肝脏 ›› 2019, Vol. 24 ›› Issue (1): 24-27.

• 论 著 • 上一篇    下一篇

肝硬化门静脉高压患者脾切除断流术后早期门静脉血栓形成的因素及预防性活血、抗凝、祛聚治疗的效果

张振, 王孟龙, 张海涛, 张其坤, 刘福全   

  1. 100069 首都医科大学附属北京佑安医院肝胆外科(张振,王孟龙,张海涛,张其坤);首都医科大学附属北京世纪坛医院肝胆外科(刘福全)
  • 收稿日期:2018-07-17 出版日期:2019-01-31 发布日期:2020-04-09
  • 基金资助:
    北京市医器局扬帆计划(XMLX201509)

Risk factors for early portal venous system thrombosis after devascularization with splenectomy and portal hypertension in cirrhotic patients with portal hypertension and preventive effects of blood activating, anticoagulation and antiplatelet therapy

ZHANG Zhen1, WANG Meng-long1, ZHANG Hai-tao1, ZHANG Qi-kun1, LIU Fu-quan2   

  1. 1. Department of Hepatobiliary surgery, Bei Jing You-An Hospital,Capital University Of Medical Sciences, Beijing 100069, China;
    2. Department of Hepatobiliary Surgery, Beijing Shijitan Hospital,Capital Medical University, Beijing 100038, China
  • Received:2018-07-17 Online:2019-01-31 Published:2020-04-09

摘要: 目的 探讨肝硬化门静脉高压患者脾切除断流术后早期门静脉血栓形成(PVST)的因素及预防性活血、抗凝、祛聚治疗的效果。方法 以2011年1月到2016年12月北京佑安医院诊治的肝硬化门静脉高压患者320例作为研究对象, 所有患者都采用脾切除断流术,记录PVST发生情况,调查所有患者病例与随访资料。PVST患者术后给予预防性活血、抗凝、祛聚治疗(低分子右旋糖酐+双嘧达莫+华法林),记录凝血指标变化情况。结果 肝硬化门静脉高压患者320例术后发生PVST 60例,发生率为18.8%。PVST组与非PVST组脾脏大小、脾静脉直径、门静脉直径、门静脉血流速度、输血量、术后血小板计数、术后D-二聚体等指标比较差异有统计学意义(P<0.05)。多因素Logistic回归分析显示术后血小板计数、术后D-二聚体、门静脉血流速度为影响PVST发生的主要独立危险因素(P<0.05)。术后D-二聚体用于诊断PVST的ROC曲线下面积为0.794,95%CI为(0.724,0.863)(P<0.05),诊断分界点为3.55 mg/L。术后血小板计数用于诊断PVST的ROC曲线下面积为0.754,95%CI为(0.672,0.836)(P<0.05),诊断分界点为435.5×109/L。60例PVST患者术后1个月的血浆PT与APTT值明显低于术后1 d(9.22±2.13) s 和(35.39±9.14) s vs (11.67±1.84) s和(41.94±10.92) s(P<0.05)。结论 肝硬化门静脉高压患者脾切除断流术后早期PVST比较常见,术后血小板计数、术后D-二聚体、门静脉血流速度为主要的危险因素,预防性活血、抗凝、祛聚治疗能起到有效的预防作用。

关键词: 肝硬化, 门静脉高压, 脾切除断流术, 门静脉血栓形成, 影响因素

Abstract: Objective To investigate the risk factors for early portal venous system thrombosis (PVST) after devascularization with splenectomy in cirrhotic patients with portal hypertension and to explore the preventive effects of blood activating, anticoagulation and antiplatelet therapy.Methods A retrospective study was conducted on 320 patients with portal hypertension post liver cirrhosis in our hospital from January 2011 to December 2016. All patients were treated with splenectomy and devascularization, and followed up after operation. Clinical data were collected including the occurrence of PVST. The patients with PVST were treated with blood activating, anticoagulation and antiplatelet therapy (low molecular dextran + vitamin K1 + dipyridamole + warfarin), and the changes of blood coagulation indexes were recorded. Results There were 60 patients developing PVST after operation in the 320 patients with an incidence of 18.8%. Parameters including spleen size, splenic vein diameter, portal vein diameter, flow velocity of portal vein blood, blood transfusion volume, postoperative platelet count and postoperative D-dimer level in PVST group (n=60) were significantly different from those in non-PVST group (n=260) (P<0.05). Multivariate logistic regression analysis showed that the postoperative platelet count, postoperative D-dimer level and blood flow velocity of portal vein were the main independent risk factors for PVST (P<0.05). The area under the receiver-operating characteristic (AUROC) curve of D-dimer for the diagnosis of PVST was 0.794 with 95% confidence interval (CI) of 0.724-0.863 (P<0.05), and the diagnostic cut-off point was 3.55 mg/L. The AUROC curve of postoperative platelet count for the diagnosis of PVST was 0.754 with 95% CI of 0.672~0.836 (P<0.05), and the diagnostic cut-off point was 435.5×109/L. The prothrombin time and activated partial thromboplastin time at month 1 were significantly lower than those at day 1 after operation in PVST group, respectively (9.22±2.13 s vs. 11.67±1.84 s and 35.39±9.14 s vs. 41.94±10.92 s, both P<0.05).Conclusion The occurrence of PVST after devascularization with splenectomy in patients with portal hypertension post liver cirrhosis is common. The postoperative platelet count, postoperative D-dimer and blood flow velocity of portal vein are the main risk factors for the PVST. The blood activating, anticoagulation and antiplatelet therapy might effectively prevent the PVST.

Key words: Liver cirrhosis, Portal hypertension, Devascularization with splenectomy, Portal venous system thrombosis, Risk factors