修回日期: 2026-06-14
接受日期: 2026-06-25
在线出版日期: 2026-06-28
急性胰腺炎(acute pancreatitis, AP)是一种常见的消化系统急症, 胃肠道是最常受累的胰外器官之一, 其功能障碍与全身炎症反应、感染并发症及多器官功能障碍密切相关, 胃肠道屏障受损导致胰腺坏死组织肠源性感染是重症AP后期死亡的主要原因. 故识别AP所致的胃肠道功能障碍机制, 评估胃肠道功能改变, 对改善AP患者临床管理及临床结局尤为重要. 随着AP相关胃肠功能紊乱病理生理机制的认识不断深化, 影像在评估AP胃肠道改变也发挥着日益重要的作用. 本文就AP胃肠道改变的临床研究进展、评估方法及相关临床结局进行综述, 旨在提高对该并发症的认识, 优化个体化诊疗策略.
核心提要: 本文就急性胰腺炎胃肠道改变的临床研究进展、评估方法及相关临床结局进行综述, 旨在提高对该并发症的认识, 优化个体化诊疗策略.
引文著录: 唐超华, 周梦婷, 钟馨月, 张婷, 张小明. 急性胰腺炎的胃肠道改变影像及临床研究进展. 世界华人消化杂志 2026; 34(6): 465-471
Revised: June 14, 2026
Accepted: June 25, 2026
Published online: June 28, 2026
Acute pancreatitis (AP) is a prevalent digestive system disorder. Among the extrapancreatic organs, the gastrointestinal (GI) tract is frequently affected during AP progression. GI dysfunction contributes critically to the development of systemic inflammatory response syndrome, infectious complications such as infected pancreatic necrosis, and subsequent multiple organ dysfunction syndrome. Intestinal infection of pancreatic necrotic tissue, arising from disruption of the GI barrier, is a leading cause of death in the late stage of severe AP. Therefore, elucidating the mechanisms underlying AP-induced GI dysfunction and assessing changes in GI function are of paramount importance for improving both the clinical management and outcomes of AP patients. As our understanding of the pathophysiological mechanisms linking GI dysfunction and AP continues to deepen, imaging has assumed an increasingly vital role in evaluating GI alterations in AP. This article reviews the clinical research progress, evaluation methodologies, and associated clinical outcomes related to GI changes in AP, with an aim to enhance the awareness of this complication and optimize individualized diagnostic and treatment strategies.
- Citation: Tang CH, Zhou MT, Zhong XY, Zhang T, Zhang XM. Assessment of gastrointestinal changes in acute pancreatitis: Advances in imaging and clinical research. Shijie Huaren Xiaohua Zazhi 2026; 34(6): 465-471
- URL: https://www.wjgnet.com/1009-3079/full/v34/i6/465.htm
- DOI: https://dx.doi.org/10.11569/wcjd.v34.i6.465
核心提要: 本文就急性胰腺炎胃肠道改变的临床研究进展、评估方法及相关临床结局进行综述, 旨在提高对该并发症的认识, 优化个体化诊疗策略.
急性胰腺炎(acute pancreatitis, AP)是临床常见的消化系统急腹症之一, 随着当代生活水平的提高和生活方式的改变,其发病率逐年上升. 其中, 约20%的AP患者可发展为急性重症胰腺炎(severe acute pancreatitis, SAP), 这些重症或坏死性胰腺炎患者死亡率高达20%[1].
胃肠道在AP的疾病进程和临床管理中有着重要地位. AP早期, 胰腺局部炎症通过释放大量炎性细胞因子导致全身炎症反应综合征并作用于远处器官, 而肠道即为重要的靶器官[2]. 早有研究表明[3], 肠道功能障碍在多器官功能障碍综合征的发生、发展中起核心作用, 约59%的AP患者存在肠道屏障功能障碍[4]. 胰腺坏死组织继发感染是SAP后期死亡的主要原因, 而大多数引起感染的细菌多由于肠道屏障功能受损, 肠道通透性增加, 菌群移位所致肠源性感染[4]. 此外, 胃肠道功能受损也是影响AP临床营养支持的重要风险因素, 肠内营养或口服喂养不耐受, 导致能量摄入不足、负氮平衡和免疫功能下降[5], 预后不良并延长住院时间.
影像学检查在AP的诊疗全过程中占据核心地位, 随着影像技术的发展, 对AP相关胃肠道改变的评估维度已显著拓宽, 同时临床对AP相关胃肠道功能障碍的机制及评估方法的研究也在不断深入. 本文将从相关临床研究进展、临床及影像评估方法、AP相关胃肠道改变所致临床结局等方面, 对AP胃肠道改变的研究现状进行系统综述, 为早期识别高风险患者, 制定临床个体化管理决策提供新的理论依据.
肠道机械屏障主要是由肠上皮细胞和细胞间连接构成. 而肠道黏液层是肠道机械屏障的第一道防线[6], 主要由杯状细胞分泌的MUC2黏蛋白构成, 体内炎症过程中产生的肿瘤坏死因子α(tumor necrosis factor-α, TNF-α)抑制MUC2的产生, 黏液层破坏使肠道上皮细胞直接暴露于肠腔内容物, 增加病原体接触和损伤风险. 紧密连接(tight junction, TJ)位于细胞间连接的顶端, 由封闭蛋白(Occludin)、突触连接蛋白(Claudin)、连接黏附分子和封闭蛋白(zonula occludens-1, ZO-1)组成, 主要封闭细胞间隙, TJ的改变是肠道屏障功能障碍的核心机制之一. AP患者中, Claudin、ZO-1表达显著下调, 且重症AP患者ZO-1表达水平显著低于轻症AP患者; 在电子显微镜观察下, 紧密连接连续性中断, 出现"开窗"现象, 部分区域甚至可见紧密连接完全缺失[7].
此外, 肠道上皮的更新对于维持肠上皮平衡至关重要, 主要由肠道干细胞和快速增殖(transient amplifying, TA)细胞组成[8]. 研究发现[9,10], TA细胞在AP组数量显著低于正常组, 并且AP患者细胞凋亡标志物和坏死性凋亡标志物表达较正常组有所增加, SAP模型大鼠细胞凋亡标志物表达显著上调, 使肠上皮细胞受到凋亡和坏死性凋亡、TA细胞增殖减少的双重打击, 致使肠道机械屏障受损. 肥大细胞位于上皮细胞附近, 在调节肠道屏障功能中也起着关键作用[11], 其可通过炎症介质的释放招募中性粒细胞和巨噬细胞至肠道屏障[12], 加剧局部炎症和组织损伤; 也可通过TNF-α诱导上皮细胞死亡[12]以及调节黏液生成损害肠道机械屏障.
肠道生物屏障主要由正常的肠道菌群组成, 在维持肠道黏膜完整性方面起着尤为重要的作用. 研究发现[13], AP患者和健康对照组之间的微生物组成发生了显著变化, 且肠道菌群的这些改变与血清白细胞介素-6和血浆内毒素水平显著相关, 这一发现提示肠道菌群失调可能与炎症反应相关. AP时, 菌群多样性下降及结构组成发生改变, 潜在致病菌如肠杆菌科和肠球菌的丰度显著增加, 而有益细菌如双歧杆菌的丰度显著降低[14,15]. 肠道菌群失调将导致肠道机械屏障功能受损, 病原菌增多, 加重TNF-α介导的炎症, 减少TJs的表达, 从而直接导致内皮细胞损伤[16]; 有益菌减少将导致短链脂肪酸生成不足. 短链脂肪酸在维持肠黏膜屏障功能中起着重要作用, 它是肠上皮细胞的主要能量来源, 增加ZO-1、Occludin等紧密连接蛋白表达[17], 增强肠道机械屏障功能等; 此外, 补充短链脂肪酸可以增加肠道跨上皮阻力, 降低肠道黏膜通透性, 并增强肠道化学屏障的功能[18].
基于上述肠道屏障功能障碍的病理机制, 临床亟需相关工具对AP患者肠屏障损伤进行评估, 但目前尚未有达成共识的准确方法. 有诸多研究发现[19,20], 一些血清标志物可反映肠道黏膜受损情况. 血清二胺氧化酶由肠上皮细胞生成和分泌, 当肠道黏膜发生损伤或炎症反应时, 二胺氧化酶由细胞内释放进入肠腔渗透入血, 故其水平升高直接反映肠黏膜损伤程度. 内毒素、D-乳酸是肠道黏膜的细菌及代谢产物, 乳果糖及甘露醇是可被肠黏膜吸收和代谢的糖类物质, AP患者肠道屏障功能受损受损时, 内毒素、D-乳酸经受损黏膜进入血液循环, 乳果糖的吸收能力增加, 而甘露醇吸收无显著改变, 故内毒素、D-乳酸、乳果糖/甘露醇比值显著升高.
腹内压(intra abdominal pressure, IAP)是腹腔密闭腔隙内的稳态压力, 正常范围为0-5 mmHg, 当IAP持续或反复超12 mmHg时, 定义为腹内高压[21]. 在所有AP患者中, 腹内高压的发病率为30%到60%[22], 胃肠道作为腹腔内最大的器官系统, 对IAP升高最为敏感, 当IAP升高至15 mmHg时, 肠道微循环血流可减少高达50%, 导致黏膜及黏膜下层组织低灌注、肠道细胞损伤, 进而导致细菌移位、内毒素释放、脓毒症及多器官功能衰竭[23]. 而胃肠功能障碍也可导致腹内高压, 二者相互作用, 形成恶性循环[24]. 经膀胱测量法是目前临床应用的首选和"金标准"方法[25].
2012年欧洲重症监护医学会提出急性胃肠道损伤(acute gastrointestinal injury, AGI)分级系统[26], 为评估AP患者胃肠功能提供了标准化的工具. AGI评分内容包括胃肠道症状(如恶心呕吐、腹胀腹痛、消化道出血等)、喂养不耐受(feeding intolerance, FI)、腹内压, 共划分为4级: AGI 0级为无胃肠功能障碍; AGI Ⅰ级为存在胃肠功能障碍风险, 表现为腹部术后早期恶心、肠鸣音减弱等自限性症状; AGI Ⅱ级为胃肠功能障碍, 表现为胃轻瘫、腹内压12-15 mmHg等需要干预的症状; AGI Ⅲ级为胃肠功能衰竭, 表现为持续喂养不耐受、腹内压15-20 mmHg等干预后仍不缓解的症状; AGI Ⅳ级为胃肠功能衰竭伴远隔器官功能障碍, 表现为腹腔间隔室综合征等(腹内压>20 mmHg). Ding等[27]研究发现, 随着AGI等级的增加, 感染性胰腺坏死、胰外感染、持续性器官衰竭和持续性多器官衰竭的发生率增加, 住院时间和入住重症监护室时间也随之延长; AGI分级是预测重症AP患者死亡率的独立危险因素, 其预测效能优于任何其他单独评分系统(如APACHE Ⅱ评分、改良马歇尔评分或Ranson评分).
临床症状观察、AGI分级及生物标志物检测虽各有价值, 但临床评估较为复杂且对腹部病理过程的诊断敏感度较低[28], 难以全面、客观地反映胃肠道结构改变和功能状态. 近年来, 随着影像学技术的快速发展, 计算机断层扫描(computed tomography, CT)、磁共振成像(magnetic resonance imaging, MRI)及超声检查在AP胃肠道评估中的应用日益受到关注. 这些技术不仅可提供胃肠道形态学信息, 还能通过功能性成像评估胃肠动力、通透性及灌注状态, 为临床决策提供重要依据.
CT是目前诊断和评估AP疾病严重程度的首选影像方法, 能较好评估胰周炎症蔓延所致的肠壁水肿及肠系膜受累. 改良CT严重程度指数(modified computed tomography severity index, MCTSI)是目前应用最广泛的AP严重程度影像学评分系统, 主要评估胰腺坏死程度及胰周炎症范围. 尽管目前少有相关评分包含胃肠功能改变, 但在熊波等[29]的研究中, MCTSI评分单独预测胃肠功能障碍的曲线下面积(area under the curve, AUC)高达0.930, 提示MCTSI评分不仅可评估胰腺局部病变及胰周病变严重程度, 还可间接反映胃肠道受累程度, 其机制可能与胰周炎症直接蔓延至肠系膜、导致肠壁水肿和动力障碍有关. Knoph等[30]曾采用CT结合不透射线标记物法客观、定量评估AP患者的胃肠道传输功能, 为临床提供了一种简便、可行的胃肠道动力评估方法.
MRI具有优越的软组织分辨率, 且无电离辐射伤害, 在鉴别肠壁水肿与缺血方面具有独特价值, 现已成为诊断评价和随访观察AP的重要影像学检查工具. 在胃肠道疾病的诊断和治疗中, MRI的应用也越来越广泛[31]. Ji等[32]研究发现, 在MRI检查中, 63%的AP患者至少存在一种胃肠道异常, 包括胃肠道壁增厚、肠腔扩张、肠壁水肿及胃肠道壁的异常强化; 并且其发生率与AP严重程度呈正相关. 肠壁水肿是AP肠壁损伤的核心表现之一, 其病理基础是紧密连接破坏导致肠屏障通透性增加, 黏液层破坏使肠上皮直接暴露于肠腔内容物, 加重局部炎症渗出. 在MRI上, 水肿表现为T2WI序列肠壁信号均匀增高、分层结构保留. 当病变进展严重, 肠上皮细胞凋亡和坏死性凋亡导致上皮完整性丧失, MRI上则可表现为肠壁分层消失、黏膜线中断或溃疡形成. 动态增强MRI则可量化肠壁异常强化反映的AP相关微循环改变: 炎症因子介导的血管扩张和血管通透性增加导致肠壁早期快速强化; 当腹内高压、微血栓形成或纤维化导致肠壁灌注不足时, 可出现强化减弱或延迟强化.
在克罗恩病的肠道研究中, 基于不相干运动扩散加权成像(incoherent motion diffusion-weighted imaging, IVIM-DWI)和动态对比增强MRI(dynamic contrast-enhanced MRI, DCE-MRI)的肠道灌注评估方法通过定量分析水弥散系数、血流及血流灌注分数及毛细血管通透性等, 可无创、动态地反映肠壁的灌注状态与炎症损伤程度. Hectors等[33]研究表明联合DCE-MRI与DWI鉴别异常肠段的AUC高达0.95, 且Alves等[34]学者在后续研究中证实, IVIM-DWI的灌注参数是监测肠壁微循环状态和治疗反应的敏感生物标志物. AP时胰周炎症释放的炎性因子可导致肠系膜微血管损伤、肠壁水肿及微循环障碍, 如在AP患者的MRI检查中常规纳入IVIM-DWI序列, 无需注射对比剂, 即可动态监测肠壁血流灌注和ADC值的变化, 早期识别微循环受损、客观评估肠屏障功能恢复情况.
Bettenworth等[35]的系统综述指出, 磁化传递MRI通过量化磁化传递率评估组织胶原含量, 其区分肠壁纤维化与炎症的能力显著优于DWI和常规增强MRI, 展现出独特优势. 在近期的学者研究[36]中发现, 磁共振弹性成像也可定量评估肠壁生物力学特性, 在肠纤维化无创诊断中展现出独特价值, 在今后评估AP后期肠壁僵硬度, 区分可逆性炎症水肿与不可逆性纤维化狭窄, AP慢性并发症的早期干预提供影像学靶点. 目前, 深度学习技术实现了肠壁的自动分割与中心线追踪, 且Liu等[37]通过建立综合肠道的影像组学和临床数据的机器学习模型在疾病诊断中发挥良好的性能, 这为未来构建AP肠壁受累的影像组学模型提供技术支撑, 整合肠壁组学特征及临床参数, 实现对喂养不耐受、肠屏障损伤和胰腺坏死感染等并发症的早期预警.
尽管超声对AP的诊断敏感性低于CT、MRI, 但超声能实时、动态的对胰腺和腹部其他器官进行探查, 因其便携、无创、可床旁操作, 在AP的诊断和随访中具有重要价值[38]. 有研究者[39]基于超声检查, 创建了急性胃肠道损伤超声(AGI ultrasonography, AGIUS)评分, 观察指标包括肠管直径、肠壁厚度、肠壁分层、肠壁皱襞改变以及肠道蠕动情况. 研究结果显示, AGIUS评分与AGI分级呈显著正相关, 且肠道异常改变(如肠道蠕动频率减低)能一定程度预测喂养不耐受发生的风险. 此外, 超声可采用非侵入性方法检测腹内压, 即通过在腹壁施加递减的外部压力, 同时用超声观察腹膜反弹消失点, 当腹膜反弹消失时, 所施加的外部压力即等于腹内压, 与膀胱内压金标准相比, 偏倚较小, 且在一定范围内具有良好的测量精度[40], 超声还可通过测量腹部前后径与横径比值等形态学指标间接评估IAP[41].
营养治疗不耐受是AP管理中常见的并发症, FI包括经口喂养不耐受和肠内喂养不耐受[42], 表现为营养治疗后出现腹痛、恶心、呕吐等症状, 研究发现[43,44], 约13%的AP患者发生经口喂养不耐受, 中重度AP患者肠内喂养不耐受可达25.8%, 发生FI的患者住院时间更长、死亡率更高及发生胰腺坏死的几率更高. 其病理机制目前尚不明确, 但多与胃肠道屏障受损、胃瘫相关[45,46]; 有研究表明胰周积聚是影响FI的相关因素, 考虑可能其占位效应压迫胃肠道, 导致胃排空障碍和胃流出道梗阻, 增加胃FI风险[47,48].
FI的发生提示着胃肠道屏障功能的损害, 而肠道屏障的崩溃, 则是连接胰腺局部炎症与全身感染并发症的关键桥梁. AP感染并发症的核心多为肠道菌群移位导致胰腺坏死组织感染, 肠源性感染是SAP后期死亡的主要原因[49,50]. Liu等[51]用乳果糖/甘露醇吸收比值检测肠道通透性, AP患者肠道通透性显著增加, 且与疾病严重程度、内毒素水平和TNF-α水平呈正相关, 肠道通透性增加不仅反映屏障功能障碍, 还与全身炎症反应密切相关. 研究发现[52], SAP患者普遍存在肠道细菌移位, 且细菌移位发生率与APACHE Ⅱ评分呈显著正相关.
在AP的相关并发症中, 上消化道出血相对少见, 在SAP中发生率约3.6%, 但一旦发生将显著增加AP患者的死亡风险[53]. 上消化道出血主要表现为急性胃黏膜病变或应激性溃疡, 其机制目前尚未完全清楚, 考虑全身炎症反应和内脏灌注不足导致胃黏膜缺血、碳酸氢盐与黏液分泌减少[54], 致使胃肠道屏障受损继发内毒素血症, 进一步加重微循环障碍[55].
值得注意的是, 某些特定人群在这一环节中可能面临更高的风险, 其中肥胖是SAP的危险因素, 且肥胖AP患者的局部和全身性并发症显著增高, 器官衰竭率也明显增高[56,57]. 其机制尚不明确, 但Ye等[58]研究发现, 胃肠道为肥胖AP患者的胰外受累的重要靶点: 肥胖组AP大鼠内毒素水平升高、肠道通透性增高、肠上皮细胞凋亡增多而增殖减少且肥胖组大鼠菌群丰富度和多样性显著低于对照组.
AP患者中, 肠道被视为全身炎症反应和多器官功能障碍的"发动机". 在临床预后方面, 肠道功能障碍的严重程度直接决定患者结局, 是SAP患者死亡的独立预测因子. 学者们已逐步认识到肠道在AP疾病发展中的重要地位, 研究胃肠道功能障碍机制, 使用多种影像及临床工具评估胃肠道异常改变, 提供AP患者治疗靶点, 保护肠道屏障、调节菌群失衡、改善胃肠动力、降低腹内压等, 为改善AP患者预后提供了重要突破口. 深入研究AP患者胃肠道异常改变不仅是理解疾病发生发展的关键, 更是优化临床管理、开发新型治疗策略的必经之路.
影像学发现可为AP胃肠道并发症的阶梯式管理提供直接决策依据. 以床旁超声为例, 若动态监测显示肠蠕动存在且肠壁血流信号正常, 提示肠屏障功能尚可, 即可积极选择早期喂养; 反之, 若肠蠕动消失伴血流信号显著减弱, 则提示腹内高压或微循环障碍, 应继续禁食、实施胃肠减压并监测腹内压, 必要时启动降低腹内压的干预措施. CT或MRI上若仅见肠壁轻度增厚及均匀强化, 反映以炎症水肿为主的可逆性改变, 可积极尝试肠内营养; 若出现肠壁延迟强化、强化减低或肠壁完整性消失, 则需警惕肠坏死风险, 应及时外科会诊. 通过将影像表型(水肿型、缺血型、纤维化型)与临床指标(AGI分级、腹内压、炎症标志物等)动态整合, 可构建从"影像评估"到"分级干预"的闭环决策路径, 实现急性胰腺炎胃肠道并发症的个体化精准管理.
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学科分类: 胃肠病学和肝病学
手稿来源地: 四川省
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科学编辑: 刘继红 制作编辑:张砚梁