经内镜胆管引流术治疗急性胰腺炎

为达到最佳治疗效果，而又减少损伤，７６例急性胰腺炎（ＡＰ）其中３例为重症急性胰腺炎（ＳＡＰ）患者接受了经内镜胆管引流术（ＥＢＤ），引流成功６９例。ＡＰ顺利治愈６７例，治愈率９７．１％，平均治愈时间８．５天。而ＥＢＤ术不成功改为其它治疗的７例，平均治愈时间长达１４．５天。结果表明ＥＢＤ具有简便、安全、疗效好、对患者打击小的优点     

急性胆石性胰腺炎内镜治疗体会

1997年 5月～ 2 0 0 0年 10月 ,我们对 2 8例急性胆石性胰腺炎 (Ａｃｕｔｅｇａｌｌｓｔｏｎｅｐａｎｃｒｅａｔｉｔｉｓ,ＡＧＰ)患者进行了内镜逆行胰胆管造影 (Ｅｎｄｏｓｃｏｐｉｃｒｅｔｒｏｇｒａｄｅｃｈｏｌａｎｇｉｏｐａｎｃｒｅａｔｏｇｒａｐｈｙ ,ＥＲＣＰ)检查 ,并进行了经鼻胆管引流 (Ｅｎｄｏｓｃｏｐｉｃｎａｓｏ ｂｉｌｌａｄｒａｉｎａｇｅ ,ＥＮＢＤ)及经内镜乳头括约肌切开术 (Ｅｎｄｏｓｃｏｐｉｃｓｐｈｉｎｃｔｅｒｏｔｏｍｙ ,ＥＳＴ)等内镜治疗 ,取得了较好的临床疗效。1　资料和方法1.1　一般资料　本组 2 8例中…     

经内镜胆管减压治疗胆源性急性胰腺炎

急性重症胆源性胰腺炎是一种病情凶险、并发症多、死亡率高的疾病。目前主要采用手术治疗,但手术创伤大,并发症较多。近年来随着内镜诊疗技术的提高,鼻胆管引流(ＥＮＤＢ)和内镜下乳头括约肌切开术(ＥＳＴ)治疗急性梗阻性化脓性胆管炎获得了较好的疗效,开始对并发症和死亡率居高不下的急性重症胰腺炎作内镜治疗。但治疗效果一直有争论[1～3]。我院自1996年以来对43例急性胆源性胰腺炎采用内镜下放置鼻胆引流管及经内镜乳头括约肌切开术治疗,现报告如下。1　临床资料1.1　一般资料　43例急性胆源性胰腺炎中,男24例,女19例,年龄21～67岁,平均…     

急性坏死型胰腺炎手术方法与时机的研究

目的探讨急性坏死型胰腺炎（ＡＮＰ）的手术方法与手术时机．方法本组ＡＮＰ２８例以入院顺序分配为早期手术多口切开多管引流缝合组（引流组）与晚期手术病灶清除伤口敞开组（敞开组），每组均１４例，进行比较研究．结果早期胰腺引流组治愈１０例（７１４％），死亡４例（２８６％）．晚期手术胰腺坏死切除敞开引流组，全部治愈为１００％，两组治愈率有高度显著差异性（Ｐ＜００１）．结论急性坏死性胰腺炎不同病期采用不同手术可提高疗效．     

急诊十二指肠镜治疗急性胆源性胰腺炎94例

目的:探讨急诊十二指肠镜行胆胰管引流治疗急性胆源性胰腺炎的价值及可行性,扩大完善内镜在胆胰疾病中的治疗范围.方法:2004-01/2005-12急诊十二指肠镜治疗急性胆源性胰腺炎94例,治疗方式以经内镜鼻胆管引流(ENBD)为主,必要时行Oddi′s括约肌切开(EST).结果:94例患者中成功91例,成功率96.81%.无发展为重症胰腺炎患者.上腹痛症状平均症状缓解时间42.3 h;尿淀粉酶平均56 h下降到正常.内镜治疗后1 wk,复查B超,61例伴有胰腺水肿患者49例水肿消退,形态恢复正常:29例伴有胰周积液患者中21例胰周积液完全吸收,8例积液量明显减少,无伴随临床症状.结论:急诊十二指肠镜治疗急性胆源性胰腺炎是安全可靠的,可以阻止胰腺向恶性转化.     

急性胰腺炎早期ERCP及内镜治疗66例

目的探讨急性胰腺炎患者早期ＥＲＣＰ及内镜治疗应用的价值及安全性．方法急性胰腺炎患者作早期（１ｄ～７ｄ内）ＥＲＣＰ及内镜治疗（ＥＲＣＰ组，６６例），并以同期保守治疗的急性胰腺炎患者６０例作对照（对照组），观察两组患者血清淀粉酶恢复时间，腹痛缓解时间、住院天数、住院费用及并发症发生情况．结果ＥＲＣＰ组中，３６例为胆道疾病患者，４例为胰管结石，４例为胰腺分裂症，３例为乳头旁巨大憩室，１７例ＥＲＣＰ未见异常．作内镜下治疗３３例，其中ＥＰＴ及取石术１７例，４例作了副乳头切开及扩张术，１２例作了鼻胆管引流术．ＥＲＣＰ组腹痛缓解天数及平均住院天数分别为１１５ｄ±３６ｄ及２１７ｄ±５０ｄ，明显短于对照组（１５４ｄ±７８ｄ及３３０ｄ±６８ｄ，Ｐ＜００１）．血清淀粉酶恢复时间及住院费用两组相差不显著．两组均未发生严重并发症．结论急性胰腺炎早期ＥＲＣＰ及内镜治疗经济安全、有效，可缩短腹痛缓解时间及住院天数，作者认为对胆源性胰腺炎应尽早行ＥＲＣＰ及内镜治疗．     

急性坏死性胰腺炎的诊断和内科治疗

急性胰腺炎（ＡｃｕｔｅＰａｎｃｒｅａｔｉｔｉｓ,ＡＰ）是胰腺的急性炎症过程,常伴上腹部剧痛。在多数情况下,血中胰酶水平包括淀粉酶和脂肪酶增高,至少达到正常值上限的３倍。在临床上,根据其严重程度,可分为轻型和重型两大类。前者在诊断和治疗上均无困难,一般疗程为１～２周,患者多在１月内恢复,胃肠胰腺功能恢复正常。重型胰腺炎又称急性重症胰腺炎（ＡｃｕｔｅＳｅｖｅｒｅＰａｎｃｒｅａｔｉｔｉｓ,ＡＳＰ）或急性出血坏死性胰腺炎（ＡｃｕｔｅＨａｅｍｏｒｒｈａｇｉｃａｎｄＮｅｃｒｏｔｉｚ－ｉｎｇＰａｎｃｒｅａｔｉ…     

内镜经十二指肠乳头引流治疗胰腺假性囊肿的临床应用疗效分析

目的评估内镜经十二指肠乳头引流治疗巨大胰腺假性囊肿（脓肿）的临床应用疗效。方法2003年6月至2006年6月取沈阳军区总医院消化内镜中心按照统一标准选择入组的胰腺假性囊肿（脓肿）病例10例，其中非感染性8例，感染性1例，胰腺脓肿1例。均采用内镜经乳头引流治疗，通过回顾性总结临床治疗和相关研究指标变化，综合评估此种治疗方法的临床应用疗效。结果内镜治疗失败1例，术后并发假性囊肿感染2例，急性胰腺炎1例。8例随访观察平均16．5个月，其中假性囊肿完全消失4例，假性囊肿残腔形成1例，假性囊肿不断缩小3例。急性重症胰腺炎2例治愈。结论内镜经乳头引流治疗胰腺炎合并巨大胰腺假性囊肿（脓肿）是一种确切有效的治疗方法。     

生长抑素对急性胰腺炎患者血小板参数的影响

目的：研究血小板参数在急性水肿型胰腺炎（ＡＥＰ）和出血坏死型胰腺炎（ＡＨＮＰ）中的变化特点及生长抑制（ＳＳ）治疗后对其影响。方法;血细胞自动分析仪检测血小板计数（ＰＬＴ）、平均血小板体积（ＭＰＶ）和血小板分布宽度（ＰＤＷ）。结果：ＡＥＰ患者血小板参数无明显变化。１周后,ＰＬＴ无明显升高,ＭＰＶ和ＰＤＷ有显著性升高;常规治疗后,对血小板参数无影响;ＳＳ治疗后,ＭＰＶ和ＰＤＷ有显著性升高。而ＡＨＮＰ患     

前列腺素E1治疗急性水肿型胰腺炎疗效观察

为了解前列腺素Ｅ１（ＰＧＥ１）治疗急性胰腺炎（ＡＰ）的疗效，将５４例ＡＰ随机分为治疗组２６例，对照组２８例。两线除禁食、输液抗生素等相同外，治疗组用ＰＧＥ１２００μｇ加５％葡萄糖液５００ｍｌ静滴，每天１次，连用３天。同时观察腹痛及血、尿淀粉酶变化。结果表明，治疗组腹痛消失及血尿淀粉酶恢复至正常时间均较对照组明显缩短（Ｐ〈０．０１）。提示ＰＧＥ１可提高ＡＰ疗效。     

Autoimmune pancreatitis： A review

Autoimmune pancreatitis has emerged over the last 40 years from a proposed concept to a well established and recognized entity. As an efficient mimicker of pancreatic carcinoma, its early and appropriate recognition are crucial. With mounting understanding of its pathogenesis and natural history, significant advances have been made in the diagnosis of autoimmune pancreatitis. The characteristic laboratory features and imaging seen in autoimmune pancreatitis are reviewed along with some of the proposed diagnostic criteria and treatment algorithms.     

Groove pancreatitis has a spectrum of severity and can be managed conservatively

Background & aimsThe natural history of groove pancreatitis is incompletely characterized. Published literature suggests a high rate of surgery. We describe the short- and long-term outcomes in a cohort of patients with groove pancreatitis treated at our institution.MethodsMedical records of patients hospitalized in the University of Pittsburgh Medical Center system from 2000 to 2014 and diagnosed with groove pancreatitis based on imaging were retrospectively reviewed. Clinical presentation and outcomes during index admission and follow-up were recorded.ResultsForty-eight patients with groove pancreatitis were identified (mean age 53.2 years, 79% male). Seventy-one percent were alcohol abusers and an equal number were cigarette smokers. Prior histories of acute and chronic pancreatitis were noted in 30 (62.5%) and 21 (43.8%), respectively. Forty-four (91.7%) met criteria for acute pancreatitis during their index admission. Alcohol was the most common etiology (68.8%). No patient experienced organ failure. The most frequent imaging findings were fat stranding in the groove (83.3%), duodenal wall thickening (52.1%), and soft tissue mass/thickening in the groove (50%). Over a mean follow-up of 5.0 years, seven (14.6%) required a pancreas-related surgery. Patients had a high burden of pancreatitis-related readmissions (68.8%, 69.4/100 patient-years). Incident diabetes and chronic pancreatitis were diagnosed in 5 (13.9% of patients at risk) and 8 (29.6% of patients at risk) respectively.ConclusionsGroove pancreatitis has a wide spectrum of severity; most patients have mild disease. These patients have a high burden of readmissions and progression to chronic pancreatitis. A small minority requires surgical intervention.     

JPN Guidelines for the management of acute pancreatitis: cutting-edge information

The JPN Guidelines for the Management of Acute Pancreatitis are organized under the subject headings: epidemiology, diagnosis, management strategy, severity assessment and transfer criteria, management of gallstone pancreatitis, nonsurgical management, and surgical management. The Guidelines contain cutting-edge information on each of these subjects, as well as a section on the Japanese medical insurance system which provides information that should prove useful to physicians in other countries. The quality of the evidence was evaluated by the evidence-based classification method used at the Cochrane Library. The levels of recommendation of the individual management methods contained in the Guidelines were determined on the basis of the evaluation of evidence by the consensus of the members of the Working Group (see below). The Japanese Society for Abdominal Emergency Medicine, the Japan Pancreas Society, and the Research Group for Intractable Diseases and Refractory Pancreatic Diseases (which is sponsored by the Japanese Ministry of Health, Labour, and Welfare) were commissioned to produce the JPN Guidelines for the Management of Acute Pancreatitis. A Working Group of 20 physicians specializing in pancreatic diseases and emergency medicine investigated and analyzed 14821 cases retrieved by means of a Medline (1960–2004) search and discussed the available literature on acute pancreatitis (limited to human pancreatitis). The Working Group held many general discussions in order to reach a consensus on the content of the Guidelines. After producing a draft, the Publishing Committee of the JPN Guidelines for the Management of Acute Pancreatitis posted it on a website and asked for comments and criticisms. Subsequently, a final version of the Guidelines was published in Japanese in 2003. The Publishing Committee is now making the Guidelines available to a much wider readership by bringing out an English version.     

Cutting-edge information for the management of acute pancreatitis

Considering that the Japanese (JPN) guidelines for the management of acute pancreatitis were published in Takada et al. (J HepatoBiliary Pancreat Surg 13:2–6, 2006), doubts will be cast as to the reason for publishing a revised edition of the Guidelines for the management of acute pancreatitis: the JPN guidelines 2010, at this time. The rationale for this is that new criteria for the severity assessment of acute pancreatitis were made public on the basis of a summary of activities and reports of shared studies that were conducted in 2008. The new severity classification is entirely different from that adopted in the 2006 guidelines. A drastic revision was made in the new criteria. For example, about half of the cases that have been assessed previously as being ‘severe’ are assessed as being ‘mild’ in the new criteria. The JPN guidelines 2010 are published so that consistency between the criteria for severity assessment in the first edition and the new criteria will be maintained. In the new criteria, severity assessment can be made only by calculating the 9 scored prognostic factors. Severity assessment according to the contrast-enhanced computed tomography (CT) grade was made by scoring the poorly visualized pancreatic area in addition to determining the degree of extrapancreatic progress of inflammation and its extent. Changes made in accordance with the new criteria are seen in various parts of the guidelines. In the present revised edition, post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis is treated as an independent item. Furthermore, clinical indicators (pancreatitis bundles) are presented to improve the quality of the management of acute pancreatitis and to increase adherence to new guidelines.     

Sclerosing pancreatitis showing rapidly progressive changes with recurrent mass formation

Summary Conclusion Sclerosing pancreatitis might develop repeatedly or might rapidly extend to the whole pancreas with recurrent mass formation. Background Nothing is known concerning course or development of sclerosing pancreatitis. Methods A 63-yr-old male was followed up for 2.5 yr. Results The patient was admitted because of a tumor in the body and tail of the pancreas. Serum pancreatic enzymes were transiently elevated, but tumor markers were all negative. Imaging studies showed a tumor 7 cm in size. The main pancreatic duct was normal in the head and obstructed at the body on endoscopic retrograde pancreatography (ERCP). The K-ras oncogene mutation was positive in pure pancreatic juice. Distal pancreatectomy was performed because pancreatic cancer was highly suspected. Pathological findings showed that the tumor was a densely fibrotic mass without malignant cells. Inflammatory cell infiltration was observed in the stroma. One year later, another mass 3 cm in size was noted in the remnant pancreatic head. ERCP revealed diffuse irregular narrowing of the main pancreatic duct, its branches, and the common bile duct. Liver dysfunction improved and an elevation of serum pancreatic enzymes subsided without any specific treatment, and the mass diminished in size. The patterns of various imaging studies on the second tumor were the same as those of the previous resected mass. Corticosteroid was not administered.     

重症急性胰腺炎的概念之争

急性胰腺炎是腹部外科最常见的急诊之一,近年来由于病理转归过程认识的深入,临床诊断方法的改进和治疗监测手段的改善,病死率已大大地降低．面对这个进展迅速的专题,理解上的“分歧”时常造成临床有关概念认识上的争议．１　重症急性胰腺炎的定义急性胰腺炎是一种在临床表现上差异很大的疾病．轻者可无并发症短期自限自愈．重者起病急骤、病情危重、病程漫长、治疗复杂、并发症多、病死率高．根据在法国的马赛（１９６３、１９８４）、英国的剑桥（１９８３）、意大利的罗马（１９８９）和美国的亚特兰大（１９９２）先后召开的五次国际…     

A study of the time course of conversion of edematous to hemorrhagic pancreatitis

We studied the conversion of acute edematous pancreatitis (AEP) to acute hemorrhagic pancreatitis (AHP) in an experimental model in cats. In the model, 16,16 dimethyl PgE₂ effects this conversion by increasing microvascular permeability. First, we induced AEP in cats and then gave PgE₂ at increasing intervalsafter the induction of AEP to see how long an interval would still allow conversion. In 6 groups of cats, PgE₂ was administered for 2 h, starting at 2, 4, 6, 8, 10, or 12 h after the creation of AEP. Twelve h later, the cats were sacrificed and the pancreases were graded for inflammation and hemorrhage. Significant pancreatic hemorrhage did not occur when the PgE₂ was administered at 12 h compared to 2 h. Next, we determined that PgE₂ still retained its ability to increase pancreatic vascular permeability when administered 12 h after the creation of AEP. This was done by perfusing a marker molecule through the MPD (fluorescein iso-thiocyanate labeled dextran: FITC-D, mol wt 20,000) and then finding it in portal venous blood (PVB). The presence of FITC-D in PVB signified increased vascular permeability, since normally none was present. We concluded that conversion of AEP to AHP was possible during the first 12 h after induction of AEP. Lack of conversion at 12 h was not caused by a lack of vascular reactivity at that time.     

Infectious causes of acute pancreatitis: A systematic review

BackgroundInfectious etiologies of acute pancreatitis (AP) are rare and include viruses, bacteria, mycobacteria, parasites, and fungi. We aimed to conduct a comprehensive review on infectious etiologies of AP analyzing the frequency, clinical features, and outcomes of individuals presenting with this condition.MethodsEligible articles reporting on AP attributed to infectious etiologies were included. A comprehensive literature search of PubMed from time of inception and until September 6,2019 was performed using all relevant MeSH (medical subject heading) keywords. Articles were assessed for eligibility and independently reviewed by two reviewers for clinical features of AP, local complications, and mortality. Methodological quality of included studies was evaluated using the Murad tool.ResultsA total of 212 articles were included, of which 168 (79.2%) were at high risk of bias. 320 cases of AP were identified. Viruses were the leading etiology of infection attributed AP (65.3%) followed by helminths (19.1%), and bacteria (12.5%). Protozoa, mycobacteria, and fungi accounted for the remaining 3.1% of cases. Mean age was 40.5 ± 18.4 years and M:F ratio was 1.94:1. Mortality occurred in 50 patients. Mortality rate was higher in the virus attributed AP patients than AP from other infectious etiologies (21.8% vs. 7.0%, p < 0.0005).InterpretationLiterature quality on infection attributed AP is limited. Virus attributed AP appears to carry a higher mortality than other etiologies of infection attributed AP.     

Current concept of pathogenesis of severe acute pancreatitis

The pathogenesis of severe acute pancreatitis is very complicated. It is a multifactorial as well as multifaceted disease. First of all, the etiologic agents initiate the pancreatic acinar injury by release of pancreatic enzymes and overstimulation of macrophages and neutrophils, then the cytokines and inflammatory mediators are liberated. There is also interaction between neutrophils and endothelial cells producing free radicals, the cytokines cause increasing vascular permeability, activating complement component, resulting in microcirculatory impairment and imbalance of thrombo-fibrinolytic system. Many of these events occur not only in the pancreas itself, but also in the other vital organs and tissues, leading to severe acute pancreatitis and complications. The sequencial events are as follows.