The original 1992 Atlanta Classification System for acute pancreatitis was revised in 2012 by the Atlanta Working Group, assisted by various national and international societies, through web-based consensus. This revised classification identifies two phases of acute pancreatitis: early and late. Acute pancreatitis can be either oedematous interstitial pancreatitis or necrotizing pancreatitis. Severity of the disease is categorized into three levels: mild, moderately severe and severe, depending upon organ failure and local/systemic complications. According to the type of pancreatitis, collections are further divided into acute peripancreatic fluid collection, pseudocyst, acute necrotic collection, and walled-off necrosis. Insight into the revised terminology is essential for accurate communication of imaging findings. In this review article, we will summarize the updated nomenclature and illustrate corresponding imaging findings using examples.
A 63-year-old man with no history of alcohol abuse presented with sudden, severe epigastric pain. The serum lipase level was elevated, a finding consistent with acute pancreatitis. Despite supportive care with fluid hydration, pain medication, and bowel rest, the patient’s condition deteriorated.
There is no question that incretin-based glucose-lowering medications have proven to be effective glucose-lowering agents. Glucagon-like peptide 1 (GLP-1) receptor agonists demonstrate an efficacy comparable to insulin treatment and appear to do so with significant effects to promote weight loss with minimal hypoglycemia. In addition, there is significant data with dipeptidyl peptidase 4 (DPP-4) inhibitors showing efficacy comparable to sulfonylureas but with weight neutral effects and reduced risk for hypoglycemia. However, over the recent past there have been concerns reported regarding the long-term consequences of using such therapies, and the issues raised are in regard to the potential of both classes to promote acute pancreatitis, to initiate histological changes suggesting chronic pancreatitis including associated preneoplastic lesions, and potentially, in the long run, pancreatic cancer. Other issues relate to a potential risk for the increase in thyroid cancer. There is clearly conflicting data that has been presented in preclinical studies and in epidemiologic studies. To provide an understanding of both sides of the argument, we provide a discussion of this topic as part of this two-part point-counterpoint narrative. In the point narrative below, Dr. Butler and colleagues provide their opinion and review of the data to date and that we need to reconsider the use of incretin-based therapies because of the growing concern of potential risk and based on a clearer understanding of the mechanism of action. In the counterpoint narrative following the contribution by Dr. Butler and colleagues, Dr. Nauck provides a defense of incretin-based therapies and that the benefits clearly outweigh any concern of risk.
PURPOSE: This study prospectively assessed whether the presence of a bull’s-eye pattern of pancreatic-duct stones on multidetector computed tomography (MDCT) correlated with gene-mutation-associated pancreatitis (GMAP) and whether other signs suggestive of GMAP can be detected with MDCT. MATERIALS AND METHODS: Forty-seven patients with chronic calcific pancreatitis underwent genetic testing for CFTR, SPINK1 and PRSS1 mutations and an MDCT scan of the abdomen. Qualitative analysis assessed the presence or absence of pancreatic-duct stones with bull’s-eye appearance. Quantitative analysis included the number and maximum diameter of stones and the diameter of the main pancreatic duct. RESULTS: Fifteen of 47 patients (32%) were positive for gene mutations (GMAP patients). The bull’s-eye pattern was found in 10/15 patients (67%) with GMAP and in 4/32 (12%) patients with chronic pancreatitis not associated with GMAP (NGMAP; p<0.0001). The mean diameter of duct stones was 15 mm in patients with GMAP and 10 mm in patients with NGMAP (p<0.04). CONCLUSIONS: The presence of duct stones with a bull's-eye pattern correlates with GMAP. Duct stones with diameter ≥15 mm are another sign suggestive of GMAP.
No association between mitochondrial disease and pancreatitis has yet been established, although diabetes mellitus and diseases caused by exocrine insufficiency, such as Pearson syndrome, are the commonest pancreatic complications of mitochondrial diseases. Here, we report 2 cases of mitochondrial disease complicated by pancreatitis as an unusual pancreatic exocrine manifestation. One patient was a 10-year-old girl with mild retardation of psychomotor development who had experienced recurrent pancreatitis since the age of 4years. Chronic progressive external ophthalmoplegia (CPEO) due to m.8344A>G mutation was diagnosed when the patient was 10years old. The other patient was a 28-year-old woman who was diagnosed with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) due to m.3243A>G mutation at 10years of age. She had experienced regular recurrent vomiting since the age of 16 and suffered an episode of critical pancreatitis at 23years. In both cases, no possible etiological, morphological, or genetic factors for pancreatitis were identified, including anomalous pancreaticobiliary duct. A combination therapy of the standard treatment for chronic pancreatitis and supportive therapy for mitochondrial energy production may be beneficial to prevent the recurrence of acute pancreatitis complicating mitochondrial diseases. The pathophysiological mechanism of pancreatitis in mitochondrial disease has not been adequately established; however, our observations suggest that pancreatitis should be included in the list of pancreatic complications of mitochondrial disease.
Acute pancreatitis is most commonly caused by gallstones or chronic alcohol use, and accounts for more than 200,000 hospital admissions annually. Using the Atlanta criteria, acute pancreatitis is diagnosed when a patient presents with two of three findings, including abdominal pain suggestive of pancreatitis, serum amylase and/or lipase levels at least three times the normal level, and characteristic findings on imaging. It is important to distinguish mild from severe disease because severe pancreatitis has a mortality rate of up to 30%. Contrast-enhanced computed tomography is considered the diagnostic standard for radiologic evaluation of acute pancreatitis because of its success in predicting disease severity and prognosis. The BALI and computed tomography severity index scores also can aid in determining disease severity and predicting the likelihood of complications. Treatment begins with pain control, hydration, and bowel rest. In the first 48 to 72 hours of treatment, monitoring is required to prevent morbidity and mortality associated with worsening pancreatitis. When prolonged bowel rest is indicated, enteral nutrition is associated with lower rates of complications, including death, multiorgan failure, local complications, and systemic infections, than parenteral nutrition. In severe cases involving greater than 30% necrosis, antibiotic prophylaxis with imipenem/cilastatin decreases the risk of pancreatic infection. In gallstone-associated pancreatitis, early cholecystectomy and endoscopic retrograde cholangiopancreatography with sphincterotomy can decrease length of hospital stay and complication rates. A multidisciplinary approach to care is essential in cases involving pancreatic necrosis.
We aimed to assess the risk of death, cancer, and comorbidities among patients with alcoholic and non-alcoholic chronic pancreatitis (CP).
Little is known regarding the optimal type of fluid resuscitation in acute pancreatitis (AP).
Patients with a first episode of acute pancreatitis can develop recurrent or chronic pancreatitis (CP). However, little is known about the incidence or risk factors for these events.
EUS-guided hepaticogastrostomy (EUS-HGS) is useful for treating obstructive jaundice. However, stent migration may sometimes occur both during and after the procedure. This report describes a patient with pancreatic cancer and massive ascites who underwent EUS-HGS combined with EUS-guided antegrade stenting (EUS-AS), with additional EUS-AS playing a role in troubleshooting for stent migration during EUS-HGS.