自发孤立性肠系膜上动脉夹层丨CT平扫征象

2022-08-02 熊猫放射 网络

总之,对急诊腹痛患者的腹部CT平扫中,存在SMA主干扩张的征象,特别是当扩张的SMA主干直径超过10mm时,应高度怀疑SISMAD。

 

自发孤立性肠系膜上动脉夹层( spontaneous isolated superior mesenteric artery dissection,SISMAD)是一种少见的血管性疾病,是指仅肠系膜上动脉( superior mesenteric artery,SMA) 发生夹层动脉瘤,而未累及主动脉或没有主动脉夹层。
 
主要临床症状为急、慢性腹痛。由于临床症状及实验室检查结果常无特殊性,易导致漏诊、误诊,以致延误治疗,甚至危及患者生命。
 
患者常由急诊发现,目前主要依靠腹部CT增强扫描、腹主动脉CT血管造影( CTA) 发现并诊断。但对所有急诊或门诊腹痛患者都进行腹部增强CT或CTA 检查是不现实的,尤其是在医疗水平及经济欠发达地区更加不现实;同时也增加对比剂肾病和CT辐射风险,故非常有必要对SISMAD的CT平扫征象进行深入研究,发现诊断SISMAD的特征性CT平扫征象,为进一步CTA或DSA检查提供诊疗依据。
图像分析
CT平扫征象及需测量数据:
(1) 扩张的SMA主干、并测量最宽处左右径;
(2) SMA管壁钙化; 
(3) SMA管壁弧形高密度征; 
(4) SMA管周脂肪浑浊;
(5) 肠壁水肿; 
(6) 腹腔血肿;
(7) SMA主干管腔CT值。
  • 为了测量准确,每例SMA 主干CT值和直径测量位置在SMA主干最宽处,测量三次取平均值。
  • SMA主干扩张的定义为SMA 主干直径>9mm。
  • SMA管壁的弧形高密度征定义为SMA管壁出现高于同层面腹主动脉管壁弧形密度。
  • 管壁钙化定义为SMA管壁出现>140HU的致密影。
  • 管壁周围脂肪浑浊定义为SMA管壁周围脂肪密度增加、模糊。
发病机制
 
高血压可能为SISMAD最重要的危险因素。SISMAD发病机制可能与SMA起始位置( 如易被胰腺头部压迫) 、解剖结构( 如血管弓弧度、与腹主动脉的夹角) 造成特殊的血流剪切力有关,导致血流动力学改变,再加上基础性疾病等危险因素导致动脉管壁损伤,而形成夹层。

 

CT征象

中国人正常肠系膜上动脉主干直径一般<9mm。本研究发现SMA主干扩张是SISMAD最具有诊断意义的征象 。SISMAD真、假腔形成,假腔管壁由于缺乏弹性层,容易扩大,导致SMA直径长范围明显扩张。

 

SMA周边脂肪浑浊为一种渗出性改变,SMA管壁的高密度可能与管壁的出血有关,这2种征象可随病程发生变化。SMA管壁周脂肪浑浊征象出现的机率除疾病因素( 如炎症、肿瘤及其他血管性疾病等) 外,可能还与病程的检查时间点有关,特别是在急性期,更容易被发现,到病程后期出现概率明显减低。

 

SMA管壁密度增高征象可能还与SMA夹层的类型有关,管壁密度高低征象还容易受到评判人的主观因素影响。SISMAD管腔CT值密度一般偏高,这可能与夹层中假腔血流缓慢或新鲜血栓形成有关。但单从SMA管壁和管腔的密度改变难以诊断SISMAD。

 

鉴别诊断

 

SMA动脉瘤常呈梭形和局限性扩张,直径常超过15mm,动脉周边脂肪间隙常清晰,除非动脉瘤破裂可发生脂肪浑浊征象; 而SISMAD常节段性扩张、累及的范围较长,管壁常呈高密度,周边脂肪模糊。

 

小结
总之,对急诊腹痛患者的腹部CT平扫中,存在SMA主干扩张的征象,特别是当扩张的SMA主干直径超过10mm时,应高度怀疑SISMAD,如果还伴有SMA周边脂肪浑浊或/和管壁的密度增高,则更有可能为SISMAD所致,应及时进行腹部增强CT或腹主动脉CTA检查,以免漏诊和误诊。

 

图1 SISMAD的Sakamoto分型: Ⅰ型夹层存在入口与出口; Ⅱ型夹层只有入口,无出口; Ⅲ型假腔已闭塞,近段或/和远段存在穿透性溃疡; Ⅳ型,假腔闭塞。

图2 诊断SISMAD的各参数的ROC曲线图,其中扩张SMA 主干诊断效能最大,其次为管腔CT值、管周脂肪间隙和管壁高密度。
图3A~D患者,男,56岁,腹痛2天。CT平扫(A)示SMA主干扩张,直径约12.4mm; 进一步行CTA( B、C) 示SMA内膜片及真假腔形成; VR(D)示SMA Sakamoto’s I型夹层。

 

 

↓ 内容来源:

 

感谢作者和期刊!

 

 

 

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    2022-07-11 jxrzshh
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    2022-07-11 zzc2216

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