Gertsch Philippe, Vandoni Riccardo E, Pelloni Angelo, Krpo Aljosa, Alerci Mario
Department of Surgery, Ospedale San Giovanni, Bellinzona, Switzerland.
Ann Surg. 2007 Dec;246(6):958-64; discussion 964-5. doi: 10.1097/SLA.0b013e31815c2a58.
To prospectively assess the frequency, severity, and extension of localized ischemia in the remaining liver parenchyma after hepatectomy.
Major blood loss and postoperative ischemia of the remnant liver are known factors contributing to morbidity after liver surgery. The segmental anatomy of the liver and the techniques of selective hilar or suprahilar clamping of the Glissonian sheaths permit identification of ischemia on the surface of the corresponding segments for precise section of the parenchyma. Incomplete resection of a segment, or compromised blood supply to the remaining liver, may result in ischemia of various extension and severity.
Patients undergoing hepatectomy received enhanced computerized tomodensitometry with study of the arterial and venous phases within 48 hours after resection. We defined hepatic ischemia as reduced or absent contrast enhancement during the venous phase. We classified the severity of ischemia as hypoperfusion, nonperfusion, or necrosis. The extension of ischemia was identified as marginal, partial, or segmental. Factors that may influence postoperative ischemia were analyzed by univariate and multivariate analyses.
One hundred fifty consecutive patients (70 F, 80 M, mean age 62 +/- 12 years) underwent 64 major and 81 minor hepatectomies and 5 wedge resections. We observed radiologic signs of ischemia in 38 patients (25.3%): 33 hypoperfusions (17 marginal, 12 partial, and 4 segmental), 3 nonperfusions (1 marginal, 1 partial, and 1 segmental), and 2 necroses (1 partial, 1 segmental). One patient with a segmental necrosis underwent an early reoperation. In all other cases, the evolution was spontaneously favorable. Postoperative peak levels of serum aspartate aminotransferase and alanine aminotransferase were significantly higher in patients with ischemia. Patients with ischemia had a significantly higher risk of developing a biliary leak (18.4% vs. 2.6%, P < 0.001). There was no correlation between liver ischemia and mortality (2%). None of the following factors were associated with ischemia after univariate and multivariate analysis: age, preoperative bilirubin level, liver fibrosis, malignant tumor, type of hepatectomy, surface of transection, weight of resected liver, Pringle maneuver, blood loss, and number of transfusions.
Some form of localized ischemia after hepatectomy was detected in 1 of 4 of our patients. Its clinical expression was discreet in the large majority of cases, even if it might have been one of the underlying causes of postoperative biliary fistulas. Clinical observation is sufficient to detect the rare patient with suspected postoperative liver ischemia that will require active treatment.
前瞻性评估肝切除术后剩余肝实质局部缺血的发生率、严重程度及范围。
大量失血和残余肝术后缺血是肝手术后导致发病的已知因素。肝脏的节段性解剖结构以及选择性肝门或肝门上方肝蒂鞘夹闭技术,有助于识别相应节段表面的缺血情况,从而精确切除肝实质。节段切除不完全或剩余肝脏血供受损,可能导致不同范围和严重程度的缺血。
接受肝切除的患者在切除后48小时内接受增强计算机断层扫描,研究动脉期和静脉期。我们将肝缺血定义为静脉期对比增强减弱或消失。我们将缺血的严重程度分为灌注不足、无灌注或坏死。缺血范围分为边缘性、部分性或节段性。通过单因素和多因素分析来分析可能影响术后缺血的因素。
150例连续患者(70例女性,80例男性,平均年龄62±12岁)接受了64例大肝切除、81例小肝切除和5例楔形切除术。我们在38例患者(25.3%)中观察到缺血的影像学征象:33例灌注不足(17例边缘性、12例部分性和4例节段性),3例无灌注(1例边缘性、1例部分性和1例节段性),2例坏死(1例部分性、1例节段性)。1例节段性坏死患者接受了早期再次手术。在所有其他病例中,病情发展呈自发好转。缺血患者术后血清天冬氨酸氨基转移酶和丙氨酸氨基转移酶的峰值水平显著更高。缺血患者发生胆漏的风险显著更高(18.4%对2.6%,P<0.001)。肝缺血与死亡率(2%)之间无相关性。单因素和多因素分析后,以下因素均与缺血无关:年龄、术前胆红素水平、肝纤维化、恶性肿瘤、肝切除类型、切面面积、切除肝脏重量、Pringle手法、失血量和输血量。
我们的患者中四分之一检测到某种形式的肝切除术后局部缺血。在大多数情况下,其临床表现不明显,即使它可能是术后胆瘘的潜在原因之一。临床观察足以发现罕见的疑似术后肝缺血患者,这类患者需要积极治疗。