Introduction

Acute pancreatitis is a common disease, characterised by painful inflammation of the pancreas. It is diagnosed if two of the following three criteria are present: abdominal pain, level of serum lipase (or amylase) three times the upper limit of normal serum levels, and characteristic finding on imaging (i.e., contrast-enhanced computed tomography [CECT]) ( Fig. 15.1 ). The clinical course and severity of acute pancreatitis varies widely. In most patients, acute pancreatitis is mild and self-limiting. With conservative therapy including adequate fluid resuscitation and analgesia, the vast majority of patients recover within days. However, approximately 20% of patients develop moderate or severe acute pancreatitis with local and/or systemic complications, such as necrosis of the (peri)pancreatic tissue and organ failure. Compared to mild acute pancreatitis, which has a mortality rate below 1%, complicated acute pancreatitis is associated with a high mortality of 10–30%, especially if necrosis becomes infected.

Figure 15.1, Algorithm for the management of acute pancreatitis. ERCP , Endoscopic retrograde cholangiopancreatography; ICU , intensive care unit.

The two most common causes of acute pancreatitis are biliary (e.g., gallstones or biliary sludge leading to temporary obstruction of the common bile duct and pancreatic duct) and alcohol. Other causes include endoscopic retrograde cholangiography (ERCP), which although a minimally invasive procedure, is associated with a risk of post-ERCP pancreatitis in 6–15% of cases. Identifying the aetiology and early detection of complications following acute pancreatitis is key to offer accurate treatment. To date, the optimal timing and type of treatment required to manage the complications of acute pancreatitis remains challenging because of the heterogeneity of the disease and the complexity of clinical decision making.

Definitions and terminology

In 1993 the Atlanta Classification of acute pancreatitis categorised disease-related definitions and enabled specialists from different backgrounds to discuss various types of acute pancreatitis. It also introduced uniformity in the assessment of acute pancreatitis.

Because of new and improved insights in the management of acute pancreatitis, the Atlanta Classification system was revised in 2012. New definitions were added for different disease-phases, disease severity and local complications.

Based on the duration of disease-related symptoms, two phases of acute pancreatitis are now defined, that is, early and late, with a cut-off of less than or more than 4 weeks. In addition, a third category was added to the severity of acute pancreatitis, resulting in mild, moderately severe or severe acute pancreatitis. The revised classification provided definitions for complications and categorised local fluid collections based on duration of symptoms, their content and whether they were sterile or infected. Several studies reported this revised classification system to be accurate and superior compared to the original Atlanta Classification. ,

Local complications of peripancreatic collections in acute pancreatitis are categorised based on duration of symptoms (with a cut-off of less than or more than 4 week) and whether this is sterile or infected.

Imaging in acute pancreatitis

Computed tomography

CECT is the standard imaging modality in acute pancreatitis to establish the diagnosis, determine the severity and identify complications. , Computed tomography (CT) is best performed beyond 72 hours from disease onset to detect (peri)pancreatic necrosis, with a sensitivity rate close to 100%. Therefore CECT on admission for acute pancreatitis is generally not recommended, except in patients with an uncertain diagnosis or with severe symptoms (e.g., organ failure). In these patients, a CT should be considered to exclude secondary peritonitis caused by perforation or mesenteric ischemia. Although concerns have been raised over the risk of post-contrast acute renal failure in severely ill patients, a recent meta-analysis showed no correlation. Follow-up CT is indicated in patients with clinical deterioration or failure of continued clinical improvement.

Magnetic resonance imaging

Magnetic resonance imaging (MRI) in acute pancreatitis is recommended in patients with allergy to iodinated contrast, patients with renal impairment caused by the lack of renal nephrotoxicity and in young or pregnant patients to avoid radiation exposure. MRI might be superior in visualising necrosis within ‘walled off necrosis’ (WON) and can be useful in evaluating the pancreatic duct and the presence of a duct rupture resulting in a disconnected pancreatic duct syndrome. MRI may also has a role in diagnosing acute pancreatitis and in assessing disease severity based on morphological changes and the (peri)pancreatic tissue.

Initial general management

Since the primary focus of this chapter is the management of complications of acute pancreatitis, the initial treatment of mild acute pancreatitis will not be addressed.

Antibiotic administration is not recommended for patients with mild pancreatitis, but should be reserved for severely ill patients, including those with systemic inflammatory response (SIRS), infected necrosis, multi-organ failure or extra-pancreatic infection. Early ERCP is not indicated in patients with mild biliary pancreatitis. In patients with predicted severe biliary pancreatitis without cholangitis, studies have shown that an early ERCP with sphincterotomy did not reduce the risk of major complications or mortality when compared to conservative management. However, ERCP should be considered in patients with cholangitis or persistent cholestasis associated with predicted severe acute biliary pancreatitis.

In acute pancreatitis, a prolonged catabolic illness is often seen, especially in patients with more complex and severe disease. It is important to anticipate nutritional insufficiency and ensure optimal nutritional support. This will positively influence the maintenance of the intestinal barrier function, inhibiting bacterial translocation and reduce the systematic inflammatory response. Multiple options for nutritional support are available. Bakker et al. found that early enteral tube feeding within 24 hours did not reduce risk of infection (25% vs. 25%) or mortality (11% vs. 7%). However, enteral tube feeding should be considered if patients have insufficient intake after 72 hours, as commonly seen in the more severe cases. Nasogastric feeding, if tolerated, has been shown to be safe but nasojejunal feeding can be undertaken if required. Enteral feeding is preferred over parental feeding because of a lower risk on infectious complications, organ failure and mortality. ,

Clinical patterns and complications

A wide variety of complications can occur in patients with acute pancreatitis and can be classified as local and/or systemic. The clinical course, disease manifestations, and prognosis of complications in acute pancreatitis is somewhat unpredictable and varies greatly between individuals. Timely diagnosis and accurate evaluation of severity are key for clinical management. Prediction of severity by surveillance of systematic inflammatory response or organ failure for a minimum of 48 hours after admission, and management by a multi-disciplinary team is therefore strongly recommended.

Classification of severity

This chapter mainly focuses on moderately severe and severe acute pancreatitis as defined by the revised Atlanta Classification. Moderately severe acute pancreatitis is defined as local or systematic complications, without persistent organ failure. Organ failure can sometimes be present at admission but can improve within 48 hours after initial treatment. Persistent organ failure distinguishes moderately severe from severe acute pancreatitis, since severe acute pancreatitis is characterised by persistent organ failure, which generally requires urgent transfer for prolonged management in an intensive care setting (ICU).

Local complications following acute pancreatitis

Acute pancreatitis can be accompanied by local complications of which (peri)pancreatic fluid collections are the most common. A clear distinction must be made between different collections based on location (peripancreatic or pancreatic area), the nature of the content (liquid, solid, gas) and the presence of a well-defined wall ( Fig. 15.2 ). Collections can be categorised as arising from either interstitial oedematous pancreatitis or collections deriving from necrotising pancreatitis.

Figure 15.2, Local complications in acute pancreatitis, defined according to the Atlanta criteria. (a) Acute peripancreatic fluid collection (≤4 weeks). (b) Acute necrotic collection: necrotising pancreatitis (≤4 weeks). (c) Pancreatic pseudocyst (≥4 weeks). (d) Walled-off necrosis (≥4 weeks).

Interstitial oedematous pancreatitis

In patients with interstitial oedematous pancreatitis, localised or diffuse enlargement of the pancreas is seen with homogeneous or slightly heterogeneous enhancement of the pancreatic parenchyma on CECT, without sings of (peri)pancreatic necrosis.

Acute peripancreatic fluids collection

One of the early complications associated with acute pancreatitis is the development of an acute peripancreatic fluid collection (APFC), defined as a non-encapsulated homogeneous peripancreatic collection that develops within the first 4 weeks after disease onset. Approximately 25% of all patients will develop APFC, which can be distinguished from other fluid collections based on morphological characteristics such as the absence of debris. APFCs are caused by (peri)pancreatic inflammation or as a consequence of rupture of small peripheral pancreatic side duct branches. In general, APFCs resolve spontaneously within a couple of weeks, remain sterile and do not require intervention. A small percentage of APFCs persist beyond 4 weeks and are then referred to as pancreatic pseudocysts.

Pancreatic pseudocyst

Pancreatic pseudocysts are defined as encapsulated fluid collections and can be either asymptomatic or symptomatic, and may cause biliary or gastric outlet obstruction, bleeding or become secondarily infected ( Fig. 15.3 ). Pancreatic pseudocysts are uncommon in patients with acute pancreatitis (approximately 10–20%), and are more frequently seen in patients with chronic pancreatitis. Although the majority of pancreatic pseudocysts will resolve spontaneously and require no further intervention, treatment is needed in selected patients depending on the size and presence of clinical symptoms. Among the treatment options available, endoscopic transluminal drainage is the first choice and is preferably performed once the collection becomes encapsulated. If there is communication with the main pancreatic duct, additional transpapillary drainage should be considered. Pancreatic pseudocysts rarely become infected and can be diagnosed on CECT by the presence of gas within the pseudocyst or by using fine-needle aspiration (FNA). Infected pseudocysts require antibiotics and either endoscopic or surgical drainage since complications of these pseudocysts include prolonged abdominal pain, sepsis, erosion into vessel leading to haemorrhage, obstruction and rupture leading to acute peritonitis.

Figure 15.3, Large pseudocyst causing gastric and extra-hepatic biliary obstruction with jaundice.

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