resulting in acinar cell damage and cytokines and other pro‐inflammatory markers that play a role in the subsequent systemic inflammatory response that results in tissue damage.5 In the majority of patients, the process is self‐limiting. However, in some patients, the disease process accelerates rapidly and can lead to pancreatic necrosis and generalized organ failure. Pancreatic necrosis can sometimes become infected by gut bacteria, which further increases the risk of mortality.
Presentation of acute pancreatitis
Patients with acute pancreatitis characteristically present with moderate to severe abdominal pain, often leading to hospital admission. The pain of pancreatitis usually occurs in the epigastrium and radiates through to the back and may be relieved by sitting forward. However, this presentation may differ in the elderly, and therefore pancreatitis may be confused with myocardial infarction or a perforated abdominal viscus.
The physical signs are those of an acute abdomen. Vomiting, fever, tachycardia, and hypotension may occur. Jaundice may also be a feature if there is concomitant biliary obstruction or cholangitis. Rarely, haemorrhagic pancreatitis can lead to retroperitoneal haemorrhage, causing bruising in the flanks (Grey Turner’s sign), around the umbilicus (Cullen’s sign) or even below the inguinal ligament (Fox’s sign).
Diagnosis of acute pancreatitis
Pancreatitis is diagnosed in patients with (i) characteristic abdominal symptoms, (ii) elevated serum amylase and/or lipase, and/or (iii) imaging demonstrating pancreatic inflammation. At least two of those three criteria must be met to render a diagnosis. Serum lipase is more specific than amylase. Lipase levels elevated three times the upper limit of normal, with characteristic abdominal pain, is considered diagnostic of pancreatitis. The serum lipase rises within 4–8 hours, peaks at 24 hours, and returns to normal in 8–14 days; but serum enzyme levels are not helpful in tracking the clinical course of the illness after the initial diagnosis is made, and daily lipase measurements are not helpful in monitoring the clinical course of pancreatitis patients.
Thoughtful use of radiologic imaging is essential in pancreatitis. An abdominal ultrasound is a helpful first step if aetiology is uncertain, to determine if gallstones or biliary dilation is present. A computed tomography (CT) scan is often performed in the early evaluation of pancreatitis, but we suggest that this should often not be necessary if the diagnosis is clear from other clinical parameters. A CT scan is often more valuable if performed on or after day 5 of a severe clinical course, at which point the presence or absence of pancreatic necrosis may be noted and has important prognostic implications. In elderly patients with mild pancreatitis, a CT scan, either at initial presentation or at four‐ to eight‐week follow‐up (once inflammation has completely diminished), can be important to rule out the rare possibility of tumour. In patients with persistent symptoms after weeks, a CT scan may also reveal the presence of a pseudocyst or walled‐off necrosis. The role of magnetic resonance cholangiopancreatography (MRCP) has expanded significantly over the years. MRCP can visualize biliary and pancreatic duct obstructions, occult lesions, microlithiasis, autoimmune pancreatitis, and complications of severe pancreatitis, e.g. peripancreatic fluid collections, necrosis, and pancreatic duct disruption. Due to its non‐invasive nature, it has largely replaced diagnostic endoscopic retrograde cholangiopancreatography (ERCP) for the investigation of suspected bile duct stones or other biliary or pancreatic ductal pathology. ERCP is now recognized as a high‐risk technique that is better suited to therapeutic indications.
In select patients, ERCP is indicated when there is a high pre‐test probability for choledocholithiasis, cholangitis, and biliary obstruction. Endoscopic ultrasound (EUS) is another highly sensitive diagnostic modality to visualize the biliary system, pancreatic duct, and parenchyma; it has had a growing role, in conjunction with MRCP, in ruling out biliary stones or sludge as a cause of pancreatitis.
Assessment of the severity of acute pancreatitis
Recognizing the disease severity of acute pancreatitis has important implications for both management and prognosis. Based on the revised Atlanta criteria, pancreatitis can be classified into mild, moderately severe, and severe disease. These categories are based on objective parameters of organ failure and local complications, e.g. peripancreatic fluid collections, pseudocyst, and necrosis. In the absence of organ failure and/or local complications, pancreatitis is considered mild. Moderately severe pancreatitis presents with transient organ failure (<48 hours) and/or the presence of local complications. Finally, severe pancreatitis is characterized by persistent organ failure beyond 48 hours. As expected, organ failure is one of the strongest predictors of prolonged hospitalization and mortality.6 Additionally, individual lab parameters, such as elevated hematocrit and blood urea nitrogen (BUN), can also help predict outcomes. Advanced age also carries a poor prognosis. Several scoring systems have been developed to predict disease severity and clinical outcomes, including the Ranson and Glasgow scores.7,8 Such prognostic indices are of proven value in predicting severe disease but suffer from the disadvantage that data collection is complex and must occur over 48 hours. In 2008, a simplified bedside clinical scoring system, the Bedside Index for Severity in Acute Pancreatitis (BISAP) score, was introduced. It was intended to simplify the prognostication of disease severity and predicting mortality by assessing only five variables: BUN, impairment of mental status, systemic inflammatory response (SIRS), age, and presence of pleural effusion. In a validation study, its performance was comparable to previous scoring systems.9 Patients with a BISAP Score >0 had an increased risk of mortality. A score of 5 predicts a mortality rate of 22%. A radiologic assessment of disease activity using CT scanning (Balthazar score) has also been studied and showed a good correlation with local complications and mortality.10
Management of acute pancreatitis
The majority of patients with pancreatitis present with mild disease and require only observation, IV fluids, and symptom control with analgesia and anti‐emetics. Antibiotics are rarely indicated. Patients with a BISAP score greater than 2 should generally be triaged to an intensive care unit for more careful monitoring.
Nutrition is another key therapeutic component. As opposed to delayed nutrition, early initiation of nutrition has shown improved outcomes, preferably using oral feeding.11 In patients with mild pancreatitis, early initiation of a low‐fat diet (versus a clear liquid diet) has been shown to reduce length of hospital stay. Patients with moderate or severe pancreatitis may not be in a clinical condition to tolerate oral feeding within 48–72 hours, so enteral feeding using a nasogastric or nasojejunal tube is recommended and should be initiated within 72 hours when possible. Several randomized controlled trials and meta‐analyses report no differences in pre‐pyloric versus post‐pyloric feeding.12 Parenteral nutrition is considered the last option for nutrition if caloric goals cannot be met through enteral means. Compared to enteral feeding, parenteral nutrition is associated with a significantly higher risk of infection in this patient population, including bacteraemia and infected necrosis.
Routine antibiotic therapy in severe acute pancreatitis is not recommended unless there is evidence of infected necrosis or persistent clinical instability concerning sepsis.13 In patients with bile duct stones, endoscopic duct clearance by ERCP is recommended, although this need not be performed urgently except in cholangitic patients. There is now clear data that patients with gallstones who develop mild acute pancreatitis should undergo cholecystectomy during their index admission to reduce the likelihood of repeated attacks and subsequent complications.14
Acute pancreatic fluid collections and pancreatic necrosis, which may develop in the first four weeks, are generally best managed conservatively. If these collections persist beyond four weeks, they can become walled off as pseudocysts (fluid) or walled‐off pancreatic necrosis (solid debris) (see Figure
