胸腔积液联合血液浓缩对急性胰腺炎严重度评估的临床价值

目的：探讨胸腔积液、血液浓缩和二者的联合应用对急性胰腺炎疾病严重程度的评估价值，并观察胸腔积液与急性胰腺炎病因，并发症及死亡率的关系。方法：对136例急性胰腺炎住院患者作回顾性分析，急性胰腺腺炎及其严重度评估的标准依据患者的临床表现，实验室检查及增强CT检查。记录患者的胸片和红细胞压积检测结果，并分析胸腔积液与急性胰腺炎患者的病因，并发症及预后的相关性。结果：轻型急性胰腺炎（MAP）96例，重症急性胰腺炎（SAP）40例。SAP患者合并胸腔积液者18例（45％），有血液浓缩现象者6例（15％），胸腔积液和血液浓缩同时存在者5例（12．5％）；MAP患者合并胸腔积液者10例（10．4％），血液浓缩者2例（2．1％），无胸腔积液和血液浓缩同时存在者，两者相比有显著性差异（P＜0．01）；此外，胆源性急性胰腺炎合并胸腔积液者11例（14．4％），酒精性急性胰腺炎合并胸腔积液者5例（48．1％），P＜0．05，结论：胸腔积液，血液浓缩均可作为SAP的独立预测指标，但以胸腔积液联合血液浓缩最为准确。胸腔积液与酒精性急性胰腺炎的病因具有明显的相关性，但未发现胰腺局部并发症如胰腺假性囊肿以及患者死亡率与胸腔积液的关系。     

重症急性胰腺炎急性液体积聚治疗体会

回顾性研究39例重症急性胰腺炎（SAP）患者的临床资料。发现全组早期皆有急性液体积聚（AFC），急性胰腺假性囊肿发生率为46．2％（18／39）。治愈组的生长抑素使用时间、中药导泻时间、血制品使用量明显高于囊肿组（P〈0．05）；而胸腹水吸收时间、住院时间皆明显低于囊肿组（P〈0．05）。提示AFC为SAP常见并发症，恰当使用生长抑素、中药导泻、血制品等对促进AFC吸收、减少SAP急性胰腺假性囊肿的发生、缩短住院时间有积极作用。     

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。     

重症急性胰腺炎的实验室和影像学诊断

根据患者的病史、症状、体征以及血、尿淀粉酶测定不难诊断急性胰腺炎。但重症急性胰腺炎常伴有脏器衰竭和全身或局部并发症,如弥散性血管内凝血（DIC）、严重代谢紊乱、胰腺坏死、脓肿和假性囊肿等,病情凶险,死亡率高,故早期识别重症急性胰腺炎具有重要临床意义。     

腹腔灌洗术在重症急性胰腺炎治疗中的应用

重症急性胰腺炎(severe acute pancreatitis，SAP)是指急性胰腺炎伴脏器功能衰竭，或出现胰腺坏死、脓肿或假性囊肿等局部并发症者，或两者皆有。SAP发病急，进展快，并发症多，经过二十多年的理论研究及临床实践，尽管疗效已有显著提高，但是仍有近20％的死亡率。由于SAP的病因不同，病程不同，治疗方法亦不完全相同。中华医学会外科学     

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。     

胰腺脓肿及胰腺坏死感染15例分析

胰腺脓肿指腹腔内邻近胰腺部位的脓液积聚，可能来源于胰腺局限性坏死液化继发感染，通常在胰腺炎发病4～6周后形成，也可来自胰腺假性囊肿继发感染或形成于胰腺炎发病很久之后。胰腺坏死感染指胰腺组织坏死30％以上又继发感染，通常发生于重症急性胰腺炎发病2～3周内。     

The etiology and clinical characteristics of 34 cases of acute recurrent pancreatitis

目的 探讨复发性急性胰腺炎患者的病因及临床特点.方法 收集我院收治的急性胰腺炎患者152例的临床资料,分析复发性急性胰腺炎患者的临床特征.结果 152例急性胰腺炎患者中,复发性急性胰腺炎组34例(22.4％),对照组即无复发组118例(77.6％).复发性急性胰腺炎患者的病因以胆源性为主(52.9％);酒精性(14.7％)、高脂血症(8.8％)和其他因素(2.9％)所占比例均低于对照组;饮食不当(8.8％)和特发性(11.9％)所占比例均高于对照组,但两组比较差异均无统计学意义(P＞0.05).复发性急性胰腺炎组患者胸水、腹水和假性囊肿形成的发生率分别为30.8％、23.1％和19.2％,对照组分别为29.2％、11.5％和3.1％,假性囊肿形成的发生率比较差异有统计学意义(P＜0.05).结论 复发性急性胰腺炎是一种常见疾病,胆道结石和酒精是其常见病因,原因不明者占较高的比例.明确病因后积极治疗原发病因,可有效减少其复发.     

应用~(111)铟标记自体白细胞鉴别胰腺脓肿和假性胰腺囊肿

胰腺脓肿是急性胰腺炎的破坏性并发症,病情甚为严重,死亡率几达100％,如立刻进行引流,死亡率可降至14～57％。急性假性胰腺囊肿亦是急性胰腺炎的并发症,需采取胃或小肠内引流。安全的囊肿-肠吻合需有一成熟或坚厚的囊壁,囊壁成熟又需要一定时间;因此,外科医生多主张推迟手术时间至少4周。另外引流时间推迟,假性囊肿也可能自行吸收。由于这二种并发症的手术时间不同,故及时鉴别两者实属重要。超声波和电子计算机断层X线照相(CT)虽能诊断出胰腺肿     

急性出血坏死性胰腺炎早期非手术治疗41例

目的介绍并讨论急性出血坏死性胰腺炎早期非手术治疗适应证，措施和中转手术指征．方法总结我院外科1988－01／1998－01收治的41例急性出血坏死性胰腺炎的诊断治疗经验．结果41例患者假性胰腺囊肿形成3例，肺部感染4例，无严重并发症34例：中转手术6例，死亡2例，死亡率4．8％．结论治疗适用于诊断明确，无胰腺及胰周感染，无明显胆道梗阻的患者非手术治疗措施除严密监护下的常规治疗外，特别强调抑制胰腺分泌促进肠道功能、肠道应用抗生素、利尿、营养、支持、中药、胰外器官损害对症治疗；在非手术治疗过程中，出现胰腺或胰周感染，假性囊肿并发症时应及时中转手术．     

生长抑素治疗重症急性胰腺炎的临床研究

目的观察生长抑素施他宁及其类似物善宁治疗重症急性胰腺炎(SAP)的治疗效果及评估其临床价值。方法按Ranson标准判断病情严重程度,将106例病情大致相近的SAP患者分成施他宁治疗组37例,善宁治疗组36例及对照组33例。对照组用一般常规治疗方法,治疗组在一般常规治疗方法治疗的基础上加用施他宁6mg／d或善宁0．6mg／d,维持治疗7～14d。观察3组血尿淀粉酶变化、平均腹痛持续时间、禁食天数、住院天数、并发症、手术率及住院费用等多项指标。结果施他宁和善宁治疗SAP均能显著降低血尿淀粉酶水平,控制腹痛,缩短禁食时间和住院天数,减少并发症和手术率,并且没有明显的增加住院费用。结论生长抑素施他宁和善宁对SAP有明显疗效,可以阻止病情进展和恶化,减少并发症,改善预后。     

急性胆源性胰腺炎早期内镜治疗价值

目的探讨急性胆源性胰腺炎早期内镜治疗的价值及其安全性。方法选择92例急性胆源性胰腺炎患者早期（72h内）行ERCP及内镜治疗（ERCP组），并与同期保守治疗40例（对照组）进行比较。结果ERCP组全部成功实施十二指肠乳头切开取石，72例胆总管结石者行网篮及气囊取石，所有92例均行鼻胆管引流，重症组10例同时行胰管支架引流。ERCP组平均腹痛消失时间、血清淀粉酶恢复时间、平均住院天数及平均费用均明显低于对照组。ERCP组重症组病死率8．3％，对照组重症组病死率33．3％。结论急性胆源性胰腺炎早期ERCP治疗是安全的，能降低患者的病死率，减少患者住院天数和费用。     

The effects of somatostatin on the microperfusion of the pancreas during acute necrotizing pancreatitis in rats

BACKGROUND/AIMS: Autodigestion and impairment of microcirculation of the pancreas play an important role in the pathogenesis of acute pancreatitis. Somatostatin with the reducing effect on the hepato-splanchnic blood flow decreases exocrine pancreatic secretion. Microcirculatory changes are central to the pathogenesis of acute pancreatitis. However, little is known about the effects of somatostatin on the pancreatic tissue oxygen pressure and acinar cell injury during acute pancreatitis. The aim was to evaluate somatostatin by measuring its effect on the pancreatic tissue oxygen pressure and acinar injury in acute pancreatitis. METHODOLOGY: Acute necrotizing pancreatitis was induced in rats by standardized intraductal bile acid infusion and cerulein hyperstimulation. Serum trypsinogen activation peptide was measured to verify comparable disease severity. After the induction of acute necrotizing pancreatitis, animals randomly received either ringer lactate or somatostatin. Monitoring included cardiorespiratory parameters, hematocrit, amylase, pancreatic tissue oxygen pressure, and trypsinogen activation peptide levels. At the end of the experiments the pancreas was removed for evaluation of acinar cell injury. RESULTS: The two study groups were comparable with regard to mean arterial pressure, heart rate, arterial blood gases, hematocrit, and serum amylase. The induction of pancreatitis resulted in the significant decrease of pancreatic tissue oxygen pressure in both groups. The use of somatostatin did not increase pancreatic tissue oxygen pressure. There were no significant differences in plasma trypsinogen activation peptide and serum amylase levels in the animals of two treatment groups. Only somatostatin decreased pancreatic damage significantly. CONCLUSIONS: The use of somatostatin did not improve pancreatic microcirculation or trypsinogen activation peptide level in acute necrotizing pancreatitis; however, it reduced pancreatic damage. Therefore, it has a limited value in the treatment of the acute pancreatitis.     

Exudative pleural effusions secondary to gastrointestinal diseases

Several different diseases of the gastrointestinal tract may have an associated exudative pleural effusion. In the acutely ill patient with a pleural effusion, the possibility of esophageal perforation should always be considered. It is important to establish this diagnosis as soon as possible since the mortality rate increases markedly if drainage of the mediastinum is delayed for even 12 or 24 hours. The best screening test for esophageal rupture is the level of amylase in the pleural fluid. All patients with undiagnosed exudative pleural effusions should have the amylase level in their pleural fluid measured to rule out a pancreatic etiology for their pleural effusion. In patients with acute pancreatitis, the clinical presentation may be dominated by chest symptoms. Such patients have small to moderately sized pleural effusions that resolve rapidly once appropriate therapy is instituted. If symptoms persist, the possibility of a pancreatic abscess or a pancreatic pseudocyst should be considered. Patients with pancreatic pseudocysts may develop a sinus tract between the pseudocyst and the pleural space. In this situation a large pleural effusion develops. Frequently there are no abdominal symptoms and the diagnosis will not be made unless a pleural fluid amylase is obtained. Patients with exudative pleural effusions that contain predominantly polymorphonuclear leukocytes should be suspected of having an intra-abdominal abscess, particularly when there is no associated parenchymal infiltrate. Subphrenic, intrahepatic, and splenic abscesses all have a high incidence of accompanying pleural effusion. Abdominal CT scanning is the method of choice to establish each of these diagnoses.     

Prophylactic antibiotic treatment in acute necrotizing pancreatitis: East wind blows no good

The thermolability of amylase was measured in saliva, pancreatic juice, urine, adult and neonatal sera. The mean percentage thermolability from these fluids was 100%, 99%, 87%, 44% and 23% respectively. In patients with acute pancreatitis and mumps the amylase was 84% and 83% thermolabile during the acute phase. On resolution of the pancreatitis this dropped towards normal. Patients with a pancreatic pseudocyst showed a high mean percentage thermolability (82%). These results could suggest that a component of amylase in human serum is not of pancreatic or salivary origin. In addition, this simple technique may be helpful in the diagnosis of pancreatic pseudocyst.     

Somatostatin in the treatment of established and severe acute pancreatitis in the rat]

The effects of somatostatin (SS) on the treatment of acute pancreatitis were studied in rats. Acute pancreatitis was established by injecting 5% sodium taurocholate in the biliopancreatic duct. Previously, pancreatic necrosis was determined in this experimental model at several intervals without treatment. Treatment was started according different groups: at 12, 16 and 20 hours after induction of acute pancreatitis (IV bolus of 4 ug/kg body weight followed by a 24h continuous infusion of 4 ug/kg body wt/hour). When somatostatin was initiated at 12 or 16h a decrease in serum amylase and lactodehydrogenase was observed, as well as in pancreatic necrosis resulting in 0% mortality after 24h of treatment. When somatostatin was started at 20h there was no changes in the lethal outcome of the disease.     

超声引导经皮置管引流治疗急性胰腺炎早期急性液体积聚疗效分析

背景：急性胰腺炎（AP）病程早期可发生急性液体积聚,积液可继发感染或形成假性囊肿。目的：评价超声引导经皮置管引流（PCD）治疗AP早期急性液体积聚的疗效和安全性。方法：2001年9月～2011年3月泰州市人民医院103例重症急性胰腺炎（SAP）伴早期胰腺、胰周急性液体积聚的住院患者纳入研究,其中42例接受保守治疗,61例在保守治疗的基础上于入院48 h内接受超声引导PCD治疗。回顾性分析两组患者的治疗效果和并发症发生情况。结果：PCD治疗组体温和血清CRP水平恢复正常时间、积液消失时间、住院天数显著短于保守治疗组（P〈0.05）,多器官功能衰竭、败血症、假性囊肿发生率以及手术率和死亡率显著低于保守治疗组（P〈0.05）：置管和引流过程中无一例患者发生内脏损伤,局部皮肤无严重感染,拔管后无瘘管形成。结论：超声引导PCD治疗胰腺、胰周积液简单、有效、安全,可作为AP早期急性液体积聚的首选治疗方法。     

A prospective study of the aetiology, severity and outcome of acute pancreatitis in Eastern India.

BACKGROUND: Acute pancreatitis is a common cause of hospital admission. The aim of this study was to evaluate the aetiology, severity and outcome of acute pancreatitis in our tertiary referral center. METHODS: Between August 2002 and December 2003, 45 cases of acute pancreatitis were admitted to the hospital. Diagnosis was ascertained by clinical examination and investigations (hyperamylasaemia). The severity was assessed by the Acute Physiology and Chronic Health Evaluation scoring system and contrast enhanced computed tomography scan. The patients were treated according to a designed protocol. The data related to aetiology, severity and outcome were noted for subsequent analysis. RESULTS: Of the 45 patients, 33 were male and 12 were female. The mean age was 30 years. Of the 45 patients, 34 patients had mild pancreatitis and 11 had severe pancreatitis. The aetiology spectrum of mild pancreatitis included the following: alcoholism in 14 (41.1%), gallstones in 8 (23.5%), trauma in 6 (17.6%), idiopathic in 4 (11.7%) and post-endoscopic retrograde cholangiopancreatography in 2 (5.8%). The causes of severe acute pancreatitis came under the following headers: trauma in 3 (27.2%), idiopathic in 2 (18.1%), gallstones in 2 (18.1%), alcoholism in 2 (18.1%) and post-endoscopic retrograde cholangiopancreatography in 2(18.1%). Mild pancreatitis led on to the following: pancreatic abscess in 1, pseudocyst in 3 and readmission for pain relapse within 6 months in 10 patients. The remainder had uneventful recoveries. There was no mortality in this group. Severe acute pancreatitis led on to the following: symptomatic sterile pancreatic necrosis in 2, infected pancreatic necrosis in 2, pancreatic abscess in 2 and presentation 8 months later with colonic stricture in 1 patient. There were 2 deaths in this group due to multi-organ failure. CONCLUSION: Although gallstones have largely been implicated as a common cause of acute pancreatitis our study found alcoholism as the main aetiological factor. Blunt abdominal trauma was also seen as a common cause of acute severe pancreatitis, particularly severe acute pancreatitits, as seen in our series. The outcome in mild pancreatitis was good, severe acute pancreatitis leads to more complications and greater mortality, thus requiring careful medical and surgical management.     

Effects of nafamostat mesilate,somatostatin, and glucagon on caerulein-induced acute pancreatitis in rats

The inhibitory effects of somatostatin (SMS) and glucagon (Gn) on acute pancreatitis were evaluated in an experimental acute pancreatitis model in male Wistar rats. The effects of these agents were compared with those of nafamostat mesilate (NM). The acute pancreatitis was induced by four serial subcutaneous injections of caerulein. The rats were divided into four groups. The first group (n=28) received SMS daily, the second group (n=28) received Gn daily, and the third group (n=28) received NM daily after the first injection of caerulein. The fourth group (n=42) received caerulein alone and served as the control group. Animals were sacrificed 4, 6, 8, 12, and 24 h, and 3 and 7 days after the first administration of caerulein and the degree of severity of the acute pancreatitis was evaluated by serial morphological and histological examinations of pancreatic tissues, as well as in terms of the serum concentrations of amylase and lipase. The characteristic findings of acute pancreatitis in the animals of all groups treated with SMS, Gn, or NM were markedly attenuated at all time points after the treatments compared with findings in the controls (caerulein alone) in terms of wet weight of pancreas, serum concentrations of amylase and lipase, formation of intracellular vacuoles in acinar cells, interstitial edema, and infiltration of an inflammatory cell component. The inhibitory effects of SMS, Gn, and NM on acute pancreatitis were similar at the doses used. These results suggest that SMS and Gn are as useful as NM, they may be of value for the treatment of acute pancreatitis.     

Necrotizing pancreatitis: Indications for surgery and surgical techniques

The term, “acute pancreatitis”, covers in terms of clinical, pathological, biochemical and bacteriological data, different entities in regard to the natural course of the disease. Interstitial edematous pancreatitis and necrotizing pancreatitis are the most frequent clinical manifestations; pancreatic abscess and postacute pseudocyst are late complications, mostly of necrotizing pancreatitis, developing after 3–5 weeks. The first choice of treatment is non-surgical management, even in patients with a severe complicated course of the disease. Patients who develop surgical acute abdomen, clinical sepsis syndrome, shock syndrome, or a severe type of mechanical or adynamic ileus must be treated surgically. Patients who do not respond to maximum intensive care measures for pulmonary, renal, cardiocirculatory, and metabolic dysfunction are candidates for surgical treatment, despite the possibility of sterile necrosis causing systemic complications. Surgical treatment is indicated in patients with infected necrosis, debridement and continuous closed lavage or open packing with re-operation being the most accepted treatment protoclos. When necrosectomy/debridement plus closed postoperative lavage was employed as a standard surgical treatment, hospital mortality was less than 20% in patients with infected necrosis as well as those with sterile necrosis. In pancreatic abscess and postacute pseudocyst, the treatment of first choice is intervention via ultrasound- or CT-guided percutaneous puncture and drainage of the abscess cavity. However, the majority of patients with a pancreatic abscess, treated interventionally, are candidates for a surgical drainage procedure because the interventional drainage fails to control the sepsis rapidly.