CHAPTER 39
Chronic pancreatitis

Mitchell L. Ramsey¹, Zarine K. Shah², Darwin L. Conwell¹, and Phil A. Hart¹

¹ Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH, USA

² Department of Radiology, The Ohio State University Wexner Medical Center, Columbus, OH, USA

Chronic pancreatitis (CP) has been described as a pathological fibroinflammatory syndrome of the pancreas in individuals with genetic, environmental, and/or other risk factors who develop a persistent inflammatory response to parenchymal injury or stress. The pathological response to injury or stress leads to a variety of abnormalities including glandular atrophy, calcifications, fibrosis, and distortions of the pancreatic duct. Along with these morphological changes of the gland, patients commonly develop functional abnormalities, including diabetes mellitus and exocrine pancreatic insufficiency. Many patients develop a chronic abdominal pain syndrome that can significantly alter their quality of life. Other local and systemic complications can arise either directly or indirectly due to the anatomical and/or functional changes in CP.

Role of imaging in the diagnosis of chronic pancreatitis

In the absence of a viable option for histological diagnosis, a pragmatic algorithm for approaching the diagnosis of CP has been proposed, which begins with a history and physical exam followed by laboratory analyses. Imaging has an indispensable role in the diagnosis of CP due to the poor specificity of symptoms, exam findings, and laboratory results. A progression of imaging studies is typically utilized, including computed tomography (CT), magnetic resonance imaging with cholangiopancreatography (MRI/MRCP) with or without secretin stimulation, and endoscopic ultrasound (EUS).

Due to its widespread availability, CT imaging is considered to be the first‐line modality for the diagnostic evaluation of CP. Many patients with CP will have a history of recurrent acute pancreatitis (Figure 39.1). Generally, pancreatic parenchymal or ductal calcifications are considered diagnostic of chronic pancreatitis (Figure 39.2). In the absence of calcifications on CT, features of glandular atrophy, dilated side‐branches, and/or an irregular main pancreatic duct seen on MRI are suggestive of CP. The Cambridge criteria were originally proposed as a scoring system for endoscopic retrograde pancreatography (ERP), and have been adapted for use with cross‐sectional imaging (primarily MRI/MRCP). Consequently, this classification relies on ductal changes and does not account for parenchymal findings, such as calcifications or atrophy (Figure 39.3, Table 39.1). Pancreatic ductal irregularity can also be demonstrated on ERP (Figure 39.4), but this is no longer recommended solely for diagnostic purposes due to the risk of complications (including acute pancreatitis). Secretin may be used to improve visualization of the pancreatic duct during an MRI/MRCP (Figure 39.5).

Role of imaging in assessing complications of chronic pancreatitis

The most common symptom of CP is pain, which may be the result of local nociceptive inputs, central sensitization, or local complications. These local complications may include blockage of the main pancreatic duct leading to ductal hypertension, which is believed to be one mechanism for causing acute or chronic pain. Ductal hypertension can directly result from a pancreatic duct obstruction (Figure 39.6) or a pancreatic duct stricture. In rare instances, ductal hypertension can contribute to the development of pancreatic fistulas, which may drain enzyme‐rich pancreatic juice into adjacent potential spaces, such as the pleura (Figure 39.7). An important consideration in patients with longstanding CP who develop pain is to exclude a pancreatic malignancy, as these patients are at increased risk for developing pancreatic ductal adenocarcinoma (Figure 39.8).

Splanchnic thromboses may occur as a consequence of acute or chronic pancreatitis. While the majority of thromboses are asymptomatic, they may lead to sinistral portal hypertension with formation of gastric varices, which can cause life‐threatening hemorrhage. Additionally, splanchnic thromboses or direct inflammation of the peripancreatic vasculature can promote aneurysm formation from the splenic or gastroduodenal arteries, which can also cause severe bleeding (Figure 39.9).

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