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。     

重症急性胰腺炎并发Wernicke脑病

Wernicke脑病由Wernicke于1881年首先提出,是指由于维生素B_1（硫胺素）缺乏所导致的中枢神经系统代谢性疾病,患者病情危重,若不能及时确诊和治疗,其病死率可高达50%以上。由于重症急性胰腺炎（SAP）禁食时间长,肠外营养及肠内营养中未注意补充维生素B_1,患者易出现维生素B_1缺乏而发生Wernicke脑病。我科收治SAP并发Wernicke脑病患者11例,经精心治疗与护理,效果满意。     

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PE37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.     

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的临床特征

急性胰腺炎出现脑损伤称为胰性脑病（pancreaticencephalopathy,PE）,其临床表现主要是在急性胰腺炎发生和发展过程中出现神经精神症状。PE临床表现具有多样性,且死亡率高,预后差,但由于发生率相对较低,故有关PE的临床报道并不多见。本文回顾性分析了我院近三年急性胰腺炎患者中8例较完整的PE临床资料,就PE的临床特征及其预后报道如下。     

水溶性维生素缺乏致迟发性胰性脑病的诊治

胰性脑病(pancreatic encephalopathy,PE)的病因复杂多样,尤其胰腺炎后期并发胰性脑病疗效较差。本文总结自1998年10月至2001年12月收治的6例急性重症胰腺炎(SAP)后期并发胰性脑病的诊治体会。     

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．     

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。     

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.     

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.     

胰性脑病的综合治疗进展

胰性脑病（PE）是重症急性胰腺炎的严重并发症之一,以脑神经症状为主要表现,虽然此并发症发生率低,但却有较高的病死率。目前,对PE的治疗尚未取得根本性进展,还缺乏特异性方法,仍以综合治疗为主,本文就PE治疗进展作一综述。     

Thiamine deficiency and wernicke's encephalopathy in AIDS

Several neuropathological reports in the last 5 years have described brain lesions characteristic of Wernicke's Encephalopathy in patients with AIDS. Using the erythrocyte transketolase activation assay, we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse nor were there clinical signs of Wernicke's Encephalopathy. Thiamine deficiency in these patients most likely results from the cachexia and catabolic state characteristic of AIDS. In view of (i) the confirmed neuropathological evidence of Wernicke's Encephalopathy in AIDS patients, (ii) the significant thiamine deficiency in these patients and (iii) the difficulties of clinical diagnosis of Wernicke's Encephalopathy, it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex.     

大剂量维生素C对急性胰腺炎患者细胞免疫功能的影响

背景：急性胰腺炎（AP）患者存在细胞免疫功能改变和血浆维生素C（Vti C)含量降低，Vit C具有抗氧化和提高机体免疫力的作用。目的：观察大剂量Vit C对AP患者细胞免疫功能的影响。方法：将84例AP患者随机分为治疗组和对照组，40例健康志愿者作为正常对照。治疗组予Vit C 10g稀释于5％葡萄糖500ml中静脉滴注，每日1次，连用5天；对照组予Vit C1g稀释于5％葡萄糖500ml中静脉滴注，每日1次，连用5天。观察正常对照组和两组患者治疗前后血浆Vit C含量和T淋巴细胞亚群的变化。结果：AP患者CD3和CD4阳性细胞百分比较正常对照组明显下降，其中重症急性胰腺炎（SAP）组的CD4阳性细胞百分比和CD4／CD8比值较轻症急性胰腺炎（MAP）组下降更为明显（P＜0．05）。大剂量Vit C治疗后，治疗组SAP患者的CD4阳性细胞百分比和CD4／CD8比值较对照组明显升高（P＜0．05）。结论：AP患者，特别是SAP患者存在细胞免疫功能损害，静脉输入大剂量Vit C对改善SAP患者的细胞免疫功能有一定作用。     

Wernicke encephalopathy hearing loss and palinacousis

Wernicke encephalopathy (WE) is a neurological emergency that develops in the setting of thiamine deficiency, and is characterised by symptoms of confusion, ophthalmoplegia and gait ataxia. Less recognised signs and symptoms include vestibular dysfunction, hearing impairment, peripheral neuropathy, and in severe cases, coma. This case study describes a non‐alcoholic patient, who presents with significant auditory and vestibular changes in addition to the classic symptoms of WE. This case report describes a non‐alcoholic patient who developed deafness, severe horizontal canal paresis and symptoms of palinacousis in the setting of WE as a complication of a recent gastric sleeve operation.     

Non-alcoholic Wernicke’s encephalopathy with cortical involvement and polyneuropathy following gastrectomy

In this study, we present the clinical manifestations, brain magnetic resonance imaging (MRI) and concurrent polyneuropathies in two patients with non-alcoholic Wernicke’s encephalopathy (WE) after gastrojejunostomy (Billroth II) anastomosis procedures. These patients developed sub-acute onset of disorientation and disturbance of consciousness following several weeks of poor intake. Peripheral neuropathy of varying severity was noted before and after the onset of WE. Brain MRI of the patients showed cerebellar vermis and symmetric cortical abnormalities in addition to typical WE changes. Electrophysiological studies demonstrated axonal sensorimotor polyneuropathy. Prompt thiamine supplement therapy was initiated and both patients gradually recovered, however mild amnesia was still noted 6 months later. We reviewed non- alcoholic WE with atypical cortical abnormalities in English language literatures and identified 29 more cases. Eight out of 31 (25.8%) patients died during follow-up. Nine patients with gait disturbance or motor paresis had showed hyporeflexia in neurological examinations. In addition to classic triad, seizure was recorded in seven patients. Dietary deprivation is a risk factor for non-alcoholic WE among elderly patients receiving gastrointestinal surgery. The prognosis is good after thiamine supplement therapy. Recognizing the MRI features and predisposing factors in patients who have undergone gastrectomy can aid in the diagnosis and management.

     

Wernicke's encephalopathy in a patient with schizophrenia

Clinically, we most often associate Wernicke's encephalopathy (WE) with an alcohol abusing population. However, it is important to consider other causes of malnutrition and vitamin deficiency as risk factors for the development of this disorder. We present a case of a 51-year-old man with schizophrenia and malnutrition who presented with delirium, ophthalmoplegia, and seizures. He responded rapidly to the administration of IV thiamine. Because of the high rate of mortality and morbidity, WE should be high on the differential of any patient at risk for malnutrition or with ophthalmoplegia, regardless of alcohol history. This is particularly important in psychiatric patients where the syndrome may be masked and thus treatment delayed.