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      American College of Gastroenterology Guideline: Management of Acute Pancreatitis :

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          Abstract

          This guideline presents recommendations for the management of patients with acute pancreatitis (AP). During the past decade, there have been new understandings and developments in the diagnosis, etiology, and early and late management of the disease. As the diagnosis of AP is most often established by clinical symptoms and laboratory testing, contrast-enhanced computed tomography (CECT) and/or magnetic resonance imaging (MRI) of the pancreas should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically. Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed. Patients with organ failure and/or the systemic inflammatory response syndrome (SIRS) should be admitted to an intensive care unit or intermediary care setting whenever possible. Aggressive hydration should be provided to all patients, unless cardiovascular and/or renal comorbidites preclude it. Early aggressive intravenous hydration is most beneficial within the first 12-24 h, and may have little benefit beyond. Patients with AP and concurrent acute cholangitis should undergo endoscopic retrograde cholangiopancreatography (ERCP) within 24 h of admission. Pancreatic duct stents and/or postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients. Routine use of prophylactic antibiotics in patients with severe AP and/or sterile necrosis is not recommended. In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis may be useful in delaying intervention, thus decreasing morbidity and mortality. In mild AP, oral feedings can be started immediately if there is no nausea and vomiting. In severe AP, enteral nutrition is recommended to prevent infectious complications, whereas parenteral nutrition should be avoided. Asymptomatic pancreatic and/or extrapancreatic necrosis and/or pseudocysts do not warrant intervention regardless of size, location, and/or extension. In stable patients with infected necrosis, surgical, radiologic, and/or endoscopic drainage should be delayed, preferably for 4 weeks, to allow the development of a wall around the necrosis.

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          Most cited references106

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          The early prediction of mortality in acute pancreatitis: a large population-based study.

          Identification of patients at risk for mortality early in the course of acute pancreatitis (AP) is an important step in improving outcome. Using Classification and Regression Tree (CART) analysis, a clinical scoring system was developed for prediction of in-hospital mortality in AP. The scoring system was derived on data collected from 17,992 cases of AP from 212 hospitals in 2000-2001. The new scoring system was validated on data collected from 18,256 AP cases from 177 hospitals in 2004-2005. The accuracy of the scoring system for prediction of mortality was measured by the area under the receiver operating characteristic curve (AUC). The performance of the new scoring system was further validated by comparing its predictive accuracy with that of Acute Physiology and Chronic Health Examination (APACHE) II. CART analysis identified five variables for prediction of in-hospital mortality. One point is assigned for the presence of each of the following during the first 24 h: blood urea nitrogen (BUN) >25 mg/dl; impaired mental status; systemic inflammatory response syndrome (SIRS); age >60 years; or the presence of a pleural effusion (BISAP). Mortality ranged from >20% in the highest risk group to <1% in the lowest risk group. In the validation cohort, the BISAP AUC was 0.82 (95% CI 0.79 to 0.84) versus APACHE II AUC of 0.83 (95% CI 0.80 to 0.85). A new mortality-based prognostic scoring system for use in AP has been derived and validated. The BISAP is a simple and accurate method for the early identification of patients at increased risk for in-hospital mortality.
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            Risk factors for post-ERCP pancreatitis: a prospective, multicenter study.

            Post-ERCP pancreatitis is poorly understood. The goal of this study was to comprehensively evaluate potential procedure- and patient-related risk factors for post-ERCP pancreatitis over a wide spectrum of centers. Consecutive ERCP procedures were prospectively studied at 11 centers (6 private, 5 university). Complications were assessed at 30 days by using established consensus criteria. Pancreatitis occurred after 131 (6.7%) of 1963 consecutive ERCP procedures (mild 70, moderate 55, severe 6). By univariate analysis, 23 of 32 investigated variables were significant. Multivariate risk factors with adjusted odds ratios (OR) were prior ERCP-induced pancreatitis (OR 5.4), suspected sphincter of Oddi dysfunction (OR 2.6), female gender (OR 2.5), normal serum bilirubin (OR 1.9), absence of chronic pancreatitis (OR 1.9), biliary sphincter balloon dilation (OR 4.5), difficult cannulation (OR 3.4), pancreatic sphincterotomy (OR 3.1), and 1 or more injections of contrast into the pancreatic duct (OR 2.7). Small bile duct diameter, sphincter of Oddi manometry, biliary sphincterotomy, and lower ERCP case volume were not multivariate risk factors for pancreatitis, although endoscopists performing on average more than 2 ERCPs per week had significantly greater success at bile duct cannulation (96.5% versus 91.5%, p = 0.0001). Combinations of patient characteristics including female gender, normal serum bilirubin, recurrent abdominal pain, and previous post-ERCP pancreatitis placed patients at increasingly higher risk of pancreatitis, regardless of whether ERCP was diagnostic, manometric, or therapeutic. Patient-related factors are as important as procedure-related factors in determining risk for post-ERCP pancreatitis. These data emphasize the importance of careful patient selection as well as choice of technique in the avoidance of post-ERCP pancreatitis.
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              Persistent organ failure during the first week as a marker of fatal outcome in acute pancreatitis.

              In predicted severe acute pancreatitis, many patients develop organ failure and recover without local complications, and mortality is only 14-30%. It has been suggested that half of patients with progressive early organ failure may die, but there are no data to relate death or local complications to duration of early (week 1) organ failure. To determine mortality rates in patients with transient ( 48 hours) early organ failure and to show whether persistent organ failure predicts death or local complications. A total of 290 patients with predicted severe acute pancreatitis previously studied in a trial of lexipafant, recruited from 78 hospitals through 18 centres in the UK. Manual review of trial database to determine: the presence of organ failure (Marshall score > or =2) on each of the first seven days in hospital, duration of organ failure, and outcome of pancreatitis (death, complications by Atlanta criteria). Early organ failure was present in 174 (60%) patients. After transient organ failure (n = 71), outcome was good: one death and 29% local complications. Persistent organ failure (n = 103) was followed by 36 deaths and 77% local complications, irrespective of onset of organ failure on admission or later during the first week. Duration of organ failure during the first week of predicted severe acute pancreatitis is strongly associated with the risk of death or local complications. Resolution of organ failure within 48 hours suggests a good prognosis; persistent organ failure is a marker for subsequent death or local complications.
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                Author and article information

                Journal
                American Journal of Gastroenterology
                American Journal of Gastroenterology
                Springer Science and Business Media LLC
                0002-9270
                2013
                September 2013
                : 108
                : 9
                : 1400-1415
                Article
                10.1038/ajg.2013.218
                23896955
                e8519958-e9b8-48a5-a287-859f998a04fd
                © 2013

                http://www.springer.com/tdm

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