非感染性坏死性胰腺炎手术时机的探讨--附62例临床病例报告

目的探讨急性重症胰腺炎非感染性胰腺坏死手术时机.方法对62例非感染性坏死性胰腺炎进行临床和CT评估以决定手术指征,根据手术发现对手术治疗的时机进行评估分析.结果经CT评估病灶大于6 cm、术前诊断为非感染性胰腺坏死41例患者中,32例发病3 ～ 4周后手术治疗.术中发现大网膜及肠系膜根部见大量皂化斑,正常胰腺与坏死胰腺组织分界清楚,10例患者胰腺坏死已合并感染,感染发生率为25%;术后5例患者死亡,病死率为12%;发病2周内手术治疗的9例患者,术中发现正常胰腺组织与坏死胰腺组织之间分界不十分清楚,胰腺及胰周组织水肿明显,术后有1例患者死亡.CT评估病灶小于6 cm,但胰周及腹膜后大片脂肪坏死、液体积聚、消化道有压迫梗阻症状的21例患者全部于发病后3 ～ 4周手术治疗,术中见4例患者胰腺坏死合并感染,3例有粘连性或压迫性消化道梗阻,术后2例死于腹腔内感染和多器官功能衰竭.结论对急性胰腺炎非感染性胰腺坏死,是否需要手术清除坏死组织,应行定期CT评估分析,对于病灶大于6 cm和/或病灶不足6 cm但胰周及腹膜后大片脂肪坏死、液体积聚并有消化道压迫梗阻症状患者,应行手术治疗.手术时机宜在发病后3 ～ 4周.过早手术,坏死组织与正常组织尚未完全分离,术中易出血,增加手术难度和再次手术的机会;过迟手术,坏死组织已合并感染,腹腔内感染严重,需再次手术甚至多次手术.     

急性胰腺炎恢复期隐匿的多发消化道瘘

急性胰腺炎发病4周后进入感染期,胰腺和胰周组织坏死合并感染可引发感染性出血、消化道瘘等并发症。该例患者经积极抗感染和营养支持治疗后仍反复出现腹痛、发热等症状,且影像学特征性表现不显著,后发现胃后壁、十二指肠旁、降结肠旁有多处点状、微小气泡征,经胃肠镜检查后发现多发消化道瘘管。最终经多学科协作会诊,对该患者行内镜超声引导...     

急性坏死性胰腺炎临床病理分期和治疗措施

目的探讨急性坏死性胰腺炎（ANP）临床病理分期和治疗措施．方法从1990－12以来，我院对23例ANP病例采用早期手术，切口开放引流，观察胰腺病理形态改变．结果通过对ANP胰腺病理形态改变的观察，将ANP的病理演变过程分为四期：①组织坏死合并急性生理紊乱期：约在术后1wk内，以胰腺坏死、胰外器官损害为主③坏死组织液化继发感染期：发生于术后4d～12d，表现为坏死组织液化感染，体温、血WBC上升，出现全身中毒症状．③胰腺感染坏死脱落及晚期并发症期：术后14d～31d，以全身性细菌性感染及随后的深部霉菌感染或双重感染为特点，并发生胰腺脓肿、胰瘘和MOF等并发症．④胰腺炎恢复期：术后40d以后，胰腺及胰周创面被健康肉芽组织代替，临床表现为严重的全身营养不良．结论治疗以改善微循环、坏死组织清除、充分引流和营养支持为主     

高渗盐水在SAP非感染性胰腺坏死患者液体复苏中的应用

目的观察对重症急性胰腺炎（SAP）非感染性胰腺坏死患者术前采用高渗盐水行液体复苏的效果。方法将同期收治的60例SAP患者随机分为观察组和对照组各30例,均禁饮禁食、卧床休息、胃肠减压、预防感染和抑制胰酶分泌、支持或替代治疗,其后均行手术治疗,其中观察组术前予7．5％高渗盐水4ml／kg行液体复苏。观察两组临床疗效及胰腺组织学评分。结果两组均顺利完成手术,无死亡;各有1例术后出现暂时性吸收热和轻微出血,经对照处理后均好转;观察组水肿、感染、出血及坏死胰腺组织学评分均显著低于对照组（P均〈0．05）。结论对SAP非感染性胰腺坏死患者术前采用高渗盐水行液体复苏可减轻胰腺组织病变程度,从而改善手术清除效果。     

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。     

喀什地区急性胰腺假性囊肿治疗体会

目的总结喀什地区急性胰腺假性囊肿的治疗经验。方法回顾性分析2010年喀什地区第二人民医院13例急性胰腺假性囊肿患者的临床资料,急性胰腺炎后12例,外伤后1例。所有病例经B超和CT提示,囊肿直径3.4-17 cm,囊肿位于胰头2例,胰尾4例,胰体尾7例。除1例胰腺外伤后手术感染患者急症行囊肿外引流术,其余12例经非手术保守治疗。结果急症手术患者5周后治愈,顺利拔管;12例非手术治疗者病情趋于稳定,痊愈7例,5例因囊肿呈渐进性增长趋势于发病后3-6个月行囊肿空肠Roux-en-Y吻合,术后恢复良好,无胰瘘及手术死亡。结论对于急性胰腺假性囊肿应因地制宜,合理选择治疗手段,以达到最佳的治疗效果。     

创口敞开引流治疗重症胰腺炎

1985～1993年6月,我们采用创口敞开引流,有计划定期清创术治疗重症胰腺炎42例,疗效显著。本组男18例、女24例,年龄16～79岁。发病至手术时间为4小时～12天。均有腹腔脓血性渗液,>1000ml者11例。胰体尾坏死5例,全胰坏死1例,余者为散在分布于胰腺的紫褐色坏死斑块。腹腔内有皂化斑块17例,休克6例,反应性左侧胸腔积液4例,消化道出血2例,低钙血症2例,多器官功能衰竭3例。 1.治疗:施行坏死组织清除术36例,全胰腺切除1例,胰腺次切除5例。死亡5例,治愈37例。术后胰瘘2例,切口疝9例,糖尿病3例,粘连性肠梗阻8例,腹腔残余感染4例。术后平均清创3次,平均住院时间70天。     

急性胰周积液和胰腺坏死对急性胰腺炎预后的影响

目的 探讨急性胰周积液和胰腺坏死对急性胰腺炎(AP)预后的影响.方法 回顾分析2003年1月至2007年12月收治的323例AP患者早期CT影像学表现,探讨急性胰周积液、胰腺坏死程度与全身炎症反应综合征(SIRS)、胰腺感染及病死率的关系.结果 发病5 d内出现SIRS并持续2 d或以上者97例(30%),12例(3.7%)在病程中、后期出现胰腺感染;病死14例(4.3%).有急性胰周积液者142例(44.0%).单个部位发生急性胰周积液者76例,其中31例发生SIRS,病死2例;多个部位急性胰周积液者66例,发生SIRS 62例,病死11例.急性胰周积液部位数量与早期SIRS发生及病死率显著相关(P＜0.01).277例(85.8%)无胰腺坏死,均未继发胰腺感染,病死4例;46例(14.2%)有不同程度胰腺坏死.胰腺坏死面积≤30%32例,胰腺感染发生率12.5%,病死率15.6%;＞30%～≤50%7例,感染发生率42.9%,病死率28.6%;＞50%7例,感染发生率为71.4%,病死率42.9%,胰腺坏死的程度与胰腺感染的发生及病死率显著相关(P＜0.05).结论 急性胰周积液和胰腺坏死对AP预后的影响不同.急性胰周积液与病程早期SIRS的发生及病死率相关;胰腺坏死与胰腺继发感染的发生及病死率有关,坏死面积越大,越容易发生胰腺感染,病死率越高.     

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．     

急性胆源性胰腺炎的诊治体会

目的：总结急性胆源性胰腺炎的诊治体会，以改进诊治方法。方法：对110例胆源性胰腺炎的临床资料进行回顾性分析。结果：110例中83例确是胆源性胰腺炎，其中入院时胆道仍有梗阻（梗阻型）34例，梗阻已解除（非梗阻型）49例。其余27例不是胆源性胰腺炎，20例只是胆源性一过性胰高压，7例乃一般胰腺炎，发病与胆道无关。结论：诊断胆源性胰腺炎要有根据，临床上不可凡遇胆道有结石，血或（和）尿淀粉酶升高就诊断为胆源性胰腺炎。要根据治疗前胆道有无梗阻对胆源性胰腺炎分型论治：梗阻型应尽早引流解除胆道梗阻，非梗阻型宜积极保守治疗，病情缓解后在同一住院期内手术。胆源性一过性胰高压和胰腺炎要按胆道或胰腺病情处理，不可一概按胆源性胰腺炎治疗。     

Hyperbaric oxygen therapy in the treatment of refractory peripancreatic abscess associated with severe acute pancreatitis

Five patients with peripancreatic abscesses associated with severe acute pancreatitis were treated by hyperbaric oxygen therapy (HBO). In 3 patients, the course after surgical mobilization of the pancreas and drainage of the pancreas bed was complicated by peripancreatic abscesses. HBO was conducted under a pressure of 2.8 atmospheres for two hours dialy. Four of the 5 patients showed a progressive improvement in their condition. In one patient who failed to respond despite seven sessions of HBO, Pseudomonas aeruginosa was isolated from the discharge, and resection of necrotic tissue and drainage were performed. The main effects of HBO were the alleviation of high spiking fever, the improvement of white blood cell count and serum amylase levels, and the reduction of the abscess size. We recognized HBO to be a successful treatment for peripancreatic abscess associated with severe acute pancreatitis and better results were obtained than in cases that did not receive HBO.     

Management of infection in acute pancreatitis

The clinical course of acute pancreatitis varies from a mild, transitory illness to a severe, rapidly fatal disease. In about 80% to 90% of cases pancreatitis presents as a mild, self‐limiting disease with low morbidity and mortality. Unlike mild pancreatitis, necrotizing pancreatitis develops in about 15% of patients, with infection of pancreatic and peripancreatic necrosis representing the single most important risk factor for a fatal outcome. Infection of pancreatic necrosis in the natural course develops in the second and third week after onset of the disease and is reported in 40% to 70% of patients with necrotizing pancreatitis. Just recently, prevention of infection by prophylactic antibiotic treatment and assessment of the infection status of pancreatic necrosis by fine‐needle aspiration have been established in the management of severe pancreatitis. Because medical treatment alone will result in a mortality rate of almost 100% in patients with signs of local and systemic septic complications, patients with infected necrosis must undergo surgical intervention, which consists of an organ‐preserving necrosectomy combined with a postoperative closed lavage concept that maximizes further evacuation of infected debris and exudate. However, intensive care treatment, including prophylactic antibiotics, reduces the infection rate and delays the need for surgery in most patients until the third or fourth week after the onset of symptoms. At that time, debridement of necrosis is technically easier to perform, due to better demarcation between viable and necrotic tissue compared with necrosectomy earlier in the disease. In contrast, surgery is rarely needed in the presence of sterile pancreatic necrosis. In those patients the conservative approach is supported by the present data.     

Severe acute pancreatitis: case-oriented discussion of interdisciplinary management.

The clinical course of an episode of acute pancreatitis varies from a mild, transitory illness to a severe often necrotizing form with distant organ failure and a mortality rate of 20-40%. Patients with severe pancreatitis, representing about 15-20% of all patients with acute pancreatitis, need to be identified as early as possible after onset of symptoms allowing starting intensive care treatment early in the disease process. An episode of severe acute pancreatitis progresses in two phases. The first 10-14 days are characterized by a systemic inflammatory response syndrome maintained by the release of various inflammatory mediators. The second phase, beginning about 10-14 days after the onset of the disease is dominated by sepsis-related morbidity due to infected peripancreatic and pancreatic necrosis. This state is associated with septic multiple organ systemic failure. The importance of infection on the outcome of necrotizing pancreatitis has been clearly delineated and the pre-emptive use of broad-spectrum antibiotics that achieve effective tissue concentrations is considered standard management of patients with severe necrotizing pancreatitis, especially if associated with organ failure or extended necrosis. Patients with infected necrosis should undergo a surgical intervention. The standard open technique consisting of an organ preserving necrosectomy followed by a postoperative concept of lavage and/or drainage to evacuate necrotic debris occurring during the further course has recently been challenged by various minimally invasive approaches.     

Magnetic resonance imaging for local complications of acute pancreatitis: A pictorial review

Acute pancreatitis is a common disease characterized by sudden upper abdominal pain and vomiting. Alcoholism and choledocholithiasis are the most common factors for this disease. The choice of treatment for acute pancreatitis might be affected by local complications, such as local hemorrhage in or around the pancreas, and peripancreatic infection or pseudoaneurysm. Diagnostic imaging modalities for acute pancreatitis have a significant role in confirming the diagnosis of the disease, helping detect the exte...     

How I do it — Necrosectomy in acute pancreatitis

Diagnostic objectives in the management of necrotizing pancreatitis include determining the anatomic extent of necrosis by computed tomography (CT) scan with vascular enhancement, the physiologic assessment of severity, ascertaining the etiology of pancreatitis, and distinguishing between patients who have sterile and infected necrosis. Treatment objectives in severe pancreatitis include: maximizing fluid resuscitation by Swan Ganz monitoring, in which the object of therapy is to create a hyperdynamic circulation maximizing cardiac index, providing mechanical ventilatory support when needed, and utilizing antibiotics on a presumptive basis in patients with more than 25% necrosis of the colon is often necessary. Triple lumen Davol catheters are used for irrigation with Chloropactin, delivered at a rate of 100–300 ml/h. Suction drainage is not employed. A No. 40 siliconized chest tube is used for gravity drainage. Open packing is preferred in patients with extensive necrosis of pancreatic and peripancreatic tissue or in patients who become infected soon after the onset of symptoms. Patients who are packed open are returned to the operating room every 2–3 days until there is no further visual or CT scan evidence of necrotic tissue or fluid. The literature shows 40%–50% of patients treated by closed drainage have room every 2–3 days until there is no further visual or CT scan evidence of necrotic tissue or fluid. The literature shows 40%–50% of patients treated by closed drainage have residual areas of necrosis and infection and require re-operation. Continued sepsis is synonymous with undrained infection and requires reoperation.     

Intra-abdominal fungal infections complicating acute pancreatitis: a review

Intra-abdominal infections of pancreatic or peripancreatic necrotic tissue complicate the clinical course of severe acute pancreatitis (SAP) and are associated with significant morbidity. Fungal infection of necrotic pancreatic tissue is increasingly being reported. The incidence of intra-abdominal pancreatic fungal infection (PFI) varies from 5% to 68.5%. Candida albicans is the most frequently isolated fungus in patients with necrotizing pancreatitis. Prolonged use of prophylactic antibiotics, prolonged placement of chronic indwelling devices, and minimally invasive or surgical interventions for pancreatic fluid collections further increase the risk of PFI. Computed tomography- or ultrasound-guided fine-needle aspiration of pancreatic necrosis is a safe, reliable method for establishing pancreatic infection. Amphotericin B appears to be the most effective antifungal treatment. Drainage and debridement of infected necrosis are also critical for eradication of fungi from the poorly perfused pancreatic or peripancreatic tissues where the antifungal agents may not reach to achieve therapeutic levels. Fungal infection adversely affects the outcome of patients with SAP and is associated with increased morbidity, although the mortality rate is not increased specifically because of PFI. Although antifungal prophylaxis has been suggested for patients on broad-spectrum antibiotics, no randomized controlled trials have yet studied its efficacy in preventing PFI.     

Quality of life following acute necrotizing pancreatitis

BACKGROUND/AIMS: The authors examine the quality of life of patients treated for acute necrotizing pancreatitis an average of 37.8 months following their illness. METHODOLOGY: The questionnaire used in the examinations was a version of the Short Form-36 (SF-36) which was adapted to a Hungarian environment and included additional questions regarding the patient's illness. During the treatment of the pancreatic necrosis, prophylactic antibiotic treatment, early nasojejunal feeding, percutaneous peripancreatic drainage, and late surgical necrectomy was used. Postoperatively the lavage of the closed omental bursa was performed. RESULTS: It was determined that 77.3% of patients considered their quality of life to be good or fair. Quality of life was considered worse in older patients, patients with complaints of abdominal distension and bowel problems, patients who had lost significant amounts of weight since their illness, patients with poor appetite, and patients who were female. CONCLUSIONS: The long-term result, and the quality of life after acute necrotizing pancreatitis is good.     

Correlation of serum amylase levels with pancreatic pathology and pancreatitis etiology

Fifty-one patients, 35 men and 16 women, with acute pancreatitis were studied prospectively with early computed tomography (CT). Etiological factors for acute pancreatitis were alcohol abuse (n = 28), gallstones (n = 14), pancreas cancer (n = 3) and miscellaneous (n = 6). Admission serum amylase levels ranged between 68-5,856 U/L with a mean of 1,090 +/- 1,369 U/L. The mean serum amylase level was significantly different between patients with alcoholic pancreatitis (439 +/- 302 U/L) and gallstone pancreatitis (2,480 +/- 1,575) (p less than 0.001). The initial pancreatic CT findings and corresponding mean serum amylase levels were in CT grade A (pancreas normal) 1,499 +/- 1,569 U/L (n = 11), in CT grade B (pancreatic enlargement with inflammation confined to pancreas) 1,144 +/- 1,542 U/L (n = 18), in CT grade C (inflammatory extension into one peripancreatic space) 722 +/- 962 U/L (n = 13) and in CT grade D (inflammatory extension into two or more peripancreatic spaces) 590 +/- 369 U/L (n = 9). However, on separating the etiology subgroups, there was no increase or decrease in the serum amylase level with increasing pancreatic inflammatory involvement. Pancreatic complications (pseudocyst, abscess, necrosis) requiring surgical intervention developed only in patients with CT grades C and D. We conclude that within the etiologic subgroups there is no correlation between the initial serum amylase level and the extent of pancreatic involvement visualized by CT. These findings provide a pathological basis for the clinical observation that the initial serum amylase level cannot predict the outcome in acute pancreatitis.     

Natural history of acute pancreatitis and the role of infection.

Bacterial infection of pancreatic necrotic tissue is a frequent complication of severe acute pancreatitis. Infected pancreatic necrotic tissue is observed in 30-70% of all patients suffering from necrotizing pancreatitis. It is the leading cause of deaths in severe acute pancreatitis, with mortality rates ranging from 15 to 30%. The incidence of infection increases with the extent of the necrotic areas and with the time after onset of pancreatitis. Compared to patients with sterile necrosis, those with infection of the necrotic areas have an increased mortality, and systemic complications occur more frequently. Standard treatment for infected pancreatic necrotic tissue is surgical debridement, whereas conservative management is feasible in approximately 30% of the patients with sterile necrosis. As bacterial infection of pancreatic necrotic tissue has a tremendous impact on the prognosis of the disease and on the patient's clinical course, efforts have been made to prevent it. Although clinical and experimental data provide evidence that prophylactic antibiotics have beneficial effects on the outcome and course of patients with severe acute pancreatitis, this topic has to be investigated further. General recommendations concerning the early use of antibiotics have to await the results of larger, double-blind studies.     

ENDOSCOPIC NECROSECTOMY UNDER DIRECT VISION AFTER ENDOSCOPIC ULTRASOUND‐GUIDED CYSTGASTROSTOMY FOR ORGANIZED PANCREATIC NECROSIS

A 56‐year‐old man was referred for an enlarging pancreatic pseudocyst that developed after severe acute pancreatitis with gallstones. Abdominal ultrasound showed a huge cystic lesion with a large amount of solid high echoic components. Arterial phase contrast‐enhanced computed tomography scan revealed arteries across the cystic cavity. Stents were placed after endoscopic ultrasound‐guided cystgastrostomy; however, the stents were obstructed by necrotic debris, and secondary infection of the pseudocyst occurred. Therefore, the cystgastrostomy was dilated by a dilation balloon, and a forward‐viewing endoscope was inserted into the cystic cavity. Many vessels and a large amount of necrotic debris existed in the cavity. Under direct vision, all necrotic debris was safely removed using a retrieval net and forceps. One year after this procedure, there was no recurrence. Our case indicates that peripancreatic fat necrosis can cause exposure of vessels across/along the cystic cavity, and blind necrosectomy should be avoided.