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Interstitial edematous pancreatitis (IEP) (70-80% of cases): Normal enhancement of pancreas without necrosis
Pancreas typically enlarged and edematous
Peripancreatic fat stranding, edema, and free fluid
Mild edematous pancreatitis can appear normal on CT
Necrotizing pancreatitis (NP) (20-30% of cases): Areas of nonenhancing parenchymal necrosis
May necrose pancreatic duct as well
Necrosis usually develops within 3-4 days after symptom onset
Complications
Infected pancreatic necrosis : Ectopic gas, in absence of intervention, is highly suggestive of infected necrosis
Central necrosis : Necrosis of central portion of gland/duct with intact pancreas/duct in head and tail
Pseudoaneurysm : Most common locations are splenic (50%) and gastroduodenal (20%) arteries
Venous thrombosis : Splenic vein most common, but portal vein or superior mesenteric vein can be involved
Fluid collections : Nomenclature depends on age of collection and edematous vs. NP
Acute peripancreatic fluid collection : Fluid collection within first 4 weeks after acute IEP
Pseudocyst : Fluid collection persisting > 4 weeks
Acute necrotic collection : Nonloculated but containing internal necrotic debris and blood
Walled-off necrosis (WON) : Loculated, complex fluid collection persisting > 4 weeks after NP
Infiltrating pancreatic adenocarcinoma
Perforated duodenal ulcer
"Shock" pancreas
Lymphoma
Alcohol and gallstones account for vast majority of cases
Many other causes, including metabolic disorders, infection, trauma, drugs, anatomic variants, neoplasm, and ERCP
Multiphasic/multiplanar CT is best for initial evaluation
MR with MRCP is better for evaluation of pancreatic duct and complex fluid collections
Acute inflammation of pancreas with variable involvement of other regional tissues or remote organs
Best diagnostic clue
Enlarged, edematous pancreas with peripancreatic fluid, fat stranding, and fluid collections
Location
Pancreas and surrounding peripancreatic soft tissues
Size
Pancreas usually increased in size (either focal or diffuse)
Morphology
2 subtypes: Interstitial edematous, and necrotizing pancreatitis
Revised Atlanta classification in 2012 standardized nomenclature used to describe acute pancreatitis
2 primary subtypes of acute pancreatitis
Interstitial edematous pancreatitis (IEP) (70-80%)
Pancreas typically enlarged and edematous
Peripancreatic fat stranding, edema, and free fluid
Usually involves entire gland but can be focal
Normal enhancement of pancreas without necrosis
Normal CT does not exclude pancreatitis
Necrotizing pancreatitis (NP) (20-30% of cases): Areas of parenchymal necrosis that are either nonenhancing or severely hypoenhancing (usually < 30 HU)
Usually more peripancreatic inflammation than IEP
Differentiate cases with ≤ 30% parenchymal necrosis from > 30% necrosis for patient prognosis
Necrosis may not be present initially but can develop within 3-4 days after symptom onset
Early CT can underestimate or miss necrosis
Necrosis both parenchymal and peripancreatic in 75%, peripancreatic alone 20%, parenchymal alone 5%
Parenchymal necrosis alone in 5%
Peripancreatic necrosis alone in 20%
Complications
Infected pancreatic necrosis
Implies superinfection of necrotic parenchyma
Ectopic gas in pancreatic bed, in absence of intervention or fistula, virtually diagnostic
No other specific findings, although inflammation usually greater in cases with infected necrosis
May require aspiration for culture
Central necrosis (disconnected duct syndrome)
Necrosis of parenchyma and duct in body with intact pancreas/duct in head and tail
Results in encapsulated fluid/debris collection with continual leakage of pancreatic fluid into collection
Diagnosis should be suggested based on distribution of necrosis
Collection may require either internal drainage or surgery (usually distal pancreatectomy)
Extrapancreatic fat necrosis
Pancreatic enzymes cause fat necrosis
Usually low density with heterogeneous fluid and solid components but can appear nodular and mass-like, mimicking carcinomatosis
Most often peripancreatic, mesenteric, retroperitoneal
Carries better prognosis than parenchymal necrosis but worse than IEP
Pseudoaneurysm
Small contrast-filled outpouching arising next to artery ± adjacent hematoma (due to leak or rupture)
Mostly splenic (50%) and gastroduodenal (20%) arteries
Unexplained hemorrhage in pancreatic bed should prompt careful search for pseudoaneurysm
Venous thrombosis
May occur due to direct intimal injury or mass effect from adjacent collections
Splenic vein > portal vein or superior mesenteric vein (SMV)
Fluid collections
Acute peripancreatic fluid collection : Fluid collection first 4 weeks after acute IEP
Simple, nonloculated with no internal debris
Pseudocyst : Fluid collection persisting > 4 weeks
Loculated with well-defined, enhancing wall usually in lesser sac or pararenal spaces
Can rarely be found in unusual locations distant from pancreas, such as thorax
Simple fluid attenuation with no internal debris
Acute necrotic collection : Fluid collection within first 4 weeks after acute NP
Nonloculated but containing internal necrotic debris and blood
Acute complex fluid collection with internal debris and solid material in setting of a normally enhancing gland suggests ANC due to extrapancreatic necrosis
Walled-off necrosis (WON) : Loculated fluid collection persisting > 4 weeks after NP
Heterogeneous collection with well-defined wall and internal necrotic debris/blood products
"Pancreatic abscess" : Term no longer utilized in revised Atlanta classification
"Hemorrhagic" pancreatitis :Term not included in Atlanta classification
Small amounts of blood frequently present in peripancreatic fluid collections and has no direct impact on disease severity
Pancreas appears enlarged with increased signal on T2WI and abnormally low signal on T1WI due to edema
Fat suppression very important in highlighting edema and fluid on T2WI
T1WI C+ images similar to CECT in detection of necrosis and nonenhancement
T2WI offers advantage (over CT) of allowing differentiation of simple fluid collections from those with internal solid debris (i.e., WON)
MRCP can evaluate integrity of pancreatic duct, unlike CT
May delineate communication between collection and pancreatic duct
Can delineate anatomic variants which might predispose to pancreatitis, including pancreatic divisum
Very sensitive for gallstones and other biliary pathology
Acute pancreatitis may be associated with restricted diffusion (lower ADC values than normal pancreas)
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