ABSTRACT
The pathophysiology of acute pancreatitis is as follows. Duodeno-pancreatic refl ux causes duodenal fl uid to enter the pancreas and activate the enzymes within it. This results in autodigestion of the pancreas by trypsin, fat necrosis by lipases and a signifi cant rise in blood amylase. Acute pancreatitis presents with an acute-onset epigastric pain that is severe and constant. It characteristically radiates through to the back and is relieved by sitting forward. Patients may also have nausea and vomiting, fever and features of shock. There may be associated infl ammatory exudates and peritonitis, presenting with a distended abdomen and absent bowel sounds. The swollen pancreas can block the distal common bile duct, resulting in jaundice. Infl ammatory exudates may collect between the stomach and pancreas, resulting in a pancreatic pseudocyst. This classically presents at day 10 of the disease. Extravasation of blood-stained exudate into the retroperitoneum results in a bluish discolouration of the skin. These can be seen as Cullen’s sign (periumbilical bruising) and Grey Turner’s sign (fl ank bruising).
