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Acute necrotizing pancreatitis occurs in about 10% of patients with acute pancreatitis, and is associated with a considerably higher mortality and morbidity than in those who have IEP. Pancreatic necrosis refers to nonviable parenchyma, and can be focal or diffuse. The Revised Atlanta Classification system has divided pancreatic necrosis into three subtypes based on anatomic location: pancreatic parenchyma, peripancreatic fat, and both pancreatic parenchyma and peripancreatic fat. Early diagnosis of pancreatic necrosis can be done using either post‐contrast CT or MRI examination [8]. Necrotizing pancreatitis is clinically diagnosed when more than 30% of the gland is affected by necrosis [9].

Parenchymal necrosis is seen as well‐demarcated low signal areas on T1‐weighted pre‐contrast sequences corresponding to nonenhancing areas on post‐contrast sequences [10]. However, evaluation of pancreatic necrosis is less accurate during the first week after the onset of acute pancreatitis. In the most acute phase of pancreatitis, increased parenchymal edema may result in decreased enhancement of viable pancreatic tissue, which limits the reliable estimation of necrosis. After a week or more, resolution of this acute parenchymal edema will improve the enhancement of any viable tissue, leaving truly nonviable tissue able to be more accurately diagnosed and quantified.

MRI is also useful in the detection of hemorrhage, as MRI is highly sensitive to the paramagnetic effect of the methemoglobin that is deposited in the setting of bleeding. Hemorrhage is recognized on MRI as high signal intensities on fat‐suppressed T1‐ and T2‐weighted images. Conversely, chronic hematoma can be hypointense on both T1‐ and T2‐weighted images due to transformation of methemoglobin into hemosiderin [11].

Table 6.1 MRI protocol for evaluating acute or chronic pancreatitis.

MRI sequence	Target organ	MRI findings
T1‐weighted gradient echo 2D or 3D. Dixon, nonfat suppressed, axial, breath‐hold. Axial slice thickness 6 mm	Parenchyma	Pancreatic inflammation: low signal
T2‐weighted single‐shot fast spin echo. 2D, nonfat suppressed, axial and coronal, breath‐hold. Axial and coronal slice thickness 4 mm	Pancreatic and biliary ducts.	Pancreatic inflammation: increased signal Fluid collection and cystic lesions: high signal intensity Ductal stones, abnormal side branches
T2‐weighted turbo spin echo 2D. Fat‐suppressed respiratory or navigator triggered. Axial slice thickness 6 mm	Parenchyma and retroperitoneum	Parenchymal and peripancreatic fat inflammation: increased signal
T2‐weighted 3D MRCP respiratory or navigator triggered high resolution. Coronal 40‐mm 3D slab	Ductal evaluation	3D MRCP provides ERCP‐like high‐resolution duct images. Disconnected duct, fistula, abnormal side branches, ductal anomalies; pancreas divisum
T2‐weighted 2D MRCP, breath‐hold, coronal 40 mm single shot	Ductal evaluation and secretin enhancement	Pancreatic abnormalities, disconnected or disrupted duct, pancreas exocrine capacity
T1‐weighted gradient echo 3D, fat suppressed, breath‐hold. Axial, 2‐mm reconstruction	Parenchymal organs and vessels	Pancreatic inflammation: decreased enhancement Pancreatic necrosis: no enhancement Vessels, active hemorrhage, pseudoaneurysm

Figure 6.1 A 44‐year‐old male presents with acute onset of severe abdominal pain and elevated lipase. (a) Axial T2‐weighted fat‐suppressed image demonstrates acute pancreatitis with hyperintense peripancreatic fluid and pancreatic parenchyma due to interstitial edema. (b) Post‐contrast T1‐weighted image demonstrates decreased enhancement of parenchyma.

Sources: (a) courtesy of Fatih Akisik; (b) Sandrasegaran et al. [7]. Reproduced with permission of American Journal of Roentgenology.

Pancreatic necrosis is responsible for approximately 40% of cases of disconnected pancreatic duct. In the presence of residual functioning pancreatic parenchyma upstream to the disconnected pancreatic duct, fluid collections or peripancreatic ascites will develop. T2‐weighted MRCP images will show a disconnected pancreatic duct often connected to adjacent fluid collection. In some cases, the pancreatic duct may not be completely disconnected but a focal rupture can cause leakage and/or fistula formation. In both entities, enlarging fluid collection(s) may be seen. Retrospective analysis of cases of pancreatic duct disruption show that MRCP identified significantly more cases than ERCP (91% vs. 74%) [12].