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主动脉夹层是一种凶险、致命的心血管外科急症,年发病率约2.9人/10万[1]。针对主动脉夹层,国际上通用分型方法有两种,即Stanford分型与Debakey分型。依据夹层累及范围分为累及升主动脉的Stanford A型和未累及升主动脉的Stanford B型[2]。由于Stanford A主动脉夹层病人数量日益增加,如何提高该类疾病手术成功率,如何简化推广相关外科技术一直是国内外专家临床研究热点[2-3]。针对上述问题,现将我院收治51例Stantord A主动脉夹层病人的围手术期临床资料进行整理和回顾性分析,将治疗经验作一总结。
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全组平均体外循环时间(231±45)min,心肌阻断时间(181±21)min,停循环时间(25±15)min,选择性脑灌注时间(36±11)min。主要并发症:肺部感染3例,急性肾损伤8例,消化道出血3例。死亡13例(25.5%),其中术后30 d内死亡9例:术前急性肺水肿,术后低心排综合征2例,术中无法控制活动性出血2例,围手术期低氧血症致心脏骤停2例,术后脑出血1例,术后脑梗死1例,多脏器衰竭1例;术后30 d以后死亡4例:骨筋膜室综合征导致多脏器衰竭1例;肺部感染,消化道应激性溃疡2例;纵隔感染1例。
与非死亡组比较,死亡组病人主动脉根部明显受累,主动脉阻断时间较长,术中输血量更多,术后需要持续肾替代治疗(CRRT)与体外膜肺氧合(ECMO)辅助治疗更多,ICU停留时间和住院时间更长(P < 0.05~P < 0.01)(见表 1)。对死亡原因进行多元回归分析提示:主动脉根部受累、术后应用CRRT和ECMO与病人死亡成相关(OR=9.714,8.831,10.997, P < 0.05)(见表 2)。
分组 非死亡组(n=38) 死亡组(n=13) t P 年龄(x±s)/岁 58.05±12.60 55.92±16.34 0.49 >0.05 男 27(71.05) 8 (62.54) 0.09# >0.05 体质量指数(x±s)/(kg/m2) 25.47±3.05 24.23±3.18 1.25 >0.05 吸烟 27(71.05) 6(46.15) 1.65# >0.05 饮酒 28(73.68) 6(46.15) 2.18# >0.05 高血压 34(89.47) 12(92.31) 0.06# >0.05 糖尿病 4(10.53) 3(23.07) 0.45# >0.05 脑血管意外 — 1(7.69) — 慢性阻塞性肺疾病 4(10.53) 3(23.07) 0.45# >0.05 主动脉根部受累 21(55.26) 12(92.31) 4.31# < 0.05 LVEF(x±s)/% 56.23±3.47 55.47±2.71 0.72 >0.05 术前丙氨酸氨基转移酶(x±s)/(U/L) 29±4.5 30±7.1 0.48* >0.05 术前天冬氨酸氨基转移酶(x±s)/(U/L) 29±1.4 29±2.5 0.69* >0.05 术前血肌酐(x±s)/(μmol/L) 98±14.7 116±7.3 5.75* >0.05 体外循环时间(x±s)/min 225±25.0 240±15.0 2.03 >0.05 主动脉阻断时间(x±s)/min 172±18.0 190±23.0 2.90 < 0.01 深低温停循环时间(x±s)/min 23.5±2.7 25.4±3.2 2.08 >0.05 术中输血量(x±s)/U 2.0±0.5 6.0±1.3 10.82* < 0.01 术后24 h内引流量(x±s)/mL 1 500±15.0 1 500±170 0.80 >0.05 术后肝损伤 12(31.58) 6(46.15) 0.38# >0.05 CRRT 4(10.53) 7(53.85) 8.34# < 0.01 ECMO治疗 2(5.26) 4(30.77) 3.86# < 0.05 ICU停留时间(x±s)/d 4±1.5 8±2.5 5.44* < 0.01 住院时间(x±s)/d 14±3 25±3 11.42 < 0.01 *示t′值;#示矫正χ2值 表 1 2组病人的围手术期比较[n; 百分率(%)]
变量 OR 95%CI P 根部严重受累 9.714 1.039~10.147 < 0.05 主动脉阻断时间 1.103 0.972~1.432 >0.05 术中输血量 1.000 0.999~1.000 >0.05 CRRT 8.831 2.737~14.573 < 0.05 ECMO 10.997 2.746~23.780 < 0.05 表 2 死亡相关因素分析
Stanford A型主动脉夹层术后早期死亡因素分析
Analysis of early death factors after surgical treatment for Stanford type A aortic dissection
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摘要:
目的 分析Stanford A主动脉夹层病人的治疗过程及结果,分析早期死亡因素。 方法 回顾性分析51例Stantord A主动脉夹层外科治疗的临床资料、治疗方案及预后。依据病人是否死亡分为死亡组与非死亡组。 结果 与非死亡组比较,死亡组病人主动脉根部明显受累,主动脉阻断时间较长,术中输血量更多,术后需要持续肾替代治疗(CRRT)与体外膜肺氧合(ECMO)辅助治疗更多,ICU停留时间和住院时间更长(P < 0.05~P < 0.01)。对死亡原因进行多元回归分析提示:主动脉根部受累、术后应用CRRT和ECMO与病人死亡成相关(OR值分别为9.714,8.831,10.997,P < 0.05)。 结论 急诊手术是治疗Stanford A型主动脉夹层最有效方法。根部“三明治”技术解决根部出血和主动脉瓣关闭不全的有效方法。主动脉远端近段吻合止血方法是手术成败的关键。 -
关键词:
- Stanford A型主动脉夹层 /
- 主动脉根部
Abstract:Objective To analyze the treatment process and outcome of patients with Stanford A aortic dissection and summarize the experience of surgical treatment. Methods Retrospective analysis was performed on the surgical data, treatment plan and prognosis of 51 cases with Stanford type A aortic dissection.Patients were divided into death group and nondeath group according to whethe they died or not. Results Compared with the non-death group, patients in the death group were significantly involved in the aortic root, the aorta occlusion time was longer, the intraoperative blood transfusion volume was higher, more postoperative adjuvant therapy was required with CRRT and ECMO, and the stay time in ICU and hospitalization time were longer(P < 0.05 to P < 0.01).Multiple regression analysis of causes of death suggested that aortic root involvement, postoperative CRRT and ECMO were correlated with death(OR=9.714, 8.831 and 10.997, P < 0.05). Conclusions Emergency surgery is the most effective treatment for Stanford A aortic dissection.Root "sandwich" technique is an effective method for root bleeding and aortic valve insufficiency.The hemostasis of distal and proximal segments of aorta is the key to the success of the operation. -
Key words:
- Stanford type A aortic dissection /
- aortic root
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表 1 2组病人的围手术期比较[n; 百分率(%)]
分组 非死亡组(n=38) 死亡组(n=13) t P 年龄(x±s)/岁 58.05±12.60 55.92±16.34 0.49 >0.05 男 27(71.05) 8 (62.54) 0.09# >0.05 体质量指数(x±s)/(kg/m2) 25.47±3.05 24.23±3.18 1.25 >0.05 吸烟 27(71.05) 6(46.15) 1.65# >0.05 饮酒 28(73.68) 6(46.15) 2.18# >0.05 高血压 34(89.47) 12(92.31) 0.06# >0.05 糖尿病 4(10.53) 3(23.07) 0.45# >0.05 脑血管意外 — 1(7.69) — 慢性阻塞性肺疾病 4(10.53) 3(23.07) 0.45# >0.05 主动脉根部受累 21(55.26) 12(92.31) 4.31# < 0.05 LVEF(x±s)/% 56.23±3.47 55.47±2.71 0.72 >0.05 术前丙氨酸氨基转移酶(x±s)/(U/L) 29±4.5 30±7.1 0.48* >0.05 术前天冬氨酸氨基转移酶(x±s)/(U/L) 29±1.4 29±2.5 0.69* >0.05 术前血肌酐(x±s)/(μmol/L) 98±14.7 116±7.3 5.75* >0.05 体外循环时间(x±s)/min 225±25.0 240±15.0 2.03 >0.05 主动脉阻断时间(x±s)/min 172±18.0 190±23.0 2.90 < 0.01 深低温停循环时间(x±s)/min 23.5±2.7 25.4±3.2 2.08 >0.05 术中输血量(x±s)/U 2.0±0.5 6.0±1.3 10.82* < 0.01 术后24 h内引流量(x±s)/mL 1 500±15.0 1 500±170 0.80 >0.05 术后肝损伤 12(31.58) 6(46.15) 0.38# >0.05 CRRT 4(10.53) 7(53.85) 8.34# < 0.01 ECMO治疗 2(5.26) 4(30.77) 3.86# < 0.05 ICU停留时间(x±s)/d 4±1.5 8±2.5 5.44* < 0.01 住院时间(x±s)/d 14±3 25±3 11.42 < 0.01 *示t′值;#示矫正χ2值 表 2 死亡相关因素分析
变量 OR 95%CI P 根部严重受累 9.714 1.039~10.147 < 0.05 主动脉阻断时间 1.103 0.972~1.432 >0.05 术中输血量 1.000 0.999~1.000 >0.05 CRRT 8.831 2.737~14.573 < 0.05 ECMO 10.997 2.746~23.780 < 0.05 -
[1] MESZAROS I, MOROCZ J, SZLAVI J, et al. Epidemiology and clinicopathology of aortic dissection[J]. Chest, 2000, 117(5): 1271. doi: 10.1378/chest.117.5.1271 [2] 郑斯宏, 孙衍庆, 孟旭, 等. Stanford A型主动脉夹层的外科治疗[J]. 中华外科杂志, 2005, 43(18): 1177. doi: 10.3760/j:issn:0529-5815.2005.18.003 [3] 孙立忠, 李建荣. 我国Stanford A型主动脉夹层诊疗进展与挑战[J]. 中华外科杂志, 2017, 55(4): 241. [4] CIFANI N, PROIETTA M, TRITAPEPE L, et al. Stanford-A acute aortic dissection, inflammation, and metalloproteinases: a review[J]. Ann Med, 2015, 47(6): 441. doi: 10.3109/07853890.2015.1073346 [5] MERKLE J, SABASHNIKOV A, DEPPE AC, et al. Impact of hypertension on early outcomes and long-term survival of patients undergoing aortic repair with Stanford A dissection[J]. Perfusion, 2018, 33(6): 463. doi: 10.1177/0267659118768147 [6] HAN L, DAI L, LI HY, et al. Elevated D-dimer increases the risk of dialysis after surgery in patients with Stanford A aortic dissection through the impact of the coagulation system[J]. J Thorac Dis, 2018, 10(12): 6783. doi: 10.21037/jtd.2018.11.138 [7] 唐杨烽, 徐激斌, 徐志云, 等. Stanford A型主动脉夹层的根部处理策略及疗效分析[J]. 中华外科杂志, 2012, 50(11): 991. doi: 10.3760/cma.j.issn.0529-5815.2012.11.007 [8] NERI E, MASSETTI M, CAPANNINI G, et al. Glue containment and anastomosis reinforcement in repair of aortic dissection[J]. Ann Thorac Surg, 1999, 67(5): 1510. doi: 10.1016/S0003-4975(99)00229-5 [9] LI Q, CHEN L, SHEN Y, et al. A modified axillo-femoral perfusion for acute type a aortic dissection accompanied with lower limb malperfusion[J]. J Cardiothorac Surg, 2020, 15(1): 10. doi: 10.1186/s13019-020-1060-2 [10] BAKER DW, CELERMAJER DS. Acute aortic dissection as a late and fatal complication of transcatheter persistent ductus arteriosus occlusion: A case report[J]. Eur Heart J Case Rep, 2020, 5(1): ytaa484. [11] NISHIGAWA K, FUKUI T, UEMURA K, et al. Preoperative renal malperfusion is an independent predictor for acute kidney injury and operative death but not associated with late mortality after surgery for acute type A aortic dissection[J]. Eur J Cardiothorac Surg, 2020, 58(2): 302. doi: 10.1093/ejcts/ezaa063 [12] HELGASON D, HELGADOTTIR S, AHLSSON A, et al. Acute kidney injury after acute repair of type A aortic dissection[J]. Ann Thorac Surg, 2021, 111(4): 1292. doi: 10.1016/j.athoracsur.2020.07.019