Groove pancreatitis has a spectrum of severity and can be managed conservatively

Background & aimsThe natural history of groove pancreatitis is incompletely characterized. Published literature suggests a high rate of surgery. We describe the short- and long-term outcomes in a cohort of patients with groove pancreatitis treated at our institution.MethodsMedical records of patients hospitalized in the University of Pittsburgh Medical Center system from 2000 to 2014 and diagnosed with groove pancreatitis based on imaging were retrospectively reviewed. Clinical presentation and outcomes during index admission and follow-up were recorded.ResultsForty-eight patients with groove pancreatitis were identified (mean age 53.2 years, 79% male). Seventy-one percent were alcohol abusers and an equal number were cigarette smokers. Prior histories of acute and chronic pancreatitis were noted in 30 (62.5%) and 21 (43.8%), respectively. Forty-four (91.7%) met criteria for acute pancreatitis during their index admission. Alcohol was the most common etiology (68.8%). No patient experienced organ failure. The most frequent imaging findings were fat stranding in the groove (83.3%), duodenal wall thickening (52.1%), and soft tissue mass/thickening in the groove (50%). Over a mean follow-up of 5.0 years, seven (14.6%) required a pancreas-related surgery. Patients had a high burden of pancreatitis-related readmissions (68.8%, 69.4/100 patient-years). Incident diabetes and chronic pancreatitis were diagnosed in 5 (13.9% of patients at risk) and 8 (29.6% of patients at risk) respectively.ConclusionsGroove pancreatitis has a wide spectrum of severity; most patients have mild disease. These patients have a high burden of readmissions and progression to chronic pancreatitis. A small minority requires surgical intervention.     

JPN Guidelines for the management of acute pancreatitis: cutting-edge information

The JPN Guidelines for the Management of Acute Pancreatitis are organized under the subject headings: epidemiology, diagnosis, management strategy, severity assessment and transfer criteria, management of gallstone pancreatitis, nonsurgical management, and surgical management. The Guidelines contain cutting-edge information on each of these subjects, as well as a section on the Japanese medical insurance system which provides information that should prove useful to physicians in other countries. The quality of the evidence was evaluated by the evidence-based classification method used at the Cochrane Library. The levels of recommendation of the individual management methods contained in the Guidelines were determined on the basis of the evaluation of evidence by the consensus of the members of the Working Group (see below). The Japanese Society for Abdominal Emergency Medicine, the Japan Pancreas Society, and the Research Group for Intractable Diseases and Refractory Pancreatic Diseases (which is sponsored by the Japanese Ministry of Health, Labour, and Welfare) were commissioned to produce the JPN Guidelines for the Management of Acute Pancreatitis. A Working Group of 20 physicians specializing in pancreatic diseases and emergency medicine investigated and analyzed 14821 cases retrieved by means of a Medline (1960–2004) search and discussed the available literature on acute pancreatitis (limited to human pancreatitis). The Working Group held many general discussions in order to reach a consensus on the content of the Guidelines. After producing a draft, the Publishing Committee of the JPN Guidelines for the Management of Acute Pancreatitis posted it on a website and asked for comments and criticisms. Subsequently, a final version of the Guidelines was published in Japanese in 2003. The Publishing Committee is now making the Guidelines available to a much wider readership by bringing out an English version.     

Cutting-edge information for the management of acute pancreatitis

Considering that the Japanese (JPN) guidelines for the management of acute pancreatitis were published in Takada et al. (J HepatoBiliary Pancreat Surg 13:2–6, 2006), doubts will be cast as to the reason for publishing a revised edition of the Guidelines for the management of acute pancreatitis: the JPN guidelines 2010, at this time. The rationale for this is that new criteria for the severity assessment of acute pancreatitis were made public on the basis of a summary of activities and reports of shared studies that were conducted in 2008. The new severity classification is entirely different from that adopted in the 2006 guidelines. A drastic revision was made in the new criteria. For example, about half of the cases that have been assessed previously as being ‘severe’ are assessed as being ‘mild’ in the new criteria. The JPN guidelines 2010 are published so that consistency between the criteria for severity assessment in the first edition and the new criteria will be maintained. In the new criteria, severity assessment can be made only by calculating the 9 scored prognostic factors. Severity assessment according to the contrast-enhanced computed tomography (CT) grade was made by scoring the poorly visualized pancreatic area in addition to determining the degree of extrapancreatic progress of inflammation and its extent. Changes made in accordance with the new criteria are seen in various parts of the guidelines. In the present revised edition, post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis is treated as an independent item. Furthermore, clinical indicators (pancreatitis bundles) are presented to improve the quality of the management of acute pancreatitis and to increase adherence to new guidelines.     

A study of the time course of conversion of edematous to hemorrhagic pancreatitis

We studied the conversion of acute edematous pancreatitis (AEP) to acute hemorrhagic pancreatitis (AHP) in an experimental model in cats. In the model, 16,16 dimethyl PgE₂ effects this conversion by increasing microvascular permeability. First, we induced AEP in cats and then gave PgE₂ at increasing intervalsafter the induction of AEP to see how long an interval would still allow conversion. In 6 groups of cats, PgE₂ was administered for 2 h, starting at 2, 4, 6, 8, 10, or 12 h after the creation of AEP. Twelve h later, the cats were sacrificed and the pancreases were graded for inflammation and hemorrhage. Significant pancreatic hemorrhage did not occur when the PgE₂ was administered at 12 h compared to 2 h. Next, we determined that PgE₂ still retained its ability to increase pancreatic vascular permeability when administered 12 h after the creation of AEP. This was done by perfusing a marker molecule through the MPD (fluorescein iso-thiocyanate labeled dextran: FITC-D, mol wt 20,000) and then finding it in portal venous blood (PVB). The presence of FITC-D in PVB signified increased vascular permeability, since normally none was present. We concluded that conversion of AEP to AHP was possible during the first 12 h after induction of AEP. Lack of conversion at 12 h was not caused by a lack of vascular reactivity at that time.     

Autoimmune pancreatitis： A review

Autoimmune pancreatitis has emerged over the last 40 years from a proposed concept to a well established and recognized entity. As an efficient mimicker of pancreatic carcinoma, its early and appropriate recognition are crucial. With mounting understanding of its pathogenesis and natural history, significant advances have been made in the diagnosis of autoimmune pancreatitis. The characteristic laboratory features and imaging seen in autoimmune pancreatitis are reviewed along with some of the proposed diagnostic criteria and treatment algorithms.     

重症急性胰腺炎的概念之争

急性胰腺炎是腹部外科最常见的急诊之一,近年来由于病理转归过程认识的深入,临床诊断方法的改进和治疗监测手段的改善,病死率已大大地降低．面对这个进展迅速的专题,理解上的“分歧”时常造成临床有关概念认识上的争议．１　重症急性胰腺炎的定义急性胰腺炎是一种在临床表现上差异很大的疾病．轻者可无并发症短期自限自愈．重者起病急骤、病情危重、病程漫长、治疗复杂、并发症多、病死率高．根据在法国的马赛（１９６３、１９８４）、英国的剑桥（１９８３）、意大利的罗马（１９８９）和美国的亚特兰大（１９９２）先后召开的五次国际…     

Infectious causes of acute pancreatitis: A systematic review

BackgroundInfectious etiologies of acute pancreatitis (AP) are rare and include viruses, bacteria, mycobacteria, parasites, and fungi. We aimed to conduct a comprehensive review on infectious etiologies of AP analyzing the frequency, clinical features, and outcomes of individuals presenting with this condition.MethodsEligible articles reporting on AP attributed to infectious etiologies were included. A comprehensive literature search of PubMed from time of inception and until September 6,2019 was performed using all relevant MeSH (medical subject heading) keywords. Articles were assessed for eligibility and independently reviewed by two reviewers for clinical features of AP, local complications, and mortality. Methodological quality of included studies was evaluated using the Murad tool.ResultsA total of 212 articles were included, of which 168 (79.2%) were at high risk of bias. 320 cases of AP were identified. Viruses were the leading etiology of infection attributed AP (65.3%) followed by helminths (19.1%), and bacteria (12.5%). Protozoa, mycobacteria, and fungi accounted for the remaining 3.1% of cases. Mean age was 40.5 ± 18.4 years and M:F ratio was 1.94:1. Mortality occurred in 50 patients. Mortality rate was higher in the virus attributed AP patients than AP from other infectious etiologies (21.8% vs. 7.0%, p < 0.0005).InterpretationLiterature quality on infection attributed AP is limited. Virus attributed AP appears to carry a higher mortality than other etiologies of infection attributed AP.     

Current concept of pathogenesis of severe acute pancreatitis

The pathogenesis of severe acute pancreatitis is very complicated. It is a multifactorial as well as multifaceted disease. First of all, the etiologic agents initiate the pancreatic acinar injury by release of pancreatic enzymes and overstimulation of macrophages and neutrophils, then the cytokines and inflammatory mediators are liberated. There is also interaction between neutrophils and endothelial cells producing free radicals, the cytokines cause increasing vascular permeability, activating complement component, resulting in microcirculatory impairment and imbalance of thrombo-fibrinolytic system. Many of these events occur not only in the pancreas itself, but also in the other vital organs and tissues, leading to severe acute pancreatitis and complications. The sequencial events are as follows.     

Clinical and pathological features of acute interstitial pancreatitis in the aged

Histological examination of the pancreas disclosed acute diffuse interstitial pancreatitis in nine cases (0.62%) out of 1457 autopsies performed in 3 yr at two general hospitals in Tokyo. In this series, there were 11 cases of necrotizing or hemorrhagic pancreatitis. In addition to diffuse phlegmonous inflammation, acute interstitial pancreatitis was characterized by rupture of the ducts and ductules associated with profuse intraluminal exudation of polymorphonuclear leukocytes and protein plugs formation. There was scarce parenchymal or fat necrosis. The interstitial type may represent characteristics of acute pancreatitis in the aged. In all nine cases, there were few clinical signs suggestive of acute pancreatitis, except for shock, that developed rapidly. Duration of the disease was rather short. Diagnosis of acute pancreatitis was not made before death. In five patients, acute pancreatitis was terminally superimposed on other serious ailments. But in the other four cases, acute pancreatitis was disclosed as the primary disease at autopsy. Although there was only one case that had a possibility of being secondary to biliary tract infection, ascending bacterial infection and impaired secretion by atrophic parenchyma seemed to be involved in its pathogenesis.     

Biochemical models as early predictors of the etiology of acute pancreatitis

In this study we observed the discriminative ability of five commonly measured laboratory tests to distinguish between gallstone-and non-gallstone-associated pancreatitis. We also assessed the ability of the lipase-amylase ratio to discriminate between alcohol-and non-alcohol-induced pancreatitis. One hundred sixty-two patients with acute pancreatitis were included in the study. Group A consisted of patients presenting to our hospital in 1988 and 1989. Group B consisted of patients presenting in 1992. Models developed using group A patients were validated using group B patients. For gallstone pancreatitis, AST (threshold value 80 IU/liter) alone and a three-factor model, ST, ALP and bilirubin (threshold values of 80 IU/liter, 115 IU/liter, and 15 mol/liter, respectively) were the best predictors, correctly classifying at least 80% of cases in group A and B. A lipase-amylase ratio of two correctly classified only 48% of cases in group A and 54% in group B. We conclude that biochemical models are useful in predicting the presence of gallstone pancreatitis but not alcoholic pancreatitis.     

Molecular mechanisms of alcohol associated pancreatitis

Alcohol abuse is commonly associated with the development of both acute and chronic pancreatitis. Despite this close association, the fact that only a small percentage of human beings who abuse alcohol develop pancreatitis indicates that alcohol abuse alone is not sufficient to initiate clinical pancreatitis. This contention is further supported by the fact that administration of ethanol to experimental animals does not cause pancreatitis. Because of these findings, it is widely believed that ethanol sensitizes the pancreas to injury and additional factors trigger the development of overt pancreatitis. How ethanol sensitizes the pancreas to pancreatitis is not entirely known. Numerous studies have demonstrated that ethanol and its metabolites have a number of deleterious effects on acinar cells. Important acinar cells properties that are affected by ethanol include: calcium signaling, secretion of zymogens, autophagy, cellular regeneration, the unfolded protein response, and mitochondrial membrane integrity. In addition to the actions of ethanol on acinar cells, it is apparent that ethanol also affects pancreatic stellatecells. Pancreatic stellate cells have a critical role in normal tissue repair and the pathologic fibrotic response. Given that ethanol and its metabolites affect so many pancreatic functions, and that all of these effects occur simultaneously, it is likely that none of these effects is "THE" effect. Instead, it is most likely that the cumulative effect of ethanol on the pancreas predisposes the organ to pancreatitis. The focus of this article is to highlight some of the important mechanisms by which ethanol alters pancreatic functions and may predispose the pancreas to disease.     

The clinical outcome of elderly patients with acute pancreatitis is not different in spite of the different etiologies and severity

The aim of this study was to investigate the overall clinical characteristics of elderly patients with acute pancreatitis. We retrospectively evaluated 227 consecutively enrolled patients who were admitted with acute pancreatitis. The clinical features, the radiological and laboratory data and the clinical outcome were analyzed according to the age groups (≥65 years vs. <65 years). Among the 227 enrolled patients with acute pancreatitis, there were 85 elderly patients and 142 non-elderly. The mean age of the elderly patients was 72.3 ± 5.5 years and that of the non-elderly was 44.7 ± 11.7 (p < 0.001). For the elderly patients, biliary pancreatitis was the most common cause (56.5%), but alcoholic pancreatitis was most common in the non-elderly patients (45.8%). Although the computed tomography (CT) severity index was significantly higher for the non-elderly patients (p < 0.001), the acute physiology and chronic health evaluation (APACHE II) score was significantly higher for the elderly than that for the non-elderly (p < 0.001). However, the duration of the hospital stay (10.3 ± 9.6 days vs. 11.9 ± 10.1 days, p = 0.619) and mortality (3.5% vs. 0.7%, p = 0.148) were not different between the age-groups. In our study, chronological age had no significant influence on the clinical outcome in spite of the different etiologies and severity of acute pancreatitis.     

Etiology of chronic calcifying pancreatitis in Brazil: a report of 329 consecutive cases

Summary The authors observed 329 consecutive cases of chronic calcifying pancreatitis (CCP) from January 1963 to January 1986. Alcoholism was the etiological agent in 282 cases (86%). In 34 patients (10%) no cause was detectable (idiopathic). Malnutrition was responsible for 10 cases (3%) and chronic familial pancreatitis was diagnosed in 3 cases (0.9%). The mean age at the apparent onset of symptoms was 36.5 ± 10.5 for the alcoholics, 22.6 ± 15.4 in the idiopathic cases and 7.3 ± 3.0 for the nutritional etiology patients. Mean age differences are statistically significant for the 3 groups. Pancreatic calcifications were found in 224 alcohol-induced cases (79%), in 32 idiopathic cases (94%), in 8 patients with malnutrition (80%) and in one patient with familial pancreatitis (33%). All cases of nutritional etiology presented severe protein-caloric deficiences with edema, and none complained of pain, but 9 had pancreatic insufficiency. Mean daily ethanol intake for the alcohol-addicted patients was 396.6 ± 286 g (range 80–1664 g) with the onset of alcoholism at 19.1 ± 6.8 yr old and 20.8 ± 8.3 (4–44) yr of alcohol indulgence. Pancreatic carcinoma developed in 7 cases. Six cases of chronic pancreatitis were seen among relatives in the group with CCP of alcoholic etiology.     

Sclerosing pancreatitis showing rapidly progressive changes with recurrent mass formation

Summary Conclusion Sclerosing pancreatitis might develop repeatedly or might rapidly extend to the whole pancreas with recurrent mass formation. Background Nothing is known concerning course or development of sclerosing pancreatitis. Methods A 63-yr-old male was followed up for 2.5 yr. Results The patient was admitted because of a tumor in the body and tail of the pancreas. Serum pancreatic enzymes were transiently elevated, but tumor markers were all negative. Imaging studies showed a tumor 7 cm in size. The main pancreatic duct was normal in the head and obstructed at the body on endoscopic retrograde pancreatography (ERCP). The K-ras oncogene mutation was positive in pure pancreatic juice. Distal pancreatectomy was performed because pancreatic cancer was highly suspected. Pathological findings showed that the tumor was a densely fibrotic mass without malignant cells. Inflammatory cell infiltration was observed in the stroma. One year later, another mass 3 cm in size was noted in the remnant pancreatic head. ERCP revealed diffuse irregular narrowing of the main pancreatic duct, its branches, and the common bile duct. Liver dysfunction improved and an elevation of serum pancreatic enzymes subsided without any specific treatment, and the mass diminished in size. The patterns of various imaging studies on the second tumor were the same as those of the previous resected mass. Corticosteroid was not administered.     

Roux-en-Y drainage of a pancreatic fistula for disconnected pancreatic duct syndrome after acute necrotizing pancreatitis

Background

After acute necrotizing pancreatitis (ANP), a pancreatic fistula may occur from disconnected pancreatic duct syndrome (DPDS) where a segment of the pancreas is no longer in continuity with the main pancreatic duct.

Aim

To study the outcome of patients treated using Roux-Y pancreatic fistula tract-jejunostomy for DPDS after ANP.

Methods

Between 2002 and 2011, patients treated for DPDS in the setting of endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopanreatography (MRCP) documented main pancreatic duct disruption with Roux-Y pancreatic fistula tract-jejunostomy.

Results

In all, seven patients with DPDS were treated. The median age was 62 years (range 49–78) and five were men. The cause of ANP was gallstones (2), alcohol (1), ERCP (1) and idiopathic (3). Pancreatic necrosectomy was done in six patients. Time from onset of pancreatitis to fistula drainage was 270 days (164–365). Pancreatic fistulae arose from DPDS in the head/neck (4) and body/tail (3). Patients had a median fistula output of 140 ml (100–200) per day before surgery. The median operative time was 142 min (75–367) and estimated blood loss was 150 ml (25 to 500). Patients began an oral diet on post-operative day 4 (3–6) and were hospitalized for a median of 7 days (5–12). The median follow-up was 264 days (29–740). Subsequently, one patient required a distal pancreatectomy. After surgery, three patients required oral hypoglycaemics. No patient developed pancreatic exocrine insufficiency.

Conclusion

Internal surgical drainage using Roux-en-Y pancreatic fistula tract-jejunostomy is a safe and definitive treatment for patients with DPDS.     

善得定治疗急性胰腺炎的体会

作者对比观察了善得定对急性胰腺炎的治疗作用，其剂量为0.1-0.15mg，每4－6h一次，皮一注射。在85例水肿型胰腺炎中，15例应用善得定治疗。结果显示，善得定治疗组转手术率显著低于非善得定组（P＜0．05），未合并感染的12例坏死性胰腺炎均采取非手术治疗，其中3例应用善得定治疗，其合并症全部消失，明显优于对照组。合并感染的67例坏死性胰腺炎均予以手术治疗，病情严重的14例，用善得定治疗，结果显示可减少并发症及其严重度。     

Clinical outcomes of acute pancreatitis in patients with cirrhosis

BackgroundAP outcomes in cirrhotic patients have not yet been studied. We aim to investigate the outcomes of cirrhotics patients with acute pancreatitis.MethodsThe National Inpatient Sample (NIS) database (2003–2013) was queried for patients with a discharge diagnosis of AP and liver cirrhosis. Cirrhosis was further classified as compensated and decompensated using the validated Baveno IV criteria. Primary outcome was inpatient mortality. The analysis was adjusted for age, gender, race, Charlson comorbidity index (CCI), median income quartile, and hospital characteristics.ResultsOver 2.8 million patients with acute pancreatitis were analyzed. Cirrhosis prevalence was 2.8% (80,093). Both compensated and decompensated cirrhosis subjects had significantly higher mortality. Highest odds ratios (OR) were: inpatient mortality (OR 3.4, P < 0.001), Shock (OR 1.5, P = 0.02), Ileus (OR: 1.3, p = 0.02, ARDS (OR 1.2, p = 0.03), upper endoscopy performed (OR 2.0, p < 0.001), blood transfusions (OR 3.1, p < 0.001), gastrointestinal bleed (OR 5.5, p < 0.001), sepsis (OR 1.3, p = 0.005), portal vein thrombosis (PVT) (OR 7.2, p < 0.001), acute cholecystitis (OR 1.3, p < 0.001). Interestingly, cirrhosis patients had lower hospital length of stay, (OR 0.16, p < 0.001), AKI (OR 0.93, p = 0.06), myocardial infarction (OR 0.31, p < 0.001), SIRS (OR 0.62, p < 0.001), parenteral nutrition requirement (OR 0.84, p = 0.002). Decompensated cirrhosis had higher inflation-adjusted hospital charges (+$3896.60; p < 0.001).ConclusionAP patients with cirrhosis have higher inpatient mortality, but it is unlikely to be due to AP severity as patients had lower incidence of SIRS and AKI. Higher mortality is possibly related to complications of cirrhosis and portal hypertension itself such as GI bleed, shock, PVT, AC and sepsis.     

Therapy of acute severe pancreatitis awaits further improvement

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Effects of nafamostat mesilate,somatostatin, and glucagon on caerulein-induced acute pancreatitis in rats

The inhibitory effects of somatostatin (SMS) and glucagon (Gn) on acute pancreatitis were evaluated in an experimental acute pancreatitis model in male Wistar rats. The effects of these agents were compared with those of nafamostat mesilate (NM). The acute pancreatitis was induced by four serial subcutaneous injections of caerulein. The rats were divided into four groups. The first group (n=28) received SMS daily, the second group (n=28) received Gn daily, and the third group (n=28) received NM daily after the first injection of caerulein. The fourth group (n=42) received caerulein alone and served as the control group. Animals were sacrificed 4, 6, 8, 12, and 24 h, and 3 and 7 days after the first administration of caerulein and the degree of severity of the acute pancreatitis was evaluated by serial morphological and histological examinations of pancreatic tissues, as well as in terms of the serum concentrations of amylase and lipase. The characteristic findings of acute pancreatitis in the animals of all groups treated with SMS, Gn, or NM were markedly attenuated at all time points after the treatments compared with findings in the controls (caerulein alone) in terms of wet weight of pancreas, serum concentrations of amylase and lipase, formation of intracellular vacuoles in acinar cells, interstitial edema, and infiltration of an inflammatory cell component. The inhibitory effects of SMS, Gn, and NM on acute pancreatitis were similar at the doses used. These results suggest that SMS and Gn are as useful as NM, they may be of value for the treatment of acute pancreatitis.