We searched PubMed for the term “acute pancreatitis”, together with “aetiology”, “pathogenesis”, “prognostic parameters”, “complications”, “death”, “treatment”, or “prognosis”. We included articles in English, French, German, and Spanish from Jan 1, 2009 to Dec 31, 2013, together with highly cited older publications that seemed necessary for full understanding. Moreover, we included several sets of guidelines, two of which cover almost the whole range of acute pancreatitis—namely, those from
SeminarAcute pancreatitis
Introduction
In this Seminar, we provide a comprehensive and balanced account of the advances since the 2008 Seminar in The Lancet on acute pancreatitis,3 highlight areas of controversy or international differences in practice, and describe concepts underlying the disease. The annual incidence of acute pancreatitis ranges from 13 to 45 per 100 000 people (appendix).4 In patients treated in hospital in the USA in 2009, acute pancreatitis was the most frequent principal discharge diagnosis in gastrointestinal disease and hepatology.5 The number of discharges with acute pancreatitis as principal diagnosis was 30% higher than in 2000. Acute pancreatitis was the second highest cause of total hospital stays, the largest contributor to aggregate costs, and the fifth leading cause of in-hospital deaths, showing the importance of accurate data for the disorder.
Section snippets
Causes
Gallstones and alcohol misuse are the main risk factors for acute pancreatitis (appendix). During 20–30 years, however, the risk of biliary pancreatitis is unlikely to be more than 2% in patients with asymptomatic gallstones6 and that of alcoholic pancreatitis is unlikely to exceed 2–3% in heavy drinkers.7 Other factors, possibly genetic, therefore probably play a part. Drugs represent an additional cause of acute pacreatitis8 (panel 1 and appendix).
Smoking might increase the risk of acute
Mechanisms of cellular injury
Pancreatic duct obstruction, irrespective of the mechanism, leads to upstream blockage of pancreatic secretion, which in turn impedes exocytosis of zymogen granules (containing digestive enzymes) from acinar cells. Consequently, the zymogen granules coalesce with intracellular lysosomes to form condensing or autophagic vacuoles containing an admixture of digestive and lysosomal enzymes. The lysosomal enzyme cathepsin B can activate the conversion of trypsinogen to trypsin. Findings from studies
Classification
The Atlanta classification45 is the standard classification of the severity of acute pancreatitis. The recently published revised classification46 provides definitions of the clinical and radiologic severity of acute pancreatitis. Clinical severity of acute pancreatitis is stratified into three categories: mild, moderately severe, and severe (table 2).
Patients with mild acute pancreatitis (no organ failure or systemic or local complications) usually do not need pancreatic imaging and are
Main diagnostic procedures
Clinicians are interested in confirmation of the diagnosis and exclusion of differential diagnoses (appendix). In accordance with the revised Atlanta classification, acute pancreatitis can be diagnosed if at least two of the following three criteria are fulfilled: abdominal pain (acute onset of persistent and severe epigastric pain, often radiating to the back); serum lipase (or amylase) activity at least three-times the upper limit of normal; or characteristic findings of acute pancreatitis on
Therapy
The patient's management begins on the emergency ward, where acute pancreatitis has to be confirmed, the risk stratified, and basic treatment initiated. This treatment includes early fluid resuscitation, analgesia, and nutritional support (appendix). Patients undergoing volume resuscitation should have the head of the bed raised, undergo continuous pulse oximetry, and receive supplemental oxygen. Supplemental oxygen has been shown to more than half mortality in patients older than 60 years.63
In
Necrosis
Prophylactic antibiotics are not indicated.87, 88, 89, 90 Surgical resection of pancreatic necroses can be achieved by open, laparoscopic, or staged necrosectomy (open-staged or closed-continuous lavage). These methods do not compete with, but rather complement, other techniques. No guidelines exist, but there is consensus that surgical intervention should be done—if at all—at a late stage, at least 2 weeks after the onset of pancreatitis.91
More conservative interventions than surgery now
Refeeding
Basic treatment of acute pancreatitis should be continued until the patient shows distinct clinical improvement (freedom from pain and normal body temperature and abdominal findings). No binding recommendation for severe acute pancreatitis exists; the decision is taken on an individual basis. In mild acute pancreatitis, oral feeding should be resumed as soon as possible according to the present European Society for Parenteral and Enteral Nutrition guidelines.111 When and how this feeding should
Prevention
One study127 showed that interventions by medical personnel (structured talks with patients by nurses trained to inform patients how and why they should stay abstinent) at 6-month intervals significantly lowered the recurrence rate of alcohol-induced pancreatitis within 2 years. In patients with mild biliary acute pancreatitis, cholecystectomy should be done before discharge. In patients with necrotising biliary acute pancreatitis, cholecystectomy should be postponed to prevent infection until
Conclusions
From the pathophysiological viewpoint, the consensus has been that exposure of acinar cells to injurious agents (alcohol or bile salts) perturbs a multitude of acinar functions (exocytosis, enzyme activation, lysosomal function, cytokine production, mitochondrial function, and autophagy); however, findings from studies suggest that the final common mechanism that mediates acinar cell death (irrespective of the cause of acute pancreatitis) might be aberrant intracellular calcium signalling.44
Search strategy and selection criteria
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