In acute pancreatitis, the overflowing pancreatic juice contains a large amount of pancreatic enzymes that spread along the tissue interstitial space and seep under the skin to dissolve the subcutaneous fat, causing the capillaries to rupture and bleed, resulting in cyanosis of the skin around the umbilicus called Cullen’s sign. What are the causes of periumbilical skin cyanosis? This petechiae is caused by blood or activated proteases crossing the peritoneum, fascia, and muscle into the subcutis, appearing late and is characteristic of necrotizing pancreatitis. Biliary tract disease is the most common cause in our country accounting for 50-80%; pancreatic duct obstruction. The pancreatic duct can be obstructed by roundworms, stones, edema, tumors or spasm; lesions adjacent to the duodenal papilla; alcoholism and overeating are the main causes in Western countries; surgery and injury; hypercalcemia and hyperparathyroidism can induce acute pancreatitis; drugs; certain infectious diseases such as mumps and viral hepatitis can be accompanied by pancreatitis. The pathogenesis of acute pancreatitis caused by various etiologies is different, but has a common pathogenesis, namely pancreatic self-digestion caused by the activation of various digestive enzymes in the pancreas. Under normal circumstances, the pancreas can prevent this self-digestion: 1. The pancreatic fluid contains a small amount of pancreatic enzyme inhibitors that can neutralize a small amount of activated pancreatic enzymes. 2. Pancreatic alveolar cells have a special metabolic function that prevents pancreatic enzymes from invading the cells. 3, the blood entering the pancreas contains substances that neutralize pancreatic enzymes. 4. The pancreatic duct epithelium has a protective layer of mucopolysaccharide. The disease can develop when the above defense mechanism is disrupted under certain circumstances. Under pathological conditions, the pancreatic duct is blocked for various reasons, and the pancreatic alveoli can still continue to secrete pancreatic juice, which can cause an increase in the intra-pancreatic ductal pressure, which destroys the mucus barrier of the pancreatic ductal system itself, and then HCO3- occurs in reverse diffusion, causing damage to the ductal epithelium. When the intraductal pressure exceeds 3.29 kPa, it can lead to rupture of pancreatic alveoli and small pancreatic ducts, and a large amount of pancreatic fluid containing various pancreatic enzymes enters the pancreatic parenchyma, pancreatic secretory protease inhibitor (PSTI) is weakened, trypsinogen is activated into protease, and pancreatic parenchyma undergoes self-digestion. Among them, trypsin has the strongest effect because after a small amount of trypsin is activated, it can activate a large number of other pancreatic enzymes including itself, thus causing edema, inflammatory cell infiltration, congestion, hemorrhage and necrosis of pancreatic tissue. Once activated by bile salts, trypsin, calcium ions and enterokinase, this enzyme can hydrolyze lecithin in the glandular cell membrane to produce fatty acids and lysolecithin, which can cause cell disintegration and release of large amounts of intracellular pancreatic enzymes, aggravating the degree of inflammation. In addition, the process of phospholipase A decomposition of cytosolic phospholipids into fatty acids and lysolecithin also produces thromboxane A2 (TXA2), which is a strong vasoconstrictor, and the imbalance of the ratio of TXA2 to PGI2 can lead to impaired blood circulation in tissues and aggravate pathological changes. Activation of lipase can lead to fat necrosis and even spread to peripancreatic tissues. Lower blood calcium indicates more severe fat necrosis, which is a sign of poor prognosis. After the activation of elastase by trypsin, in addition to the general protein hydrolysis, it has a specific digestive effect on elastic fibers, causing the lysis of elastic fibers in the vascular wall, pancreatic vascular necrosis, rupture and hemorrhage, which is also the pathophysiological basis for the development of edema type into hemorrhagic necrotizing pancreatitis. Vasoproteinogen is activated by trypsin to form vasoprotein, which can release bradykinin and tryptokinin, which can increase vasodilation and permeability and eventually cause shock.