皮质类固醇治疗严重急性胰腺炎
Int J Clin Exp Pathol 2015;8(7):7654-7660 /ISSN:1936-2625/IJCEP0007864Review ArticleCorticosteroid therapy for severe acute pancreatitis: a meta-analysis of randomized, controlled trialsLi-Hua Dong1,2, Zhong-Min Liu1, Shi-Ji Wang1, Shu-Jie Zhao1, Dong Zhang1, Ying Chen1, Yu-Shan Wang11Intensive Care Unit, First Affiliated Hospital of Jilin University, Changchun 130021, China; 2Intensive Care Unit, Second Affiliated Hospital of Jilin University, Changchun 130041, ChinaReceived March 12, 2015; Accepted June 10, 2015; Epub July 1, 2015; Published July 15, 2015Abstract: Background: Recent reports about the benefits of corticosteroid therapy in patients with severe acute pancreatitis (SAP) have shown conflicting results. We aimed to explore the effects of corticosteroid therapy in SAP patients on patient outcomes by performing a meta-analysis. Methods: Databases (Medline, EMBASE, Web of Sci-ence, PubMed, Cochrane Library, Chinese Biomedicine Database, and China Academic Journal Full-Text Database) were queried for all relevant, randomized, controlled trials investigating corticosteroid therapy in patients with SAP. Results: Six randomized, controlled trials including 430 SAP patients were identified. Corticosteroid therapy for SAP was associated with reductions in the length of hospital stay, the need for surgical intervention, and the mortality rate (weighted mean difference[WMD]: -9.47, 95% confidence interval [CI]: -16.91 to -2.04, P = 0.01; odds ratio [OR]: 0.35, 95% CI: 0.18-0.67, P = 0.002; OR: 0.45, 95% CI: 0.22-0.94, P = 0.03). There were no significant differ-ences in the complication rates or Physiology and Chronic Health Evaluation II (APACHE II) scores in patients with or without corticosteroid therapy. Conclusion: Corticosteroid therapy may improve outcomes in patients with SAP. Keywords: Corticosteroid, severe acute pancreatitis, meta-analysisIntroductionAcute pancreatitis (AP) is initiated by autodiges-tion, defined as the activation of proteolytic and lipolytic enzymes within acinar cells and/or pancreatic ducts, which leads to inflammation and destruction of the pancreatic tissue. AP is associated with a high mortality rate, and its incidence has been increasing in recent years. Standard therapy for AP includes bowel rest, pain control, intravenous fluids, and correction of electrolyte and metabolic abnormalities. Patients with more severe presentations are treated with early enteral nutrition and are closely monitored to maintain adequate organ perfusion.Despite these therapeutic interventions, ap- proximately 20% of patients with severe acute pancreatitis (SAP) will progress to systemic inflammatory response syndrome (SIRS), com-plicated by shock, multiorgan failure, and even death, within the first 72 hours after admission [1, 2]. SIRS is a response to the widespread systemic effects of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin (IL)-β, IL-6, and phospholipase A2 (PLA2). These circulating cytokines play major roles in SAP progression to a systemic process by activating the vascular endothelium, increas-ing capillary permeability, and triggering the migration of leukocytes into tissues throughout the entire body [3, 4]. Inhibitors of these proin-flammatory cytokines can be beneficial for reducing the severity of SAP. Corticosteroids have shown beneficial effects in animal models of AP and SAP [5-7], poten-tially due to their effects on inflammatory medi-ators, such as cytokines, endotoxins, and free radicals [8, 9]. Corticosteroids were initially reported to induce pancreatitis in susceptible patients [10]. However, in 1952, corticosteroids were used successfully as nonspecific anti-inflammatory agents to treat AP [11]. Following this report, additional studies showed that cor-ticosteroids suppress the release of inflamma-tory cytokines in AP [12-14]. In 1997, Lazar and colleagues found that rats treated with hydro-cortisone showed diminished IL-6 levels [15].Corticosteroid and SAPSAP patients exhibit an influx of leukocytes into the pancreas [16].Corticosteroids may relieve disease symptoms by inhibiting leuko-cyte activation[17]. Corticosteroids increase the activity of selected protease inhibitors [17, 18] and indirectly inhibit PLA 2 synthesis [19].Administration of glucocorticoids attenuatespancreatic damage by protecting acinar cells[20]. When administered shortly before endo -toxin, hydrocortisone greatly reduced the clini-cal response to endotoxin in normal volunteers[21]. This interaction with endotoxin may repre-sent another mechanism by which corticoste-roids act.Despite the positive results in animal models,the impact of corticosteroid therapy in patientswith SAP remains unclear. Wan et al [22] foundthat corticosteroid therapy in SAP patients withSIRS decreased the risk of developing acuterespiratory distress syndrome and shortenedthe length of hospitalization. Similarly, Xiang etal [23] reported that corticosteroid therapyameliorated and abbreviated pathogenesis.However, most studies have not concludedwhether corticosteroid therapy is useful inreducing rates of complications, surgery, andmortality in SAP patients. Therefore, given thepositive effects in animal experiments [24, 25],sone OR hydrocortisone OR prednisone ORprednisolone acetate OR methylprednisolo- ne)” AND “(“pancreatitis” [MeSH] AND “gluco-corticoids” [MeSH])”. References of selected studies were searched by hand.Inclusion and exclusion criteria Studies were included in the meta-analysis if they were randomized controlled trials (RCTs) enrolling participants, of any sex or ethnic ori -gin, who had been diagnosed with SAP on the basis of clinical findings, elevated C-reactive protein and serum amylase concentrations, and computed tomography (CT) results. SAP was defined by a history of typical abdominal pain associated with an increase in serum lipase values of at least twofold. SAP diagnosis was confirmed by CT. Severity was predicted by Ranson’s score (≥ 3), Balthazar CT (≥ II), Acute Physiology and Chronic Health Evaluation II (APACHE II) scores (> 8), local complications (e.g., pancreatic necrosis, pseudocyst, and pancreatic abscess), or organ failure. Data on at least one of the following outcomes was required for inclusion: complication rates, changes in APACHE II scores, length of hospital stay, need for surgical intervention, or mo-rtality.Figure 1. Six original RCTs were selected from 430 articles obtained from theelectronic searches of MEDLINE, EMBASE, Web of Science, PubMed, CochraneLibrary, Chinese Biomedicine Database, and China Academic Journal Full-Text Database. These RCTs were published from 2002 to 2010 and included 320 patients with SAP.we performed a meta-anal -ysis to explore the potential effects of corticosteroids in patients with SAP.Methods Search strategyWe performed a literature search in several electronic databases (i.e., MEDLINE, EMBASE, Web of Science, PubMed, Cochrane Library, Chinese Biomedicine Da- tabase, and China Acade- mic Journals Full-Text Da- tabase), without any lan-guage restriction. The fol -lowing search terms were used: “(acute pancreatitis OR severe acute pancreati-tis) AND (steroid OR cortico-steroid OR cortisol OR glu-cocorticoid OR dexametha-Data extraction and methodological quality Two reviewers independently extracted the study data, including authors, publication year, study design, population, intervention, dura-tion, and outcome. Disagreement was resolved by discussion. Methodological quality of the studies was scored by the Jadad scale, on the basis of the randomization method, allocation concealment, blinding of outcome assessment, and follow-ups. All included studies had a Jadad score of at least 2.Statistical analysisData were analyzed with Review Manager 5.0. Dichotomous data were presented as odds ratios (ORs) with 95% confidence intervals (CIs). Statistical heterogeneity was measured using the chi-squared test and the inconsistency index (I2). A P-value < 0.05 in the chi-squared test was considered to indicate statistically sig-nificant heterogeneity. The random-effects model was applied when obvious heterogeneity was present; otherwise, the fixed-effects model was used.ResultsThe literature search yielded 430 articles pub-lished from 1996 to 2013. After reviewing each publication, we selected six original RCTs that met the study criteria. These RCTs were pub-lished from 2002 to 2010 and included 320 SAP patients (Figure 1). Characteristics of each study are shown in Table 1. Allocation conceal-ment was adequate in three studies. Blinding was not mentioned in any study. Follow-ups were completed in all studies. Baseline charac-teristics of patients included in each study were well matched between the treatment and con-trol groups.There was no significant difference in the com-plication rate between the experimental and control groups (OR: 0.65, 95% CI: 0.11 to 3.85, P = 0.64). Three RCTs [26-28] reported this out-come, with significant heterogeneity being observed among them (I2 = 83%, P = 0.003, Figure 2A). There was no significant difference in the APACHE II score changes between the two groups (weighted mean difference [WMD]: 1.07, 95% CI: -2.75 to 4.9, P = 0.58). Three RCTs [23, 28, 29] reported this outcome, with significant heterogeneity being observed among them (I2 = 96%, P < 0.00001, Figure 2B). Corticosteroid therapy had a significant effect on the length of hospital stay in patients with SAP (WMD: -9.47 95% CI: -16.91 to -2.04, P = 0.01). Six RCTs [22, 23, 26-29] reported this outcome, with significant heterogeneity being observed among them (I2 = 96%, P < 0.00001, Figure 2C).Significantly fewer patients in the experimental group required surgery compared to the control group (OR: 0.35, 95% CI: 0.18-0.67, P = 0.002). Included studies [22, 26-28]were homoge-neous (I2 = 0%, P = 0.40, Figure 2D). Four RCTs [22, 26, 28, 29] assessed the effect of cortico-steroid therapy on reducing the incidence of mortality.The mortality rate was significantly lower in the experimental group than in the con-trol group(OR 0.45, 95% CI: 0.22-0.94, P = 0.03). Homogeneity among the studies was observed (I2 = 0%, P = 0.68, Figure 2E). DiscussionIn this meta-analysis of six RCTs, corticosteroid therapy reduced the length of hospitalization, the need for surgical intervention, and the mor-tality rate. Corticosteroid use not only lowered pain and hospitalization expenses, but also extended the survival of SAP patients. However, some researchers found an increased mortality rate after administering a high dose of h ydro-cortisone treatment (100 mg/kg) [30]. Thus, we conclude that a relatively low dose (10 mg/ kg)corticosteroids is helpful in the treatment of SAP.Five of the six RCTs examined the effect of dexamethasone in the treatment of SAP, and one investigated the effect of methylpredniso-lone. The dexamethasone dosages differed in each study (range: 20-120 mg/day), and the duration of treatment ranged from 3 to 14 days. Wan et al. [22] studied the compound effect of dexamethasone and a Chinese herb decoction. Zhang et al. [28] studied the combined use ofFigure 2. Forest plots of the effects of corticoid treatment for patients with severe acute pancreatitis. Forest plots display values of the weighted mean difference (WMD), 95% confidence interval (CI), and odds ratio (OR). The dia-mond indicates the global estimate and its 95% CI.6% hydroxyethyl starch, dexamethasone, and furosemide. Such combined interventions may have complicated the results, but the number of studies was limited. The diagnosis of SAP was based on similar, but not identical, criteria. Studies diagnosed SAP according to the “Atlanta” criteria [31], the National Conference for Pancreatic Diagnosis Standards [32], and the Guide to Diagnosis and Treatment of Acute Pancreatitis in China [33]. Although all of the studies were prospective and randomized, none was blinded. Therefore, the possibility of investigator bias must be considered.In conclusion, corticosteroid therapy can bene-fit SAP patients by reducing the length of hospi-tal stay, the need for surgical intervention and the mortality rate. Future well-designed RCTs of adequate size and duration are needed to explore the effects of corticosteroids in SAP patients.AcknowledgementsThis study was supported by a grant from National Health and Family Planning Com- mission of the People’s Republic of China (Special Fund for Health Scientific Research in the Public Interest). Program: No. 201202011. Disclosure of conflict of interestNone.Address correspondence to: Yu-Shan Wang, In- tensive Care Unit, First Affiliated Hospital of Jilin University, Changchun 130021, China. E-mail: don-gleehua@References[1] Rau BM, Bothe A, Kron M, Beger HG. 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犬急性胰腺炎的诊断与治疗
犬急性胰腺炎的诊断与治疗王兴华（山东省烟台市海阳市二十里店镇畜牧兽医站山东烟台265100）胰腺炎是指胰腺分泌的胰酶被激活后对自身器官的消化作用所引起的炎症。
在犬的内科病中，胰腺炎较为常见。
随着国内外对犬胰腺炎的研究，犬胰腺炎的诊断与治疗已经取得很大进展，不过因为资料有限，目前人们对犬胰腺炎的发病机理仍然不是十分明朗。
本文中的犬急性胰腺炎典型病例，通过基础检查和实验室检查确诊为犬的急性胰腺炎，然后对其进行"饮食调理为主，药物治疗为辅"的治疗方法进行治疗，最终病犬完全康复。
腺炎；犬；诊断；治疗现阶段犬胰腺炎是犬内科病中发病率最高的一种内科病，犬胰腺炎临床的典型症状是腹痛、呕吐、拉稀多还伴有脱水，有急性胰腺炎和慢性胰腺之分[1]。
急性胰腺炎是胰腺外分泌腺酶被激活，引起胰腺组织自身及周围组织消化、水肿、出血甚至坏死的炎症反应。
临床主要以急性腹痛、呕吐、血胰酶增高、病情重、并发症多等为特点[2]。
病情轻者以胰腺水肿为主，临床多见，病情常呈自限性，预后良好；病情重者胰腺出血坏死，常继发感染、腹膜炎和休克等，病死率高。
犬胰腺炎的发病机制主要有胰腺微循环障碍、胰腺胰酶自身消化、肠道细菌移居到胰腺组织内，还有全身的炎症反应，其中最主要考虑的发病机制就是胰腺分泌的胰液把自己消化了[3]。
目前临床上较为常见的病例大多可能是暴饮暴食导致高脂蛋白血症有关，并且临床上这类病例多呈急性，并且有典型的“作揖”样姿势，其发生的机制可能与血液中高脂、高蛋白引起胰液大量分泌有关，还有一种较为常见的情况是某些病犬患有其他胃肠道疾病并发的胰腺炎，这类病例大多可能是因为十二指肠内容物反流引起的。
十二指肠液反流进入胰管，十二指肠液中含有肠肽酶、激活的胰酶、细菌和胆汁都可以引起胰腺炎的发生[4]，具体可能诱发胰腺炎的因素见表1。
1材料与方法1.1材料病例：贵宾犬，雌性，2岁，体重7kg ，已绝育。
1）主要仪器威尔德兽用B 超、SEDECAL 兽用DR 、爱德士血常规、爱德士生化分析仪、cPL 试板。
重症急性胰腺炎如何治疗
重症急性胰腺炎如何治疗作者：谭忠桦来源：《幸福家庭》2020年第13期重症急性胰腺炎对人体生理扰乱较大，极易损害患者体内的重要脏器，有较高的致死率，严重时甚至会导致患者骤然死亡。
重症急性胰腺炎病因复杂，治疗难度较大。
医生需要对患者病情做全方位评估，从而选取最适合的方案进行治疗。
本文主要介绍重症急性胰腺炎的治疗方法。
重症急性胰腺炎的发作病理为人体局部酶被激活，导致区域性炎症迅速升级为全身性急性炎症，若未及时治疗会导致组织严重损伤，自身器官也会因此衰竭，从而对患者生命安全造成极大的威胁。
重症急性胰腺炎会引发各种感染性并发症，导致患者死亡风险呈直线上升。
所以重症急性胰腺炎患者要尽快去医院就诊，并在重症监护室（ICU）内接受全天候生命体征监测。
重症急性胰腺炎的治疗原则为确定病因、控制炎症。
一般情况下，重症急性胰腺炎患者病情较重，通常会采取静脉补液、镇痛、维持机体电解质平衡、营养干预等常见方式，本质上即先确保患者生命体征，再去尽可能地治愈患者，以挽救患者生命。
1.医生通常选择生理盐水或者脓毒症相关药液对患者进行静脉补液，防止重症急性胰腺炎患者肾脏等脏器衰竭。
在此基础上，医生要全程做好患者的体征监测工作，明确其血管外肺水等基本参数，以确保治疗的针对性。
2.胰腺以及胰腺外感染是重症急性胰腺炎复杂化的根本。
为防止胰腺坏死引发单器官或者多器官衰竭，医生要根据患者病情实况，合理计算抗菌药物使用时间。
相关医学文献研究表明，并发患者症状显现3天以内使用抗菌药物，其病死率和感染性胰腺坏死发生风险会有效减低。
1/3重症急性胰腺炎患者都会发生胰腺外感染，多以菌血症或者肺部感染为主要表现。
所以科学使用抗菌药物，也是治疗重症急性胰腺炎的主要方式。
3.营养干预也是临床医学认可的一种治疗重症急性胰腺炎的方法。
患者进入重症监护室后1～2天，其肠内营养吸收率降低，而营养干预可以有效防止患者病情恶化。
但该方法的治疗效果受限于患者病情和机体素质。
急性胰腺炎(外科)
急性胰腺炎（外科）【概述】急性胰腺炎为腹部外科常见病，近年来重型胰腺炎发病率逐渐增多。
由于它对生理扰乱大，而且对各重要脏器损害明显，故死亡率甚高。
有时可引起骤然死亡。
重型胰腺炎死亡率为20％，有并发症者可高达50％。
临床病理常把急性胰腺炎分为水肿型和出血坏死型两种。
这种分类法固然可以说明其病理状况，但胰腺炎的病情发展不是静止的，随着胰管的梗阻程度，以及胰腺间质血管（动、静脉及淋巴管）的改变，其病理变化是在动态发展着。
因此，以急性轻型胰腺炎和重型胰腺炎分类的方法，较适合于临床的应用。
重型胰腺炎（如出血坏死型）临床医生往往十分重视，但轻型胰腺炎（如水肿型）亦不能忽视，它可以发展为重型胰腺炎。
【诊断】急性胰腺炎分为轻型及重型两类。
前者胰腺的损害轻微为单纯性水肿，少有渗出，CT上几无阳性发现，后者胰腺的损害十分严重，为广泛的出血、坏死。
急性水肿型胰腺炎发病率约占90%，死亡者较少。
而出血坏死型胰腺炎死亡率甚高可达20～50%。
多年来人们对急性出血坏死性胰腺炎进行了深入研究，特别是对其早期诊断以及全身生理的扰乱，提出了一些指标，拟求将死亡率降低到最低水平。
由于出血坏死性胰腺炎的病理变化、病理生理改变的轻重程度不一，当前几乎找不到某一个单项指标：如临床表现、化验结果、影像检查等，能够作为确定诊断的依据，更不可能用某一指标能阐明其病理变化的严重性和预后的变化。
自从1974年Ranson提出对出血坏死型胰腺炎用几个指标来衡量其病变程度、手术指征和/或预后的估计以来，相继有许多学者提出对急性出血坏死性胰腺炎的判断，以及对其预后的评估，各有其代表性。
现将临床常用的几种标准简介于下：1.Ranson标准：Ranson于1974年提出预测急性胰腺炎严重性的指标11项（表一）。
表一 Ranson标准此标准已应用了20年，目前仍用于临床。
在这11项中，阳性指标越多越能肯定病变的严重性，而且预后越差。
6年报一（1980年）Ranson总结了一些重型胰腺炎的病理与临床后，提出：具备11项指标中的1～2项为轻型，可采取姑息疗法治疗，死亡率为0.9%；若上述11项指标中具备3项以上者为重型胰腺炎，应予以手术治疗，死亡率很高，可达50～60%。
急性胰腺炎用药指南1
急性胰腺炎用药指南【概述】急性胰腺炎是多种原因导致胰酶在胰腺内被激活后引起胰腺组织自身消化、水肿、出血甚至坏死的炎症反应。
临床上以急性上腹痛、呕吐、腹胀、发热和血中胰酶升高等为主要特点，病情程度轻重不等，轻者以胰腺水肿为主，临床多见，病情常呈自限性，预后良好，又称为轻型急性胰腺炎。
少数重症患者的胰腺出血坏死，常继发感染、腹膜炎和休克等多种并发症，病死率高，称为重症急性胰腺炎。
【诊断要点】1.有引起胰腺炎的相关致病因素如胆石症等胆道疾病、大量饮酒、暴食暴饮、手术、创伤、高钙血症、高脂血症等。
约15%胰腺炎的原因不明，称为特发性胰腺炎。
2.临床表现典型的急性胰腺炎腹痛特点为突发、程度较剧烈、持续性，可有阵发性加剧，主要位于中上腹，可伴有腰背部带状放射，弯腰和蜷曲体位常可好转，进食后易加剧。
可伴有呕吐、腹胀、发热，重症患者可出现低血压、呼吸困难、休克等。
轻症患者主要体征为中上腹压痛，重症患者常可出现肠麻痹、腹膜刺激征等体征。
3.实验室检查血清和尿中的淀粉酶和脂肪酶明显升高，一般高于正常值上限的3倍以上。
4.影像学检查腹部B超和增强CT常可显示肿胀的胰腺，胰腺周围渗出以及是否存在出血坏死等。
5.区分重症胰腺炎在临床上十分重要，具有评价预后和指导治疗的价值，有以下改变时应考虑重症胰腺炎，如休克表现、腹膜刺激征表现、Cullen征、Grey-Turner征、血钙＞2mmol/L、血糖＞11.22mmol/L、C反应蛋白明显升高、影像学检查提示胰腺受损严重等。
【药物治疗】药物治疗应建立在病因治疗和基本治疗基础之上，包括禁食、胃肠减压、静脉输液支持等。
1.抗菌药物主要用于胆源性胰腺炎、重症胰腺炎和有感染证据的胰腺炎患者。
比如如头孢菌素（如头孢硫脒、头孢西丁、头孢唑肟等），静脉滴注（8-12小时一次），疗程不定，一般随着病情好转或感染控制而停用。
一般联合应用奥硝唑，以加强抗厌氧菌效果，一般剂量为1g每日1次，静脉滴注。
急性胰腺炎(Acute Pancreatitis)
2）上腹压痛： 反跳痛
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3）上腹肿块：压痛性 胰腺肿大 粘连性
囊肿性
4）手足搐搦
少数起病急:症状→休克,似心源性/失血性
猝死 暴发性胰腺炎
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五、预后
水肿型：3~5天好转 →1W左右症状完全消失 出血坏死型: 2~3W恢复，易成慢性 少数起病急:症状→休克,似心源性/失血性
猝死 暴发性胰腺炎
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四、临床表现：
发病率：占尸检1%，占住院27% 年龄：20-60 男30-50 女较男轻 性别：男：女 < 1 相近或女多 1、症状： 1）腹痛 轻重不一 性质：钝 、剧、绞、刀割 持续性或阵发性加重 餐后1~2小时或脂肪餐后逐渐加重 部位：剑下，左右季肋，向腰背部扩散 特殊体位：仰卧加重；屈曲位稍缓。
急性坏死型：局限或弥漫实质坏死
胰表面、大网膜、后腹膜、肠系膜 →黄白色坏死灶 重症在坏死灶加出血 胰黑褐色、粥状、崩毁坏死
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胰腺黑褐色崩毁坏死
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重症在坏死灶加出血
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继发感染时： 化脓 脓肿 镜下：腺泡细胞凝固坏死，消失 实质出血，小叶间水肿，淋巴管炎， 血管炎，血栓 炎细胞浸润 临床：危重 并发症多 常导致死亡
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X线：肠麻痹时 → 液面
EKG： 胰腺T波：低平或倒
ST：↓与休克，电解质紊乱有关， 病好立好。
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影像学在诊断及分级中的作用
增强CT是目前诊断AP最佳影像检查 -A级：正常，计0分； -B级：胰腺肿大，少量胰周积液，计1分； -C级：除B级变化外，胰腺周围软组织轻度改 变，计2分； -D级：除C级变化外，胰腺周围软组织明显改 变，胰周积液不超过一个部位，计3分； -E级：胰周多部位积液或积脓，计4分。
急性胰腺炎治疗方案
急性胰腺炎治疗方案急性胰腺炎是一种严重的胰腺疾病，其特征为胰腺的炎症和组织损伤。
这种疾病通常由胆石堵塞胰管或胰腺组织受损引起。
急性胰腺炎的治疗需要全面的方法和一系列的治疗措施。
首先，治疗急性胰腺炎的第一步是停止胰酶的活动。
由于胰酶会导致胰腺自身消化，停止或减少其分泌对于治疗急性胰腺炎非常重要。
为此，病人通常需要暂时禁食，并使用胰酶抑制剂。
这些药物可以减少胰酶的产生，并减轻胰腺的压力。
其次，控制疼痛是治疗急性胰腺炎的关键。
急性胰腺炎往往伴随着严重的胰腺和上腹部疼痛。
为了减轻疼痛，医生通常会给患者开具止痛药，如阿片类药物和非甾体抗炎药。
但需要注意的是，这些止痛药物不能超过推荐剂量，并应在医生的指导下使用，以避免引起副作用。
另外，液体的管理也是治疗急性胰腺炎的重要方面。
由于胰腺炎导致的炎症反应和胰腺组织损伤，往往造成体内大量的液体丢失。
为了补充体内的液体和预防脱水，病人通常需要静脉输液。
在特殊情况下，可能需要通过胃肠道或肠外途径进行营养补充。
除了上述治疗措施，药物治疗也是管理急性胰腺炎的重要手段之一。
例如，抗生素可用于预防和治疗胰腺炎相关的细菌感染。
然而，对于无细菌感染的病例，存在使用抗生素的争议。
在某些情况下，可能需要使用其他药物，如抗炎药、抗氧化剂和免疫调节剂等，以减轻炎症反应和胰腺组织损伤。
在严重的病例中，可能需要手术干预来治疗急性胰腺炎。
手术的目的是清除胰腺周围的炎性渗出物和坏死组织，减轻胰腺的压力，恢复胰腺的功能。
手术干预还可以通过石切除或改善胆道引流来预防将来的胰腺炎发作。
总的来说，治疗急性胰腺炎需要综合考虑病情的严重程度和个体特点。
医生通常会根据患者的条件制定个性化的治疗方案。
早期诊断和及时治疗对于急性胰腺炎的疗效和预后至关重要。
因此，患者在出现胰腺炎相关症状时，应及时就医并遵循医生的治疗建议，以期获得最佳的治疗效果。
输甲强龙的副作用
输甲强龙的副作用甲强龙用于某些内分泌疾病的替代治疗，糖皮质激素仅仅是一种对症治疗的药物，不知道大家对输甲强龙的副作用了解吗?下面是店铺为你整理的输甲强龙的副作用的相关内容，希望对你有用!输甲强龙的副作用可能会观察到全身性副反应。
尽管在短期治疗时很少出现，但仍应仔细随访。
这是类固醇治疗的随访工作的一部分，并不针对某一药物。
糖皮质激素(如甲泼尼龙)可能的不良反应为：感染和侵袭：感染、机会性感染。
免疫系统异常：药物过敏，(包括类似严重过敏反应或严重过敏反应，伴有或不伴有循环虚脱、心脏停搏、支气管痉挛)。
内分泌异常：类库欣综合征、垂体功能减退症、类固醇停药综合征。
代谢和营养异常：葡萄糖耐量受损、低钾性碱中毒，血脂异常、增加糖尿病患者对胰岛素或口服降糖药的需求。
钠潴留、体液潴留、负氮平衡(由蛋白质分解造成)、血尿素氮增高、食欲增加(可能会导致体重增加)、脂肪过多症。
精神异常：情感障碍(包括情绪不稳定、情绪低落、欣快、心理依赖、自杀意念)、精神病性异常(包括躁狂、妄想、幻觉、精神分裂症[加重])、意识模糊状态、精神障碍、焦虑、人格改变、情绪波动、行为异常、失眠、易激惹。
神经系统异常：颅内压增高(可能出现视神经乳头水肿[良性颅高压]、惊厥、健忘、认知障碍、头晕、头痛。
眼部异常：眼球异常、青光眼、白内障。
耳和迷路异常：眩晕。
心脏异常：充血性心力衰竭(易感患者)、心律失常。
血管异常：高血压、低血压。
呼吸系统、胸和纵隔异常：呃逆。
胃肠道异常：胃出血、肠穿孔、消化道溃疡(可能出现消化性溃疡穿孔和消化性溃疡出血)、胰腺炎、腹膜炎、溃疡性食管炎、食管炎、腹痛、腹胀、腹泻、消化不良、恶心。
皮肤和皮下组织异常：血管性水肿、外周水肿、瘀斑、瘀点、皮肤萎缩、条纹状皮肤、皮肤色素减退、多毛、皮疹、红斑、瘙痒、荨麻疹、痤疮、多汗症。
肌肉骨骼和结缔组织异常：骨坏死、病理性骨折、发育迟缓(儿童)、肌肉萎缩、肌病、骨质疏松症、神经病性关节病、关节痛肌肉痛、肌无力。
危重病皮质类固醇使用指南(全文)
危重病皮质类固醇使用指南（全文）一、脓毒症1.成人脓毒症住院患者无休克时是否应使用皮质内固醇？推荐意见：不建议在没有休克的成人脓毒症住院患者中使用皮质类固醇（条件性推荐，中等质量证据）。
2.脓毒性休克住院患者是否应使用皮质类固醇？推荐意见：脓毒性休克患者对液体复苏无反应及其使用中至高剂量血管加压药时，建议使用皮质类固醇（条件性推荐，低质量证据）。
3.成人脓毒性休克住院患者若使用皮质类固醇进行治疗，其推荐剂量与治疗时间是多少？推荐意见：如果使用皮质类固醇治疗脓毒性休克，建议使用长疗程和低剂量：氢化可的松iv＜400mg/d，疗程≥3d，而不是短疗程和高剂量（条件性推荐，低质量证据）。
原理：促炎细胞因子或通过抑制皮质醇对ACTH的反应，或与细胞内糖皮质激素功能相竞争从而导致脓毒症相关的CIRCI，后者反过来引起器官衰竭，并使血管加压药治无反应。
因此，皮质类固醇治疗脓毒症的潜在获益在几十年的观察研究和试验中得到了验证。
对纳入3176例伴或不伴休克的脓毒症患者的27项随机临床试验的分析显示，接受皮质类固醇治疗的患者28d死亡率为29.3％，安慰剂组患者死亡率为31.8％，相对危险度0.87（95％CI ：0.76－1.0）。
由于结果的不一致和不严密，证据质量是低的。
对纳入826例伴或不伴休克的脓毒症患者的6项随机临床试验的分析显示，接受皮质类固醇治疗的患者28d死亡率为33.8％，安慰剂组患者死亡率为30.6％，相对危险度1.11（95％CI：0.91－1.34）。
最近，HYPRESS多中心试验对190例脓毒症患者(不包括休克患者)接受连续注射200mg氢化可的松5d，然后逐渐减量直到第11d，另190例患者接受安慰剂治疗。
主要观察终点是在14d内发生的脓毒性休克，结果显示与接受安慰剂治疗的患者相比，接受氢化可的松治疗的患者在14d 内进展为脓毒性休克的比例没有差异(差异1.8％；95％CI：10.7－7.2％，p = 0.70)。
重症急性胰腺炎合并真菌感染的临床诊治研究进展
.综述.重症急性胰腺炎合并真菌感染的临床诊治研究进展彭越岭综述，高青#审校（重庆医科大学附属第一医院消化内科，重庆400016）［摘要］重症急性険腺炎（SAP）是临床•见的急腹症之一，其在治疗中•因合并真菌感染，导致病死率较高、治疗困难。
早期限制广谱抗菌药物的使用，尽早引入肠内营养，及时更换中心静脉导管等侵入性管道，已成为早期预防真菌感染的重要措施。
该文将近年来BI内外对SAP合并真菌感染的危险因素、临床诊断及治疗预防等研究进展进行了综述&［关键词］重症急性険腺炎；真菌感染；危险因素；预防#综述DOI：10.3969/j.issn.1009-5519.2021.05.019中图法分类号：R657.51文章编号：1009-5519（2021）05-0786-04文献标识码：A急性胰腺炎（AP）具有急性起病和疾病过程多变的临床特征&多数AP患者病情较轻，仅有胰腺实质的局灶性炎症，机体常可恢复正常少数患者进展为重症AP（SAP）,并发全身性疾病。
持续性的器官衰竭及全身炎性反应，是SAP患者早期死亡的重要原因&随着对SAP认识的提高、广谱抗菌药物的使用，以及肠外营养、机械通气、中心静脉导管、血液透析治疗等多种全身综合治疗方式的广泛应用，SAP合并多器官功能障碍综合征的病死率明显下降，继发性感染及其相关并发症逐渐成为SAP死亡的主要病因之一⑵。
近年来，真菌感染的发病率逐渐升高，但发病率报道不一，为5.0%〜68.5%，以念珠菌感染最为常见3&由于真菌感染临床表现缺乏特异性，早期诊断困难，易导致患者的死亡风险增加4&本文就近年来国内外对SAP合并真菌感染的危险因素、临床诊断及治疗预防的研究进展进行简要综述&1SAP合并真菌感染的发病机制动物实验和人体研究发现，即使暴露在具有传染力的繁殖体环境中，具有正常免疫能力的个体极少感染真菌$%&SAP患者免疫功能低下，同时由于病程中长期禁食、禁饮，采取静脉肠外营养输入，导致肠内营养严重不足，肠黏膜细胞、绒毛萎缩，微绒毛脱落，肠上皮细胞间紧密连接破坏，肠上皮二胺氧化酶活性下降，肠道通透性增加，肠黏膜屏障受损，局部抵抗力下降及肠道菌群易发生移位，从而引起全身感染6&同时,长疗程广谱抗菌药物的使用，使肠道菌群失调，导致肠道真菌扩增，而且侵入性操作可增加导管相关真菌感染的风险因此，真菌感染是多方面因素共同作用的结果&1.1机体免疫功能低下高龄患者、合并多种疾病及长期处于免疫低下的患者，真菌感染风险更高间&长期使用糖皮质激素时，皮质类固醇抑制嗜中性粒细胞和单核细胞巨噬细胞募集至炎症部位，抑制单核细胞和嗜中性粒细胞的杀菌活性，会增加真菌感染风险&对于糖尿病患者，较高的血糖水平会对机体的免疫功能造成不利影响，尤其是在合并SAP时，机体处于应激状态&持续高血糖状态抑制了中性粒细胞对真菌的识别和黏附能力，降低了巨噬细胞对真菌芽抱的吞噬作用$10%&另一方面，高糖环境为真菌的生长提供了有利条件，因此，糖尿病患者更易继发真菌感染&1.2长期肠外营养在SAP治疗过程中，应综合评估患者疾病严重程度和肠道功能恢复情况⑴%&由于SAP患者处于高分解代谢状态，营养支持是预防感染（包括真菌感染）的重要步骤，因此应早期（入院48h 内）开始肠内营养$12。
糖尿病酮症酸中毒并发急性胰腺炎26例临床救治分析
糖尿病酮症酸中毒并发急性胰腺炎26例临床救治分析1. 引言1.1 研究背景糖尿病酮症酸中毒是一种严重并发症，常见于1型糖尿病患者，尤其是在胰岛素治疗不当或剂量不足的情况下。
急性胰腺炎是一种常见的急腹症，与糖尿病酮症酸中毒的并发表现较为罕见。
对于同时合并糖尿病酮症酸中毒和急性胰腺炎的患者，临床救治具有一定的挑战性。
在目前的临床实践中，对于这一罕见并发症的病例报道相对较少，对其诊断和治疗策略尚未形成统一的指南。
有必要对糖尿病酮症酸中毒并发急性胰腺炎的临床救治情况进行深入研究和分析，以提高对该病情的认识，并为临床医生提供更为全面有效的救治策略。
本研究旨在探讨糖尿病酮症酸中毒并发急性胰腺炎的临床特点、诊断与鉴别诊断、治疗方法、并发症及预后评估，总结临床救治经验并展望未来的研究方向。
通过对该并发症的深入了解和研究，有助于提高其治疗水平，降低并发症发生率，改善患者的预后结果。
1.2 目的糖尿病酮症酸中毒是一种严重的糖尿病并发症，常见于糖尿病患者未经过适当治疗或发生应激情况下。
而糖尿病酮症酸中毒并发急性胰腺炎的情况较为罕见，但危害性较大，容易导致患者出现严重的代谢紊乱和器官功能损害。
本研究旨在探讨糖尿病酮症酸中毒并发急性胰腺炎的临床特点、诊断与鉴别诊断、治疗方法、并发症及预后评估等方面的问题。
通过总结分析26例病例的临床资料，以期为临床治疗提供依据和经验，同时加深对该病病理生理机制的认识，提高诊治水平，降低患者的死亡率和并发症发生率。
希望通过本研究的开展，为临床医生提供更多有益的信息，为进一步完善该病的治疗方案和预防措施提供参考。
1.3 方法引言中的方法部分主要包括研究设计、受试者选取、数据采集和分析等内容。
在本研究中，我们采用回顾性病例分析的方法，共纳入了26例糖尿病酮症酸中毒并发急性胰腺炎的患者。
所有病例的临床资料、检查结果、治疗方案以及随访数据均被完整记录。
数据采集过程中严格遵循医疗伦理规范，并确保患者个人信息的保密性。