠段和正常肠段的CT值分别为28.58 HU±9.28 HU、58.97 HU±12.50 HU, 在静脉期分别为33.93 HU±11.16 HU、76.25 HU±13.56 HU, 强化比值在动脉期≤0.32, 静脉期≤0.81. 张昌立等[37]应用双源CT做动物实验后发现, 缺血肠管栓塞后CT值显著降低, 栓塞前后CT值分别是141.42 HU±23.81 HU、76.17 HU±7.68 HU, 正常与缺血肠壁强化值分别是108.43 HU±8.82 HU、36.40 HU±6.67 HU. 另外, AMI的病因病理(动脉阻塞/静脉阻塞)、缺血程度(肠壁黏膜缺血/全层缺血坏死)和部位(小肠/大肠)不同, 有无肠壁出血/感染, 其CT表现复查多样.
4.2.1 动脉阻塞性AMI: 初期, CTA即可见肠系膜动脉狭窄、闭塞, 分支血管变细、减少, 肠管收缩、萎陷, 肠壁和肠腔显示不清, 增强后肠壁强化降低, 无肠系膜水肿、渗出和腹腔积液, 仅凭肠管表现CT难以与正常收缩肠管鉴别[38]. 但结合增强后肠系膜血管充盈缺损、CTA及临床腹痛剧烈和体征轻微的表现可做出正确诊断. 这个阶段CT正确诊断非常重要, 因为肠缺血损伤可以完全愈合. 第二阶段, CT表现为低张性肠梗阻, 肠壁菲薄如纸, 厚度<1 mm, 强化明显降低或消失, 肠腔扩张、积气, 坏死肠管充满混杂多发气泡的未消化的内容物, 似结肠内的粪便, 称之为小肠"积粪征"或"粪便征". 粪便征诊断急性肠梗死的敏感性27%, 特异性达94%[39]. 这时, CT容易误诊为其他原因引起的肠管积气扩张. 肠系膜动脉主干栓塞或血栓形成CTA容易诊断, 而远端小动脉阻塞, 手术病理才能发现的细小栓子, 常常造成严重的肠梗死[16,34], 须提高警惕. 第三阶段, 肠壁全层坏死、穿孔, 腹膜炎, CT表现为肠管广泛扩张、积气, 肠壁菲薄, 强化消失; 肠系膜浑浊, 腹腔积液, 肠壁、肠系膜静脉及门静脉积气.
4.2.2 静脉阻塞性AMI: 静脉阻塞性AMI, 早期CTA就可见肠系膜静脉主干和属支内低密度血栓, 管腔狭窄、闭塞, 甚至伴门静脉血栓形成, 肠系膜小血管淤血扩张[40]. 肠壁增厚、水肿是静脉阻塞性AMI最常见的征象, 容易并发肠壁内出血, 在CT平扫呈高密度, 边缘模糊. 肠壁出血诊断AMI的特异度达100%, 敏感度为56%[41]. 肠壁黏膜下层水肿明显, 强化降低, 而黏膜层血管丰富、伴出血和溃疡, 正常或稍增厚的肌层强化亦相对明显, 肠壁呈两层的"晕征"和三层的"靶征", 肠腔扩张, 大量积液、积气. 进一步发展, 肠壁水肿及强化降低更加明显, 肠系膜脂肪水肿浑浊、腹腔积液. 后期发生透壁性肠梗死, 肠壁强化消失, 可见肠壁和肠系膜静脉、门静脉积气, 肠系膜水肿及腹腔积液更加明显. CT肠壁强化降低或消失, 临床伴有腹膜刺激征, 患者死亡率达57%-59%[42]. 肠壁强化降低和肠壁积气诊断AMI的特异度高达97%-100%, 敏感度为42%; 肠系膜动脉或静脉狭窄、闭塞伴肠系膜静脉和门静脉积气诊断AMI的特异度达94%-100%, 但敏感度仅12%-15%[21,43]. Milone等[44]报道肠壁积气伴静脉积气发生透壁梗死的特异度达83%, 但敏感度仅为17%. 肠梗阻、肠管扩张和炎症, 如憩室炎、结肠炎, 由于肠壁黏膜完整性破坏, 也可发生肠壁及静脉积气[45-47], 在诊断AMI时要予以排除. 因此, 肠系膜血管狭窄、闭塞伴肠壁强化降低, 或伴肠壁、肠系膜静脉积气诊断AMI特异度高, 但敏感度低. 双源CT应用双能量成像, 可增加缺血与正常肠壁的对比, 有利于早期检出缺血肠壁, 提高AMI的诊断敏感性[36,37]. 另外, CT检查前临床怀疑AMI, 针对AMI的CT扫描方案和诊断思路, 可将AMI的诊断准确度由80%提高到97%[48].
4.2.3 非阻塞性AMI: 非阻塞性AMI的整个肠道都可能缺血, 但小肠和右半结肠、结肠脾区更容易受累. CT表现为肠系膜动脉主干及分支变细、分支显示减少, 无血栓形成; 肠管表现与动脉阻塞性AMI相同, 即肠管痉挛后扩张、积气, 肠壁变薄、强化减低、消失. 如病因纠正, 心输出量增加, 肠管再灌注, 出现肠壁水肿, 增强后呈"晕征"或"靶征". 黏膜强化正常, 为肠管存活的标志, 肠壁强化消失, 表明肠壁梗死. 再灌注损伤可加重AMI, 引起透壁性肠梗死和麻痹性肠梗阻[35]. 此外, 非阻塞性AMI可同时伴发肝脏、脾脏和肾脏缺血表现.
4.2.4 继发性AMI: 多层CT可见肠系膜动脉或/和静脉狭窄、闭塞, 如果是远端细小分支或肠壁小血管损伤、闭塞, 则主干及大分支通畅; 肠管、肠系膜缺血和腹腔积液, 以及原发病的征象, 如闭袢性肠梗阻狭窄的梗阻点, 血管狭窄周围侵犯的肿瘤或炎性渗出, 或有明确的外伤、放化疗病史. 但是, CT鉴别肠壁增厚是炎症还是AMI较困难, 必须结合肠系膜血管狭窄或闭塞做出AMI诊断. 肠梗阻继发AMI较常见, CT直接征象为平扫肠壁出血、密度增高, 肠壁强化降低或消失, 肠系膜局限性积液和肠壁积气, 间接征象为肠袢呈C形或U形, 系膜血管纠集聚拢, 漩涡征, 其中肠壁强化降低或消失征象最重要, 特异度高达96%, 敏感度为78%[41,49].
4.2.5 AMI病因的多层CT诊断: AMI的病因、缺血程度和持续时间是影响患者预后的重要因素[7], 不同的病因和病程阶段, 选择的治疗方法不同, 如抗凝、溶栓、介入血管内溶栓、取栓或外科手术血管重建、坏死肠管切除[50-53]. CT既要尽早诊断有无肠缺血和肠梗死, 又要诊断其病因. 动脉或静脉阻塞性AMI的CT和CTA可见血管内栓子或血栓, 动脉夹层可见主动脉或肠系膜动脉真、假腔和撕裂的内膜片. 系统性血管炎引起的AMI, 广泛累及小肠和结直肠, 十二指肠和直肠缺血为其特点, 肠壁明显水肿、增厚、分层, 肠系膜血管主干通畅, 小血管充血、增粗呈"梳征" [18,19], 患者较年轻, 有自身免疫性疾病史和实验室自身免疫检查异常. 非血管阻塞性AMI, 有休克、心输出量降低的病史. 继发性肠缺血, 有外伤、放化疗、介入栓塞术等病史或肠梗阻和肿瘤征象. CT对肠系膜动脉栓塞、动脉粥样硬化及静脉血栓的检出率分别为92%、100%及100%, 对肠系膜动脉栓塞、动脉粥样硬化、非阻塞性及静脉血栓形成的AMI的肠壁异常检出率分别为92%、100%、100%及67%[46], 部分动脉栓塞和静脉血栓形成的肠管CT表现正常, 需要根据肠系膜血管阻塞(狭窄、闭塞)做出AMI的诊断. 因此, CT只要发现肠系膜动脉或静脉阻塞, 就要高度怀疑AMI, 需结合肠管CT和患者临床表现明确诊断[54].
AMI病因不同, 其发展过程和病理改变不同, CT表现复杂多样. 肠系膜血管阻塞性AMI, CTA可见肠系膜动脉或静脉狭窄、闭塞; 动脉阻塞性AMI, 发展过程为痉挛、低张和麻痹性肠梗阻、肠梗死, CT上肠管先后表现为萎陷、扩张, 肠壁强化减低或消失, 随后肠壁变薄. 静脉阻塞性AMI, CT表现为肠壁出血、水肿、增厚, 强化减低, 呈"靶征"和"晕征", 肠腔积液、积气, 肠系膜水肿和腹腔积液. 非阻塞性AMI, 临床为休克、心输出量降低后, 肠缺血累及小肠和大肠, 肠管的CT表现与动脉阻塞性AMI相同, 休克纠正、心输出量增加后, 肠系膜血流再灌注, 肠管的CT表现又与静脉阻塞性AMI相同. 继发性AMI, 肠管各种缺血表现, 结合病史和临床可做出诊断. 因此, AMI的多层CT诊断应以CTA肠系膜血管狭窄、闭塞为主要依据, 结合肠管和肠系膜缺血的形态和强化改变做出诊断, 提高对AMI的认识和警惕, 注意早期CT征象, 早期诊断AMI; 根据肠壁强化消失或肠壁、肠系膜静脉积气诊断肠梗死, 并根据肠系膜血管形态和病史诊断出病因, 指导临床保守或手术治疗.
急性肠缺血(acute mesenteric ischemia, AMI)发病急, 死亡率高, 常被误诊. 64层以上多层CT快速、薄层扫描和精细的三维重建, 可清楚显示肠系膜血管有无狭窄和闭塞, 评估肠壁及肠系膜有无缺血, 快速准确诊断AMI、肠梗死及其病因.
任刚, 副主任医师, 上海交通大学医学院附属新华医院放射科
提高肠壁血供减少、强化降低和肠系膜血管细小血栓的检出率, 在AMI初期做出诊断, 是该研究领域中的研究重点以及亟待研究的问题.
Potretzke等应用双源CT薄层扫描和肠灌注碘成像, 提高缺血肠壁的分辨率和检出率以早期诊断AMI; 应用磁共振弥散加权成像在动物实验中可在AMI 30 min后早期检出病变肠壁.
本文重点阐述了各种原发性AMI各个阶段的多层CT表现及一些重要征象的诊断价值, 分析了不同病因的多层CT诊断, 强调AMI的诊断方法及早期诊断和诊断肠梗死的征象, 以更好指导临床治疗.
AMI的多层CT诊断应以CT血管造影(CT angiography, CTA)肠系膜血管狭窄、闭塞为主要依据, 结合肠管和肠系膜形态和强化改变做出诊断, 注意AMI的早期CT征象, 根据肠壁强化消失或肠壁、肠系膜静脉积气诊断肠梗死, 并根据肠系膜血管形态和病史诊断出病因.
CT血管造影(CTA): 是静脉注射含碘对比剂, CT薄层、大范围、快速扫描后, 经计算机对图像后处理, 三维显示血管完整形态, 对血管变异、血管疾病以及显示病变和血管关系有重要价值.
该研究的内容有重要的临床研究价值, 研究提供了较充足的有意义的信息, 但研究不具有新颖性.
手稿来源: 邀请约稿
学科分类: 胃肠病学和肝病学
手稿来源地: 陕西省
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