Pancreas typically enlarged and edematous with loss of normal fatty lobulation
• Necrotizing pancreatitis (20-30% of cases): Areas of parenchymal necrosis which are either nonenhancing or severely hypoenhancing
• Complications
Infected pancreatic necrosis: Ectopic gas, in absence of intervention, highly suggestive of infected necrosis
Central necrosis: Necrosis of central portion of gland/duct with intact pancreas/duct in head and tail









IMAGING
General Features
CT Findings
• Revised Atlanta classification in 2012 standardized nomenclature used to describe acute pancreatitis
• 2 primary subtypes of acute pancreatitis
Interstitial edematous pancreatitis (70-80% of cases)

– Peripancreatic fat stranding, edema, and free fluid (with fluid most often localized to lesser sac, anterior pararenal spaces, and paracolic gutters)
• Complications
Infected pancreatic necrosis
Central necrosis (disconnected duct syndrome)
Extrapancreatic fat necrosis
Pseudoaneurysm
Venous thrombosis
Fluid collections


– Necrosis of central portion of gland and pancreatic duct with intact upstream and downstream pancreas/duct in head and tail


– Small contrast-filled outpouching arising next to artery ± adjacent hematoma (due to leak or rupture)


– Acute peripancreatic fluid collection: Fluid collection first 4 weeks after acute edematous pancreatitis
– Pseudocyst: Fluid collection persisting > 4 weeks after acute edematous pancreatitis
– Acute postnecrotic fluid collection: Fluid collection first 4 weeks after acute necrotizing pancreatitis
MR Findings
• Pancreas appears enlarged with increased signal on T2WI and abnormally low signal on T1WI due to edema
• T2WI offers advantage (over CT) of allowing differentiation of simple fluid collections from collections with internal solid debris (i.e., walled off necrosis)
DIFFERENTIAL DIAGNOSIS
Infiltrating Pancreatic Carcinoma
• Heterogeneous, hypoenhancing mass with abrupt obstruction of upstream pancreatic duct and upstream pancreatic atrophy
• Presence of dilated pancreatic duct or biliary obstruction should prompt further investigation for underlying mass
• Pancreatic cancer infiltrates dorsally into retroperitoneum, unlike pancreatitis, which infiltrates anteriorly and laterally
• Usually other signs of malignancy, including vascular encasement, metastatic disease (most often liver), etc.
PATHOLOGY
General Features
• Etiology
Many other causes, including metabolic disorders (e.g., hypertriglyceridemia, hypercalcemia), infection, trauma, drugs, anatomic variants (e.g., pancreatic divisum, annular pancreas), neoplasm (e.g., pancreatic adenocarcinoma or IPMN), iatrogenic (e.g., ERCP), etc.
Exact pathogenesis of acute pancreatitis unclear and may vary depending on etiology


– Possibilities include reflux of pancreatic enzymes, bile, and duodenal contents into pancreatic duct, increased ductal pressure due to ampullary obstruction, or activation of intracellular/extracellular homeostatic factors
CLINICAL ISSUES
Presentation
• Most common signs/symptoms
Natural History & Prognosis
• Prognosis
• Natural evolution of fluid collections
Treatment
• Initial treatment is conservative, including fluid resuscitation, pain control, n.p.o. (nothing by mouth) with nutritional support until patient can resume oral diet, and antibiotics (only if infection is suspected)
Early ERCP and sphincterotomy in patients with suspected gallstone pancreatitis only in setting of cholangitis or cholestasis

• Infected pancreatic necrosis may require surgical debridement (necrosectomy), although surgery typically deferred until 4 weeks after presentation to allow collections to become walled off















































































































