Acute pancreatitis is a common acute disease in gastroenterology, which is essentially a systemic inflammatory response syndrome with two main pathogenic mechanisms: 1. 2, microcirculatory disorders (e.g.: hyperlipidemic pancreatitis, pancreatitis caused by blood volume changes after major cardiothoracic surgery). Therefore, clinically we often encounter some patients who do not have severe inflammation of the pancreas itself, or even normal amylase, but have severe systemic clinical manifestations, or even systemic multi-organ failure. From this perspective, it is possible to change the name of acute pancreatitis, and this topic is left to medical doctors. Traditional medical thinking, including classical textbooks, proposes the “pancreatic enzyme self-digestion theory” and the “common channel theory”, which are both correct and very classical, but explain the pathogenesis of pancreatitis from different levels (chemical inflammation, anatomy). In recent years, the more popular “inflammatory factor theory” better explains the pathogenesis of acute pancreatitis from the perspective of molecular biology. It is due to the full understanding of the nature of acute pancreatitis and the further improvement of clinical management (including the renewal of drugs), the mortality rate of acute pancreatitis has been greatly reduced, and the proportion of surgical interventions required has been greatly reduced, and the vast majority of patients can be cured through conservative medical treatment. Among the patients with acute pancreatitis that I have treated personally since I started my medical career (including the tertiary and teaching hospitals where I worked during my postgraduate studies), there have been no fatal cases. There was only one case that required surgical treatment due to the combination of bile duct cell carcinoma in the left lobe of the liver. As gastroenterologists, it is no longer difficult to diagnose pancreatitis, but we have the duty and obligation to find the causes of the onset of acute pancreatitis in patients and remove these causative factors to prevent patients from being admitted to the hospital again for similar conditions. For example, performing ERCP to release stones in the common bile duct, removing the gallbladder if necessary, and persuading patients to stop drinking, eat a low-fat diet, and lose weight. The principles of treatment for acute pancreatitis are clear: fasting, supervision, gastrointestinal decompression, acid control, massive fluid replacement, improvement of microcirculation, enema and laxative …… These are generally known by heart to medical students. However, the difficulty in the diagnosis and treatment of acute pancreatitis actually lies in the early identification of mild and severe pancreatitis. We have a series of scoring criteria such as Ranson, APACHE, CT grading, BISAP scoring system, etc. Some scholars believe that acute pancreatitis can be transformed from mild to severe, and some scholars believe that there is no mutual transformation between mild and severe acute pancreatitis, only that a small proportion of severe pancreatitis has atypical initial clinical manifestations, and I personally agree with the latter. Because, we know that mild acute pancreatitis, has a certain self-limiting, some patients can partially heal themselves after fasting, paying attention to rest and diet at home (of course, this proportion is not much). Therefore, early identification of those seemingly mild cases of severe pancreatitis (some arguments) is crucial for front-line clinicians. That is why it is very important to strengthen the questioning of medical history and physical examination, to go to the bedside more often in the first three days of admission to observe the patient’s mental status, respiratory condition and abdominal condition, and to ask more questions about urine output, etc. (Most of the acute pancreatitis will get better as long as the first 3-5 days are not aggravated) For growth inhibitors as well as octreotide application, the current foreign guidelines and literature mostly do not advocate it and it is overpriced. In fact, we check the manual of Sunnin (imported octreotide), we can see that it can cause pancreatitis itself, and such drugs may aggravate the local microcirculatory disorder of patients, in fact, long-term use of octreotide can make bile sticky and induce the occurrence of gallstones, if non-severe pancreatitis, I generally do not advocate the use of such drugs. For the issue of antibiotics, the use of antibiotics is generally not advocated in non-biliary pancreatitis (non-severe) unless there is evidence of co-infection, such as fever, etc. For the issue of TCM, after the restoration of bowel sounds, the use of drugs such as Da Cheng Qi Tang and Qing Pancreatic Tang can help the patient to pass stool and exhaust as early as possible, which is conducive to the early opening of the diet, therefore, they can be used appropriately, but the actual use must be grasped, otherwise it will aggravate the patient’s abdominal distension and even acute gastric dilatation and vomiting.