区域性动脉灌注四联给药治疗重症急性胰腺炎的临床研究

目的探讨区域性(胰腺及胰周)动脉灌注(RAI)给药治疗重症急性胰腺炎(SAP)，以提高胰腺及胰周的给药浓度，从而缩短疗程、减少治疗费用、降低死亡率。方法从1994年11月至2002年8月共收治100例重症急性胰腺炎病人，按Seldinger法，经股动脉插管，置管并固定于腹腔动脉干内，用输液泵加压持续给药。结果本组100例病人中，死亡3例，死亡率为3％，平均住院时间25d，平均住院费用4．25万元／人。结论区域性动脉灌注(RAI)四联给药治疗重症急性胰腺炎方法简单、疗效显著、住院时间短、费用低，有较好的社会效益和经济效益。     

重症急性胰腺炎时胰腺血管造影的影像学表现及其临床意义

目的 探讨重症急性胰腺炎时胰腺血管造影的影像学表现及其临床意义。方法 对25例重症急性胰腺炎病人和20例胰腺无疾患志愿者,按Seidinger法将导管插入至胃十二指肠动脉行胰腺血管造影。结果 重症急性胰腺炎时胰腺血管造影的影像学表现为：(1)主干动脉／分支动脉的直径比增大;(2)“树枝状”结构的“树枝”数目明显减少;(3)“网络状”结构模糊;(4)胰腺“轮廓”的消失,或成片状、模糊不清。结论 (1)胰腺血管造影是一种比较客观、直观地反映胰腺血供情况的影像学手段;(2)重症急性胰腺炎时,胰腺血管造影有较明显的影像学异常表现;(3)其临床意义在于：对重症急性胰腺炎病情严重度有一定的评估作用;预测区域动脉灌注治疗的疗效;为临床应用改善胰腺微循环药物提供客观的影像学证据。     

重症急性胰腺炎微循环障碍的治疗现状

胰腺微循环障碍是导致急性胰腺炎发展的重要因素,其在重症急性胰腺炎发病中的作用越来越引起人们的重视,针对改善胰腺微循环的治疗方法会减少胰腺组织的坏死程度和病变的演进。本文针对重症急性胰腺炎微循环障碍提出相关的治疗策略。     

区域动脉灌注治疗重症急性胰腺炎的适应证探讨

目的 探讨早期区域动脉灌注治疗重症急性胰腺炎的适应证.方法 分析各种类型的重症急性胰腺炎患者的区域动脉灌注治疗的疗效.结果 ①45 例重症急性胰腺炎患者采用区域动脉灌注治疗,治愈43 例,治愈率95.6%.② 10 例入院时合并有胰外脏器功能障碍的患者采用区域动脉灌注治疗,治愈9 例,治愈率90%.③13 例在治疗过程中继发感染的病例采用区域动脉灌注抗生素治疗,治愈12 例,治愈率为92.3%.④2 例腹腔室间隔综合征患者采用早期手术联合区域动脉灌注治疗,1 例治愈,1 例病死.结论 ①适应早期非手术治疗者可采用区域动脉灌注治疗.②早期未局限化的胰腺坏死继发感染病例可采用区域动脉灌注抗生素治疗.③排除腹腔室间隔综合征后诊断"暴发性胰腺炎"者也是区域动脉灌注的适应证.④需要早期手术的危重患者如腹腔室间隔综合征可联合区域动脉灌注治疗,以提高疗效.     

区域动脉灌注5-FU诱导大鼠急性胰腺炎腺泡细胞凋亡及Caspase-3表达

目的 探讨区域动脉灌注（regional arterial infusion,RAI）5-氟尿嘧啶（5-fluorouracil,5-FU）对大鼠急性胰腺炎（acute pancreatitis,AP）胰腺腺泡细胞凋亡的影响及其对急性胰腺炎的治疗作用。方法 18只健康成年SD大鼠随机分成3组：对照组（C组）、急性胰腺炎组（AP组）和5-FU治疗组（5-FU组）。各组均行胃左动脉置管,AP组和5-FU组以大剂量雨蛙素（每小时腹腔注射50 μg/kg,连续6 h）诱导建立大鼠急性胰腺炎模型,对照组注射同等剂量的生理盐水。5-FU组在第一次腹腔注射雨蛙素1 h后立即区域动脉灌注5-FU（40 mg/kg）治疗,C组和AP组区域动脉灌注等量的生理盐水。建模成功后3 h取标本并处死大鼠,检测血淀粉酶浓度,RT-PCR法检测胰腺组织内TNF-α、IL-1β、IL-6 mRNA表达水平,胰腺标本送病理学检查,Western blotting法检测胰腺组cleaved Caspase-3的蛋白表达,同时TUNEL法检测大鼠胰腺腺泡细胞凋亡情况。结果 与AP组比较,5-FU组血淀粉酶浓度明显降低（P＜0.05）;胰腺组织内TNF-α、IL-1β、IL-6  mRNA表达水平下降（P＜0.05）;胰腺组织病理学改变减轻;胰腺组织cleaved Caspase-3的蛋白表达增加;胰腺腺泡细胞凋亡增加（P＜0.05）。结论 区域动脉灌注5-FU对大鼠急性胰腺炎有改善作用,其作用机制可能与诱导胰腺腺泡细胞凋亡有关。     

重症急性胰腺炎区域动脉灌注的序贯治疗选择

自武田和宪报告区域动脉灌注(RAI)治疗急性坏死性胰腺炎至今已历经16年[1],目前RAI作为治疗重症急性胰腺炎(SAP)的一种增效非手术方法正逐渐被胰腺外科所接受.     

重症急性胰腺炎区域动脉灌注的序贯治疗选择

自武田和宪报告区域动脉灌注(RAI)治疗急性坏死性胰腺炎至今已历经16年[1],目前RAI作为治疗重症急性胰腺炎(SAP)的一种增效非手术方法正逐渐被胰腺外科所接受.     

重症急性胰腺炎区域动脉灌注的序贯治疗选择

自武田和宪报告区域动脉灌注(RAI)治疗急性坏死性胰腺炎至今已历经16年[1],目前RAI作为治疗重症急性胰腺炎(SAP)的一种增效非手术方法正逐渐被胰腺外科所接受.     

特殊营养膳对重症急性胰腺炎患者的血糖调控作用

目的探讨特殊营养膳对重症急性胰腺炎患者的血糖调控作用。方法将60例重症急性胰腺炎患者随机分为对照组和治疗组,分别给予常规营养膳及特殊营养膳。在不同时间监测急性期反应、胰腺病变、血糖变化、感染及其相关并发症的发生率、病死率和住院天数。结果两组急性期反应指标及胰腺病变无明显差异,但治疗组各时间点血糖平均水平及胰岛素用量、感染及其相关并发症的发生率及住院天数显著低于对照组,但病死率无显著差别。结论特殊营养膳能有效缓解重症急性胰腺炎急性期反应,通过对血糖的调控减少感染及其相关并发症的发生。     

区域性动脉灌注5－FU治疗急性坏死性胰腺炎

作者自１９９２年８月至１９９３年１２月，无选择地对１９例急性坏死性胰腺炎患者采用Ｓｅｌｄｉｎｇｅｒ法，将Ｃｏｒｄｉｓ导管置于胰腺病变的供血动脉内。如坏死病变位于胰头部，导管置于胃十二指肠动脉或胰十二指肠动脉；坏死病变限于胰体尾部，导管置于脾动脉或腹腔动脉；全胰散在性坏死病变，置管于腹腔动脉。经导管内区域性灌注５－ＦＵ为主的药物，自发病起２０天内为灌注治疗时间。全组病例治疗后获得满意效果，并与以手术治疗为主的６８例作对照，结果两组死亡率分别为１０．５％、３０．９％；器官功能衰竭发生率分别为５．３％、４２．７％；继发性细菌感染发生率分别为５．３％、４４．１％；有显著差异。作者认为区域性动脉灌注５－ＦＵ治疗急性坏死性胰腺炎是一种有效的疗法，且给延期手术，清除残留坏死胰腺组织提供了基础，术后病情恢复平衡。文中对方法、时间、作用和体会均作了详细的阐述。     

急性感染性坏死性胰腺炎的外科治疗进展

【摘要】〓感染性坏死性胰腺炎(infected necrotizing pancreatitis, INP)是以胰腺局部炎症、感染和坏死为特征的一种常见的临床急症,它起病急、病情重、进展快,治疗时间长,花费多,病死率高。通过近十年国内外文献统计研究发现虽然近年来坏死性胰腺炎综合治疗已取得巨大进展,从最初的胰周引流到坏死部分手术切除、由传统的外科开腹胰腺坏死组织清创术进展至微创手术治疗,但是病死率仍居高不下,通过文献研究比对发现,临床上最佳治疗方案还存在争议。急性坏死性胰腺炎的非手术疗法已得到充分肯定。感染坏死性胰腺炎是目前公认的手术治疗急性胰腺炎的适应证,本文就坏死性胰腺炎的外科治疗做一综述。     

Pathogenesis and prevention of early pancreatic infection in experimental acute necrotizing pancreatitis.

OBJECTIVE: The authors test antibiotic strategies aimed at either mitigating bacterial translocation from the gut or delivering antibiotics specifically concentrated by the pancreas for prevention of early secondary infection after acute necrotizing pancreatitis. BACKGROUND: Infection currently is the principal cause of death after severe pancreatitis. The authors have shown that the risk of bacterial infection correlates directly with the degree of tissue injury in a rodent model of pancreatitis. Bacteria most likely arrive by translocation from the colon. METHODS: Severe acute necrotizing pancreatitis was induced in rats by a combination of low-dose controlled intraductal infusion of glycodeoxycholic acid superimposed on intravenous cerulein hyperstimulation. At 6 hours, animals were randomly allocated to five treatment groups: controls, selective gut decontamination (oral antibiotics and cefotaxime), oral antibiotics alone, cefotaxime alone, or imipenem. At 96 hours, surviving animals were killed for quantitative bacterial study of the cecum, pancreas, and kidney. RESULTS: The 96-hour mortality (35%) was unaffected by any treatment regimen. Cecal gram-negative bacteria were significantly reduced only by the oral antibiotics. Pancreatic infection was significantly reduced by full-gut decontamination and by imipenem, but not by oral antibiotics or by cefotaxime alone. Renal infection was reduced by both intravenous antibiotics. CONCLUSIONS: Early pancreatic infection after acute necrotizing pancreatitis can be reduced with a full-gut decontamination regimen or with an antibiotic concentrated by the pancreas (imipenem) but not by unconcentrated antibiotics of similar spectrum (cefotaxime) or by oral antibiotics alone. These findings suggest that 1) both direct bacterial translocation from the gut and hematogenous seeding interplay in pancreatic infection while hematogenous seeding is dominant at extrapancreatic sites and 2) imipenem may be useful in clinical pancreatitis.     

Frequency and time course of pancreatic and extrapancreatic bacterial infection in experimental acute pancreatitis in rats

BACKGROUND: Infectious complications in severe pancreatitis are the main factors determining clinical course and outcome. The taurocholate model for acute necrotizing pancreatitis was evaluated for frequency and time course of pancreatic and extrapancreatic bacterial infection. METHODS: Sixty-five male Wistar rats were divided into 5 groups of 13 animals each. Specimens for bacteriologic examination were taken, and pancreatitis was induced by intraductal infusion of 3% taurocholate under sterile conditions. Animals were killed 8, 16, 24, or 32 hours thereafter, and bacteriologic examination was performed. A control group of animals with intraductal infusion of 0.9% saline solution were killed after 32 hours. RESULTS: There was no significant pancreatic infection in the control group and in the 8-hour group (1 of 13 rats). Sixteen and 24 hours after induction of pancreatitis, infection and inflammation of the pancreas were found in 77% (10 of 13 rats), and after 32 hours pancreatic infection occurred in 69% (9 of 13 rats). Extrapancreatic bacterial infection after 16 hours occurred in the liver (62%), spleen (62%), and mesenteric lymph nodes (46%). Bacteria infecting the pancreas reflected the bacterial spectrum of the large bowel and terminal ileum before induction of pancreatitis (Escherichia coli [77%], Proteus [43%], Enterococcus [37%], and Staphylococcus [23%]). CONCLUSIONS: Pancreatic infection is an early and frequent finding in the taurocholate model of acute necrotizing pancreatitis. Infection occurs between 8 and 16 hours after induction of pancreatitis. The source of infecting bacteria seems to be the large bowel or the terminal ileum. We present a useful model of severe pancreatitis in which to study bacterial translocation, the further route of spread, and therapeutic approaches.     

Early enteral feeding in severe acute pancreatitis: can it prevent secondary pancreatic (super) infection?

Sepsis continues to account for a second peak in mortality in patients with severe acute pancreatitis. The prevention of these septic complications and subsequent development of multiple organ dysfunction syndrome remains a major focus for investigators, yet despite considerable clinical and experimental work addressing its etiology, septic complications remain high. Several studies have been designed to demonstrate the mechanism of origin of these septic complications with an attempt to define strategies for their prevention to improve patient outcomes. There is clear evidence that the origin of this secondary bacterial infection arises from enteric bacterial translocation secondary to disruption of the gut mucosal barrier during acute pancreatitis. Strategies designed to prevent secondary pancreatic infection include aggressive fluid resuscitation to maximize organ perfusion, early systemic antibiotic treatment or selective gut decontamination, and recently attempts to block mediators of the systemic inflammatory response. This discussion will summarize our present understanding of the etiopathogenesis of secondary bacterial 'superinfection' of necrotizing pancreatitis and how the initiation of enteral feeding early in the course of acute pancreatitis may prove to be an effective means of preventing and/or reversing the breakdown of the gut mucosal defense barrier.     

Controlled clinical trial of selective decontamination for the treatment of severe acute pancreatitis.

OBJECTIVE: A randomized, controlled, multicenter trial was undertaken in 102 patients with objective evidence of severe acute pancreatitis to evaluate whether selective decontamination reduces mortality. SUMMARY BACKGROUND DATA: Secondary pancreatic infection is the major cause of death in patients with acute necrotizing pancreatitis. Controlled clinical trials to study the effect of selective decontamination in such patients are not available. METHODS: Between April 22, 1990 and April 19, 1993, 102 patients with severe acute pancreatitis were admitted to 16 participating hospitals. Patients were entered into the study if severe acute pancreatitis was indicated, on admission, by multiple laboratory criteria (Imrie score > or = 3) and/or computed tomography criteria (Balthazar grade D or E). Patients were randomly assigned to receive standard treatment (control group) or standard treatment plus selective decontamination (norfloxacin, colistin, amphotericin; selective decontamination group). All patients received full supportive treatment, and surveillance cultures were taken in both groups. RESULTS: Fifty patients were assigned to the selective decontamination group and 52 were assigned to the control group. There were 18 deaths in the control group (35%), compared with 11 deaths (22%) in the selective decontamination group (adjusted for Imrie score and Balthazar grade: p = 0.048). This difference was mainly caused by a reduction of late mortality (> 2 weeks) due to significant reduction of gram-negative pancreatic infection (p = 0.003). The average number of laparotomies per patient was reduced in patients treated with selective decontamination (p < 0.05). Failure of selective decontamination to prevent secondary gram-negative pancreatic infection with subsequent death was seen in only three patients (6%) and transient gram-negative pancreatic infection was seen in one (2%). In both groups of patients, all gram-negative aerobic pancreatic infection was preceded by colonization of the digestive tract by the same bacteria. CONCLUSION: Reduction of gram-negative colonization of the digestive tract, preventing subsequent pancreatic infection by means of selective decontamination, significantly reduces morbidity and mortality in patients with severe acute necrotizing pancreatitis.     

Die akute Pankreatitis Klassifikation – Diagnostik – Therapie

Acute pancreatitis is a multietiologic entity with rather diverse clinical courses. Whereas edematous pancreatitis has a mortality of less than 1%, nowadays; still approximately 20% of all patients with the necrotizing form succumb to the disease. To further improve therapeutic results a standardized approach should be used. For effective treatment the differentiation between edematous and necrotizing pancreatitis is crucial. All patients with signs of pancreatic necroses during abdominal ultrasound and patients with organ insufficiencies should undergo a CT-scan to define exactly the nature and the extent of the disease. Primarily all patients are treated conservatively. Main indications for operative intervention are signs for infection of pancreatic necroses and an acute abdomen due to local complications of acute pancreatitis. In cases of biliary origin an elective cholecystectomy has to be performed during a free interval to prevent a recurrence.     

一种新的小鼠急性胰腺炎动物模型

目的　建立一种新的急性胰腺炎小鼠模型。方法　应用显微外科技术 ,对实验组动物行胰管导入及低浓度胆盐低压注射 ;术后 2 4h杀活评估胰腺炎症程度。对照组仅行剖腹术。结果　实验组动物表现为血清淀粉酶增高、胰腺组织髓过氧化物酶 (MPO )活性增高 ,胰腺的病理改变为组织水肿、出血、坏死及炎性细胞浸润。结论　该小鼠模型具有典型的急性胰腺炎病理特征 ,可用于急性胰腺炎实验研究。     

Liver Transplantation for Acute-on-Chronic Liver Failure Associated With Acute Necrotizing Pancreatitis: A Case Report

Liver transplantation (LT) for acute-on-chronic liver failure (ACLF) accompanied by acute necrotizing pancreatitis is still unclear. We have a reported case of LT for ACLF associated with acute necrotizing pancreatitis. The postoperative multiorgan dysfunction and secondary infection were successfully managed under close supervision. The patient was a 47-year-old man with chronic hepatitis B virus infection presented with ACLF and acute necrotizing pancreatitis. After receiving LT from a deceased donor, the patient's liver functioning rapidly reverted to a normal level, and the acute pancreatitis was simultaneously stabilized. However, the patient later developed multiorgan dysfunction secondary to multidrug resistant bacteria infection, which was treated successfully with repeated percutaneous drainage, sensitive antibiotics, continuous renal replacement therapy, microbial balance, and best supportive care. LT can be considered for ACLF associated with acute necrotic pancreatitis without absolute contraindication. Moreover, we recommend a close observation of possible postoperative severe infection, and cautious multidisciplinary management was needed for the prevention of organ dysfunction.     

Effects of omega-3 fatty acids on acute necrotizing pancreatitis in rats

The aim of this study was to investigate the influence of omega-3 fatty acids (omega3FA) on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. The induction of ANP resulted in significant increases in mortality rate, intestinal permeability, bacterial infection in pancreas and extrapancreatic organs, and serum activity of urea and amylase, alanine transferase (ALT), interleukin (IL)-6, tumor necrotizing factor-alpha (TNF-alpha), lactate dehydrogenase (LDH) in bronchoalveolar lavage (BAL) fluid, tissue activity of myeloperoxidase (MPO) and malondialdehyde (MDA) in the pancreas and lung, and a considerable decrease of concentrations of calcium, protein and albumin. The use of omega3FA reduced mortality, phenol sulfophthalein excretion in urine, bacterial infection in pancreas, liver, spleen, MPO and MDA levels in pancreatic and lung tissue, LDH level in BAL fluid and serum IL-6 and TNF-alpha values. Serum triglyceride increased only in the omega3FA groups. Serum amylase, ALT, calcium, urea, protein, IL-1, and degree of pancreatic damage indicated no difference between the pancreatitis groups. Increased intestinal permeability and cytokine levels, and free radical damage play an important role during the course of acute pancreatitis. The treatment with omega3FA improves these effects. omega3FA may be useful in the treatment during ANP in rats. Therefore, it can be beneficial in patients with pancreatitis.     

8种抗生素透入犬胰组织能力的实验研究

为了解抗生素渗透胰组织的能力,以便为选择合适的抗生素治疗继发性胰腺感染提供参考依据。作者在建立犬急性出血坏死性胰腺炎模型的基础上,应用高效液相色谱法测定犬血清和胰组织中抗生素的浓度,并计算出它们的胰组织渗透率。结果：头孢噻肟,氧氟沙星,丁胺卡那霉素,氧哌嗪肯青霉素,头孢哌酮,氨苄青霉素,甲硝唑和环丙沙星的胰组织渗透率由小到大依次为１２％,１９％,２０％,４６％,５５％,６３％,７１％和１３２％。