There has been a proliferation and divergence of imaging-based tumor-specific response criteria over the past 3 decades whose purpose is to achieve objective assessment of treatment response in oncologic clinical trials. The World Health Organization (WHO) criteria, published in 1981, were the first response criteria and made use of bidimensional measurements of tumors. The Response Evaluation Criteria in Solid Tumors (RECIST) were created in 2000 and revised in 2009. The RECIST criteria made use of unidimensional measurements and addressed several pitfalls and limitations of the original WHO criteria. Both the WHO and RECIST criteria were developed during the era of cytotoxic chemotherapeutic agents and are still widely used. However, treatment strategies changed over the past decade, and the limitations of using tumor size alone in patients undergoing targeted therapy (including arbitrarily determined cutoff values to categorize tumor response and progression, lack of information about changes in tumor attenuation, inability to help distinguish viable tumor from nonviable components, and inconsistency of size measurements) necessitated revision of these criteria. More recent criteria that are used for targeted therapies include the Choi response criteria for gastrointestinal stromal tumor, modified RECIST criteria for hepatocellular carcinoma, and Immune-related Response Criteria for melanoma. The Cheson criteria and Positron Emission Tomography Response Criteria in Solid Tumors make use of positron emission tomography to provide functional information and thereby help determine tumor viability. As newer therapeutic agents and approaches become available, it may be necessary to further modify existing anatomy-based response-assessment methodologies, verify promising functional imaging methods in large prospective trials, and investigate new quantitative imaging technologies.

Comparison of tumor volumes at serial CT examinations reveals a very wide range of growth rates. Some tumors grow so slowly that biopsy is required to prove they are malignant.

It is difficult to identify normal peritoneal folds and ligaments at imaging. However, infectious, inflammatory, neoplastic, and traumatic processes frequently involve the peritoneal cavity and its reflections; thus, it is important to identify the affected peritoneal ligaments and spaces. Knowledge of these structures is important for accurate reporting and helps elucidate the sites of involvement to the surgeon. The potential peritoneal spaces; the peritoneal reflections that form the peritoneal ligaments, mesenteries, and omenta; and the natural flow of peritoneal fluid determine the route of spread of intraperitoneal fluid and disease processes within the abdominal cavity. The peritoneal ligaments, mesenteries, and omenta also serve as boundaries for disease processes and as conduits for the spread of disease.

A discrete intrapancreatic fluid collection along the expected course of the main pancreatic duct with viable upstream pancreatic parenchyma suggests the diagnosis of DPDS. ERCP findings of ductal obstruction at the level of this fluid collection with or without contrast extravasation confirm this diagnosis. Treatment is surgical and requires either internal drainage or distal pancreatic resection for complete resolution.

Given the technologic advances of the past decade, pancreatic MRI protocols have evolved. Most sequences can now be performed in one or a few breath-holds; 3D sequences with thin, contiguous slices offer improved spatial resolution; and better fat and motion suppression allow improved contrast resolution and image quality. The diagnostic potential of MRCP is now almost as good as ERCP, with pancreatic MRI as the main imaging technique to investigate biliopancreatic pain, chronic pancreatitis, and cystic pancreatic tumors at many institutions. In addition, functional information is provided with secretin-enhanced MRCP.

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In patients with severe acute pancreatitis, the percentage of necrosis of pancreatic glandular parenchyma is an important predictor of prognosis. However, little attention has been paid to necrosis of ductal epithelium, which may result in disconnection of the main pancreatic duct. In pancreatic duct disconnection, a viable segment of the pancreatic body or tail is isolated from the gastrointestinal tract; the result is a persistent end fistula, that is, an uncontrolled leak of pancreatic secretions into peripancreatic spaces without communication to the gastrointestinal tract. The authors present their experience with clinical and radiologic follow-up of 85 patients with necrotic pancreatitis who either did (n = 46) or did not (n = 39) have pancreatic duct disconnection at surgery. Confident preoperative diagnosis of a disconnected duct requires both imaging tests (computed tomography or magnetic resonance imaging) and pancreatography. However, not all peripancreatic collections signify ductal disconnection, and imaging has poor accuracy in differentiation between pancreatic and peripancreatic necrosis. Early recognition of disconnected pancreatic duct obviates unnecessary and potentially harmful drainage procedures.