巨大自发性脾肾分流道栓塞联合抗凝治疗门静脉血栓1例报告

黄菊 ,  王小泽 ,  罗薛峰 ,  杨丽

临床肝胆病杂志 ›› 2025, Vol. 41 ›› Issue (08) : 1639 -1642.

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临床肝胆病杂志 ›› 2025, Vol. 41 ›› Issue (08) : 1639 -1642. DOI: 10.12449/JCH250825
病例报告

巨大自发性脾肾分流道栓塞联合抗凝治疗门静脉血栓1例报告

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Large spontaneous splenorenal shunt embolization combined with anticoagulant therapy in treatment of portal vein thrombosis: A case report

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摘要

门静脉血栓是肝硬化患者常见且严重的并发症,门静脉血流动力学的改变与门静脉血栓的发生密切相关。合并巨大的自发性脾肾分流时门静脉灌注减少、血流速度减慢,极有可能削弱门静脉血栓的抗凝效果。本文将报道1例通过栓塞自发性脾肾分流道联合抗凝治疗策略,实现了门静脉的完全再通,然而,仍需高质量的临床研究进一步验证和支持这一策略的有效性。

Abstract

Portal vein thrombosis (PVT) is a common and severe complication in patients with liver cirrhosis, and alterations in portal hemodynamics are closely associated with the development of PVT. The presence of large spontaneous splenorenal shunt (SSRS) may lead to reductions in portal vein perfusion and blood flow velocity, which may compromise the anticoagulant effect on PVT. This article reports the treatment strategies of SSRS embolization combined with anticoagulant therapy that help to achieve complete recanalization of the portal vein; however, high-quality clinical studies are still needed to further validate and support the effectiveness of this strategy.

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关键词

门静脉 / 静脉血栓形成 / 栓塞, 治疗性

Key words

Portal Vein / Venous Thrombosis / Embolization, Therapeutic

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黄菊,王小泽,罗薛峰,杨丽. 巨大自发性脾肾分流道栓塞联合抗凝治疗门静脉血栓1例报告[J]. 临床肝胆病杂志, 2025, 41(08): 1639-1642 DOI:10.12449/JCH250825

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门静脉血栓(portal vein thrombosis,PVT)是肝硬化患者常见的严重并发症之一,门静脉血流量减少是血栓形成的重要影响因素1。自发性门体分流(spontaneous portosystemic shunts,SPSS)是指门静脉系统绕过肝脏与体循环系统直接交通,一定程度上缓解门静脉压力,但随着SPSS的直径及分流量增大,肝脏血流灌注减少,门静脉血流缓慢,这可能加速肝损伤并增加PVT的风险2-4。其中,自发性脾肾分流(spontaneous splenorenal shunt,SSRS)是SPSS较为常见类型。抗凝治疗是PVT的一线治疗方法,但在本病例中,因SSRS的存在,其疗效可能会受到影响。本文将报道1例通过栓塞SSRS来辅助治疗PVT的方法。

1 病例资料

患者女性,53岁,于2023年4月4日因“发现HBsAg阳性10年,PVT 5个月”入住本院。入院前10年,患者体检发现HBsAg阳性,于当地医院进一步检查,确诊乙型肝炎肝硬化,先后予以恩替卡韦、富马酸替诺福韦酯抗病毒治疗。病程中无呕血、黑便、意识障碍、腹胀、腹痛等。入院前5个月,患者无特殊不适,本院门诊规律复诊,完善腹部彩超提示门静脉右支未见血流信号(图1),完善上腹部CT血管造影(computed tomography angiography,CTA)提示门静脉右支闭塞,门静脉主干及左支细小,且存在一个较大的SSRS(图2a)。嘱患者口服利伐沙班(10 mg,1次/d)抗凝治疗后门诊复查。治疗4个月后门诊随访发现PVT情况无好转,门静脉左支也闭塞(图3a),考虑SSRS的存在可能是该患者抗凝效果差的重要影响因素,建议入院行分流道栓塞手术,遂收入本科室。既往史、个人婚育史、家族史、流行病学史均无异常。入院查体:神清,对答切题,无皮肤黄染,腹软,无压痛及反跳痛,双下肢无水肿。

本院辅助检查结果:血小板减少(73×109/L),而血红蛋白水平和白细胞计数在正常范围内。总胆红素66.7 μmol/L,直接胆红素13.5 μmol/L,丙氨酸转氨酶24 U/L,天冬氨酸转氨酶46 U/L,碱性磷酸酶160 U/L,白蛋白34.4 g/L;凝血酶原时间14.6 s,国际标准化比值1.29;输血前全套:HBsAg、抗-HBc阳性,余阴性。高精度HBV病毒载量阳性(<20 U/mL)。甲胎蛋白、异常凝血酶原阴性。入院后行脾肾分流道栓塞术:局麻下穿刺右侧股静脉,经左肾静脉插管至脾肾分流道内,交换9F长鞘,使用3个Amplatzer血管塞(18、20、22 mm,Abbott,Plymouth,MN,US)封堵分流道,复查造影血管塞在位,分流道栓塞确切(图2b)。出院后持续口服利伐沙班(10 mg,1次/d)治疗。

5个月后复查结果提示:总胆红素39.5 μmol/L,直接胆红素8.6 μmol/L,丙氨酸转氨酶、天冬氨酸转氨酶、碱性磷酸酶、谷氨酰转肽酶、白蛋白正常;凝血酶原时间13.2 s,国际标准化比值1.24。Child-Pugh评分从8分降至6分。腹部CTA提示门静脉主干及左右分支完全再通,SSRS未再显影(图2c)。截至2024年9月随访,未见血栓复发及出血(图3b)。

2 讨论

PVT是指门静脉主干和(或)门静脉左、右分支发生血栓,伴或不伴肠系膜静脉及脾静脉血栓形成5。随着肝硬化的严重程度增加,其发病率也随之上升。一项荟萃分析显示,在Child-Pugh A级肝硬化患者中,PVT的患病率为13.54%6,而在Child-Pugh B/C级肝硬化患者中,上升到23.72%6,年发病率在3.7%~24.4%7。研究表明PVT增加了肝硬化患者远期死亡风险、出血、腹水以及肝移植后死亡的风险8-10

研究显示,无论血栓严重程度如何,应尽早抗凝,抗凝治疗可以带来生存获益11-12。抗凝治疗能够显著提高(部分或完全)再通率(71% vs 42%,P<0.000 1),减缓进展(9% vs 33%,P<0.000 1)13。根据国内外的指南514,PVT占据主干>50%时,推荐抗凝治疗。因此,该患者抗凝是有必要的。

理论上,SPSS被视为肝硬化患者门静脉高压的一种代偿机制。然而,SPSS一定程度上减少了门静脉灌注,导致门静脉血流速度减慢1,这可能增加PVT的风险2-4。肝硬化患者PVT的发展主要由Virchow血栓形成三要素变化所驱动:门静脉血流减少、高凝状态和内皮损伤15。同时,有研究发现,合并SSRS的患者,门静脉主干及右支直径更细16。故当SSRS存在时,本例患者影像学应提示门静脉右支细小,但表现为门静脉右支闭塞、门静脉主干部分血栓及左支细小,且在抗凝治疗的过程中逐渐演变为左支闭塞,说明SSRS影响该病例PVT的形成与发展。因此,考虑SSRS引起的“盗血现象”继发门静脉血流较少可能是促进本病例中血栓形成的重要因素17

虽然抗凝治疗是肝硬化PVT患者治疗的基石18,但由于PVT的复杂性,单独的抗凝治疗并不能产生最佳效果,抗凝治疗后门静脉再通率为66%~71%813。影响抗凝治疗有效性的因素包括血栓的严重程度和位置、肝硬化的阶段以及开始抗凝治疗的时机19-20。SSRS作为本病例中血栓形成的重要因素,其导致的门静脉血流动力学的改变可能削弱了抗凝本身治疗的有效性,进入门静脉系统内的抗凝药大多经SSRS至体循环,未能完全作用于PVT。目前的研究表明,经颈内静脉肝内门体分流中应联合栓塞较大的SPSS,以避免过度分流,降低肝性脑病、肝衰竭和支架早期功能障碍的风险21。此外,SPSS栓塞已被证明可以改善肝功能并改变疾病的自然进展15。尽管通过栓塞改善了血流动力学,但患者门静脉左右分支已完全闭塞,实现自发再通可能性较低,单纯栓塞可能不足以恢复血流12。因此,栓塞联合抗凝治疗是有必要的。

综上,对于PVT患者,应尽早进行腹部血管影像评估,若存在较大自发性门体分流道,应在抗凝的基础上联合分流道栓塞,尽早恢复门静脉血流,改善肝功能的同时有助于提高门静脉再通成功率。

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基金资助

四川大学华西医院“1·3·5”高端人才支持计划(ZYGD23031)

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