Volume 126, Issue 3, Pages 715-723 (March 2004) Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis  Marianna Arvanitakis, Myriam Delhaye, Viviane De Maertelaere, Monia Bali, Catherine Winant, Emmanuel Coppens, Jacques Jeanmart, Marc Zalcman, Daniel Van Gansbeke, Jacques Devière, Celso Matos  Gastroenterology  Volume 126, Issue 3, Pages 715-723 (March 2004) DOI: 10.1053/j.gastro.2003.12.006

Figure 1 Acute pancreatitis with peripancreatic exudates. Axial T2-weighted (A) and arterial phase gadolinium-enhanced T1-weighted (B) MRI sections display increased signal intensity of peripancreatic fat tissues (arrows) in A and no enhancement of pancreatic parenchyma compared with the spleen in B. Nonenhanced MRCP (C) does not show the full length of the main pancreatic duct, whereas on secretin-enhanced MRCP (D), the main pancreatic duct is completely filled allowing disruption to be ruled out. Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)

Figure 2 Acute biliary pancreatitis. Axial T2-weighted (A), nonenhanced (B), and gadolinium-enhanced (C) T1-weighted MRI sections show areas of signal heterogeneity within the pancreatic parenchyma and heterogeneous glandular enhancement as well as a peripancreatic exudate. Gallstones are also displayed (arrow). Secretin-enhanced MRCP (D) displays a filling defect in the common bile duct corresponding to a stone (arrow), a nondilated main pancreatic duct not filled in the head, and periduodenal exudates (arrowhead). Areas of necrosis are also seen in the parenchyma. Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)

Figure 3 Same patient as Figure 2, 7 days later. Axial T2-weighted (A), nonenhanced (B), and gadolinium-enhanced (C) T1-weighted sections now display a peripancreatic fluid collection (hyperintense in A and nonenhancing in C) associated with decreased parenchymal enhancement (arrows). Secretin-enhanced MRCP (D) clearly shows the topography of the fluid collections and the full length of the main pancreatic duct. Necrotic areas in the head are increased in size. Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)

Figure 4 Severe necrotizing acute pancreatitis, 7 days after admission. (A) Contrast-enhanced T1-weighted axial MRI sections showing areas of hypoperfusion in the head and body of the pancreas appearing as zones of decreased signal intensity (arrow) and peripancreatic acute fluid collections (arrowhead). (B) T2 heavily weighted coronal MRI sections following secretin injection (S-MRCP) showing main pancreatic duct rupture (arrow). Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)

Figure 5 Spearman’s correlation between MRSI and CTSI on admission in 39 patients with acute pancreatitis. Numbers in parentheses indicate the number of patients represented by the adjoining square. Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)

Figure 6 Spearman’s correlation between MRSI on admission and the Ranson score for 39 patients with acute pancreatitis. Numbers in parentheses indicate the number of patients represented by the adjoining square. Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)

Figure 7 Spearman’s correlation between MRSI on admission and clinical outcome for 39 patients with acute pancreatitis. Clinical outcome is defined on a scale from 0 to 3 as follows: 0: restitution to normal, 1: local complications, 2: systemic complications, 3: death. Numbers in parentheses indicate the number of patients represented by the adjoining square. Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)

Figure 8 Clinical outcome of 39 patients with acute pancreatitis. Gastroenterology 2004 126, 715-723DOI: (10.1053/j.gastro.2003.12.006)