Practice Guidelines in Acute Pancreatitis

Abstract

INTRODUCTION Guidelines for the diagnosis and treatment of acute pancreatitis were published by the American College of Gastroenterology in 1997 (1). These and subsequent guidelines (2–7) have undergone periodic review (6, 8–13) in accordance with advances that have been made in the diagnosis and treatment of acute pancreatitis. Guidelines for clinical practice are intended to apply to all health-care providers who take care of patients with acute pancreatitis and are intended to be flexible, and to suggest preferable (but not the only) approaches. Because there is a wide range of choices in any health-care situation, the physician should select the course best suited to the individual patient and the clinical situation. These guidelines have been developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. The world literature in English was reviewed using a MEDLINE search and also using the Cochrane Library. The ratings of levels of evidence for these guidelines are indicated in Table 1. The final recommendations are based on the data available at the time of the publication of this document and may be updated with appropriate scientific development at a later time. The following guidelines are intended for adult and not pediatric patients. The main diagnostic guidelines include an assessment of risk factors of severity at admission and determination of severity. The major treatment guidelines include supportive care, fluid resuscitation, transfer to intensive care unit, enteral feeding, use of antibiotics, treatment of infected pancreatic necrosis, treatment of sterile pancreatic necrosis, treatment of associated pancreatic duct disruptions, and role of magnetic resonance cholangiopancreatography (MRCP), endoscopic ultrasound (EUS), and endoscopic retrograde cholangiopancreatography (ERCP) with biliary sphincterotomy for detection and treatment of choledocholithiasis in biliary pancreatitis.Table 1: Ratings of Evidence Used for This GuidelinePATHOPHYSIOLOGY The pathophysiology of acute pancreatitis is generally considered in three phases. In the first phase, there is premature activation of trypsin within pancreatic acinar cells. A variety of mechanisms have been proposed including disruption of calcium signaling in acinar cells (14–18), cleavage of trypsinogen to trypsin by the lysosomal hydrolase cathepsin-B, and decreased activity of the intracellular pancreatic trypsin inhibitor (17, 18). Once trypsin is activated, it activates a variety of injurious pancreatic digestive enzymes. In the second phase, there is intrapancreatic inflammation through a variety of mechanisms and pathways (16, 18–28). In the third phase, there is extrapancreatic inflammation including acute respiratory syndrome (ARDS) (16, 19–21, 29). In both phases, there are four important steps mediated by cytokines and other inflammatory mediators: 1) activation of inflammatory cells, 2) chemoattraction of activated inflammatory cells to the microcirculation, 3) activation of adhesion molecules allowing the binding of inflammatory cells to the endothelium, and 4) migration of activated inflammatory cells into areas of inflammation. In the majority of patients, acute pancreatitis is mild. In 10–20%, the various pathways that contribute to increased intrapancreatic and extrapancreatic inflammation result in what is generally termed systemic inflammatory response syndrome (SIRS) (Table 2). In some instances, SIRS predisposes to multiple organ dysfunction and/or pancreatic necrosis. The factors that determine severity are not clearly understood, but appear to involve a balance between proinflammatory and anti-inflammatory factors. Recent evidence suggests that the balance may be tipped in favor of proinflammatory factors by genetic polymorphisms of inflammatory mediators that increase severity of acute pancreatitis (27, 30, 31).Table 2: Systemic Inflammatory Response Syndrome (SIRS)CLINICAL CONSIDERATIONS Clinical Diagnosis It has been estimated that in the United States there are 210,000 admissions for acute pancreatitis each year (13). Most patients with acute pancreatitis experience abdominal pain that is located generally in the epigastrium and radiates to the back in approximately half of cases. The onset may be swift with pain reaching maximum intensity within 30 min, is frequently unbearable, and characteristically persists for more than 24 h without relief. The pain is often associated with nausea and vomiting. Physical examination usually reveals severe upper abdominal tenderness at times associated with guarding (32). is that a diagnosis of acute pancreatitis of the following three 1) abdominal pain of acute 2) and/or times the upper of and 3) of acute pancreatitis on This for the that an and/or be times the upper of in acute pancreatitis. In a patient with abdominal pain of acute pancreatitis and levels that are than times the upper of a be