This week we'll discuss intraoperative risk factors for renal dysfunction.
1.Are there operations which are commonly associated with postoperative renal failure?
2.What is the mechanism for postoperative renal dysfunction following aortic surgery?
3.Does deliberate hypotensive anesthesia increase the risk of postoperative renal dysfunction?
4.Do regional and general anesthetic techniques affect the incidence of postoperative renal dysfunction?
1 是否有些手术与术后肾功衰竭有关？
2 主动脉手术后肾功障碍发生机制是什么？
3 麻醉过程中控制性降压，是否会增加术后肾衰风险？
4 局麻和全麻技术是否影响术后肾功障碍发生率？
1 是否有些手术与术后肾功衰竭有关？
心脏手术、主动脉瘤手术、大的创伤或烧伤手术、胆道手术和器官移植（肝、肾、心脏）等手术过程通常与术后肾功衰竭有关，心肺转流，尤其是体外循环时间过长时(超过130-180 min)、应用主动脉内球囊泵和低心输出量综合征也可导致急性肾功衰竭。
2 主动脉手术后肾功障碍发生机制是什么？
近期前瞻性研究报导主动脉手术后发生肾功不全的几率是2.7-15%。此种肾功不全的发病机制可能如下：
• 手术：主动脉阻段的平面和时间
• 生理：
o 肾素血管紧张素系统兴奋
o 交感神经系统兴奋
o 前列腺素类
o 氧自由基
o 补体系统激活
o 细胞因子和其他炎性因子
值得注意的是，超过30 min的肾脏缺血和术中失血量需输注5 u压缩红细胞时，预示着主动脉手术后可能发生急性肾功衰竭。主动脉手术后发生急性肾功衰竭的患者，不仅仅是肾功并发症增多，死亡率可达50-60%。
3 麻醉过程中控制性降压，是否会增加术后肾衰风险？
控制性降压常用于术中可能大量失血的手术中。然而此种低血压可能使平均动脉压低于肾脏的自主调节范围。Williams-Russo 等在研究此问题时，应用两种平均动脉压水平(45-55 mmHg or 55-70 mmHg)评估了235名伴有心脏病、高血压或糖尿病的超过70岁的高龄患者和中年患者在硬膜外麻醉和控制性降压下行全髋置换时发生肾功不全的风险，结果发现把肌酐水平高于基础值20％定义为肾功障碍时，两组患者肾功无统计学差异。因此作者得出结论认为即使在高风险人群，控制性降压不会增加术后肾功不全几率。
4 局麻和全麻技术是否影响术后肾功障碍发生率？
有学者已经对前述Williams-Russo的研究及硬膜外麻醉可能没有肾功保护作用的研究进行了阐述。比较明确的是，这些研究表明交感神经系统（或其被抑制）在调节肾小球滤过率和肾血流中的作用有限。
谈起全麻，争论的焦点集中在应用七氟烷时氟离子和Compound A分解产物潜在的肾毒性上。然而，在临床资料显示，即使使用七氟烷、且时间较长、低流量麻醉、控制性降压并伴有术前肾功不全病史，这些均与术后肾功衰竭无相关性。近期证据表明，早期的实验证据显示的七氟烷的肾毒性可能与七氟烷在种族间代谢差异有关
英文参考答案
1 Are there operations which are commonly associated with postoperative renal failure?Cardiac surgery, aortic aneurysm surgery, major trauma or burn surgery, biliary tract surgery and transplantation (liver, kidney, heart) surgery are all procedures which are commonly associated with postoperative renal failure. Cardiopulmonary bypass, especially when associated with longer bypass times (greater than 130-180 min), the use of intraaortic balloon pumps, and low output syndromes, is particularly associated with acute renal failure (1).
2 What is the mechanism for postoperative renal dysfunction following aortic surgery?
The incidence of renal dysfunction following aortic surgery ranges from 2.7-15% in recent prospective studies (2). The mechanisms believed to play a role in the pathogenesis of this renal dysfunction include (3):
• Surgical: level and duration of cross clamping
• Physiological:
o renin-angiotensin stimulation
o sympathetic stimulation
o prostaglandins
o oxygen free radicals
o complement cascade mediators
o cytokines and other inflammatory mediators.
In particular, more than 30 minutes of renal ischemia and an intraoperative blood loss requiring more than 5 units of PRBCs, are predictive of acute renal failure following aortic surgery (2). Morbidity is not limited to renal function; individuals who sustain acute renal failure after aortic surgery have a 50-60% chance of mortality (4).
3 Does deliberate hypotensive anesthesia increase the risk of postoperative renal dysfunction?
Deliberate hypotensive anesthesia (DHA) is often utilized in surgeries which may potentially result in large blood loss. However, this hypotension has been speculated to result in mean arterial pressures below renal autoregulatory abilities. Williams-Russo et al. (5), in attempting to study this question, evaluated a high risk population of 235 patients older than 70 years of age or middle aged patients with cardiac, hypertensive or diabetic processes, undergoing total hip replacement under epidural anesthesia and DHA. Using two separate levels of mean arterial pressure (45-55 mmHg or 55-70 mmHg), the authors noted no differences in renal function, as defined by a 20% increase in serum creatinine level from baseline. They concluded that even in a high risk population, DHA does not create differences in postoperative renal function.
4 Do regional and general anesthetic techniques affect the incidence of postoperative renal dysfunction?
Some have interpreted the Williams-Russo study cited above, and other studies as failing to show a renal protective effect of epidural anesthesia. More specifically, these studies may suggest that the sympathetic system (or its inhibition) may play a less critical role in regulating GFR and renal blood flow (5).
In terms of general anesthesia, controversy has surrounded the use of sevoflurane due to experimental data demonstrating potentially nephrotoxic free fluoride and Compound A breakdown products. Despite these data, however, clinical data in patients receiving sevoflurane, even with prolonged exposure, low flow rates, DHA, and a history of preoperative renal insufficiency, have not correlated with postoperative renal dysfunction (6,7). Recent evidence suggests that the earlier experimental evidence demonstrating sevoflurane nephrotoxicity may be due to species differences in sevoflurane metabolism .
References:
1.Conlon PJ, Stafford-Smith M, White WD, et al. Acute renal failure following cardiac surgery. Nephrol Dial Transplant. 1999;14(5):1158-62.
2.Godet G, Fleron MH, Vicaut E, et al. Risk factors for acute postoperative renal failure in thoracic or thoracoabdominal aortic surgery: a prospective study. Anesth Analg 1997;85:1227-32.
3.Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology. 1995;82(4):1026-60.
4.Williams-Russo P, Sharrock NE, Mattis S, et al. Randomized trial of hypotensive epidural anesthesia in older adults. Anesthesiology. 1999;91(4):926-35.
5.Rothenberg DM. Postoperative renal dysfunction. Problems in Anesthesia 2000;12:314-25.
6.Hara T, Fukusaki M, Nakamura T, Sumikawa K. Renal function in patients during and after hypotensive anesthesia with sevoflurane. J Clin Anesth. 1998;10(7):539-45.
7.Artru AA. Renal effects of sevoflurane during conditions of possible increased risk. J Clin Anesth. 1998;10(7):531-8.
8.Kharasch ED, Jubert C. Compound A uptake and metabolism to mercapturic acids and 3,3,3-trifluoro-2-fluoromethoxypropanoic acid during low-flow sevoflurane anesthesia: biomarkers for exposure, risk assessment, and interspecies comparison. Anesthesiology 1999;91(5):1267-78.
