急性胰腺炎(acute pancreatitis，AP)是一种全身性疾病，其始动因素为胰腺局部的化学性炎症，而后炎症级联反应累及呼吸、循环、泌尿等多个系统器官^[1,2]。按照亚特兰大标准修订版，将AP分为间质水肿性胰腺炎与坏死性胰腺炎^[1]。既往文献报道坏死性胰腺炎约占AP的20%～30%^[1,2]，但是，随着新分类系统的重新定义，仅胰周坏死性胰腺炎也加入了坏死性胰腺炎的队列，故而国内外最新文献统计坏死性胰腺炎可占AP的40%～80%^{[3, 4, 5]}。对于临床医生而言，坏死性胰腺炎的诊断就对应新分类下的中度重症胰腺炎或重症胰腺炎。所以，早期识别胰腺坏死以及坏死病灶的动态演变至关重要。

       近十年来，随着医学影像学的飞速发展，使得计算机断层摄影(computered tomography，CT)和磁共振成像(magnetic resonance imaging，MRI)在胰腺疾病的诊疗方面有了长足的进展^{[3,5, 6, 7, 8]}。尤其是MRI，目前它被视为AP胰胆管显影、严重程度评估、局部并发症检出的重要影像学检查手段^[3,5,7]。正因为MRI具有良好的软组织分辨率和对液体信号的高敏感性，使得胰腺坏死的动态变化能很好地可视化，从而为临床治疗决策提供重要的参考依据。本文从影像学的角度，着重阐述MRI示踪的坏死性胰腺炎的一种动态演变规律——“透壁性胰腺坏死—胰管中断—包裹性坏死”三部曲，旨在促进放射科医生和临床医生的相关学术交流。

1 胰腺坏死之透壁性胰腺坏死

       按照新的分类标准^[1,2]，坏死性胰腺炎在影像学上被划分为三类：胰腺和胰周坏死型、仅胰周坏死型^[9,10]、仅胰腺坏死型。而胰腺坏死的范围仍然沿用CT严重指数评分方式^[11,12]，即胰腺坏死面积＜30%、30%～50%、＞50%。对于放射科医生而言，我们要清楚识别胰腺坏死的黄金时间应该是患者发病72 h～96 h以后，行影像学检查譬如增强CT或MRI^[13,14]；诚然，更加确凿的影像学诊断则推荐AP发病后5～7天的影像学检查，这是因为胰腺坏死要经历“缺血-半实性(凝固性坏死)-液体(液化性坏死)”的动态过程^[15]。

       通过我们的前期临床观察，首次增强CT或MRI上，除了胰腺坏死的面积占比外^[11]，坏死灶的深度同样重要。如图1所示，胰腺实质坏死常散在分布，有时位于腺体表浅的部分，不侵犯主胰管，称之为浅表性胰腺坏死；当胰腺实质坏死范围较大(左右径＞2 cm)且胰腺坏死灶较深在，其深度接近穿透或完全覆盖整个胰腺腺体，则称之为“透壁性胰腺坏死”(图2)，多伴有主胰管受累。

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图1  A：浅表性胰腺坏死示意图。胰腺内散在坏死灶(箭)，未累及主胰管(PD)。B：透壁性胰腺坏死示意图。胰腺实质内坏死灶较深在，贯穿或接近穿透整个胰腺腺体(箭头)，主胰管(PD)受累　图2　女，50岁，重症急性胰腺炎。增强MRI静脉期横轴位(A)与冠状位(B)示坏死性胰腺炎，胰头实质坏死灶几乎贯穿整个腺体(箭头)，可视为透壁性胰腺坏死
Fig. 1  A：Schematic diagram of superficial necrosis of the pancreas. Intra-pancreatic scattered necrosis lesions (arrows) were shown, without involvement of the pancreatic duct (PD). B：Schematic diagram of transmural necrosis of the pancreas. Pancreatic necrosis lesions (arrowheads) are deeper, along with roughly entire pancreas involvement, as well as the involved PD. Fig. 2　A 50-year-old female with severe acute pancreatitis. Contrast-enhanced MRI in venous phase (A) and (B) images depict necrotizing pancreatitis, and nearly entire pancreatic parenchyma of head (arrowheads) involved. It can be considered as transmural necrosis of pancreas.

2 主胰管之胰管中断改变

       主胰管系胰腺组织内部，从胰尾向胰头方向走行的细管状结构，沿途收集众多分支胰管内的胰液，最终经瓦特氏壶腹汇入十二指肠腔。正常情况下，主胰管直径约2～3 mm，行MRCP检查时可清晰显影^[14]。如图3所示，当透壁性胰腺坏死发生后，走行于胰腺组织中央的细小主胰管常常受到累及出现胰管损伤、坏死，继而主胰管发生破裂、中断改变。这种病理过程能被MRI和MRCP所检出(图4)。

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图3  透壁性胰腺坏死进展合并主胰管中断示意图。透壁性胰腺坏死可侵犯胰腺组织中央细小的主胰管(PD) (箭)，常出现胰管损伤、坏死，继而主胰管破裂、中断(弯箭)　图4　男，39岁，中度重症急性胰腺炎。A：增强MRI静脉期示胰腺体部透壁性胰腺坏死(箭)，同时累及胰尾部中央走行的主胰管(弯箭)；B：2D-MRCP像示胰尾部主胰管(PD)轻微扩张，且走行至胰腺体部区域时出现中断改变(弯箭)
Fig. 3  Schematic diagram of transmural pancreatic necrosis complicating main pancreatic duct (PD) disruption. Transmural parenchyma necrosis can result in the ductal invasion (arrow). And then, the disruption and cut-off change may occur (curved arrow). Fig. 4　A 39-year-old male with moderately severe acute pancreatitis. A：Contrast-enhanced MRI in the venous phase image reveals transmural necrosis of (arrow), along with the involvement of main pancreatic duct (curved arrow). B：Two-dimensional MRCP shows the mildly dilated pancreatic duct (PD) in the tail, as well as a cut-off sign (curved arrow) due to the pancreatic body lesion.

3 后期并发症之包裹性坏死

       在2012亚特兰大标准修订版中，明确提出了AP的四种局部并发症^[1]。它们主要是依据AP的影像学分型以及发病时间长短来界定的^[16]。其中，胰腺包裹性坏死(walled-off necrosis，WON)就是一个新术语。它是指坏死性胰腺炎患者在起病4周后，胰腺内、外出现的包裹性液性积聚，积聚内含有不等量的固体坏死物和脂肪碎屑^[1,2]。如图5所示，透壁性胰腺坏死合并主胰管中断改变出现后，随着时间的迁移，局部坏死更加彻底即形成液化性坏死区，胰腺实质彻底断裂。但是，胰尾部尚存活力的腺体组织仍然会源源不断地分泌胰液，胰尾部主胰管引流的胰液缓慢地向液化坏死区溢出，形成胰瘘。而后，病变区局部逐渐形成液性积聚，积聚缓慢长大且具备占位效应，大约在AP症状发作后3～4周，局部液性积聚周围形成一完整的纤维肉芽组织壁将其包裹，即后期并发症WON形成(图6)。依据影像学表现，尤其是MRI特征，可以将WON再细分为胰腺和胰周WON、胰外WON、胰内WON^[15,17,18]。临床上，较小的WON可以保守治疗或随访复查。若WON直径＞6 cm、WON合并感染、WON压迫胆管(出现黄疸)和胃肠管(出现梗阻症状) (图7)、WON合并出血(假性动脉瘤形成)、WON破裂形成胰源性腹水、WON并发肠瘘形成等，则需要外科治疗^[15,19,20]。

       综上所述，坏死性胰腺炎是一种动态演变的疾病，随着病程的进展，坏死的腺体组织从实性到半实性、再到液化性坏死。而深在的胰腺实质坏死贯穿或几近覆盖胰腺的全层时，大多会导致主胰管的坏死、破裂，形成所谓的“胰管中断综合征”。胰体、尾部残存的活性腺体不断分泌胰液，经主胰管引流从坏死断裂处缓慢溢出；当AP病程至发病后4周左右时，影像学检查即可发现胰腺WON。以上的序贯性演变，笔者将其命名为“透壁性胰腺坏死—胰管中断—包裹性坏死”三部曲。

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图5  “透壁性胰腺坏死—胰管中断—包裹性坏死”三部曲示意图。透壁性胰腺坏死(N)合并主胰管中断改变出现后，随着时间的推进，局部坏死更加彻底。胰尾部腺体组织仍会不断地分泌胰液，胰尾部主胰管(PD)引流的胰液向液化坏死区溢出形成胰瘘。而后，局部形成液性积聚且不断变大；约在发病3～4周后，局部液性积聚完全纤维性包裹，即后期并发症WON形成　图6　女，55岁，重症急性胰腺炎。患者首次住院期间行增强MRI静脉期(A)示胰腺头体部广泛透壁性胰腺坏死(N)，且致主胰管中断；患者腹胀不断加重，发病后近2月再入院复查MRI压脂T2WI (B)示原胰腺坏死区域及网膜囊下隐窝巨大包裹性坏死(WON)形成　图7　女，50岁，重症急性胰腺炎。患者发病后首次入院MRI增强静脉期(A)示胰腺头颈部大面积透壁性胰腺坏死(N)，致胰腺体部断裂(箭)、主胰管中断；发病后3周复查CT增强静脉期(B)示胰腺头颈部完全液化性坏死(箭头)，胰体尾部部分组织尚存在；患者发病后约8周再次入院复查CT增强静脉期(C)示原坏死区形成一个11.8 cm×7.2 cm的巨大包裹性坏死(WON)，因病灶不断长大且已经对胃造成明显挤压(箭)，故拟行外科治疗
Fig. 5  Drawings of "Transmural pancreatic necrosis-Pancreatic duct disruption-Walled-off necrosis" trilogy. Step one: transmural necrosis (N) occurrence; Step two: secondary pancreatic leakage owing to the main pancreatic duct (PD) disruption; Step three: approximately three to four weeks later, the late complication, called walled-off necrosis (WON) (arrowheads), will be formed. Fig. 6　A 55-year-old female with severe acute pancreatitis. Contrast-enhanced MRI in the venous phase (A) during the first hospitalization shows large areas of transmural pancreatic necrosis (N) in the head and body of the pancreas. As the second hospitalization (nearly two months after AP onset), repeated MRI T2WI (B) demonstrates a large well-rounded WON formation. Fig. 7　A：50-year-old woman with severe acute pancreatitis. Contrast-enhanced MRI in the venous phase (A) during the first hospitalization shows large zones of transmural pancreatic necrosis (N) in the head and neck of the pancreas, as well as pancreatic ductal disruption (arrow). On the three weeks after AP onset, repeated CT image (B) reveals the completely liquefied necrosis (arrowheads). During approximate eight weeks after onset, the following CT image (C) demonstrates a walled-off necrosis (WON) with a size of 11.8 cm×7.2 cm in the omental sac and the pancreatic head, neck and body, as well as necrotic fragments within WON. The lesion was closely adjacent to the gastric body (arrow). Therefore, the patient underwent surgery management.