胰腺炎并发胰性脑病 37 例临床分析

目的 探讨胰腺炎并发胰性脑病(PE)的临床表现、诊断、鉴别诊断及可能诱因.方法 回顾性分析5年来上海6所医院急性胰腺炎并发PE 37例患者的临床资料.结果 37例PE中男性24例,女性13例,平均年龄53岁(25 ～ 80岁).按Ranson诊断标准33例为重症急性胰腺炎(SAP),4例为轻症急性胰腺炎(MAP),其中迟发性PE(DPE)6例,15例发病前有胰腺手术史.PE死亡率56.8%,DPE为66.7%.临床表现和诊断无特异性,血淀粉酶水平与PE严重程度无相关性.PE出现时常伴发低氧血症和急性呼吸窘迫综合征、水电解质紊乱、氮质血症、消化道出血等并发症.结论 PE是胰腺炎发病过程中的严重并发症,死亡率高,多在重症胰腺炎中伴发.在PE的发病过程中,有些因素也可引起胰腺炎患者的精神症状,如低氧血症、Wernicke脑病等,临床上较易混淆,为确诊带来困难.     

胰性脑病的诊治探讨

胰性脑病（pancreatic encephalopathy，PE）是急性胰腺炎（AP）．尤其是重症急性胰腺炎（SAP）的少见严重并发症，一旦发生，预后差．死亡率高．故提高对本病的早期诊断及临床治疗水平至关重要。现对2001年1月～2005年12月诊治的10例PE患进行回顾分析。     

胰性脑病与韦尼克脑病

目的和方法 通过对急性重症胰腺炎伴发中枢神经系统症状的9例典型病例介绍,加上文献检索30篇共185例急性重症胰腺炎合并脑病患者的临床分析,对并发脑病进行分类。结果 185例脑病中大多为重症（84％）,男性略多,且胆源性胰腺炎居多。早期发生脑病者为急性全身炎症反应所致多脏器衰竭的一部分,为胰性脑病（PE）,有107例,死亡61例（57％）;2周以上甚至在恢复期发生脑病者与长期禁食缺乏维生素B1（Vit B1)有关,为韦尼克（Wernicke)脑病（WE）,共有78例,死亡26例（33％）;两组病死率的差异有显著性（P＜0．01）。WE组病死率较低系近年来注意及时补充Vit B1,文献加本组3例,给予VitB1治疗的17例全部存活,而未给VitB1的WE患者中病死率达43％,与PE组病死率相比差异无显著性（P＞0．05）。结论 本文详述了PE与WE的发病机制、诊断要点及处理原则,提出对于PE应早期诊断、综合强化治疗,而对于禁食时间较长者应给予VitB1肌肉注射以预防WE发生,已发生者则应补充大剂量VitB1,这是降低急性胰腺炎并发脑病病死率的关键。     

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胰性脑病(pancreatic encephalopathy,PE),指急性胰腺炎并发中枢神经系统的损害,是胰腺炎少见的严重并发症,常发生于急性胰腺炎的病程中,也可以发生在轻型胰腺炎或慢性胰腺炎的急性发作过程中。1923年Lowell首次在临床观察中发现,其定义于1941年由Rothemich提出,主要临床表现为定向力障碍、烦躁不安、妄想、幻觉、意识不清或反应迟钝、表情淡漠、抑郁等精神神经障碍,亦称酶性脑病。1发病机制目前对PE发病机制的研究虽然取得了一定的进展,但尚未完全清楚[1-3]。一般认为,与胰腺脂酶、磷脂酶A2、炎症介质及其它因素如低氧血症和急性呼吸窘…     

急性胰腺炎合并胰性脑病3O例临床分析

胰性脑病（pancreatic encephalopathy，PE）是急性胰腺炎（acute pancreatitis，AP）时出现的以精神症状和神经系统体征为主要临床表现的并发症，死亡率高（57％），预后差。我们回顾分析了从1997年1月至2003年12月南京军区总医院普通外科研究所SICU收治的448例AP的临床资料，其中30例AP患并发PE。现将结果报告如下，并对其治疗体会进行探讨。     

重症急性胰腺炎并发胰性脑病的发病机制

胰性脑病(pancreatic encephalopathy,PE)是重症急性胰腺炎 (severe acute pancreatitis,SAP)病程中的严重并发症,其发病机制尚未完全明确,阐明引起和加剧PE的各种因素对有效防治PE具有重要意义．目前认为PE的发病机理与以下几方面因素有关:胰酶激活;细胞因子、氧自由基的过度释放; 血流动力学紊乱导致微循环障碍;ET-1／NO比值失调;低氧血症;细菌感染;水、电解质紊乱及VitB1缺乏等,上述因素可参与PE的发病过程．我们对PE上述发病机制研究进行阐述．     

胰性脑病的诊治探讨

胰性脑病(pancreatic encephalopathy, PE)是急性胰腺炎(AP),尤其是重症急性胰腺炎(SAP)的少见严重并发症,一旦发生,预后差,死亡率高,故提高对本病的早期诊断及临床治疗水平至关重要.现对2001年1月～ 2005年12月诊治的10例PE患者进行回顾分析.     

舒血宁联合奥曲肽对急性坏死性胰腺炎大鼠脑损伤的保护作用

重症急性胰腺炎（SAP）并发脑损伤,又称胰性脑病（pancreatic encephalopathy,PE）,是SAP常见的并发症之一,主要表现为定向力障碍、意识模糊、幻觉等精神状态异常。临床SAP并发PE约占同期患者的18．2％,病死率达67．0％。     

急性胰腺炎并发胰性脑病和韦尼克脑病

目的探讨急性胰腺炎（AP）并发胰性脑病（PE）和韦尼克脑病（WE）的临床特征和治疗方法。方法回顾性分析8年来收治AP病人394例的临床资料。结果AP中重症急性胰腺炎（SAP）78例，发生脑病8例，其中PE5例，WE3例。死亡3例。PE2例，WE1例，2例WE经注射维生束B1而治愈。结论PE多发生在SAP的早期或病情反复时；WE发生于SAP或AP的恢复期。禁食时间长、反复呕吐及全胃肠外营养中未补充维生素B1是导致急性胰腺炎者维生素B1缺乏，从而发生WE的重要原因。     

迟发性胰腺脑病的临床特征及处理

胰腺脑病(Pancreatic encephalopathy,PE)是胰腺炎,尤其是重症急性胰腺炎(severe acute pancreatiris,SAP)的严重并发症,死亡率高达67%～100%.     

Pathogenesis of pancreatic encephalopathy in severe acute pancreatitis

BACKGROUND: Pancreatic encephalopathy (PE) is a serious complication of severe acute pancreatitis (SAP). In recent years, more and more PE cases have been reported worldwide, and the onset PE in the early stage was regarded as a poor prognosis sign of SAP, but the pathogenesis of PE in SAP still has not been clarified in the past decade. The purpose of this review is to elucidate the possible pathogenesis of PE in SAP. DATA SOURCES: The English-language literature concern- ing PE in this review came from the Database of MEDLINE (period of 1991-2005), and the keywords of severe acute pancreatitis and pancreatic encephalopathy were used in the searching. RESULTS: Many factors were involved in the pathogenesis of PE in SAP. Pancreatin activation, excessive release of cytokines and oxygen free radicals, microcirculation abnormalities of hemodynamic disturbance, ET-1/NO ratio, hypoxemia, bacterial infection, water and electrolyte imbalance, and vitamin B1 deficiency participated in the development of PE in SAP. CONCLUSIONS: The pathogenesis of PE in SAP has not yet been fully understood. The development of PE in SAP may be a multi-factor process. To find out the possible inducing factor is essential to the clinical management of PE in SAP.     

Pancreatic encephalopathy and Wernicke encephalopathy in association with acute pancreatitis： A clinical study

AIM: To investigate clinical characteristics and therapy of pancreatic encephalopathy (PE) and Wernicke encephalopathy (WE). METHODS: In a retrospective study of 596 patients with acute pancreatitis (AP), patients with PE were compared to those with WE in regards to history, clinical manifestation, diagnosis, treatment and outcome. RESULTS: There were 93 patients with severe acute pancreatitis (SAP). Encephalopathies were discovered in 10 patients (1.7%). Six patients with PE all developed in SAP (6.5%), and three of them died (3% of SAP, 50% of PE). Four patients with WE developed in AP (0.7%), and two of them died (0.3% of AP, 50% of WE). Two patients with WE were treated with parenteral thiamine and survived. Global confusions were seen in all patients with encephalopathy. Ocular abnormalities were found. Conjugate gaze palsies were seen in 1 of 6 (16.7%) patients with PE. Of 4 patients with WE, one (25%) had conjugate gaze palsies, two (50%) had horizontal nystagmus, three (75%) had diplopia, and one (25%) had myosis. Ataxia was not seen in all patients. None of patients with WE presented with the classic clinical triad. CSF examinations for 2 patients with WE showed lightly-increased proteins and glucose. CT and MRI of the brain had no evidence of characteristic abnormalities. CONCLUSION: PE occurs in early or reiteration stage of SAP, and WE in restoration stage of SAP/AP. Ocular abnormalities are the hallmarks of WE, and horizontal nystagmus is common. It is difficult to diagnose earlier an encephalopathy as PE or WE, as well as differentiate one from the other. Long fasting, hyperemesis and total parenteral nutrition (TPN) without thiamine are main causes of thiamine deficiency in the course of pancreatitis.     

重症急性胰腺炎并发胰性脑病诊治的探讨（附11例报告）

目的：探讨重症急性胰腺炎并发胰性脑病的临床特点和诊断治疗方法。方法：回顾分析11例SAP并发PE患的临床资料。结果：本组共11例，占同期SAP的13．8％（11／80）；男性5例，女性6例；手术8例，非手术保守治疗3例；急性期PE7例，迟发性PE4例；死亡4例，存活7例，其中治愈3例，好转4例。结论：本病主要依据临床症状及排除性诊断。治疗除手术、抑制胰酶分泌、抗感染、支持疗法外，辅以强有力的脱水剂、中枢神经营养药、激素冲击治疗至关重要。     

GP-2在急性胰腺炎诊断中的临床价值

目的对血清GP-2(glycoprotein2)浓度在急性胰腺炎中的诊断价值进行研究。方法通过临床症状、血清酶学、影像学和病理学诊断的48例急性胰腺炎患者分为重症急性胰腺炎(n=28)和轻症急性胰腺炎(n=20)两组,另选择20例非胰腺炎腹痛患者作为对照组,测定他们血清中的GP-2浓度,并和他们的血清酶学结果进行比较。结果GP-2诊断急性胰腺炎的特异性为100%,高于淀粉酶(83.3%)和脂肪酶(89.6%);淀粉酶和脂肪酶水平分别在入院后的第3及第4天降至正常值上限的3倍以下,而在观察的第6天,GP-2水平仍然维持在诊断标准的5倍以上;同时在轻症急性胰腺炎和重症急性胰腺炎患者,GP-2平均水平分别为4.71U和11.30U,后者明显高于前者(P<0.05)。结论GP-2对急性胰腺炎的早期诊断特异性高,持续时间长,同时对病情的判断有一定的帮助,因此有相当的I临床应用价值。     

急性胰腺炎诊治的新理念、新技术及临床面临的难点与困惑

急性胰腺炎（AP）是最常见的消化系统急腹症之一,其中约20%为重症急性胰腺炎（SAP）,病情凶险,治疗棘 手。按病程分期进行个体化治疗的治疗理念和多学科诊治（MDT）的治疗模式的应用,显著降低了SAP的病死率。重 视AP合并症和并发症的治疗,及时选择外科手术治疗,开展高质量的临床研究,将有益于降低病死率,改善患者预后。 关键词：急性胰腺炎;多学科诊治;合并症与并发症     

The use of antibiotics for acute pancreatitis: Is there a role?

Infections due to pancreatic necrosis and abscesses are observed in one third of patients with severe acute pancreatitis (SAP). Based on results of double-blind, randomized, placebo-controlled trials, antibiotic prophylaxis in SAP is ineffective for reducing the frequency of infected necrosis and to decrease hospital mortality. Antibiotic treatment using carbapenems and quinolones is indicated on demand in patients with SAP and multiorgan failure at admission and in those with hemodynamic shock. Patients with biliary acute pancreatitis (AP) and clinically acute cholecystitis and/or cholangitis benefit from antibiotic treatment. Patients with AP associated with bacteremia, positive bronchoalveolar lavage, and urinary tract infection should receive antibiotics. In necrotizing pancreatitis, evidence-based data do not support late use of antibiotic prophylaxis after onset. Further high-quality, randomized, controlled trials are needed to evaluate antibiotic prophylaxis in the first 24 to 48 hours after SAP onset.     

Factors influencing mortality in acute pancreatitis: can we alter them?

Severe acture pancreatitis (SAP), a multisystem disease, is characterized by multiple organ system failure and additionally by local pancreatic complications such as necrosis, abscess, or pseudocyst. The rate of mortality in SAP, which is about 20% of all cases of acute pancreatitis (AP), may be as high as 25%, as in infected pancreatic necrosis. The factors that influence mortality in different degrees are various. Etiology for the episode, age, sex, race, ethnicity, genetic makeup, severity on admission, and the extent and nature of pancreatic necrosis (sterile vs. infected) influence the mortality. Other factors include treatment modalities such as administration of prophylactic antibiotics, the mode of feeding (TPN vs. enteral), ERCP with sphincterotomy, and surgery in selected cases. Epidemiological studies indicate that the incidence of AP is increasing along with an increase in obesity, a bad prognostic factor. Many studies have indicated a worse prognosis in idiopathic AP compared to pancreatitis induced by alcoholism or biliary stone. The risk for SAP after ERCP is the subject of extensive study. AP after trauma, organ transplant, or coronary artery bypass surgery is rare but may be serious. Since Ranson reported early prognostic criteria, a number of attempts have been made to simplify or add new clinical or laboratory studies in the early assessment of severity. Obesity, hemoconcentration on admission, presence of pleural effusion, increased fasting blood sugar, as well as creatinine, elevated CRP in serum, and urinary trypsinogen levels are some of the well-documented factors in the literature. The role of appropriate prophylactic antibiotic therapy although still is highly controversial, in properly chosen cases appears to be beneficial and well accepted in clinical practice. Early enteral nutrition has gained much support and jejunal feeding bypassing the pancreatic stimulatory effect of it in the duodenum is desirable in selected cases. The limited role for endoscopic sphincterotomy in patients with demonstrated dilated CBD with impacted stone and evidence of impending cholangitis is well documented. Surgery in AP other than for removal of the gallbladder is often limited to infected pancreatic necrosis, pseudocysts, and pancreatic abscess and in some cases of traumatic pancreatitis with a ruptured duct system. The progress in the understanding of the role of cytokines will over us opportunities to use immunomodulatory therapies to improve the outcome in SAP.     

Clinical characteristics and management of patients with early acute severe pancreatitis： Experience from a medical center in China

AIM: To study clinical characteristics and management of patients with early severe acute pancreatitis (ESAP). METHODS: Data of 297 patients with severe acute pancreatitis (SAP) admitted to our hospital within 72 h after onset of symptoms from January 1991 to June 2003 were reviewed for the occurrence and development of early severe acute pancreatitis (ESAP). ESAP was defined as presence of organ dysfunction within 72 h after onset of symptoms. Sixty-nine patients had ESAP, 228 patients without organ dysfunction within 72 h after onset of symptoms had SAP. The clinical characteristics, incidence of organ dysfunction during hospitalization and prognosis between ESAP and SAP were compared. RESULTS: Impairment degree of pancreas (Balthazar CT class) in ESAP was more serious than that in SAP (5.31+/-0.68 vs 3.68+/-0.29, P<0.01). ESAP had a higher mortality than SAP (43.4% vs 2.6%, P<0.01), and a higher incidence of hypoxemia (85.5% vs 25%, P<0.01), pancreas infection (15.9% vs 7.5%, P<0.05), abdominal compartment syndrome (ACS) (78.3% vs 23.2%, P<0.01) and multiple organ dysfunction syndrome (MODS)(78.3% vs 10.1%, P<0.01). In multiple logistic regression analysis, the main predisposing factors to ESAP were higher APACHE II score, Balthazar CT class, MODS and hypoxemia. CONCLUSION: ESAP is characterised by MODS, severe pathological changes of pancreas, early hypoxemia and abdominal compartment syndrome. Given the poor prognosis of ESAP, these patients should be treated in specialized intensive care units with special measures such as close supervision, fluid resuscitation, improvement of hypoxemia, reduction of pancreatic secretion, elimination of inflammatory mediators, prevention and treatment of pancreatic infections.     

Gastrointestinal dysmotility in patients with acute pancreatitis

BACKGROUND AND AIMS: Gut-origin bacterial translocation is one of the major causes of pancreatic necrotic tissue infection in patients with severe acute pancreatitis (SAP). The gastrointestinal dysmotility is supposed to be the fundamental event in this process. To test this hypothesis, alteration of colonic transit time (CTT) in patients with acute pancreatitis (AP) was investigated. In order to evaluate the possible mechanisms involved in gastrointestinal dysmotility, changes of serum motilin (MTL), cholecystokinin (CCK) and vasoactive intestinal peptide (VIP) in patients with AP were also measured. METHODS: Twenty-four non-consecutive patients with AP and 25 controls were included in this study. The diagnosis of AP was based upon clinical features, biochemical indices and radiological investigation. The severity of AP at admission was evaluated according to the APACHE-II and Balthazar computed tomography (CT) scoring system. Total and segmental CTT in patients with AP and in controls were determined by ingestion of radiopaque markers (Sitzmarks(R)) according to the modified Metcalf's method. Meanwhile, serum MTL and CCK were assessed using radioimmunoassay (RIA), and serum VIP was measured by using ELISA in this study. RESULTS: Compared to the controls, the total CTT and segmental CTT (mainly right and left hemicolon) were prolonged significantly in 10 patients with SAP and 14 patients with MAP; P < 0.05. Moreover, the total CTT and segmental CTT were markedly more delayed in patients with SAP than in patients with MAP; P < 0.05. The concentrations of serum MTL and CCK were significantly decreased in both MAP and SAP patients compared with those in controls (P < 0.01). There was no significant differences in serum MTL and CCK levels between the SAP and MAP groups; P > 0.05. In addition, the concentration of serum VIP was increased in AP patients, and it reached statistical significance in patients with SAP (P < 0.05). CONCLUSIONS: In conclusion, gastrointestinal dysmotility often occurred in patients with AP, especially more severely in SAP patients. One of the possible mechanisms might be related to the synergic actions of gut hormones, such as MTL, CCK and VIP.