急性胰腺炎早期液体复苏应注意的问题

过去数十年,液体复苏在急性胰腺炎早期治疗中具有重要作用,是急性胰腺炎早期治疗的基石。急性胰腺炎病人对液体治疗的反应有较大的差异性,目前急性胰腺炎尚无统一的早期液体复苏方案。复苏过程中须关注以下几个问题：如何选择液体、如何控制复苏总量以及如何评估复苏效果。急性胰腺炎早期液体复苏时,应优先选择晶体液进行快速补液,坚持早期目标导向治疗的液体复苏理念,密切监测临床指标以评估补液效果,及时调整液体复苏的速度与总量,进而提高急性胰腺炎整体治疗效果。     

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过去数十年,液体复苏在急性胰腺炎早期治疗中具有重要作用,是急性胰腺炎早期治疗的基石。急性胰腺炎病人对液体治疗的反应有较大的差异性,目前急性胰腺炎尚无统一的早期液体复苏方案。复苏过程中须关注以下几个问题:如何选择液体、如何控制复苏总量以及如何评估复苏效果。急性胰腺炎早期液体复苏时,应优先选择晶体液进行快速补液,坚持早期目标导向治疗的液体复苏理念,密切监测临床指标以评估补液效果,及时调整液体复苏的速度与总量,进而提高急性胰腺炎整体治疗效果。     

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胰腺炎病人原则上应住院接受治疗,需密切监测病人的意识状态、心肺功能及尿量的变化,给予充分的液体复苏和镇痛等,同时要进行病因学评估和疾病严重性评估。对于重症急性胰腺炎病人应进入重症医学科治疗,接受器官功能监护、血液净化以及营养支持等。胰腺炎诊断48 h内应反复评估病情的严重程度,参考血流动力学指标的变化,给予病人充分的液体复苏,恢复血流动力学稳定。重症急性胰腺炎病人在行液体复苏时,通常需要大量的液体才能稳定病人的血流动力学指标。为防治重症急性胰腺炎病人的感染性并发症,建议预防性应用抗生素。为防治器官功能障碍和其他并发症,可应用大剂量的合成蛋白酶抑制剂。重症急性胰腺炎病人的营养支持应首选肠内营养。对于重症急性胰腺炎病人,可选择应用持续动脉灌注治疗和持续血液净化治疗。     

不同液体复苏对重症急性胰腺炎患者预后的影响分析

目的探讨不同液体复苏对重症急性胰腺炎患者预后的影响。方法回顾性分析2009年3月-2012年10月我院SICU 172例重症急性胰腺炎患者的临床资料,根据患者入院后24h内液体复苏量将患者分成A组与B组,各86例。A患者给予充分性液体复苏治疗,B组患者给予限制性液体复苏治疗,比较两组患者的临床治疗效果和预后。结果 A组患者的急性肾损伤（AKI）发生率、AKI持续时间、肌酐峰值及连续肾脏替代疗法（CRRT）使用率均较B组有明显升高,两组比较具有统计学意义（P〈0.05）;A组患者与B组患者在多器官功能衰竭综合征（MODS）发生率、CRRT使用时间、机械通气率、开腹手术率、住院时间及死亡率等方面无统计学意义（P〉0.05）。结论对于重症急性胰腺炎患者给予限制性液体复苏能够显著降低患者的AKI发生率和持续时间以及肌酐峰值,减少CRRT的使用率,减少并发症的发生,较充分性液体复苏具有更好的临床疗效,对于重症胰腺炎患者疾病的治疗和预后具有重要的意义。     

连续性血液净化在急性重症胰腺炎中的应用与护理

急性重症胰腺炎(SAP)为外科重症,多发病凶险,病死率高,其治疗趋势是采用非手术的综合性治疗,重点是液体复苏,纠正内稳态失调,维护器官功能[1],我院自2004年至今曾对6例急性重症胰腺炎患者进行连续性血液净化治疗(CBP),效果明显,现报告如下:     

早期重症加强治疗在预防急性重症胰腺炎继发感染中的意义

急性重症胰腺炎继发胰腺感染将导致病人住院时间延长,病死率增加.ICU在SAP发病早期从氧代谢水平对休克加以认识并给予充分的液体复苏,主张更积极的进行重要脏器功能的支持和(或)替代治疗,并强调多种治疗措施之间的相互协调和配合等.这些治疗理念和措施将有助于减少MODS的发生,从而降低SAP继发感染的发生率.     

重症急性胰腺炎的非手术治疗进展

重症急性胰腺炎是普通外科及ICU常见的一种重症疾病,其起病急、并发症多、病死率高。既往其病死率常高达40%,近年来,重症急性胰腺炎病死率有大幅度降低,其治疗原则也从以手术为主逐渐向早期炎症调控、代谢失衡与内环境紊乱的调节等综合治疗转变。本研究从重症急性胰腺炎的内科治疗和中医治疗方面进行综述,有助于对重症急性胰腺炎治疗的研究。     

重症急性胰腺炎外科干预时机与策略的研究进展

重症急性胰腺炎的诊治在过去的一个多世纪以来反复在内、外科之间徘徊, 经过多学科的共同努力, 现已取得了重大突破。早期主要治疗方法包括液体复苏、营养支持和胰腺炎相关并发症预防等。重症急性胰腺炎患者可出现局部并发症, 如假性囊肿、包裹性坏死等, 其中感染性胰腺坏死是重症急性胰腺炎的严重并发症。现已形成采用创伤递升式策略治疗感染性胰腺坏死的共识, 即首先采用经皮穿刺置管引流, 对引流不佳的患者再采取进一步的外科或者内镜的微创治疗, 而开腹手术不再是干预的首选方法。本文总结了国内外在重症急性胰腺炎诊治方面的进展, 并分享了笔者团队在重症急性胰腺炎诊疗过程中的心得体会。     

重症急性胰腺炎的腹腔镜治疗现状

近些年,外科领域干预重症急性胰腺炎的方式、理念有了显著变化.以腹腔镜技术为代表的各种微创技术被不断被应用于重症急性胰腺炎的治疗,使其病死率及术后并发症发病率有了明显下降.目前国内外各中心报道的用腹腔镜治疗重症急性胰腺炎的方式却并不相同,总体来说各有特点,在本文中笔者就其不同方式的研究现状做一综述.     

急性胰腺炎临床研究进展与展望

近20年来，多个急性胰腺炎相关诊治指南相继颁布，急性胰腺炎的治疗模式及理念发生了很大变化。重症急性胰腺炎病程中的“两次死亡高峰”是临床治疗中的一大挑战。早期为炎症反应期，应进行ICU为主体的多学科综合救治，包括脏器功能维持、早期液体复苏、合理使用抗生素、营养支持及腹腔间隔室综合征的处理；后期以感染性并发症为主，外科医师对于外科干预指征、时机及方式的掌控尤为重要。现代重症急性胰腺炎的外科干预呈现微创化、阶段化、多学科化、专业化和多元化5大特点，临床医生应建立以疾病为中心的综合治疗模式。此外，还应重视重症急性胰腺炎的病因治疗及后期并发症，防患于未然。     

暴发性急性胰腺炎的诊断与治疗

With the unremitting efforts of researchers for the past 40 years, the survival of patients with severe acute pancreatitis (SAP) has been improved to 86%. Patients with SAP, although had been given fluid resuscitation and formal non-operative therapy in 72 hours after the onset, still progress to organ dysfunction can be diagnosed with fulminant acute pancreatitis (FAP). The treatment methods for FAP include sufficient fluid resuscitation, formal non-operative therapy and removing etiological factors. If patients have the tendency toward deterioration of organ function or incidence of abdominal compartment syndrome (ACS), creating conditions for early surgical drainage is essential, and the surgical procedure should be as simple as possible. The survival rate of patients with FAP is still unsatisfactory, and the advanced age, high scores of acute physiology and chronic health enquiry ( APACHE Ⅱ ), sequential organ failure assessment (SOFA) and Balthazar, and the incidence of ACS are the indicators for a poor prognosis of patients with FAP.     

感染性胰腺坏死的诊治进展

感染性胰腺坏死（IPN）是急性胰腺炎最严重的并发症之一，常引起严重的脓毒症和器官功能衰竭，甚至导致患者死亡。近年来，随着急性胰腺炎治疗理念和技术的不断进步，IPN的病死率有所下降。但IPN的诊断，尤其是早期诊断仍十分困难，IPN的干预时机、干预方式和干预策略仍有较多争议。并且，由于IPN的诊治往往涉及多学科合作，因此，统一认识、充分发挥多学科诊疗模式的优势显得十分重要。笔者通过文献复习并充分结合本单位的实践经验，就IPN的诊断、病原学变化及治疗进展等进行系统阐述。     

Early enteral feeding in severe acute pancreatitis: can it prevent secondary pancreatic (super) infection?

Sepsis continues to account for a second peak in mortality in patients with severe acute pancreatitis. The prevention of these septic complications and subsequent development of multiple organ dysfunction syndrome remains a major focus for investigators, yet despite considerable clinical and experimental work addressing its etiology, septic complications remain high. Several studies have been designed to demonstrate the mechanism of origin of these septic complications with an attempt to define strategies for their prevention to improve patient outcomes. There is clear evidence that the origin of this secondary bacterial infection arises from enteric bacterial translocation secondary to disruption of the gut mucosal barrier during acute pancreatitis. Strategies designed to prevent secondary pancreatic infection include aggressive fluid resuscitation to maximize organ perfusion, early systemic antibiotic treatment or selective gut decontamination, and recently attempts to block mediators of the systemic inflammatory response. This discussion will summarize our present understanding of the etiopathogenesis of secondary bacterial 'superinfection' of necrotizing pancreatitis and how the initiation of enteral feeding early in the course of acute pancreatitis may prove to be an effective means of preventing and/or reversing the breakdown of the gut mucosal defense barrier.     

Metabolic Management of Severe Acute Pancreatitis

The metabolic management of severe acute pancreatitis involves early identification of patients with severe pancreatitis, aggressive fluid resuscitation, organ support, and careful monitoring in an intensive care environment. Recent evidence has helped to define the roles of enteral feeding, prophylactic antibiotics, endoscopic retrograde cholangiopancreatography, computed tomography, and fine-needle aspiration for bacteriology. The most difficult decision in the management of these patients is whether surgery is required and which of the complementary approaches to necrosectomy and drainage is appropriate. Key metabolic events in the acinar cell, pancreas, and intestines are now being unraveled, as is the basis for the systemic manifestations and organ dysfunction associated with pancreatitis. This gives hope for the development of more specific metabolic interventions, which will likely target the maintenance of intestinal integrity and function, preservation of pancreatic microcirculation, and balanced modulation of the inflammatory response.     

Dynamic nature of early organ dysfunction determines outcome in acute pancreatitis

BACKGROUND: All patients with organ dysfunction are currently classified as having severe acute pancreatitis. The aim of this study was to characterize the systemic inflammatory response syndrome (SIRS) and early organ dysfunction in patients with acute pancreatitis and the relationship with overall mortality. METHODS: Patients with predicted severe acute pancreatitis of less than 48 h duration had daily organ dysfunction scores and SIRS criteria calculated. These features were then correlated with outcome. RESULTS: Of 121 patients, 68 (56 per cent) did not develop organ dysfunction; only two of these patients died (mortality rate 3 per cent). Fifty-three (44 per cent) had early organ dysfunction, of whom 11 died (21 per cent). Organ dysfunction and persistent SIRS were both associated with an increased mortality rate, but on multivariate analysis only deteriorating organ dysfunction was an independent determinant of survival. CONCLUSION: Early organ dysfunction in acute pancreatitis usually resolves and in itself has no significant influence on mortality. In contrast, worsening organ dysfunction was associated with death in more than half of the patients (11 of 20); it is this group of patients who should be classified as having severe acute pancreatitis.     

外科常见腹腔感染多学科诊治专家共识

腹腔感染是临床常见的急危重症之一,其诊治涉及外科、重症医学、感染、检验、临床药学等多个学科,包括局部病灶处置、病原学检测、抗菌药物合理应用及因感染导致的全身各系统异常状况纠正等过程,具有特殊性及复杂性。本共识参考国内外最新进展并结合临床经验,以问题为导向,以循证为基础,对急性阑尾炎、上消化道穿孔、下消化道穿孔、急性胆道感染、肝脓肿、重症急性胰腺炎、胰瘘、胆瘘、吻合口瘘、内镜诊治后消化道穿孔等外科常见腹腔感染的诊断、病原学检测、外科及抗菌药物治疗等临床热点问题进行评述,并根据证据等级提出诊治相关的推荐意见,旨在规范外科常见腹腔感染的诊疗行为,在临床决策、抗菌药物应用等方面为临床医师提供参考及指导,以提高诊治水平并改善患者预后。     

Vascular endothelial growth factor increases in serum and protects against the organ injuries in severe acute pancreatitis

BACKGROUND: We have demonstrated that apoptosis was detected in liver and kidney cells in severe acute pancreatitis and that cellular injury because of apoptosis may be involved in the mechanism of multiple organ dysfunction syndrome. Vascular endothelial growth factor (VEGF) is a glycoprotein with potent angiogenic, mitogenic, and vascular permeability-enhancing activities specific for endothelial cells. It has been reported that VEGF is implicated in many diseases such as cancer and inflammation. METHODS: Serum VEGF concentrations were determined in patients with acute pancreatitis at the time of admission, and the relationships with severity, blood biochemical parameters on admission, organ dysfunction during the clinical course, and prognosis were analyzed. Moreover, to clarify the role of VEGF in acute pancreatitis, effects of VEGF were investigated in experimental severe acute pancreatitis. RESULTS: Serum VEGF levels were significantly elevated in patients with acute pancreatitis. Serum VEGF levels were not related to severity or prognosis. In male patients, among the various blood biochemical parameters, serum lactate dehydrogenase, and blood urea nitrogen levels were positively correlated with serum VEGF levels. Serum VEGF levels with organ dysfunction (liver and kidney) were higher than those without organ dysfunction. In rat experimental severe acute pancreatitis, serum VEGF levels were significantly elevated. Recombinant VEGF did not affect the lung water content, volume of ascitic fluid, hematocrit, or serum amylase, but improved the hepatic and renal dysfunctions. Apoptosis of liver and kidney was significantly inhibited by the administration of VEGF. CONCLUSIONS: These results suggest that VEGF is closely related to organ dysfunction in severe acute pancreatitis, and that VEGF may function as not a vascular permeability factor, but a protective factor via the anti-apoptotic effect against the organ injuries in this disease.