Gastroenteritis, acute adrenal insufficiency, sickle cell crisis, diabetic ketoacidosis, acute porphyria, pelvic inflammatory disease, kidney stones, and pyelonephritis.

Grey Turner’s sign refers to a blue-black discoloration in the flanks. It is considered a sign of retroperitoneal hemorrhage due to acute pancreatitis. Cullen’s sign is a blue-red discoloration at the umbilicus, and the appearance is a result of digested blood products in the retroperitoneum, forming methemalbumin, that then travel towards the anterior abdominal wall.

Epigastric pain radiating to the back, worsened with food, nausea/vomiting (90 % of cases), anorexia, or decreased oral intake. Physical exam frequently reveals fever, tachycardia, epigastric tenderness with localized guarding, and hypoactive bowel sounds secondary to reactive ileus.

One can remember these structures with the following mnemonic, “DID KAPA (the kangaroo) go retro”: Descending colon, IVC, Duodenum (2nd & 3rd segments), Kidney, Aorta, Pancreas, Ascending colon.

It initially occurs as a result of inappropriate activation of pancreatic enzymes leading to peripancreatic inflammation. Intraparenchymal extravasation of enzymes causes autodigestion of pancreatic parenchyma but primarily damages the peripancreatic tissues and vasculature. The inflammatory response is out of proportion to the insult and, with time, potentiates further damage leading to fluid sequestration, fat necrosis, vasculitis, and hemorrhage.

“GET SMASHED” will help you remember the causes of acute pancreatitis

The exact mechanism is not entirely clear. The most prevailing theory is the Opie’s common channel theory (in which the pancreatic and common bile ducts end in a common channel at the ampulla of Vater). A gallstone passes from the gallbladder down into the common bile duct. The theory attributes the inflammation to a transient impaction at the ampulla which not only causes increased pancreatic duct pressure but results in reflux of duodenal juices and bile into the pancreatic duct. Whether it is the increased pressure or the stasis of duct contents that leads to acute pancreatitis is undetermined.

The gallstones that cause pancreatitis are usually small, and as such, in the majority of cases, the stone remains impacted very briefly, only transiently obstructing the ampulla of Vater, and soon after passes into the duodenum. As such, persistence of a common bile duct (CBD) stone is uncommon and therefore Endoscopic retrograde cholangiopancreatography (ERCP) is not usually needed. This differs from gallstones that cause acute cholangitis, where the stones are usually large and usually need ERCP for removal.

The mechanism whereby alcohol causes acute pancreatitis is unclear. Interestingly, it usually occurs only after many years of alcohol abuse and not after single episodes of binge drinking in an alcohol-naïve pancreas. Intra-acinar activation of proteolytic enzymes seems to be one of the central requirements in all cases of pancreatitis. It has been proposed that the products of ethanol metabolism results in pancreatic hypoxia and oxidative damage, leading to an excessive increase in the calcium ion concentration in pancreatic cells (explaining low serum calcium that develops). Over time, this sensitizes the cells to respond to cholecystokinin (CCK) prematurely, leading to the inappropriate activation of zymogens in the cells.

There are three phases in acute pancreatitis, though not every patient goes through all three. Phase one consists of premature activation of trypsin within the pancreatic acinar cells. The second phase involves intrapancreatic inflammation, whereas phase three consists of extrapancreatic inflammation (affecting multiple organ systems).

The severity of pancreatitis is classified as mild and severe. Most patients (80–90 %) have mild pancreatitis, which is characterized by the absence of multiorgan failure and local/systemic complications. It usually resolves in 2–5 days. Severe pancreatitis is defined by the development of systemic complications (organ failure) and/or local (pancreatic) complications such as pancreatic pseudocyst, abscess, and necrosis (worst prognosis).