腹高压对重症急性胰腺炎胰腺损伤及器官功能的影响
摘要
腹高压(Intra-abdominal hypertension, IAH)在重症急性胰腺炎(severe acute pancreatitis,SAP)患者中的发生率大约为60-80%,在病程的不同阶段SAP发生腹高压的原因不一。早期由于炎症反应、毛细血管渗漏等原因导致腹腔急性液体积聚、肠管壁、腹壁水肿引起腹内压升高,中后期由于腹腔感染、休克、肠梗阻、肠功能障碍导致腹高压。既往的研究中,由于腹内压测定方法以及腹高压定义的不一致,SAP合并IAH时对患者预后的影响结果不一。到目前为止,关于SAP患者发生IAH和腹腔间隔综合征(abdonimal compartment syndrome,ACS)的危险因素以及不同程度IAH对SAP患者胰腺损伤及器官功能影响程度有待进一步研究；而且关于不同程度腹腔高压及不同减压指征、减压时点对SAP胰腺损伤及器官功能的影响尚缺乏大动物基础实验研究。
在本系列研究中,我们首先回顾分析SAP急性期住院患者的临床资料。探究SAP患者发生IAH的危险因素以及对预后的影响。在临床研究的基础上,为研究SAP合并腹高压时对主要器官功能的损伤及其机制,并确定最优化腹腔减压的指征,我们进行了第二部分实验研究,在国际上首次制作SAP猪合并腹腔高压动物模型,通过动物实验分析不同程度的腹高压对SAP模型猪胰腺损伤、肾脏功能及循环、呼吸的影响程度,从而确立SAP合并IAH时的减压指征。在第三部分,根据前期动物研究的基础结合专家及相关指南的意见,进一步研究25mmHg腹高压不同时点减压对模型猪胰腺损伤、器官功能及血流动力学的影响及损伤机制,确定SAP合并IAH时的最佳减压时点。
第一部分临床研究
重症急性胰腺炎腹高压危险因素分析及对患者预后的影响
背景：腹高压(Intra-abdominal hypertension, IAH)是重症急性胰腺炎(severe acute pancreatitis,SAP)常见并发症；2002年Pupelis G首次描述了重症急性胰腺炎患者腹内压升高的临床意义,期间有多篇文献就SAP与IAH之间的相关性进行了研究,并就IAP的持续升高所导致的机体心肺功能的障碍、肾损伤及胃肠道缺血及对患者的预后产生的影响进行了阐述。同时文献记录了SAP患者降低IAH的多种方法,其中包括保守或手术等不同的减压方式。但是,由于对IAH及腹腔间隔综合征(abdonimal compartment syndrome,ACS)的定义及测量方法的不一致；并且到目前为止,关于SAP患者发生IAH及ACS的危险因素及确切机制尚不明确,有待进一步研究。2006年世界腹腔间隔室综合征协会(、orld Society of the Abdominal Compartment Syndrome, WSACS)通过大量文献,就IAH、ACS的定义及测量方法进行了统一。因此,本研究根据该指导意见,按照IAH、ACS的定义及测量方法分析SAP患者发生腹腔高压的危险因素,并就SAP患者是否合并腹高压对其预后的影响进行研究。
方法：回顾分析58例SAP住院患者的临床资料。采用Logistic回归分析患者年龄、性别、Balthazar CT评分、CT液体积聚数目,入院第一个24h液体平衡以及入院72h内以下参数的平均数值：平均动脉压、APACHEII评分、血淀粉酶、红细胞压积、血肌酐、白细胞数、血钙、入院血糖、国际标准化比值(INR)、C-反应蛋白、白蛋白值等因素与IAP的相关性。并根据患者入院后测定的腹内压值,分析腹内压对患者胰腺坏死、胰腺感染、手术率、血管活性药物使用、机械通气、急性肾损伤、住院时间及病死率等预后指标的影响。
结果：IAH单因素Logistic回归分析显示,SAP患者IAH组与未发生IAH组在入院第一个24h液体平衡、BalthazarCT评分、APACHEII评分以及血清钙浓度之间存在显著性差别；进一步通过IAH多因素Logistic回归分析显示入院第一个24h液体平衡(OR,1.003；95%CI,1.001-1.006；P=0.013)、CT液体积聚数目(OR,1.652；95%CI,1.023-2.956；P=0.046)及血清钙浓度(OR,0.132；95%CI,0.012-0.775；P=0.033)是SAP患者发生腹内压升高的独立危险因素；而腹高压的发生对患者胰腺坏死、胰腺感染、手术率、血管活性药物使用、机械通气、急性肾损伤、住院时间及病死率等预后指标产生显著影响。
结论：SAP患者腹内压的升高与多个因素有关,入院24h液体平衡、CT液体积聚数目以及血清钙浓度是SAP患者发生IAH的独立危险因素。腹高压的程度对重症急性胰腺炎患者器官功能及预后产生明显影响。加强监测SAP患者的腹内压,及时解除可能引起腹内压升高的危险因素是胰腺炎治疗的重要环节之一。
第二部分：实验研究不同程度腹高压对重症急性胰腺炎猪胰腺损伤、器官功能、血流动力学及呼吸功能的影响
背景：重症急性胰腺炎(SAP)出现病情加重与出血、微血栓及腹高压(IAH)有关。ACS和IAH是SAP患者的常见并发症,不同程度的腹高压对SAP患者胰腺损伤、循环、呼吸、肾脏等器官功能产生什么程度影响尚不明确,有待进一步研究,本研究旨在评价不同腹高压状态对重症急性胰腺炎模型猪胰腺损伤、循环、呼吸及其他器官功能损伤的影响。
方法：将24只家猪进行麻醉、气管插管/切开后接呼吸机辅助呼吸,使用含5%牛磺胆酸钠和0.5%胰蛋白酶生理盐水1ml/kg胰管内注射制作重症急性胰腺炎模型,随机分为四组(n=6),其中三组分别采用氮气气腹法制作15、25、30mmHg腹高压模型,持续12小时(腹高压组)；另一组未叠加腹高压(胰腺炎组)均置入动脉导管和Swan-Ganz导管动态监测心率(Hr)、平均动脉压(MAP)、心排量(CO)、中心静脉压(CVP)等血流动力学指标并行血气分析检查。观察腹高压对胰腺炎猪血流动力学和氧代谢的影响；同时在不同时点采取血标本,检测天门冬氨酸氨基转移酶(Aspartate aminotransferase, AST)、淀粉酶、乳酸、肌酐等；记录每小时模型猪尿量。实验结束留取胰腺、肝脏、肺等组织标本。标本立即予磷酸盐酸福尔马林固定2-3天后予石蜡包埋。将石蜡块4um切片后以苏木精伊红染色(HE)由病理科医师在光镜下观察结果。将电镜检查用的新鲜组织标本固定于2.5%戊二醛溶液中,由病理科医生进行包埋烘干后,进行超薄切片通过电子显微镜镜检。
结果：1只30mmHg腹高压模型猪在造模后11h死亡,另23只持续观察12h。25、30mmHg腹高压组对重症急性胰腺炎模型猪胰腺、肺脏等器官组织及血流动力学产生明显影响：与15mmHg腹高压组及胰腺炎组相比,25、30mmHg组3h、6h、12h时,胰腺腺泡坏死,出血,微血栓形成；肺泡不张,间质大量出血,炎细胞浸润；Hr加快、CVP上升；12h时CO、MAP明显下降(P均<0.05)；血气分析比较,25mmHg及30mmHg组6h、12h时PH值、氧分压(P02)明显下降；血乳酸(LAC)和二氧化碳分压(PC02)显著上升,与15mmHg腹高压组及胰腺炎组相比差异有显著性(P均<0.05)
结论：25mmHg以上腹高压对SAP模型猪胰腺损伤、循环、呼吸等器官功能产生明显影响,及时采用合适的方式减轻、解除25mmHg以上腹高压是SAP治疗的重要环节之一。
第三部分：实验研究不同时点减压对重症急性胰腺炎腹高压猪模型胰腺损伤、器官功能及血流动力学的影响
目的：评价不同时点减压对重症急性胰腺炎腹高压模型猪胰腺损伤、器官功能及血流动力学的影响。
方法：将32只家猪进行麻醉、气管切开后接呼吸机辅助呼吸,使用含5%牛磺胆酸钠和0.5%胰蛋白酶生理盐水1ml/kg胰管内注射制作重症急性胰腺炎模型,分为四组(n=8)。其中24只关腹后采用氮气气腹法制作25mmHg腹高压模型,随机分为三组,第一组腹高压持续6小时后减压(6h组)；第二组腹高压持续9小时后减压(9h组)；第三组腹高压持续12小时后减压(12h组)。均置入动脉导管和Swan-Ganz导管动态监测心率(Hr)、平均动脉压(MAP)、心排量(CO)、中心静脉压(CVP)等血流动力学指标并行血气分析检查。同时在不同时点采取血标本,检测天门冬氨酸氨基转移酶(Aspartate aminotransferase, AST)、乳酸、肌酐及TNF-a、IL-6水平；记录每小时模型猪尿量。持续24h观察不同时点减压对上述指标的影响。实验结束留取胰腺、肺等组织标本。标本立即予磷酸盐酸福尔马林固定后予石蜡包埋。将石蜡块4um切片后以苏木精伊红染色(HE)由病理科医师在光镜下观察结果。
结果：6h组减压后血流动力学指标与胰腺炎组相比差异无显著性；9h组减压后Hr和CO与胰腺炎组相比有明显差异(P<0.05)；12h组减压后Hr和CO与胰腺炎组及6h组相比有明显差异(P<0.05)；血气分析显示：6h组减压后与胰腺炎组相比氧分压(P02)无明显差异。9h组及12h组减压后P02仍低于胰腺炎组及6h组(P均<0.05)。血乳酸及尿量比较：6h组及胰腺炎组无显著性差异；9h组及12h组在减压后血乳酸及尿量与另两组相比有统计学差异。天门冬氨酸氨基转移酶及血肌酐监测显示：9h组及12h组在减压后天门冬氨酸氨基转移酶及血肌酐水平持续高于胰腺炎组(P<0.05)；TNF-α及IL-6水平在25mmHg腹高压状态下明显高于胰腺炎组。9h组及12h组在减压后TNF-α水平持续高于胰腺炎组及6h组(P<0.05)；IL-6水平在实验18h时12组明显高于胰腺炎组、6h组及9h组；24h时IL-6水平四组之间无显著性差别。病理评分显示：9h组与12h组在胰腺、肺脏损伤评分明显高于胰腺炎组、6h组；9h组一只模型猪在21h时循环衰竭死亡,生存率87.5%(7/8)；12h组先后有5只猪死亡,生存率37.5%(3/8)。12h组生存率与9h组相比差异有显著性(P=0.037)；12h组生存率与6h组相比有显著性差异(P=0.008)。
结论：25mmHg腹高压6h内减压能减轻腹高压对SAP猪胰腺、肺脏等器官功能的损伤及血流动力学的影响,并改善生存率。9h后减压对重症急性胰腺炎腹高压模型猪的血流动力学及氧代谢的改善存在不确定性；不同时点减压对25mmHg腹高压SAP猪生存率产生明显影响。
The incidence rate of intra abdominal hypertension(IAH) ranges from60%to80%in patients with severe acute pancreatitis(SAP). During different phases of SAP, IAH has different causes such as inflammation, capillary leakage and abdominal wall swelling in the acute phase and abdominal infection, septic shock and intestinal dysfunction in the latter phase. There are several previous studies regarding the different outcome between SAP patients with or without IAH, but the results are quite confusing due to different standards of IAH and different methods for measuring intra abdominal pressure. Therefore, the risk factors of IAH in SAP patients and the effect of different levels of IAH on the outcome of SAP need to be further studied according to the standards established by the World Society of Abdominal Compartment Syndrome(WSACS). Additionally, the optimal timing and indication of surgical decompression remains unknown, hence animals studies are warranted to address these issues.
In our serial studies, we retrospectively reviewed the clinical data of SAP patients admitted in the acute phase to explore the risk factors and outcome of SAP patients in combination with IAH. On the basis of clinical results, we set up a brand new animal model to assess the effect of sustained different levels of IAH combined with SAP on global hemodynamics, systemic oxygenation and organ functions. Furthermore, we also studied the effect of decompression at different time point in a porcine model of25mmHg IAH incorporating SAP to help optimize the timing for surgical intervention in this special patient population.
Part I:Risk factors and Outcome of Intra Abdominal Hypertension in Patients with Severe Acute Pancreatitis
Objective:Intra-abdominal hypertension(IAH) is common in patients with severe acute pancreatitis(SAP). The aim of this study was to investigate the risk factors of IAH in SAP patients and assess the prognosis of SAP combined with IAH.
Methods:To analyze the data from patients with SAP, both univariate and multivariate logistic regression analyses were applied, using16indices including age, gender, Acute Physiology and Chronic Health Evaluation Ⅱ scores(APACHE Ⅱ),24-hour fluid balance, hematocrit, serum calcium level and so on. Clinical prognosis such as mortality, hospital duration, etc. of SAP patients with or without IAH was also compared.
Results:First24-hour fluid balance (OR,1.003;95%CI,1.001-1.006), number of fluid collections(OR,1.652;95%CI,1.023-2.956) and serum calcium level(OR,0.132;95%CI,0.012-0.775) were found to be independent risk factors for IAH in patients with SAP. Moreover, patients with SAP and IAH had significantly longer average length of hospital and intensive care unit duration, higher rates of systemic and local complications and more invasive treatments.
Conclusion:The significant risk factors for IAH in patients with SAP include24-hour fluid balance (first day), number of fluid collections and serum calcium level. Additionally, IAH is associated with extremely bad prognosis evidenced by high rates of death, complications and invasive interventions.
Part II:The effect of different intra-abdominal pressures (IAP) on pancreatic necrosis, organ function, hemodynamics and oxygen metabolism in severe acute pancreatitis porcine model
Objective:The deterioration of severe acute pancreatitis (SAP) is associated with abdominal bleeding, formation of microthrombus and intra-abdominal hypertension (IAH). Abdominal compartment syndrome (ACS) and IAH are common complications in patients with SAP. However, the effects of different degrees of IAH on pancreatic necrosis, organ function including heart, lung and kidney are unclear. Our research is aimed to evaluate the effects of different degrees of IAH on pancreatic necrosis and organ function in severe acute pancreatitis in a porcine model.
Methods:24swine were divided into4groups randomly as follows (N=6):A) IAP=15mmHg for12hours with SAP, B) IAP=25mmHg for12hours with SAP, C) IAP=30mmHg for12hours with SAP, D) no IAH with SAP. The swine were anaesthetized, endotracheally intubated and placed on mechanical ventilation. SAP was induced by retrograde infusion of5%sodium taurocholate and0.5%trypsin solution via pancreatic duct with a dose of1ml/kg. IAP is raised by intraperitoneal insufflation with N2. An artery catheter and a Swan-Ganz catheter were placed to monitor mean arterial pressure (MAP), cardiac output (CO), central vein pressure (CVP). Arterial blood was also collected via the artery catheter for blood gas measurement. At different time points, blood sample was collected for determination of aspartate aminotransferase (AST), amylase, lactic acid (Lac) and serum creatinine. At the end of the experiment, pancreas, liver and lung tissue were harvested. The tissue samples were immediately transferred into10%phosphate-buffered saline (PBS) buffered formalin and embedded in paraffin. Sections measuring4um in thickness were cut, placed on glass slides, and stained with hematoxylin and eosin (H&E). Images were obtained using a light microscope and analyzed by pathologist.
Results:One swine in30mmHg group died after11hours, while other23swine were alive during the12-hour experiment period. The results of group B and C were significantly changed due to the IAH. Comparing with group A, the histological appearance demonstrated pancreatic acinus necrosis, bleeding, formation of microthrombus and alveolar collapse, interstitial bleeding and inflammatory cells infiltration after3,6and12hours. The heart rate, CVP were increased while CO and MAP were decreased significantly after12hours (P<0.05). The blood gas measurements manifested that blood pH, PaO2were decreased while blood Lac and PaCO2were increased significantly in group B and C (P<0.05).
Conclusions:ACS has detrimental effect on SAP in a porcine model, including pancreatic lesion, circulation and respiratory function. Relief of ACS is one of the key strategies in the treatment of SAP.
PART Ⅲ:Effect of decompression in different time on pancreatic necrosis, organ function and hemodynamics of porcine model with severe acute pancreatitis combined intra-abdominal hypertension
Objective:The aim of this study was to assess the effect of decompression in different time on systemic hemodynamics and oxygen metabolism in a24h lasting porcine model of severe acute pancreatitis incorporating intra-abdominal hypertension(IAH).
Methods:Following baseline registrations, SAP was induced in all32animals. We used a N2pneumoperitoneum to increase the intra-abdominal pressure (IAP) to25mmHg in24of32SAP animals (n=8). After6hours, we applied decompression in8of these pigs and the other16animals received decompression at9h and12h respectively since the induction of IAH. For decompression, the nitrogen gas was pumped out slowly to avoid sudden drop of abdominal pressure which could lead to acute cardiac failure due to sudden increase of venous return. The investigation period was24h. Heart rate (HR), cardiac output (CO) and mean arterial pressure (MAP) were continuously recorded with the aid of Swan-Ganz catheter and electrocardiography monitor; Oxygen partial pressure of artery (PaO2) was measured by blood-gas analysis. Besides that, the level of serum TNF-α and IL-6were taken every6h; Plasma samples were frozen at-70℃degrees for later measurements. Serum cytokine concentrations(TNF-α and IL-6) were determined by enzyme-linked immunosorbent assay (ELISA) with commercial kit (R&D Systems, Munich, Germany under the same experimental conditions.The urine output was recorded every1h。 At different time points, blood sample was collected for determination of aspartate aminotransferase (AST), lactic acid (Lac) and serum creatinine. At the end of the experiment, pancreas and lung tissue were harvested. The tissue samples were immediately transferred into10%phosphate-buffered saline (PBS) buffered formalin and embedded in paraffin. Sections measuring4um in thickness were cut, placed on glass slides, and stained with hematoxylin and eosin (H&E). Images were obtained using a light microscope and analyzed by pathologist.
Results:After induction of IAH+SAP, CO in all three study groups was much more significantly reduced than SAP group in the first a few hours. Decompression could increase CO remarkably in both6h and9h groups but slightly in the12h group. In the latter phase of observation, the SAP group as well as6h group showed higher CO when compared with9h and12h groups, although very few statistical differences were reached. MAP in all groups decreased gradually over time, but no significant between-group difference could be detected throughout the experiment. Similar to CO, HR dropped more profoundly in6h and9h group than12h group after abdominal decompression and statistical differences could hardly be seen during the second half as well. Blood gas results showed that arterial PO2in the SAP group ranged without significant differences in the first6hours and decreased gradually thereafter. Differently, the combination of IAH decreased PO2more significantly in other3groups and decompression especially early intervention could help PO2back to a higher level which is still lower than the baseline value but similar to SAP group. The induction of IAH also led to much higher lactate levels in3study groups, although SAP animals showed an upbeat trend as well. Decompression could slow down or even slightly reverse the increase of lactate evidenced by that6h group and SAP group presented very similar levels of lactate during the last9hours. The application of SAP+IAH dramatically decreased UO over time and decompression at6h could regain the UO to a level similar to the SAP group. Regarding the9h and12h groups, although UO increased substantially after decompression, the levels of these two groups were still lower than other2groups during the rest of the observation. After induction of SAP and IAH, concentration of plasma cytokines increased significantly and reached peak at different time points (6h for6h,9h and SAP group,12h for12h group) and different levels. Early decompression resulted in statistically lower levels of both TNF-a and IL-6during the second half of experiment. Indicators of liver and kidney injury, including AST and creatinine increased more significantly in IAH groups compared with SAP alone animals.Compared with the6h group and9h group, the survival time of animals in12h group was significantly reduced(P=0.037vs.9h and P=0.008vs.6h).
Conclusions:There were remarkable and relatively irreversible effects on global hemodynamics and oxygen metabolism in response to the decompression in different time after sustained25mmHg IAH with the underlying condition of SAP.The results of this study are in favor of a decompression in SAP with IAH in an early time.
在本系列研究中,我们首先回顾分析SAP急性期住院患者的临床资料。探究SAP患者发生IAH的危险因素以及对预后的影响。在临床研究的基础上,为研究SAP合并腹高压时对主要器官功能的损伤及其机制,并确定最优化腹腔减压的指征,我们进行了第二部分实验研究,在国际上首次制作SAP猪合并腹腔高压动物模型,通过动物实验分析不同程度的腹高压对SAP模型猪胰腺损伤、肾脏功能及循环、呼吸的影响程度,从而确立SAP合并IAH时的减压指征。在第三部分,根据前期动物研究的基础结合专家及相关指南的意见,进一步研究25mmHg腹高压不同时点减压对模型猪胰腺损伤、器官功能及血流动力学的影响及损伤机制,确定SAP合并IAH时的最佳减压时点。
第一部分临床研究
重症急性胰腺炎腹高压危险因素分析及对患者预后的影响
背景：腹高压(Intra-abdominal hypertension, IAH)是重症急性胰腺炎(severe acute pancreatitis,SAP)常见并发症；2002年Pupelis G首次描述了重症急性胰腺炎患者腹内压升高的临床意义,期间有多篇文献就SAP与IAH之间的相关性进行了研究,并就IAP的持续升高所导致的机体心肺功能的障碍、肾损伤及胃肠道缺血及对患者的预后产生的影响进行了阐述。同时文献记录了SAP患者降低IAH的多种方法,其中包括保守或手术等不同的减压方式。但是,由于对IAH及腹腔间隔综合征(abdonimal compartment syndrome,ACS)的定义及测量方法的不一致；并且到目前为止,关于SAP患者发生IAH及ACS的危险因素及确切机制尚不明确,有待进一步研究。2006年世界腹腔间隔室综合征协会(、orld Society of the Abdominal Compartment Syndrome, WSACS)通过大量文献,就IAH、ACS的定义及测量方法进行了统一。因此,本研究根据该指导意见,按照IAH、ACS的定义及测量方法分析SAP患者发生腹腔高压的危险因素,并就SAP患者是否合并腹高压对其预后的影响进行研究。
方法：回顾分析58例SAP住院患者的临床资料。采用Logistic回归分析患者年龄、性别、Balthazar CT评分、CT液体积聚数目,入院第一个24h液体平衡以及入院72h内以下参数的平均数值：平均动脉压、APACHEII评分、血淀粉酶、红细胞压积、血肌酐、白细胞数、血钙、入院血糖、国际标准化比值(INR)、C-反应蛋白、白蛋白值等因素与IAP的相关性。并根据患者入院后测定的腹内压值,分析腹内压对患者胰腺坏死、胰腺感染、手术率、血管活性药物使用、机械通气、急性肾损伤、住院时间及病死率等预后指标的影响。
结果：IAH单因素Logistic回归分析显示,SAP患者IAH组与未发生IAH组在入院第一个24h液体平衡、BalthazarCT评分、APACHEII评分以及血清钙浓度之间存在显著性差别；进一步通过IAH多因素Logistic回归分析显示入院第一个24h液体平衡(OR,1.003；95%CI,1.001-1.006；P=0.013)、CT液体积聚数目(OR,1.652；95%CI,1.023-2.956；P=0.046)及血清钙浓度(OR,0.132；95%CI,0.012-0.775；P=0.033)是SAP患者发生腹内压升高的独立危险因素；而腹高压的发生对患者胰腺坏死、胰腺感染、手术率、血管活性药物使用、机械通气、急性肾损伤、住院时间及病死率等预后指标产生显著影响。
结论：SAP患者腹内压的升高与多个因素有关,入院24h液体平衡、CT液体积聚数目以及血清钙浓度是SAP患者发生IAH的独立危险因素。腹高压的程度对重症急性胰腺炎患者器官功能及预后产生明显影响。加强监测SAP患者的腹内压,及时解除可能引起腹内压升高的危险因素是胰腺炎治疗的重要环节之一。
第二部分：实验研究不同程度腹高压对重症急性胰腺炎猪胰腺损伤、器官功能、血流动力学及呼吸功能的影响
背景：重症急性胰腺炎(SAP)出现病情加重与出血、微血栓及腹高压(IAH)有关。ACS和IAH是SAP患者的常见并发症,不同程度的腹高压对SAP患者胰腺损伤、循环、呼吸、肾脏等器官功能产生什么程度影响尚不明确,有待进一步研究,本研究旨在评价不同腹高压状态对重症急性胰腺炎模型猪胰腺损伤、循环、呼吸及其他器官功能损伤的影响。
方法：将24只家猪进行麻醉、气管插管/切开后接呼吸机辅助呼吸,使用含5%牛磺胆酸钠和0.5%胰蛋白酶生理盐水1ml/kg胰管内注射制作重症急性胰腺炎模型,随机分为四组(n=6),其中三组分别采用氮气气腹法制作15、25、30mmHg腹高压模型,持续12小时(腹高压组)；另一组未叠加腹高压(胰腺炎组)均置入动脉导管和Swan-Ganz导管动态监测心率(Hr)、平均动脉压(MAP)、心排量(CO)、中心静脉压(CVP)等血流动力学指标并行血气分析检查。观察腹高压对胰腺炎猪血流动力学和氧代谢的影响；同时在不同时点采取血标本,检测天门冬氨酸氨基转移酶(Aspartate aminotransferase, AST)、淀粉酶、乳酸、肌酐等；记录每小时模型猪尿量。实验结束留取胰腺、肝脏、肺等组织标本。标本立即予磷酸盐酸福尔马林固定2-3天后予石蜡包埋。将石蜡块4um切片后以苏木精伊红染色(HE)由病理科医师在光镜下观察结果。将电镜检查用的新鲜组织标本固定于2.5%戊二醛溶液中,由病理科医生进行包埋烘干后,进行超薄切片通过电子显微镜镜检。
结果：1只30mmHg腹高压模型猪在造模后11h死亡,另23只持续观察12h。25、30mmHg腹高压组对重症急性胰腺炎模型猪胰腺、肺脏等器官组织及血流动力学产生明显影响：与15mmHg腹高压组及胰腺炎组相比,25、30mmHg组3h、6h、12h时,胰腺腺泡坏死,出血,微血栓形成；肺泡不张,间质大量出血,炎细胞浸润；Hr加快、CVP上升；12h时CO、MAP明显下降(P均<0.05)；血气分析比较,25mmHg及30mmHg组6h、12h时PH值、氧分压(P02)明显下降；血乳酸(LAC)和二氧化碳分压(PC02)显著上升,与15mmHg腹高压组及胰腺炎组相比差异有显著性(P均<0.05)
结论：25mmHg以上腹高压对SAP模型猪胰腺损伤、循环、呼吸等器官功能产生明显影响,及时采用合适的方式减轻、解除25mmHg以上腹高压是SAP治疗的重要环节之一。
第三部分：实验研究不同时点减压对重症急性胰腺炎腹高压猪模型胰腺损伤、器官功能及血流动力学的影响
目的：评价不同时点减压对重症急性胰腺炎腹高压模型猪胰腺损伤、器官功能及血流动力学的影响。
方法：将32只家猪进行麻醉、气管切开后接呼吸机辅助呼吸,使用含5%牛磺胆酸钠和0.5%胰蛋白酶生理盐水1ml/kg胰管内注射制作重症急性胰腺炎模型,分为四组(n=8)。其中24只关腹后采用氮气气腹法制作25mmHg腹高压模型,随机分为三组,第一组腹高压持续6小时后减压(6h组)；第二组腹高压持续9小时后减压(9h组)；第三组腹高压持续12小时后减压(12h组)。均置入动脉导管和Swan-Ganz导管动态监测心率(Hr)、平均动脉压(MAP)、心排量(CO)、中心静脉压(CVP)等血流动力学指标并行血气分析检查。同时在不同时点采取血标本,检测天门冬氨酸氨基转移酶(Aspartate aminotransferase, AST)、乳酸、肌酐及TNF-a、IL-6水平；记录每小时模型猪尿量。持续24h观察不同时点减压对上述指标的影响。实验结束留取胰腺、肺等组织标本。标本立即予磷酸盐酸福尔马林固定后予石蜡包埋。将石蜡块4um切片后以苏木精伊红染色(HE)由病理科医师在光镜下观察结果。
结果：6h组减压后血流动力学指标与胰腺炎组相比差异无显著性；9h组减压后Hr和CO与胰腺炎组相比有明显差异(P<0.05)；12h组减压后Hr和CO与胰腺炎组及6h组相比有明显差异(P<0.05)；血气分析显示：6h组减压后与胰腺炎组相比氧分压(P02)无明显差异。9h组及12h组减压后P02仍低于胰腺炎组及6h组(P均<0.05)。血乳酸及尿量比较：6h组及胰腺炎组无显著性差异；9h组及12h组在减压后血乳酸及尿量与另两组相比有统计学差异。天门冬氨酸氨基转移酶及血肌酐监测显示：9h组及12h组在减压后天门冬氨酸氨基转移酶及血肌酐水平持续高于胰腺炎组(P<0.05)；TNF-α及IL-6水平在25mmHg腹高压状态下明显高于胰腺炎组。9h组及12h组在减压后TNF-α水平持续高于胰腺炎组及6h组(P<0.05)；IL-6水平在实验18h时12组明显高于胰腺炎组、6h组及9h组；24h时IL-6水平四组之间无显著性差别。病理评分显示：9h组与12h组在胰腺、肺脏损伤评分明显高于胰腺炎组、6h组；9h组一只模型猪在21h时循环衰竭死亡,生存率87.5%(7/8)；12h组先后有5只猪死亡,生存率37.5%(3/8)。12h组生存率与9h组相比差异有显著性(P=0.037)；12h组生存率与6h组相比有显著性差异(P=0.008)。
结论：25mmHg腹高压6h内减压能减轻腹高压对SAP猪胰腺、肺脏等器官功能的损伤及血流动力学的影响,并改善生存率。9h后减压对重症急性胰腺炎腹高压模型猪的血流动力学及氧代谢的改善存在不确定性；不同时点减压对25mmHg腹高压SAP猪生存率产生明显影响。
The incidence rate of intra abdominal hypertension(IAH) ranges from60%to80%in patients with severe acute pancreatitis(SAP). During different phases of SAP, IAH has different causes such as inflammation, capillary leakage and abdominal wall swelling in the acute phase and abdominal infection, septic shock and intestinal dysfunction in the latter phase. There are several previous studies regarding the different outcome between SAP patients with or without IAH, but the results are quite confusing due to different standards of IAH and different methods for measuring intra abdominal pressure. Therefore, the risk factors of IAH in SAP patients and the effect of different levels of IAH on the outcome of SAP need to be further studied according to the standards established by the World Society of Abdominal Compartment Syndrome(WSACS). Additionally, the optimal timing and indication of surgical decompression remains unknown, hence animals studies are warranted to address these issues.
In our serial studies, we retrospectively reviewed the clinical data of SAP patients admitted in the acute phase to explore the risk factors and outcome of SAP patients in combination with IAH. On the basis of clinical results, we set up a brand new animal model to assess the effect of sustained different levels of IAH combined with SAP on global hemodynamics, systemic oxygenation and organ functions. Furthermore, we also studied the effect of decompression at different time point in a porcine model of25mmHg IAH incorporating SAP to help optimize the timing for surgical intervention in this special patient population.
Part I:Risk factors and Outcome of Intra Abdominal Hypertension in Patients with Severe Acute Pancreatitis
Objective:Intra-abdominal hypertension(IAH) is common in patients with severe acute pancreatitis(SAP). The aim of this study was to investigate the risk factors of IAH in SAP patients and assess the prognosis of SAP combined with IAH.
Methods:To analyze the data from patients with SAP, both univariate and multivariate logistic regression analyses were applied, using16indices including age, gender, Acute Physiology and Chronic Health Evaluation Ⅱ scores(APACHE Ⅱ),24-hour fluid balance, hematocrit, serum calcium level and so on. Clinical prognosis such as mortality, hospital duration, etc. of SAP patients with or without IAH was also compared.
Results:First24-hour fluid balance (OR,1.003;95%CI,1.001-1.006), number of fluid collections(OR,1.652;95%CI,1.023-2.956) and serum calcium level(OR,0.132;95%CI,0.012-0.775) were found to be independent risk factors for IAH in patients with SAP. Moreover, patients with SAP and IAH had significantly longer average length of hospital and intensive care unit duration, higher rates of systemic and local complications and more invasive treatments.
Conclusion:The significant risk factors for IAH in patients with SAP include24-hour fluid balance (first day), number of fluid collections and serum calcium level. Additionally, IAH is associated with extremely bad prognosis evidenced by high rates of death, complications and invasive interventions.
Part II:The effect of different intra-abdominal pressures (IAP) on pancreatic necrosis, organ function, hemodynamics and oxygen metabolism in severe acute pancreatitis porcine model
Objective:The deterioration of severe acute pancreatitis (SAP) is associated with abdominal bleeding, formation of microthrombus and intra-abdominal hypertension (IAH). Abdominal compartment syndrome (ACS) and IAH are common complications in patients with SAP. However, the effects of different degrees of IAH on pancreatic necrosis, organ function including heart, lung and kidney are unclear. Our research is aimed to evaluate the effects of different degrees of IAH on pancreatic necrosis and organ function in severe acute pancreatitis in a porcine model.
Methods:24swine were divided into4groups randomly as follows (N=6):A) IAP=15mmHg for12hours with SAP, B) IAP=25mmHg for12hours with SAP, C) IAP=30mmHg for12hours with SAP, D) no IAH with SAP. The swine were anaesthetized, endotracheally intubated and placed on mechanical ventilation. SAP was induced by retrograde infusion of5%sodium taurocholate and0.5%trypsin solution via pancreatic duct with a dose of1ml/kg. IAP is raised by intraperitoneal insufflation with N2. An artery catheter and a Swan-Ganz catheter were placed to monitor mean arterial pressure (MAP), cardiac output (CO), central vein pressure (CVP). Arterial blood was also collected via the artery catheter for blood gas measurement. At different time points, blood sample was collected for determination of aspartate aminotransferase (AST), amylase, lactic acid (Lac) and serum creatinine. At the end of the experiment, pancreas, liver and lung tissue were harvested. The tissue samples were immediately transferred into10%phosphate-buffered saline (PBS) buffered formalin and embedded in paraffin. Sections measuring4um in thickness were cut, placed on glass slides, and stained with hematoxylin and eosin (H&E). Images were obtained using a light microscope and analyzed by pathologist.
Results:One swine in30mmHg group died after11hours, while other23swine were alive during the12-hour experiment period. The results of group B and C were significantly changed due to the IAH. Comparing with group A, the histological appearance demonstrated pancreatic acinus necrosis, bleeding, formation of microthrombus and alveolar collapse, interstitial bleeding and inflammatory cells infiltration after3,6and12hours. The heart rate, CVP were increased while CO and MAP were decreased significantly after12hours (P<0.05). The blood gas measurements manifested that blood pH, PaO2were decreased while blood Lac and PaCO2were increased significantly in group B and C (P<0.05).
Conclusions:ACS has detrimental effect on SAP in a porcine model, including pancreatic lesion, circulation and respiratory function. Relief of ACS is one of the key strategies in the treatment of SAP.
PART Ⅲ:Effect of decompression in different time on pancreatic necrosis, organ function and hemodynamics of porcine model with severe acute pancreatitis combined intra-abdominal hypertension
Objective:The aim of this study was to assess the effect of decompression in different time on systemic hemodynamics and oxygen metabolism in a24h lasting porcine model of severe acute pancreatitis incorporating intra-abdominal hypertension(IAH).
Methods:Following baseline registrations, SAP was induced in all32animals. We used a N2pneumoperitoneum to increase the intra-abdominal pressure (IAP) to25mmHg in24of32SAP animals (n=8). After6hours, we applied decompression in8of these pigs and the other16animals received decompression at9h and12h respectively since the induction of IAH. For decompression, the nitrogen gas was pumped out slowly to avoid sudden drop of abdominal pressure which could lead to acute cardiac failure due to sudden increase of venous return. The investigation period was24h. Heart rate (HR), cardiac output (CO) and mean arterial pressure (MAP) were continuously recorded with the aid of Swan-Ganz catheter and electrocardiography monitor; Oxygen partial pressure of artery (PaO2) was measured by blood-gas analysis. Besides that, the level of serum TNF-α and IL-6were taken every6h; Plasma samples were frozen at-70℃degrees for later measurements. Serum cytokine concentrations(TNF-α and IL-6) were determined by enzyme-linked immunosorbent assay (ELISA) with commercial kit (R&D Systems, Munich, Germany under the same experimental conditions.The urine output was recorded every1h。 At different time points, blood sample was collected for determination of aspartate aminotransferase (AST), lactic acid (Lac) and serum creatinine. At the end of the experiment, pancreas and lung tissue were harvested. The tissue samples were immediately transferred into10%phosphate-buffered saline (PBS) buffered formalin and embedded in paraffin. Sections measuring4um in thickness were cut, placed on glass slides, and stained with hematoxylin and eosin (H&E). Images were obtained using a light microscope and analyzed by pathologist.
Results:After induction of IAH+SAP, CO in all three study groups was much more significantly reduced than SAP group in the first a few hours. Decompression could increase CO remarkably in both6h and9h groups but slightly in the12h group. In the latter phase of observation, the SAP group as well as6h group showed higher CO when compared with9h and12h groups, although very few statistical differences were reached. MAP in all groups decreased gradually over time, but no significant between-group difference could be detected throughout the experiment. Similar to CO, HR dropped more profoundly in6h and9h group than12h group after abdominal decompression and statistical differences could hardly be seen during the second half as well. Blood gas results showed that arterial PO2in the SAP group ranged without significant differences in the first6hours and decreased gradually thereafter. Differently, the combination of IAH decreased PO2more significantly in other3groups and decompression especially early intervention could help PO2back to a higher level which is still lower than the baseline value but similar to SAP group. The induction of IAH also led to much higher lactate levels in3study groups, although SAP animals showed an upbeat trend as well. Decompression could slow down or even slightly reverse the increase of lactate evidenced by that6h group and SAP group presented very similar levels of lactate during the last9hours. The application of SAP+IAH dramatically decreased UO over time and decompression at6h could regain the UO to a level similar to the SAP group. Regarding the9h and12h groups, although UO increased substantially after decompression, the levels of these two groups were still lower than other2groups during the rest of the observation. After induction of SAP and IAH, concentration of plasma cytokines increased significantly and reached peak at different time points (6h for6h,9h and SAP group,12h for12h group) and different levels. Early decompression resulted in statistically lower levels of both TNF-a and IL-6during the second half of experiment. Indicators of liver and kidney injury, including AST and creatinine increased more significantly in IAH groups compared with SAP alone animals.Compared with the6h group and9h group, the survival time of animals in12h group was significantly reduced(P=0.037vs.9h and P=0.008vs.6h).
Conclusions:There were remarkable and relatively irreversible effects on global hemodynamics and oxygen metabolism in response to the decompression in different time after sustained25mmHg IAH with the underlying condition of SAP.The results of this study are in favor of a decompression in SAP with IAH in an early time.
引文
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18. Pitchumoni CS, Patel NM, Shah P. Factors influencing mortality in acute pancreatitis:can we alter them? J Clin Gastroenterol 2005; 39(9):798-814.
19. Singh VK, Wu BU, Bollen TL, et al. Early systemic inflammatory response syndrome is associated with severe acute pancreatitis. Clin Gastroenterol Hepatol 2009; 7(11):1247-51.
20. De Winter BY, De Man JG. Interplay between inflammation, immune system and neuronal pathways:effect on gastrointestinal motility. World J Gastroenterol 2010; 16(44):5523-35.
21. Ranson JH, Lackner H, Berman IR, et al. The relationship of coagulation factors to clinical complications of acute pancreatitis. Surgery 1977; 81(5):502-11.
22. Garcia M, Barbachano EH, Lorenzo PH, et al. Saline infusion through the pancreatic duct leads to changes in calcium homeostasis similar to those observed in acute pancreatitis. Dig Dis Sci 2009; 54(2):300-8.
23. Wilson C, Heath DI, Imrie CW. Prediction of outcome in acute pancreatitis:a comparative study of APACHE H, clinical assessment and multiple factor scoring systems. Br J Surg 1990; 77(11):1260-4.
24. Mayerle J, Hlouschek V, Lerch MM. Current management of acute pancreatitis. Nat Clin Pract Gastroenterol Hepatol 2005; 2(10):473-83.
25. De Waele JJ, Leppaniemi AK. Intra-abdominal hypertension in acute pancreatitis. World J Surg 2009; 33(6):1128-33.
26. Olofsson PH, Berg S, Ahn HC, et al. Gastrointestinal microcirculation and cardiopulmonary function during experimentally increased intra-abdominal pressure. Crit Care Med 2009; 37(1):230-9.
27. Toens C, Schachtrupp A, Hoer J, et al. A porcine model of the abdominal compartment syndrome. Shock 2002; 18(4):316-21.
28. Al-Bahrani AZ, Darwish A, Hamza N, et al. Gut barrier dysfunction in critically ill surgical patients with abdominal compartment syndrome. Pancreas 2010; 39(7):1064-9.
29. Talmor D, Sarge T, Malhotra A, et al., Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med,2008.359(20):2095-2104.
30. Peng, Z. Y.Critchley, L. A.Joynt, G. M.Effects of norepinephrine during intra-abdominal hypertension on renal blood flow in bacteremic dogs. Crit Care Med.2008;36(3):834-41.
31. van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010; 362(16):1491-502.
32. Hartwig W, Maksan SM, Foitzik T, et al. Reduction in mortality with delayed surgical therapy of severe pancreatitis. J Gastrointest Surg 2002; 6(3):481-7.
[1]王春友,赵玉沛。从治疗观点演变和技术变革看重症急性胰腺炎疗效进步。中华外科杂志,2006,44：872-874.
[2]Cheatham ML, Malbrain ML, Kirkpatrick A,et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med,2007,33:951-962。
[3]De Waele JJ, Hoste E, Blot SI, et al. Intra-abdominal hypertension in patients with severe acute pancreatitis. Crit Care,2005,9:R452-457.
[4]Al-Bahrani AZ, Abid GH, Holt A, et al. Clinical relevance of intra-abdominal hypertension in patients with severe acute pancreatitis. Pancreas,2008,36:39-43.
[5]Rosas JM, Soto SN, Aracil JS, et al. Intra-abdominal pressure as a marker of severity in acute pancreatitis. Surgery,2007,141:173-178.
[6]Bloomfield GL, Ridings PC, Blocher CR, et al.Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion. J Trauma, 1996,40:936-941.
[7]Kashtan J, Green JF, Parsons EQ, et al.Hemodynamic effect of increased abdominal pressure. JSurg Res,1981,30,249-255.
[8]Diebel LN, Wilson RF, Dulchavsky SA, et al. Effect of increased intra abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma,1992,33,279-282.
[9]Otto J, Afify M, Jautz U, et al.Histomorphologic and ultrastructural lesions of the pancreas in a porcine model of intraabdominal hypertension.Shock.,2010,33:639-645.
[10]Toens C, Schachtrupp A, Hoer J, et al.A porcine model of the abdominal compartment syndrome. Shock,2002,18:316-321.
[11]Simon RJ, Friedlander MH, Ivatury RR,et al.Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma,1997,42:398-403.
[12]Cheatham M, Malbrain M.Cardiovascular implications of abdominal compartment syndrome. Acta Clin Belg Suppl,2007,1:98-112.
[13]Kotzampassi K, Paramythiotis D, Eleftheriadis E. Deterioration of visceral perfusion caused by intra-abdominal hypertension in pigs ventilated with positive end-expiratory pressure. Surg Today.2000;30:987-92.
[14]Kubiak BD, Gatto LA, Jimenez EJ, Silva-Parra H, Snyder KP, Vieau CJ, Barba J, Nasseri-Nik N, Falk JL, Nieman GF. Plateau and transpulmonary pressure with elevated intra-abdominal pressure or atelectasis. J Surg Res,2010,Mar;159:e 17-24.
[15]Schachtrupp A. Fluid resuscitation preserves cardiac output but cannot prevent organ damage in a porcine model during 24 h of intra abdominal hypertension. Shock. 2005;24:153-158.
[16]Peng ZY.Effects of norepinephrine during intra-abdominal hypertension on renal blood flow in bacteremic dogs. Crit Care Med 2008;36:834-841.
[17]Schachtrupp A, Wauters J, and Wilmer A. What is the best animal model for ACS? Acta Clin Belg Suppl,2007,1:225-232.
[18]Olofsson PH, Berg S, Ahn HC, et al. Gastrointestinal microcirculation and cardiopulmonary function during experimentally increased intra-abdominal pressure. Crit Care Med,2009. 37:230-39.
1.王春友,赵玉沛。从治疗观点演变和技术变革看重症急性胰腺炎疗效进步。中华外科杂志,2006,44：872-874.
2.Schwarte LA, Scheeren TW, Lorenz C, et al. Moderate increase in intraabdominal pressure attenuates gastric mucosal oxygen saturation in patients undergoing laparoscopy. Anesthesiology 2004,100(5):1081-1087.
3.Diebel LN, Dulchavsky SA, Brown WJ:Splanchnic ischemia and bacterialtranslocation in the abdominal compartment syndrome. J Trauma 1997,43(5):852-855.
4.De Waele JJ, Leppaniemi AK. Intra-abdominal hypertension in acute pancreatitis. World J Surg. 2009;33(6):1128-33.
5.De Waele JJ, Hoste EA, Malbrain ML. Decompressive laparotomy for abdominal compartment syndrome--a critical analysis.Crit Care.2006;10(2):R51. Review.
6.Rosas JM, Soto SN, Aracil JS, et al. Intra-abdominal pressure as a marker of severity in acute pancreatitis. Surgery,2007,141:173-178.
7.Malbrain ML, Chiumello D, Pelosi P, et al:Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients:a multiple-center epidemiological study. Crit Care Med 2005;33(2):315-322.
8.倪海滨,李维勤,柯路等,腹腔高压对急性坏死性胰腺炎模型猪血流动力学影响的实验研究。中华外科杂志,2011,34(5)
9.Ackland GL, Yao ST, Rudiger A, et al.Cardioprotection, attenuated systemic inflammation, and survival benefit of betal-adrenoceptor blockade in severe sepsis in rats. Crit Care Med. 2010;38(2):388-94.
10. Mentula P, Hienonen P, Kemppainen E, et al. Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Arch Surg.2010;145(8):764-769.
11. Gudmundsson FF, Heltne JK. Respiratory changes during prolonged increased intra-abdominal pressure in pigs.Acta Anaesthesiol Scand.2004;48(4):463-8.
12. Talmor D, Sarge T, Malhotra A,et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med.2008;359(20):2095-2104.
1.Malbrain, M.L.N.G., et al., Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients:A multiple-center epidemiological study. Critical care medicine, 2005.33(2):p.315-322.
2.Malbrain, M.L.N.G., et al., Prevalence of intra-abdominal hypertension in critically ill patients:a multicentre epidemiological study. Intensive Care Medicine,2004.30(5):p.822-829.
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4.Reintam, A., et al., Primary and secondary intra-abdominal hypertensioniadifferent impact on ICU outcome. Intensive Care Medicine,2008.34(9):p.1624-1631.
5.Cheatham, M.L., It is time to pay attention?Now more than ever!. Critical care medicine,2007. 35(6):p.1629-1630.
6.Vivier, E., Effects of increased intra-abdominal pressure on central circulation. British Journal of Anaesthesia,2006.96(6):p.701-707.
7. Madigan, M.C., et al., Secondary Abdominal Compartment Syndrome After Severe Extremity Injury:Are Early, Aggressive Fluid Resuscitation Strategies to Blame? The Journal of Trauma: Injury, Infection, and Critical Care,2008.64(2):p.280-285.
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9. Rivers, E., et al., Early goal-directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine,2001.345(19):p.1368.
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12. Cheatham, M., et al., Right Ventricular End-Diastolic Volume As A Predictor of Preload Status in Abdominal Compartment Synorome. Critical care medicine,1998.26(1):p.38A.
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17.Cheatham, M. and M. Malbrain, Cardiovascular implications of abdominal compartment syndrome. Acta Clinica Belgica,2007.62:p.98-112.
18.Durham, R., et al., Right ventricular end-diastolic volume as a measure of preload. The Journal of trauma,1995.39(2):p.218.
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24.Enomoto, T.M. and L. Harder, Dynamic Indices of Preload. Critical Care Clinics,2010.26(2): p.307-321.
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26.Duperret, S., et al., Increased intra-abdominal pressure affects respiratory variations in arterial pressure in normovolaemic and hypovolaemic mechanically ventilated healthy pigs. Intensive Care Medicine,2007.33(1):p.163-171.
27.Tournadre, J., et al., Estimation of cardiac preload changes by systolic pressure variation in pigs undergoing pneumoperitoneum. Acta Anaesthesiologica Scandinavica,2000.44(3):p. 231-235.
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29.Monnet, X., et al., Passive leg raising predicts fluid responsiveness in the critically ill*. Critical care medicine,2006.34(5):p.1402-1407.
30.Mahjoub, Y., et al., The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension*. Critical care medicine,2010.38(9): p.1824-1829.
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34.Bloomfield GL, Ridings PC, Blocher CR, et al.Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion[J]. J Trauma 1996,40(6):936-941.
35. Kashtan J, Green JF, Parsons EQ, et al.Hemodynamic effect of increased abdominal pressure. [J] J Surg Res 1981,30(3),249-255.
36. Diebel LN, Wilson RF, Dulchavsky SA, et al. Effect of increased intra abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow[J]. J Trauma 1992,33(2),279-282.
37. Otto J, Afify M, Jautz U, et al.Histomorphologic and ultrastructural lesions of the pancreas in a porcine model of intraabdominal hypertension[J]。Shock.2010,33(6):639-645.
38.Toens C, Schachtrupp A, Hoer J, et al.A porcine model of the abdominal compartment syndrome. Shock[J].2002,18(4):316-321.
39.Simon RJ, Friedlander MH, Ivatury RR,et al.Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction[J]. J Trauma 1997,42(3):398-403.
40.Cheatham M, Malbrain M.Cardiovascular implications of abdominal compartment syndrome[J]. Acta Clin Belg Suppl 2007,1(1):98-112.
41. Schachtrupp A, Wauters J, and Wilmer A. What is the best animal model for ACS? [J] Acta Clin Belg Suppl,2007,1(1):225-232.
42.Olofsson PH, Berg S, Ahn HC, et al. Gastrointestinal microcirculation and cardiopulmonary function during experimentally increased intra-abdominal pressure[J]. Crit Care Med.2009. 37(1):230-39.
43.Kubiak BD, Gatto LA, Jimenez EJ, Silva-Parra H, Snyder KP, Vieau CJ, Barba J, Nasseri-Nik N, Falk JL, Nieman GF. Plateau and transpulmonary pressure with elevated intra-abdominal pressure or atelectasis. J Surg Res,2010,Mar;159:e 17-24.
44.Talmor DS, Fessler HE.Are esophageal pressure measurements important in clinical decision-making in mechanically ventilated patients? Respir Care.2010 Feb;55(2):162-72; discussion 172-4.
45. Loring SH, O'Donnell CR, Behazin N, Malhotra A, Sarge T, Ritz R, Novack V, Talmor D.Esophageal pressures in acute lung injury:do they represent artifact or useful information about transpulmonary pressure, chest wall mechanics, and lung stress? J Appl Physiol.2010 Mar; 108(3):515-22
46.Sarge T, Talmor D.Targeting transpulmonary pressure to prevent ventilator induced lung injury. Minerva Anestesiol.2009 May;75(5):293-9. Review
47.Talmor D, Sarge T, Malhotra A, O'Donnell CR, Ritz R, Lisbon A, Novack V, Loring SH.Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008 Nov 13;359(20):2095-104.
48. Verzilli D, Constantin JM, Sebbane M, Chanques G, Jung B, Perrigault PF, Malbrain M, Jaber S.Positive end-expiratory pressure affects the value of intra-abdominal pressure in acute lung injury/acute respiratory distress syndrome patients:a pilot study. Crit Care.2010;14(4):R137o
49. Krebs J, Pelosi P, Tsagogiorgas C, Zoeller L, Rocco PR, Yard B, Luecke T. Open lung approach associated with high-frequency oscillatory or low tidal volume mechanical ventilation improves respiratory function and minimizes lung injury in healthy and injured rats. Crit Care. 2010;14(5):R183.
[2].Malbrain ML, Chiumello D, Pelosi P, et al:Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients:a multiple-center epidemiological study. Crit Care Med 2005;33(2):315-322.
[3].Diebel LN, Dulchavsky SA, Brown WJ:Splanchnic ischemia and bacterialtranslocation in the abdominal compartment syndrome. J Trauma 1997,43(5):852-855.
[4]. De Waele JJ, Hoste E, Blot SI, et al. Intra-abdominal hypertension in patients with severe acute pancreatitis. Crit Care,2005,9:R452-457.
[5]. Al-Bahrani AZ, Abid GH, Holt A, et al. Clinical relevance of intra-abdominal hypertension in patients with severe acute pancreatitis. Pancreas,2008,36:39-43.
[6].Rosas JM, Soto SN, Aracil JS, et al. Intra-abdominal pressure as a marker of severity in acute pancreatitis. Surgery,2007,141:173-178.
[7].Cheatham ML, Malbrain ML, Kirkpatrick A,et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med,2007,33:951-962。
[8].De Waele JJ, Hoste EA, Malbrain ML. Decompressive laparotomy for abdominal compartment syndrome--a critical analysis.Crit Care.2006;10(2):R51. Review.
[9].Mentula P, Hienonen P, Kemppainen E, et al. Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Arch Surg.2010;145(8):764-769.
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2. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006; 32(11):1722-32.
3.De Waele JJ, Hoste E, Blot SI, et al., Intra-abdominal hypertension in patients with severe acute pancreatitis. Crit Care,2005.9(4):R452-457.
4. Al-Bahrani AZ, Abid GH, Holt A, et al. Clinical relevance of intra-abdominal hypertension in patients with severe acute pancreatitis. Pancreas 2008;36(1):39-43.
5. Rosas JM, Soto SN, Aracil JS, et al. Intra-abdominal pressure as a marker of severity in acute pancreatitis. Surgery 2007; 141(2):173-8.
6. Leppaniemi A, Mentula P, Hienonen P, et al. Transverse laparostomy is feasible and effective in the treatment of abdominal compartment syndrome in severe acute pancreatitis. World J Emerg Surg 2008; 3:6.
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9. Bradley EL,3rd. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13,1992. Arch Surg 1993; 128(5):586-90.
10. Uhl W, Warshaw A, Imrie C, et al. IAP Guidelines for the Surgical Management of Acute Pancreatitis. Pancreatology 2002; 2(6):565-73.
11. Jones AE, Trzeciak S, Kline JA. The Sequential Organ Failure Assessment score for predicting outcome in patients with severe sepsis and evidence of hypoperfusion at the time of emergency department presentation. Crit Care Med 2009; 37(5):1649-54.
12. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference:definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992; 20(6):864-74.
13. De Waele, J. J.Leppaniemi, A. K. Intra-abdominal hypertension in acute pancreatitis. World J Surg 2009; 33(6):1128-1133..
14. Pupelis G, Plaudis H, Snippe K, et al. Increased intra-abdominal pressure:is it of any consequence in severe acute pancreatitis? HPB (Oxford) 2006; 8(3):227-32.
15. Keskinen P, Leppaniemi A, Pettila V, et al. Intra-abdominal pressure in severe acute pancreatitis. World J Emerg Surg 2007; 2:2.
16. Company L, Saez J, Martinez J, et al. Factors predicting mortality in severe acute pancreatitis. Pancreatology 2003; 3(2):144-8.
17. Baron TH. Predicting the severity of acute pancreatitis:is it time to concentrate on the hematocrit? Am J Gastroenterol 2001; 96(7):1960-1.
18. Pitchumoni CS, Patel NM, Shah P. Factors influencing mortality in acute pancreatitis:can we alter them? J Clin Gastroenterol 2005; 39(9):798-814.
19. Singh VK, Wu BU, Bollen TL, et al. Early systemic inflammatory response syndrome is associated with severe acute pancreatitis. Clin Gastroenterol Hepatol 2009; 7(11):1247-51.
20. De Winter BY, De Man JG. Interplay between inflammation, immune system and neuronal pathways:effect on gastrointestinal motility. World J Gastroenterol 2010; 16(44):5523-35.
21. Ranson JH, Lackner H, Berman IR, et al. The relationship of coagulation factors to clinical complications of acute pancreatitis. Surgery 1977; 81(5):502-11.
22. Garcia M, Barbachano EH, Lorenzo PH, et al. Saline infusion through the pancreatic duct leads to changes in calcium homeostasis similar to those observed in acute pancreatitis. Dig Dis Sci 2009; 54(2):300-8.
23. Wilson C, Heath DI, Imrie CW. Prediction of outcome in acute pancreatitis:a comparative study of APACHE H, clinical assessment and multiple factor scoring systems. Br J Surg 1990; 77(11):1260-4.
24. Mayerle J, Hlouschek V, Lerch MM. Current management of acute pancreatitis. Nat Clin Pract Gastroenterol Hepatol 2005; 2(10):473-83.
25. De Waele JJ, Leppaniemi AK. Intra-abdominal hypertension in acute pancreatitis. World J Surg 2009; 33(6):1128-33.
26. Olofsson PH, Berg S, Ahn HC, et al. Gastrointestinal microcirculation and cardiopulmonary function during experimentally increased intra-abdominal pressure. Crit Care Med 2009; 37(1):230-9.
27. Toens C, Schachtrupp A, Hoer J, et al. A porcine model of the abdominal compartment syndrome. Shock 2002; 18(4):316-21.
28. Al-Bahrani AZ, Darwish A, Hamza N, et al. Gut barrier dysfunction in critically ill surgical patients with abdominal compartment syndrome. Pancreas 2010; 39(7):1064-9.
29. Talmor D, Sarge T, Malhotra A, et al., Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med,2008.359(20):2095-2104.
30. Peng, Z. Y.Critchley, L. A.Joynt, G. M.Effects of norepinephrine during intra-abdominal hypertension on renal blood flow in bacteremic dogs. Crit Care Med.2008;36(3):834-41.
31. van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010; 362(16):1491-502.
32. Hartwig W, Maksan SM, Foitzik T, et al. Reduction in mortality with delayed surgical therapy of severe pancreatitis. J Gastrointest Surg 2002; 6(3):481-7.
[1]王春友,赵玉沛。从治疗观点演变和技术变革看重症急性胰腺炎疗效进步。中华外科杂志,2006,44：872-874.
[2]Cheatham ML, Malbrain ML, Kirkpatrick A,et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med,2007,33:951-962。
[3]De Waele JJ, Hoste E, Blot SI, et al. Intra-abdominal hypertension in patients with severe acute pancreatitis. Crit Care,2005,9:R452-457.
[4]Al-Bahrani AZ, Abid GH, Holt A, et al. Clinical relevance of intra-abdominal hypertension in patients with severe acute pancreatitis. Pancreas,2008,36:39-43.
[5]Rosas JM, Soto SN, Aracil JS, et al. Intra-abdominal pressure as a marker of severity in acute pancreatitis. Surgery,2007,141:173-178.
[6]Bloomfield GL, Ridings PC, Blocher CR, et al.Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion. J Trauma, 1996,40:936-941.
[7]Kashtan J, Green JF, Parsons EQ, et al.Hemodynamic effect of increased abdominal pressure. JSurg Res,1981,30,249-255.
[8]Diebel LN, Wilson RF, Dulchavsky SA, et al. Effect of increased intra abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma,1992,33,279-282.
[9]Otto J, Afify M, Jautz U, et al.Histomorphologic and ultrastructural lesions of the pancreas in a porcine model of intraabdominal hypertension.Shock.,2010,33:639-645.
[10]Toens C, Schachtrupp A, Hoer J, et al.A porcine model of the abdominal compartment syndrome. Shock,2002,18:316-321.
[11]Simon RJ, Friedlander MH, Ivatury RR,et al.Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma,1997,42:398-403.
[12]Cheatham M, Malbrain M.Cardiovascular implications of abdominal compartment syndrome. Acta Clin Belg Suppl,2007,1:98-112.
[13]Kotzampassi K, Paramythiotis D, Eleftheriadis E. Deterioration of visceral perfusion caused by intra-abdominal hypertension in pigs ventilated with positive end-expiratory pressure. Surg Today.2000;30:987-92.
[14]Kubiak BD, Gatto LA, Jimenez EJ, Silva-Parra H, Snyder KP, Vieau CJ, Barba J, Nasseri-Nik N, Falk JL, Nieman GF. Plateau and transpulmonary pressure with elevated intra-abdominal pressure or atelectasis. J Surg Res,2010,Mar;159:e 17-24.
[15]Schachtrupp A. Fluid resuscitation preserves cardiac output but cannot prevent organ damage in a porcine model during 24 h of intra abdominal hypertension. Shock. 2005;24:153-158.
[16]Peng ZY.Effects of norepinephrine during intra-abdominal hypertension on renal blood flow in bacteremic dogs. Crit Care Med 2008;36:834-841.
[17]Schachtrupp A, Wauters J, and Wilmer A. What is the best animal model for ACS? Acta Clin Belg Suppl,2007,1:225-232.
[18]Olofsson PH, Berg S, Ahn HC, et al. Gastrointestinal microcirculation and cardiopulmonary function during experimentally increased intra-abdominal pressure. Crit Care Med,2009. 37:230-39.
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