1= spread into the lesser sac will deform the poserior gastric wall 2 = spread into the transverse mesocolon will cause deformity along the inferior border of the colon 3 = spread into the root of the bowel mesentery will cause deformity of the small bowel loops 4 = extension into the duodenum will cuse deformity and mucosal abnormalities 5= spread into the remainder of the retroperitoneum will cause changes in the anterior pararenal space
Fat necrosis sign is due
Due to high attenuation exudates, presence of pancreatic necrosis cannot be assessed unless the gland is imaged during late arterial-early portal venous phase of rapid bolus intra venous injection of contrast patchy areas of absence of enhancement, fragmentation, and liquefaction necrosis can be seen. Poorly defined peripancreatic exudates obliterate the peripancreatic fat, envelop the pancreas, dissect fascial planes, and penetrate through fascial and peritoneal boundaries and ligaments.
Acute Pancreatitis Pathophysiology Gore and Levine, Textbook of Gastrointestinal Radiology• Blockage of the pancreatic duct leads to increased pressure in pancreatic duct and rupture.• Pancreatic fluid (proteolytic and lipolytic enzymes) ruptures into pancreas parenchyma and anterior pararenal space
Anterior Pararenal Space• Kidney –like pancreas-is retroperitoneal• Shares Anterior pararenal space with duodenum, ascending and descending colon• Anterior to Aorta, IVC, and kidneys Robbins and Cotran, Pathologic Basis of Disease
The long range inflammatory missiles• Peripancreatic fluid can spread through diaphragmatic hiatuses ,peritoneal recesses, or retropritoneal fascial planes to present in remote sites.
Targets of Inflammatory spread in Acute Pancreatitis• 1= spread into the lesser sac• 2 = spread into the transverse mesocolon• 3 = spread into the root of the bowel mesentery• 4 = extension into the duodenum• 5= inferior spread into the remainder anterior pararenal space• 6=RP fluid colecting down to scrotum,or even thigh Gore and Levine, Textbook of Gastrointestinal Radiology
Imaging Goals in Pancreatitis1. Exclude other abdominal disorders that can mimic acute pancreatitis – DDx: acute cholecystitis, bowel obstruction or infarction, perforated viscus, renal colic, duodenal diverticulitis, aortic dissection, appendicitis, and ruptured abdominal aortic aneurysm2. Confirm clinical diagnosis of acute pancreatitis3. Staging the disease, by evaluation of the extent and nature of pancreatic injury and peripancreatic inflammation
Abdominal Plain FilmFindings of Acute Pancreatitis on Abdominal Plain Film – Duodenal ileus in 42% of patients – Colon cutoff (paucity of gas distal to splenic flexure due to spasm of colon affected by spread of pancreatic inflammation) – Pancreatic abscess (gas bubbles) – Abdominal fat necrosis and saponification (effects of activated lipase on fatty tissues)
Plain Chest Film• 1/3 of acute pancreatitis patients have pulmonary changes secondary to superior spread of pancreatic inflammation to diaphragm and lung bases • Findings of Acute Pancreatitis on Plain Chest Film: – pleural effusions (seen on 10% of chest films) – basal atelectasis – pulmonary infiltrates – elevated diaphragm – Acute Respiratory Distress Syndrome Gore and Levine, Textbook of Gastrointestinal Radiology
Ultrasound• Indications – Good screening test in mild disease, suspected biliary pancreatitis, and thin patients lacking fat planes for good CT evaluation• Uses – Exclude a diagnosis of gallstones – Follow up of pseudocysts – Doppler of cystic masses to rule out pseudoaneurysm• Major Limitations – Bowel gas – US cannot specifically reveal areas of necrosis
Computed Tomography“CT is the premier imaging test in the diagnosis and management of patients with acute pancreatitis. It visualizes the gland, the retroperitoneum, the abdominal ligaments, the mesenteries, and the omenta in their entirety.”
Bilateral renal halo sign• The halo appears as ground- glass attenuation on imaging, due to enhancement of the perirenal fat from the retroperitoneal collection of pancreatic exudates. Bilateral perirenal fluid collections are rare and suggest pancreatitis.
Pseudocyst in Lesser Sac or Gastric Wall ROI: •12 HU (simple fluid) •69mm x 36mm
Evaluation for Pancreatic Necrosis Focal areas of necrosis show enhancement of less than 30 HU in early arterial phase Due to high attenuation exudates, presence of pancreatic necrosis cannot be assessed unless the gland is imaged during late arterial-early portal venous phase of rapid bolus intravenous injection of contrast patchy areas of absence of enhancement, fragmentation, and liquefaction necrosis can be seen.
Inflammation Spreads to the Transverse ColonNormal Bowel Wall Edematous, Inflamed Bowel Wall Inflamed Fat Normal Fat
Splenic Vein thrombosisSplenic vein thrombosisoccurs in 2% to 4% ofpatients with chronicpancreatitis. This eventleads to isolated gastricvarices with resultinggastrointestinalhemorrhage.
Fluid Collections ROI: 16 HUCourse: Superolateral to (simple fluid) the region of the lesser sac, becoming contiguous with the greater curvature of the stomachStructure: ill-defined, with indistinct margins Image courtesy Dr. Anne Kim
Pancreatic AscitesDependent fluidcollectionbetween liverand diaphragmROI: 14 HU
I-Pancreatic cancer presenting as acute pancreatitis
II-Hemorrhagic Pancreatitis• Rare• Noted clinically by ↓ in hematocrit
70 year-old woman with hemorrhagic pancreatitisCT scan demonstrates hemorrhagic pancreatitis as a heterogeneous mass inthe area of the pancreatic bed (*). Arrow indicates active extravasation(hemorrhage).
III-Autoimmune pancreatitis in 1995 researchers described a form of pancreatitis associated with autoimmune manifestations. Today its known that about 5- 6 percent of all cases of chronic pancreatitis are autoimmune in nature.• Focal or diffuse enlargement• Delayed enhancement.• Capsule like rim.