Mistakes in the management of acute pancreatitis and how to avoid them
Critical decision-making points & pitfalls
Acute pancreatitis is a common inflammatory disorder of the pancreas and its incidence is increasing among hospitalized patients worldwide.
The main symptoms include severe upper abdominal pain (often sudden onset), nausea, vomiting, bloating and the development of ileus. In many cases jaundice will also be present. The diagnosis, as agreed by international consensus, can be established by fulfilling two of the following three criteria: upper abdominal pain of sudden onset, elevation of either serum lipase or amylase activity to greater than three times the upper limit of normal, and imaging findings consistent with inflammation of the pancreas.4–6
By far the most common risk factors for the development of acute pancreatitis are excessive alcohol consumption and gallstone disease. Several mutations have been identified that, in combination with nongenetic factors or alone, can lead to pancreatitis. Certain drugs are known to be associated with the development of pancreatitis and smoking might also increase the probability of it developing. 80–85% of patients diagnosed with the disease will have mild disease and make an uneventful recovery with little more than adequate fluid therapy and analgesia needed to support them. The remaining patients, however, will suffer from moderately severe to severe acute pancreatitis, with the development of pancreatic necrosis, severe sepsis or abdominal compartment syndrome. These patients are at immediate danger of multiorgan failure and death and require multidisciplinary intensive care, organ support and often pancreatic interventions conducted by experienced investigators. Since it is difficult to predict outcomes and complications develop during the disease course, treatment in specialized centres that have a high case load is recommended.4
Here, we discuss critical decision-making points and pitfalls frequently occurring when managing patients with acute pancreatitis. The discussion is based on the medical literature and many years of clinical experience.
In 2009, it was the most frequent diagnosis in patients discharged from GI services in the US and the fifth leading cause of in-hospital mortality.1 Because of this high disease burden, acute pancreatitis is also a substantial contributor to healthcare spending, accounting for an estimated annual spend of US$4–7 million per million inhabitants in western countries.2,3
NAFLD and diabetes—are they symptoms of gut dysbiosis?
Connecting changes in gut microbiota to metabolic and hepatic diseases
The idea that obesity is a direct consequence of changes in gut microbiota structure and function that lead to enhanced extraction of energy from the host diet has been discussed for some years. Studies now suggest that associated diseases such as non-alcoholic fatty liver disease (NAFLD) and diabetes may also be considered consequences of intestinal dysbiosis.A leading cause of liver transplantation, NAFLD may now top the list of the most common liver diseases in developed countries. In an article published in Gastroenterology earlier this year, Betrapally and colleagues argue that “…the development and progression of fatty liver, alcoholic fatty liver disease, and NAFLD all appear to be influenced by the composition of the [gut] microbiota.”1 The way the gut microbiota influences the progression of these diseases appears to be complex, potentially involving diet-induced changes in bacterial metabolomes and microbial interactions with, for instance, bile acids and gut hormones such as glucagon-like peptide 1 (GLP1).1,2 An incretin secreted by enteroendocrine L cells, GLP1 induces pancreatic β-cell proliferation, maintains glucose-dependent insulin secretion and inhibits glucagon release, gastric emptying and food intake. Short-chain fatty acids (SCFAs) synthesized by certain bacteria activate the G-protein-coupled receptors GPR41 and GPR43, promoting secretion of GLP1.1 This was exemplified in a randomized controlled trial (RCT), in which Alisi and colleagues investigated the effect of the probiotic VSL#3, a mixture of eight probiotic strains (Streptococcus thermophilus, bifidobacteria [B. breve, B. infantis, B. longum], Lactobacillus acidophilus, L. plantarum, L. paracasei, and L. delbrueckii subsp. bulgaricus) in children with NAFLD, using changes in the severity of the fatty liver disease as the primary outcome.2 They found that a 4-month supplement of VSL#3 significantly improved NAFLD, probably through VSL#3-dependent reversal of dysbiosis. Of note, however, is the fact that no data were included on gut microbiota profiling prior to or after intervention. Nevertheless, the authors speculated that restoration of normal gut flora led to reduced intestinal permeability, increased production of SCFAs and anorexogenic gut hormones, including GLP1, as well as enhanced insulin sensitivity. The effect of consuming 300g of probiotic yoghurt containing Lactobacillus acidophilus La5 and Bifidobacterium lactis Bb12 every day for 8 weeks on selected metabolic parameters was studied in an RCT comprising 72 NAFLD patients.3 Patients consuming the probiotic yoghurt exhibited a reduction in the levels of serum hepatic enzymes (alanine aminotransferase and aspartate aminotransferase), serum total cholesterol, and low-density lipoprotein cholesterol. Again, no microbiota profiling was performed in order to try to link the findings with potential restoration of gut eubiosis. Meanwhile, other studies—although not intervention studies—have taken to investigating the gut microbiota profiles of patients with NAFLD lesions such as non-alcoholic steatohepatosis and fibrosis. These studies have identified independent associations between the predominance of certain bacterial groups and the presence of fatty liver disease.4,5 The fact remains, however, that we still need intervention studies that include pre-intervention and post-intervention gut microbiota profiling, preferably including data on the gut metabolome as well. And, as pointed out by Wieland and colleagues,6 we still need data in order to be able to delineate causality and obtain a mechanistic understanding of how in fact obesity and related metabolic and hepatic disease might reflect changes in gut microbiota structure and function.
We still need intervention studies that include pre-intervention and post-intervention gut microbiota profilingOn a different—yet related—note, a study has just been published in Nature identifying Prevotella copri as a driver of insulin resistance and potentially the development of type-2 diabetes.7 Mice fed P. copri developed increased serum levels of branched-chain amino acids, insulin resistance and reduced glucose tolerance. Hence, P. copri was identified as one of the bacterial species most critical to the development of insulin resistance. This finding suggests that type-2 diabetes is effectively the result of intestinal dysbiosis with predominance of certain bacteria such as P. copri. The results of future research will reveal the extent to which obesity and associated metabolic and hepatic diseases may be alleviated and perhaps even treated via gut microbiota manipulation with prebiotics, probiotics, synbiotics, antibiotics or other compounds such as SCFAs.8 If you are interested in the role of the gut microbiota in the development of NAFLD, especially changes in SCFA metabolism, I highly recommend perusing the review by Leung and colleagues in Nature Reviews Gastroenterology & Hepatology.9 For even more information on microbiota-associated pathogenesis of liver disease and its complications, I suggest reading the reviews by Schnabel and Brenner,10 Boursier and Diehl,11 Quigley and Monsour,12 and Abdou and colleagues.13 To find out more about the use of probiotics in the therapy of NAFLD, the reviews by Putignani et al.14 and Tarantino and Finelli15 are also worth consulting. References
- Betrapally NS, Gillevet PM and Bajaj JS. Changes in the intestinal microbioma and alcoholic and nonalcoholic liver diseases: Causes of effects? Gastroenterology 2016; 150: 1745–1755.
- Alisi A, Bedogni G, Beviera G, et al. Randomised clinical trial: the beneficial effects of VSL#3 in obese children with non-alcoholic steatohepatitis. Aliment Pharmacol Ther 2014; 39: 1276–1285.
- Nabavi S, Rafraf M, Somi MH, et al. Effects of probiotic yogurt consumption on metabolic factors in individuals with nonalcoholic fatty liver disease. J Dairy Sci 2014; 97: 7386–7393.
- Boursier J, Mueller O, Barret M, et al. The severity of nonalcoholic fatty liver disease is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota. Hepatology 2016; 63: 764–775.
- Jiang W, Wu N, Wang X, et al. Dysbiosis gut microbiota associated with inflammation and impaired mucosal immune function in intestine of humans with non-alcoholic fatty liver disease. Sci Rep 2015; 5: 8096.
- Wieland A, Frank DN, Harnke B, et al. Systematic review: microbial dysbiosis and non-alcoholic fatty liver disease. Aliment Pharmacol Ther 2015; 42: 1051–1063.
- Pedersen HK, Gudmundsdottir V, Nielsen HB, et al. Human gut microbes impact hos serum metabolome and insulin sensitivity. Nature 2016; 535: 376–381.
- Jin CJ, Sellmann C, Engstler AJ, et al. Supplementation of sodium butyrate protects mice from the development of non-alcoholic steatohepatitis (NASH). Br J Nutr 2015; 114: 1745–1755.
- Leung C, Rivera L, Furness JB, et al. The role of the gut microbiota in NAFLD. Nat Rev Gastroenterol Hepatol 2016; 13: 412–425.
- Schnabl B and Brenner DA. Interactions between the intestinal microbiome and liver diseases. Gastroenterology 2014; 146: 1513–1524.
- Boursier J and Diehl AM. Implication of gut microbiota in nonalcoholic fatty liver disease. PLoS Pathog 2015; 11: e1004559.
- Quigley EM and Monsour HP. The gut microbiota and nonalcoholic fatty liver disease. Semin Liver Dis 2015; 35: 262–269.
- Abdou RM, Zhu L, Baker RD, et al. Gut microbiota of nonalcoholic fatty liver disease. Dig Dis Sci 2016; 61: 1268–1281.
- Putignani L, Alisi A and Nobili V. Pediatric NAFLD: the future role of patient-tailored probiotics therapy. J Pediatr Gastroenterol Nutr 2016; 63 Suppl 1: S6–8.
- Tarantino G and Finelli C. Systematic review on intervention with prebiotics/probiotics in patients with obesity-related nonalcoholic fatty liver disease. Future Microbiol 2015; 10: 889–902.
The ABC of E-learning
How UEG E-learning fills a gap in Continuing Medical Education and how you can get the most out of our Online Education offer.
Mistakes in endoscopic retrograde cholangiopancreatography and how to avoid them
Endoscopic retrograde cholangiopancreatography (ERCP) is a widespread technique used for the treatment of different diseases of the bile and pancreatic ducts.
Endoscopic retrograde cholangiopancreatography (ERCP) is a widespread technique used for the treatment of different diseases of the bile and pancreatic ducts. The technique is, however, associated with rare but potentially severe morbidity.Some of the adverse events associated with ERCP are directly linked to commonly made mistakes and can, therefore, be prevented. Here, we discuss 10 common and/or high-impact mistakes that are made during ERCP and how they can be avoided.
Updates on calprotectin and IBD—where to look?
Endoscopy with biopsy is the gold standard for detection and monitoring of intestinal inflammation.
Endoscopy with biopsy is the gold standard for detection and monitoring of intestinal inflammation. Meanwhile, the use of surrogate markers (biomarkers) enables gastroenterologists to reduce costs and inconvenience in the management of intestinal disorders by eliminating the need for invasive procedures. Hence, efficient application of biomarkers for disease detection and assessment of treatment response is critical to cost-effective control of gastrointestinal disease. In this setting, elevated levels of C-reactive protein are a general sign of inflammation and widely used in combination with faecal calprotectin for the detection and monitoring of inflammatory bowel disease (IBD).Calprotectin is a protein found particularly in neutrophils but also in monocytes. Neutrophil disruption results in the release of calprotectin, although some of it is actively secreted.1 Detection of calprotectin in stool indicates neutrophil migration and infiltration in the intestinal tract, including the gut mucosa. Resisting enzymatic degradation, calprotectin is highly stable and can be detected in stool kept at room temperature for at least 7 days.2 Calprotectin levels in stool (usually expressed as µg/g of faeces) correlate well with endoscopic scoring systems for IBD, such as the ulcerative colitis endoscopic index of severity (UCEIS) and Crohn’s disease endoscopic index of severity (CDEIS), and may even perform better than the Crohn’s Disease Activity Index (CDAI).2 In his comprehensive Gastroenterology review on biomarkers of inflammation in IBD, Bruce Sands summarized the applicability and relevance of using faecal calprotectin to distinguish between IBD and irritable bowel syndrome, and also for categorizing IBD activity, ascertaining response to treatment and predicting clinical relapse.3 Reviews in leading journals are, of course, an excellent tool for updating yourself on state-of-the-art knowledge within a given area; however, the plethora of material present in the UEG Education Library may also prove highly useful. For example, searching the library for calprotectin currently returns no fewer than 338 hits, including 214 conference abstracts, 64 presentations, 55 posters, and 4 syllabus contributions submitted by leading gastroenterologists and rising stars. Among the four syllabus contributions, there is one specifically focused on calprotectin by Christoph Beglinger; for this particular syllabus contribution you have the option to read the pdf or view the associated presentation from UEG Week 2013.4 If you’re looking for the latest progress on the use of calprotectin, filtering your 338 hits by year narrows the results to 59 items for 2015. Among these hits, there are three abstracts from UEG Week 2015 on a smartphone-based calprotectin home test—a technology that was developed to try to eliminate the need for patients to bring stool samples to the clinic for analysis and to allow them to play a more active role in their disease management. Another great place to search for relevant information is in the ‘Standards and Guidelines’ that are also now available via the UEG Education Library. There are currently 17 IBD standards and guidelines available for you to access. One of these articles is “Second European evidence-based consensus on the diagnosis and management of ulcerative colitis Part 1: Definitions and diagnosis”, which you can use to update yourself on consensus opinion on the application of calprotectin.5 Finally, the UEG 24/7 pathway gives you access to all core scientific lectures from UEG Week 2015 in Barcelona. Here, you have the option to select the IBD pathway or you can narrow the results by entering the word biomarker in the filter by title’ search box. Any interesting hits? References:
- Ikhtaire S, et al. Fecal calprotectin: its scope and utility in the management of inflammatory bowel disease. J Gastroenterol 2016; 51: 434–446.
- Dhar A. Faecal calprotectin—ready for prime time? Frontline Gastroenterol 2015; 6: 11–13.
- Sands BE. Biomarkers of inflammation in inflammatory bowel disease. Gastroenterology 2015; 149: 1275–1285.
- “Utility of faecal markers in IBD clinical practice” syllabus contribution at UEG Week 2013
- Dignass A, et al. Second European evidence-based consensus on the diagnosis and management of ulcerative colitis Part 1: Definitions and diagnosis. J Crohn’s Colitis 2012; 6: 965–990.
Recordings covering hot topics in experimental GI cancer
Highlight recordings from the Basic Science Course 2016 in Munich are now online.
Mistakes in IBD and reproduction and how to avoid them
Find out more about the major mistakes and misperceptions!
Inflammatory bowel disease (IBD) is a chronic relapsing gastrointestinal disease, often affecting young people during their fertile years. The chronic character of IBD means that lifelong medical treatment is often required. As such, it is not surprising that questions often arise about fertility and pregnancy in patients with IBD.The most important risk factor for adverse pregnancy outcomes in IBD patients is the presence of disease activity during pregnancy. Indeed, negative pregnancy outcomes (e.g. spontaneous abortion, preterm delivery and low birth weight) are associated with disease activity at the time of conception and during pregnancy.1–4 The majority of pregnancies in women with quiescent IBD are uncomplicated. This demonstrates the importance of maintaining remission by continuing medication during pregnancy. Counselling patients before pregnancy on the effects of IBD drugs and disease activity on the child in utero is, therefore, of utmost importance. Although much is known about reproduction and IBD, misbeliefs regarding pregnancy and IBD still persist. Here, we present 10 major mistakes and misperceptions that are made when treating IBD patients who wish to reproduce. The list and discussion are evidence based and integrated in our clinical practice.
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Find out more
Get access to recorded lectures from Summer School Prague 2016.This intense clinical-based weekend course is perfect for trainees and early career medical professionals and can now be attended from home.
EDS Surgery Course Recordings
Discover the highlights of the 10th EDS Postgraduate Course featuring a large variety of surgical state-of-the-art lectures.
Mistakes in upper gastrointestinal bleeding and how to avoid them
Discover more about the most frequent mistakes!
Faecal microbiota transplantation
Learn about FMT—the transfer of gut microbiota from a healthy donor to a recipient.
Primer in capsule endoscopy
Discover more about the procedure, indications, potential complications and how to use capsule reporting software.
Understand the role of liver biopsy in diagnosis and indications, contraindications, different techniques and steps involved.
Mistakes in mouse models of IBD and how to avoid them
Learn how to get the most from experimental colitis models!
In general, mouse models of colitis are used to study its pathophysiology and for the development of new treatment modalities for inflammatory bowel disease (IBD). For the latter it is essential to select a mouse model that has many overlapping features with human IBD.More than 50 experimental colitis models have been developed and they have provided us with very useful insights into IBD physiology, as reviewed by Bouma and Strober1 and others,2–4 but they have limited use in predicting the clinical relevance of therapeutic targets in IBD.5 Experimental colitis models broadly fit into four different groups. First is spontaneous colitis, resulting from a naturally occurring genetic abnormality. Second is induced colitis occurring as a consequence of a targeted mutation or the introduction of a transgene. Third is induced colitis resulting from administration of different exogenous causative agents. Fourth is induction of colitis by manipulation of the immune system. We have learned a great deal from these models about the involvement of genetics, the microbiota and the role of different cells and the mucus layer in the development of IBD. Here we discuss the major mistakes that are made using experimental colitis models, based on our own experience and the scientific literature. Recently increased awareness has developed for the necessity to improve the methodological quality of animal studies.
ERCP & EUS Symposium
Recordings from the last Quality in Endoscopy series cover topics including “Conquering the papilla”, “Diagnostic EUS” and “Pancreatitis”.
Scientific writing practice
32 aspiring researchers met at the House of European Gastroenterology to practice how to craft research papers and abstracts.
Mistakes in colorectal cancer and how to avoid them
Specialist tips on diagnosis, prevention and treatment!
Colorectal cancer (CRC) is one of the most common malignancies and the second leading cause of cancer death in both sexes in developed countries. Over the past 30 years, a great advance in the understanding of this disease has occurred, from colorectal carcinogenesis to diagnosis, prevention and treatment.Although the majority of CRCs are related to environmental factors, up to 25% of cases have a familial component and potential genetic basis, and highly penetrant monogenic germline mutations account for up to 5% of all CRC cases1. Identification and characterization of these hereditary disorders have allowed modification of their natural history, with a substantial decrease in morbidity and mortality among high-risk patients1. Nonetheless, the majority of patients who are at high risk of CRC remain undiagnosed due to lack of suspicion. On the other hand, studies from the past two decades have suggested that besides adenomas, serrated polyps are also precursors of CRC, responsible for up to 15–30% of all malignancies.2 Several studies have demonstrated that serrated polyps are common precursors of colonoscopy interval cancers (cancers diagnosed within the surveillance interval after a complete colonoscopy), mainly due to their challenging clinical management.2 Finally, strategies for CRC prevention have shown efficacy in reducing CRC incidence and mortality, and colonoscopy is an integral part of CRC screening strategies. The main objective of screening colonoscopy is the detection and removal of premalignant lesions or early CRC.3 However, colonoscopy is not perfect, and some lesions may be missed. Colonoscopy quality is an emerging concept, and some quality indicators have been demonstrated to be directly related to the development of interval CRC.3 Here we discuss the major mistakes that are made when gastroenterologists deal with CRC diagnosis, prevention and treatment, and how to avoid them. The list of mistakes and the discussion that follows is evidence based and integrated with our longstanding clinical experience.
Mistakes in dyspepsia and how to avoid them
Expert knowledge at your fingertips!
Dyspepsia refers to upper abdominal discomfort that is thought to arise from the upper gastrointestinal tract. Symptoms include epigastric pain or discomfort, bloating, early satiety and/or fullness after meals, repeated belching or regurgitation (often rumination), nausea and heartburn.1 The symptoms of dyspepsia are nonspecific, but most commonly result from one of four underlying disorders: functional (nonulcer) dyspepsia, gastro-oesophageal reflux disease (GORD; 10–20% erosive esophagitis), peptic ulcer disease (5–15%) and malignancy (~1%).2 Dyspeptic symptoms may also result from other problems, such as medication intolerance, pancreatitis, biliary tract disease or motility disorders (e.g. gastroparesis or gastric dumping).Clinical guidelines recommend that endoscopy is not always required for diagnosis; a positive diagnosis of GORD and functional dyspepsia can be based on clinical presentation in the absence of alarm symptoms or features (see below).3,4 In many cases symptoms are increased after meal ingestion (postprandial distress syndrome), being triggered by impaired gastric accommodation and visceral hypersensitivity to gastric distension.5 Other patients have an epigastric pain syndrome in which discomfort is independent of food intake and gastrointestinal function.6 There is an important overlap between functional dyspepsia and other functional gastrointestinal diseases (e.g. irritable bowel syndrome [IBS]) and chronic pain syndromes (e.g. fibromyalgia).7 Psychological disease (e.g. anxiety or somatization disorder) and/or psychosocial stress are also present in a significant proportion of patients who seek medical attention.8,9 Notwithstanding the constructive advice provided by published reviews and guidelines, the broad definition of dyspepsia, lack of diagnostic investigations, uncertain cause of disease, psychosocial issues and paucity of specific treatments make the management of dyspepsia challenging. Here, I discuss 10 common and/or high-impact mistakes that are made in the diagnosis and treatment of patients with dyspeptic symptoms: five related to diagnosis, five related to treatment.
Mistakes in coeliac disease diagnosis and how to avoid them
Learn from leaders in the field!