elevations in lipase or amylase are more common and may not be of clinical significance. 15–25% of pancreatitis episodes are categorized as idiopathic. Cholecystectomy has been shown to reduce recurrence of idiopathic pancreatitis, suggesting that some ‘idiopathic’ pancreatitis may be due to microlithiasis.
In the elderly – and indeed, in all patients – medications are often considered as a possible cause of pancreatitis when no other cause is identified. In fact, with the exception of a small group of anti‐retroviral and immunomodulator medications, true drug‐related pancreatitis is likely very uncommon. Most reports of drug‐related pancreatitis are anecdotal, and the potential severity of the disease precludes drug challenges. A large retrospective German study of acute pancreatitis implicated drugs as a possible cause in only 1.4% of pancreatitis patients.3
Finally, autoimmune pancreatitis can be seen in the elderly, but rather than presenting as acute pancreatitis more often presents as a suspected pancreatic mass, with or without painless jaundice, raising concern for adenocarcinoma.4 There are two recognized entities of this condition: Type 1 and 2. Type 1, also known as IgG4‐related pancreatitis, is more prevalent in the older population. On imaging, it is typically characterized by a diffuse ‘sausage‐shaped’ pancreatic enlargement with an irregular narrow pancreatic duct. Histologically, there is lymphoplasmacytic infiltrate with ‘swirling fibrosis’ and obliterative phlebitis. The tissue stains positive for IgG4‐positive cells. Serum levels of IgG4 are often elevated (typically to at least two times the upper limit of normal). Extra‐pancreatic involvement can be seen, including biliary stricturing, retroperitoneal fibrosis, mediastinal lymphadenopathy, and infiltration of the kidneys, salivary glands, and parotids. This condition is typically highly responsive to steroid treatment.
Pathophysiology of acute pancreatitis
The underlying pathophysiological mechanism in acute pancreatitis varies based on the inciting event. The central theory of pancreatitis revolves around the activation of intrapancreatic trypsinogen, 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