Acute pancreatitis

Acute pancreatitis is an acute inflammation of the pancreas caused by reasons such as pancreatic duct obstruction, sudden increase in intraductal pressure, and insufficient blood supply to the pancreas. The main clinical manifestations include upper abdominal pain, accompanied by nausea, vomiting, and bloating, lumbar muscle tension, tenderness, rebound pain, reduced or absent bowel sounds, and elevated blood and urine amylase levels. About half of the patients have biliary tract diseases.
This disease is one of the common acute abdominal diseases. There are two types: edematous and hemorrhagic types, which are essentially two stages of lesion development. The edematous type of lesion is relatively mild and more common. The hemorrhagic type, also known as the necrotic type, has severe lesions, is prone to shock, has more complications, has a high mortality rate, but is rare. Therefore, early diagnosis and early treatment are crucial.

　　Mild acute pancreatitis rarely has complications, while severe acute pancreatitis often has various complications.

　　1. Local complications

　　(1) Pancreatic abscess: Refers to encapsulated abscess around the pancreas, formed by secondary infection of necrotic and liquefied pancreatic tissue. It usually appears 2 to 3 weeks after onset, at which time the patient has high fever with toxic symptoms, severe abdominal pain, palpable mass in the upper abdomen, and significantly elevated white blood cell count. The puncture fluid is purulent, and culture shows bacterial growth.

　　(2) Pancreatic pseudocyst: The accumulation of fluid around the pancreas that is not absorbed is encapsulated by fibrous tissue to form a pseudocyst. It usually forms 3 to 4 weeks after the onset, and a mass in the upper abdomen can often be palpated during physical examination. Large cysts can compress adjacent tissues, causing corresponding symptoms.

　　2. Systemic complications

　　(1) Organ dysfunction failure: One to multiple organs may experience varying degrees of functional failure, with severe cases presenting as multiple organ failure (MOF). The main ones are:

　　① Circulatory failure, manifested as shock.

　　② Arrhythmia and heart failure.

　　③ Acute respiratory failure or acute respiratory distress syndrome, manifested by rapid onset of dyspnea, cyanosis, and conventional oxygen therapy cannot alleviate it.

　　④ Acute renal failure, manifested as oliguria, progressive elevation of blood urea nitrogen and creatinine.

　　⑤ Gastrointestinal bleeding, manifested as hematemesis, melena, or hematochezia, with positive fecal occult blood test.

　　⑥ Disseminated intravascular coagulation.

　　⑦ Pancreatic encephalopathy, manifested as mental and consciousness disorders, even coma.

　　(2) Infection: Infection may occur in the abdominal cavity, respiratory tract, urinary tract, etc., during the course of the disease. The spread of infection can lead to sepsis. In the later stage, due to extremely low body resistance, combined with the extensive use of antibiotics, fungal infections are easy to occur.

　　(3) A few cases may evolve into chronic pancreatitis.

⒈ There is an abrupt, severe pain in the upper abdomen, which is persistent and may worsen intermittently, radiating to the back and waist.
⒉ Nausea, vomiting, and abdominal distension.
⒊ There is abdominal or generalized muscle tension, tenderness, rebound pain, and decreased or absent bowel sounds.
⒋ In severe cases, high fever, jaundice, or shock may occur.
⒌ The periumbilical area turns blue, known as Cullen's sign. Blue or brown large, irregular ecchymoses on both sides or the left side of the腰部 are called Grey-Turner's sign.

　　Methods for preventing acute pancreatitis

　　1) Biliary tract diseases: Prevention lies in avoiding or eliminating biliary tract diseases. For example, preventing intestinal ascaris infection, timely treating biliary tract stones, and avoiding acute exacerbations of biliary tract diseases are important measures to prevent acute pancreatitis.

　　2) Excessive alcohol consumption: People who habitually drink alcohol may suffer liver and pancreatic damage due to chronic alcoholism and malnutrition, leading to a decrease in their ability to resist infection. On this basis, acute pancreatitis can occur due to a single bout of heavy drinking, so avoiding excessive alcohol consumption is also a preventive measure.

　　3) Overeating and overdrinking can lead to gastrointestinal dysfunction, impairing the normal activity and emptying of the intestines. This hinders the normal drainage of bile and pancreatic juices, causing pancreatitis. Therefore, when attending a feast, one should be aware of acute pancreatitis and avoid overeating and overdrinking.

　　4) Abdominal damage or surgery, as well as endoscopic retrograde cholangiopancreatography, can also cause acute pancreatitis. Both doctors and patients should be vigilant in such cases.

　　5) Other causes include infection, diabetes, mood disorders, and medication. There are also acute pancreatitis cases with unknown causes, which are difficult to prevent.

　　1. White blood cell count In cases of mild pancreatitis, it may not increase or only slightly increase, but in severe cases and those with infection, it often increases significantly, along with an increase in neutrophils.

　　2. Amylase measurement This is one of the important objective indicators for diagnosing acute pancreatitis, but it is not a specific diagnostic method. In the early stage of the disease, when there is thrombosis of the pancreatic vessels or certain hemorrhagic necrotic pancreatitis, due to severe destruction of the pancreatic tissue, it may not increase. Sometimes, in cases of shock, acute renal failure, pneumonia, mumps, ulcer perforation, and infections of the intestines and bile ducts, amylase can also increase. Therefore, when amylase increases, it is necessary to combine medical history, symptoms, and signs to exclude the increase in amylase caused by non-pancreatic diseases in order to diagnose acute pancreatitis. The increase in amylase is also related to the onset time of pancreatitis. According to clinical observations, the following manifestations can be present:

　　① Within 24 hours after onset, serum amylase reaches its peak, and 48 hours later, urine amylase appears at its peak.

　　② Within a short period after onset, urine amylase reaches its peak, while serum amylase may not increase or only slightly increase.

　　③ Serum amylase and urine amylase increase simultaneously, but gradually return to normal thereafter.

　　④ The rise and fall curve of amylase is wavy or persistently high, indicating the occurrence of complications.

　　During the acute phase of severe pain, back pain, nausea, and vomiting, it is necessary to avoid water and food intake to prevent the stimulation of pancreatic juice secretion. As the condition improves, one should start with a diet of sugar-containing liquid foods, beginning with easily digestible carbohydrate-rich foods. Even if food intake is possible, the digestive capacity is low. Therefore, appropriate meals should be prepared. In summary, the basic dietary principle for acute pancreatitis is to provide small amounts of easily swallowed and digestible, low-protein and low-fat carbohydrate-rich foods. In some cases, fat intake should be strictly controlled. When symptoms are normal, protein intake can be gradually increased. Salt intake should be limited when there is edema. During the treatment of acute pancreatitis, it is necessary to follow principles such as low-fat, high-protein, high-vitamin, high-carbohydrate, non-irritating, and easily digestible foods. During the acute attack phase, fasting for 1-3 days is recommended, and parenteral nutrition can be administered to avoid stimulating the pancreas; after remission, fat-free and low-protein liquid foods such as fruit juices, rice gruel, lotus root powder, soup, honey water, tomato juice, watermelon juice, mung bean soup, etc., can be provided; after the condition stabilizes, low-fat semi-liquid foods such as fish, shrimp, chicken, duck, lean meat, beans, and soy products, as well as fresh vegetables and fruits rich in vitamin A, B, and C, can be given. It is important to adhere to the principle of small and frequent meals. Abstain from: Absolutely avoid alcohol, fried foods, high-fat foods, and spicy foods. Acute pancreatitis can be cured if the condition is mild; however, if it worsens further, it may threaten life. Even after recovery, if dietary habits are not changed, it is difficult to eliminate the risk of recurrence. But by avoiding alcohol, controlling high-fat and high-calorie diets, and allowing the pancreas to rest sufficiently, it is possible to delay the progression of the disease and prevent further decline in pancreatic function, which is the key to dietary therapy. Regular diet: It is both common and very important.

　　Diet should be quantified and timed, with a certain regularity; overeating can impose the greatest burden on the gallbladder and pancreas. Pancreatitis patients should aim for 4 to 5 meals a day, even up to 6 meals. Because this multiple and small amount of eating reduces the stimulation to the pancreas, making the inflammation tend to stabilize. The daily fat intake should be controlled at 20 to 40 grams. Sugar is mainly obtained from grains. Sugar is the best nutrient for both the gallbladder and pancreas. Sugar stays in the stomach for the shortest time, and does not cause excessive secretion of bile and pancreatic juice, thus reducing the burden on the gallbladder and pancreas. However, excessive intake of fructose or sucrose may also lead to obesity, promote cholesterol synthesis, and easily lead to diabetes. Therefore, fruits should be eaten in moderation. Grains and tubers rich in vitamins, minerals, and dietary fiber should be the main sources of sugar. Actively consuming fat-soluble vitamins for a long time can cause a deficiency of fat-soluble vitamins A, D, E, and K, manifested as malnutrition. Some vitamin supplements can be taken under the guidance of a doctor or a nutritionist, and vitamins should be obtained as much as possible from food. Green and yellow vegetables contain a wealth of fat-soluble vitamins, so it is best to consume about 150 grams of green and yellow vegetables daily.

　　Acute pancreatitis tends to recur, and preventive measures include eliminating the cause and avoiding triggers, such as abstaining from alcohol, avoiding overeating, and treating hyperlipidemia. Gallstones play an important role in the onset of acute pancreatitis, so patients with a history of acute pancreatitis should consider gallbladder removal and common bile duct exploration at an appropriate time.

　　Western medicine treatment

　　The treatment of acute pancreatitis is still a challenge to this day. Firstly, the choice of treatment method: non-surgical treatment or surgical treatment? How can non-surgical treatment reasonably supplement blood volume and reduce complications, and how to grasp the timing of surgical treatment and how to implement surgery reasonably. The non-surgical treatment and/or surgical treatment of acute pancreatitis has been discussed for decades. With a deeper understanding of the pathophysiological changes of acute pancreatitis, the treatment of acute pancreatitis has become relatively clear so far: the main treatment for acute edematous pancreatitis is palliative treatment, while hemorrhagic necrotic pancreatitis should be treated according to the situation. The former accounts for about 80-90% of acute pancreatitis, and the latter accounts for about 10-20%. However, the boundary between acute edematous pancreatitis and hemorrhagic necrotic pancreatitis cannot be clearly separated. Acute edematous pancreatitis can transform into acute hemorrhagic necrotic pancreatitis, and statistics show that about 10% can transform. Therefore, during the non-surgical treatment of acute edematous pancreatitis, the evolution of the disease course needs to be strictly observed.

　　The treatment views for acute edematous pancreatitis and acute hemorrhagic necrotic pancreatitis have become relatively consistent. However, there is still some controversy about the treatment views for localized pancreatic necrosis. One view is that surgical drainage should be performed, while another view is that palliative treatment can be adopted. From some literature reports and our experience in treatment, we believe that surgical 'debridement' should also be performed for this type of pancreatitis. The reasons are: on the one hand, necrosis is irreversible, and necrotic tissue is difficult to absorb, even if it can be absorbed, the course of the disease is also very long. The long-term absorption of toxins may lead to persistent clinical symptoms such as persistent abdominal pain and fever. On the other hand, toxic substances in the necrotic tissue, such as vasoactive peptides, elastin, phospholipase A, etc., will cause the pancreas to undergo progressive self-digestion, and the lesion may continue to expand, leading to further aggravation of systemic toxic symptoms, and even multiple organ dysfunction leading to failure. Some methods of non-surgical treatment are also preoperative preparations for hemorrhagic necrotic pancreatitis.

　　Firstly, non-surgical therapy

　　The rational application of non-surgical therapy for acute pancreatitis can treat most cases of acute edematous pancreatitis, and also provides a good preoperative preparation for hemorrhagic necrotic pancreatitis. Non-surgical therapy includes: prevention and treatment of shock, improvement of microcirculation, antispasmodic, analgesic, inhibition of pancreatic enzyme secretion, anti-infection, nutritional support, prevention of complications, and some measures for strengthening intensive care, as shown in Table 10.

　　The main measures for the non-surgical treatment of acute pancreatitis are as follows:

　　Firstly, anti-shock

　　1. Supplementing blood volume to improve microcirculation

　　2. Antispasmodic, analgesic, maintain electrolyte and acid-base balance

　　Secondly, control the development of inflammation

　　1. Inhibition of pancreatic juice secretion

　　Fasting, nasal gastric tube decompression

　　Drugs: anticholinergic drugs, glucagon, etc.

　　Inhibition of RNA, DNA synthesis: 5-Fu,

　　Low temperature

　　Pancreatic irradiation △

　　2. Inhibition of pancreatic enzymes: antipain, atropine, soybean trypsin inhibitor

　　Antivenom Antitoxin Sandate

　　3. Corticosteroids

　　III. Prevention of Complications

　　1. Antibiotics

　　2. Insulin

　　3. Antacids

　　4. Heparin, Fibrinolytic Enzymes

　　5. Low Molecular Weight Dextran

　　6. Vasopressin

　　IV. Support and Monitoring

　　1. ICU Monitoring and Protection of the Lung and Kidney

　　2. Nutritional Support

　　△ In the trial stage, used for severe pancreatitis

　　(I) Prevention and Treatment of Shock and Improvement of Microcirculation

　　Hours after the onset of acute pancreatitis, due to a large amount of inflammatory exudation around the pancreas (within the omental cavity), and in the abdominal cavity, there is a significant loss of body fluids, especially the loss of fluids due to the 'chemical burn' of the retroperitoneum caused by pancreatitis is particularly large. Therefore, in a severe case of pancreatitis, the exudation around the pancreas, in the abdominal cavity, and retroperitoneally, can reach 5-6 liters of fluid loss per 24 hours. Additionally, due to paralytic ileus caused by peritonitis, vomiting, and the accumulation of contents in the intestinal lumen, the daily loss will far exceed 5-6 liters. In addition to fluid loss, it also causes a large loss of electrolytes and leads to acid-base imbalance. Within 24 hours, it is necessary to infuse 5-6 liters of fluid, as well as a large amount of electrolytes, and if infused too quickly, it can cause pulmonary edema. Therefore, for large fluid infusions, and to reduce the complications brought about by fluid infusion, it is necessary to monitor central venous pressure (CVP) and urine output, infusing fluid based on the changes in central venous pressure and urine volume and specific gravity. To improve microcirculation, dextran should be infused in appropriate amounts. Dextran has a large and small molecular weight, which can be flexibly controlled; high molecular weight is used to rapidly expand the充血 volume, and then it is changed to low molecular weight to improve microcirculation. Additionally, drugs to dilate microvessels such as 654-2 are administered. To expand blood volume and reduce inflammatory exudation, albumin is infused. Furthermore, potassium and calcium ions are supplemented, and acid-base imbalance is corrected based on the electrolyte changes detected by blood biochemistry and the acid-base results obtained from blood gas analysis.

　　(II) Inhibition of Pancreatic Secretion

　　1. H2 receptor blockers: Medications such as cimetidine, ranitidine, and famotidine can reduce the secretion of gastric acid and inhibit the action of pancreatic enzymes. Some people use H2 receptor blockers concurrently with 5-Fu, believing that it has a better inhibitory effect on exocrine pancreas, administered intravenously at 500-1000 mg per day.

　　2. Trasylol: Since its large-dose clinical application by Trapnell in 1974, Trasylol has been widely used in clinical practice to inhibit the secretion of pancreatic enzymes in large doses. In addition to inhibiting trypsin secretion, it can also inhibit the secretion of kallikrein and fibrinolytic enzymes. The current dose is 20,000 units per kilogram of body weight, infused intravenously, with a course of treatment lasting one week. According to Trapnell's report, the mortality rate in the high-dose Trasylol group was significantly lower than that in the control group. It has a good effect on edematous acute pancreatitis, but the effect on hemorrhagic necrotizing pancreatitis has not been fully confirmed. As early as the 1970s and 1980s, we were also enthusiastic about using it (but in smaller quantities), but did not find it to have a significant effect, and it also posed a risk of allergic reactions.

　　3.5-Fu (5-fluorouracil): 5-Fu can inhibit the synthesis of ribonucleic acid (DNA) and deoxyribonucleic acid (RNA). During acute pancreatitis, it can be used to block the synthesis and secretion of pancreatic enzymes by exocrine pancreatic cells. The use of 5-Fu for the treatment of acute pancreatitis began in the 1970s and has gradually been used in clinical practice. In 1979, Mamm used enterokinase for intraductal injection into the pancreas, which induced acute pancreatitis and hyperamylasemia. When 5-Fu is injected into the pancreatic duct along with enterokinase, it can prevent the occurrence of pancreatitis. From 1978 to 1981, scholars reported the use of 5-Fu to treat over 300 cases of acute pancreatitis, which could block the progression of the disease, reduce the levels of amylase and trypsin, and decrease mortality and recovery time.

　　Huang Yanting et al. reported in 1989 that in 10 cases of hemorrhagic necrotic pancreatitis, 5 cases treated with 5-Fu had no deaths, and the blood and urine amylase levels returned to normal within an average of 2 to 10 days. In the other 5 cases that did not use 5-Fu, the treatment was conventional, and only 3 patients survived while 2 died. All died from toxic shock and multiple organ failure. The dosage is: 500mg dissolved in 500ml of liquid for intravenous infusion, for a continuous period of 1 week, with a few cases that may require 10 days. Dandong First Hospital (1989) reported 17 cases of necrotic pancreatitis, where only 1 case died after surgical drainage and treatment with 5-Fu.

　　The key points of the action of 5-Fu should be noted:

　　① Immunosuppressed patients with severe pancreatitis but with normal amylase levels, or those who have undergone partial pancreatectomy, should not use 5-Fu.

　　② For patients with edematous pancreatitis and very high amylase levels, and for some patients who have undergone 'debridement', the use of 5-Fu is effective and the recovery is smooth.

　　Fasting and gastrointestinal decompression: This measure is commonly used in patients with acute abdominal pain. During acute pancreatitis, the use of a nasogastric tube for decompression can not only relieve abdominal distension and vomiting caused by paralytic ileus but is also more importantly, it can reduce the stimulatory effect of gastric juice and acid on the secretion of pancreatic enzymes, thereby limiting the progression of pancreatitis. Due to the stimulation of chyme to the antrum and duodenum, leading to the secretion of pancreatic enzymes, it is usually necessary to fast for a longer period of time. After amylase returns to normal, fasting for another 1 to 2 weeks is required; otherwise, recurrence of pancreatitis may occur due to early eating.

　　(Three) Antispasmodic and Analgesic Treatment

　　Acute severe pancreatitis is characterized by extremely severe abdominal pain, which in severe cases can lead to painful shock and may cause coronary spasm through the reflex of the vagus nerve. Therefore, analgesics should be administered regularly, and the traditional method is to intravenously drip 0.1% procaine for venous occlusion. It is also possible to use Durodin and atropine in combination at regular intervals, which can both relieve pain and relax the Oddi sphincter spasm. Isosorbide dinitrate, nitroglycerin, and other drugs can be used in cases of severe pain, especially in older patients, which can not only relax the Oddi sphincter spasm but also be of great benefit to the coronary blood supply.

　　(Four) Nutritional support

　　Nutritional support is very important in acute pancreatitis, if used appropriately, it can significantly reduce mortality, and if used improperly, it may sometimes increase mortality. In severe acute peritonitis, the body's catabolic metabolism is high, inflammatory exudation, long-term fasting, high fever, etc., the patient is in a negative nitrogen balance and hypoproteinemia, so nutritional support is needed, and at the same time, the pancreas should not secrete or secrete less. Therefore, it is necessary to master its inherent laws to maximize the effect of nutritional support.

　　1. The following points should be considered for nutritional support in acute pancreatitis:

　　① Mild pancreatitis without complications does not require nutritional support

　　② Moderate to severe acute pancreatitis should start nutritional support early (when hemodynamics and cardiovascular stability allow)

　　③ Initial nutritional support should be through an extraintestinal route, with sufficient calories

　　④ The patient has a jejunostomy during surgery to provide enteral feeding

　　⑤ When the symptoms, physical examination, and CT images of the pancreas show that the patient is basically normal, oral diet can be initiated, but with less fat.

　　2. Nutritional support for acute severe pancreatitis can be summarized into three stages: In the first stage, total parenteral nutrition (TPN) should be the main method, generally requiring 2-3 weeks; in the second stage, through a jejunostomy, intestinal elemental diet is administered for 2-3 weeks, enteral feeding with intestinal elemental diet (EEN), which still has a certain stimulating effect on pancreatic enzymes, so EEN should not be used prematurely; in the third stage, a gradual transition to oral diet. The timing of starting oral diet is very important, and it must be started after a comprehensive assessment of the patient's overall condition.

　　3. One of the important mechanisms of onset of acute pancreatitis is that activated pancreatic enzymes cause autodigestion of the gland and pancreatic tissue, so one of the important means of treatment is to make the pancreas secrete 'static' or 'rest'. When using nutritional support, it is necessary to grasp which nutrient components enter the body through which route, so that the pancreas does not secrete or secretes less (referring to digestive enzymes). The following issues are discussed below.

　　(1) Intestinal nutrition and pancreatic secretion: Gastric and intestinal pancreatic reflexes can stimulate pancreatic exocrine secretion. Some studies have been conducted on dogs with infused elemental diets (containing glucose, fat, and amino acids) into the stomach, duodenum, or jejunum, compared with infused water. After intragastric infusion of elemental diet, the amount of pancreatic secretion, protein, and bicarbonate secretion increased. After intraduodenal infusion of elemental diet, the amount of pancreatic secretion increased, but there was no significant change in the secretion of protein and bicarbonate. After intrajejunal infusion of elemental diet, the exocrine pancreatic secretion, protein, and bicarbonate secretion increased. In the control group, there was no increase in exocrine pancreatic secretion after jejunal infusion. Stabile injected different doses of emulsified fat (Intralipid) into the duodenum of experimental dogs and found that the relationship between the amount of emulsified fat exceeding the baseline and the excretion of protein and bicarbonate was significant. Therefore, during the recovery period of acute pancreatitis, the amount of oral fat diet should be low. In enteral feeding, directly infusing fat diet into the jejunum, avoiding the reflexes of gastric and intestinal pancreas, can reduce exocrine pancreatic secretion.

　　(2) Parenteral nutrition and pancreatic secretion:

　　Glucose: Klein reported that intravenous infusion of glucose can inhibit the exocrine secretion of the pancreas, which may be related to increased serum osmotic pressure.

　　Amino acids: Fried infused 1-aminocellulose into a canine fistula model and found that there was no change in the amount of pancreatic protein secretion. Stabile infused a mixture of amino acids and found that it did not increase the excretion of pancreatic secretion, protein, or bicarbonate. This indicates that intravenous infusion of amino acids does not stimulate human pancreatic secretion.

　　Fatty acids: research has confirmed that the injection of fatty acids into the duodenum has a significant stimulatory effect on pancreatic secretion. However, the intravenous infusion of fatty acids does not stimulate the exocrine secretion of the pancreas.

　　The above-mentioned explanation states that intravenous injection of amino acids and glucose, or the use of fat emulsion alone, does not stimulate the exocrine secretion of the pancreas.

　　(3) The role of nutritional support in acute pancreatitis: TPN has been used as a nutritional support and treatment method for the treatment of acute pancreatitis, but how effective is it? Feller reviewed 200 cases of acute pancreatitis and believed that high-level nutritional support has a direct therapeutic effect, reducing the mortality rate from 22% to 14%. Motton reported in 1982 on 68 cases of acute necrotizing pancreatitis, where the mortality rate was 15.6% for those treated with TPN and 22.4% for those untreated, with the former hospital stay of 32 days and the latter of 45 days. TPN plays a positive role in reducing pancreatic exocrine secretion, turning negative nitrogen balance into positive nitrogen balance, and preventing complications. The amount of sugar should not be excessive when TPN is applied to avoid raising blood sugar levels.

　　In recent years, somatostatin octapeptide (Sandostatin) has been used in clinical practice, especially in the treatment of acute necrotizing pancreatitis and pancreatic leaks (fistulas), achieving good results. It is now widely used in pancreatic diseases, upper gastrointestinal bleeding, gastrointestinal fistulas, and endocrine tumors of the digestive system.

　　Sandostatin (Sandoz) is an artificial octapeptide cyclic compound that retains the pharmacological activity of the natural somatostatin and has a long-lasting effect. It can inhibit the pathological hypersecretion of growth hormone and gastrointestinal pancreatic endocrine hormones; Sandostatin can significantly improve the microcirculation of the pancreas, inhibit the release of pancreatic enzymes, and also reduce the water content in the lungs and the extrapancreatic vascular water, thereby achieving the purpose of treating pancreatitis and preventing pulmonary edema (but high doses of Sandostatin can lead to a decrease in pancreatic microcirculatory blood volume); the effect of Sandostatin on the Oddi sphincter has recently been found through animal experiments, which can reduce its pressure. The pressure begins to decrease 3 minutes after the injection of Sandostatin, and it decreases particularly明显 in 5, 10, and 15 minutes, with a duration of up to 4 hours, thereby reducing the reflux of bile into the pancreatic duct.

　　(Five) The application of antibiotics

　　The application of antibiotics in acute pancreatitis is one of the indispensable contents of comprehensive treatment. The application of antibiotics in acute hemorrhagic necrotic pancreatitis is uncontroversial. In acute edematous pancreatitis, as a preventive measure against secondary infection, a certain amount of antibiotics should be used rationally. Beger reported that in 138 cases of necrotizing pancreatitis, the tissue bacterial culture of pancreas resection had a positive rate of 40%, and the more severe the necrosis and the longer the time, the higher the positive rate. Pancreatic necrosis complicated with suppurative infection has a variety of bacterial species, the most common being Gram-negative bacilli from the intestines, such as Escherichia coli, Klebsiella pneumoniae, Streptococcus faecalis, Alcaligenes faecalis, Pseudomonas aeruginosa, Proteus, Pseudomonas aeruginosa, Staphylococcus aureus, etc. The mortality rate is very high when pancreatitis is complicated with infection. Therefore, how to correctly use antibiotics in acute pancreatitis is an important issue.

　　1. The blood-pancreatic barrier of antibiotics: The content of antibiotics in pancreatic juice and serum is determined by microbiological methods, enzyme immunoassay, and high-performance liquid chromatography. It is found that the penetration of antibiotics into pancreatic juice is influenced by many factors, the most important of which is the existence of a blood-pancreatic barrier similar to the blood-brain barrier in the pancreas. When antibiotics penetrate the blood-pancreatic barrier, they first penetrate the capillary endothelial cell layer and basement membrane, and then penetrate the cell membrane of the pancreatic acini and ducts to enter the pancreatic juice. Since the cell membrane contains a large amount of lipids, polar and liposoluble antibiotics are more easily penetrate than polar and hydrophilic ones. The serum protein binding rate of antibiotics, the size of the binding protein molecules as carriers, and the pH value of antibiotics can all affect their entry into the pancreatic juice. Therefore, during acute pancreatitis, inflammation affects the change in cell membrane permeability and also affects the penetration of antibiotics into the pancreatic juice. Since antibiotics are present in pancreatic juice, they should also be present in pancreatic tissue. However, whether the concentration of antibiotics in the pancreatic juice can represent the concentration in the pancreatic tissue has been proven by experiments that the concentrations of antibiotics in the pancreatic tissue and pancreatic juice are parallel. To date, only 1/3 of the 30 or so antibiotics studied can enter the pancreas and reach effective concentrations. Under the action of the blood-pancreatic barrier, some antibiotics such as penicillin G and some cephalosporin antibiotics cannot enter the pancreatic tissue. Tetracycline, gentamicin, and ampicillin enter the pancreatic tissue rarely and cannot form effective concentrations.

　　2. The principles of antibiotic application in acute pancreatitis: able to penetrate the blood-pancreatic barrier; able to form effective concentrations in pancreatic tissue; able to effectively inhibit known pathogenic bacteria. In recent years, the frequency of bacterial species appearing in pancreatic infections is as follows: Escherichia coli, Klebsiella pneumoniae, Enterococcus, Staphylococcus aureus, Pseudomonas aeruginosa, Pseudomonas fluorescens, Streptococcus, Enterobacter aerogenes, Bacteroides fragilis, etc. In recent years, fungal (candida) infections have increased. Research has shown that broad-spectrum antibiotics, imipenem (Tianning) and ciprofloxacin can inhibit the above bacteria (except for Bacteroides fragilis); cefoperazone (Fudaxin), cefotaxime, cefamandole, rifampicin, and cotrimoxazole can inhibit 5 of the 9 kinds of bacteria, clindamycin can inhibit 3 kinds of bacteria, and metronidazole can only inhibit Bacteroides fragilis.

　　The incidence of infection in the first week of acute pancreatitis is about 5%, and the incidence rate of infection in the 2nd to 3rd weeks is 50%. Therefore, the type of antibiotic to be used, when to start using it, and how long to use it are for reference. With the deepening of research, continuous corrections will be made.

　　3. The source of bacteria in acute pancreatitis is mainly due to the following two aspects:

　　① Due to the damage of the intestinal mucosal barrier function, decreased immunity, and imbalance of the intestinal flora, some pathogenic bacteria grow and reproduce, leading to intestinal bacterial translocation.

　　② Factors of TPN, infection is very easy to occur during TPN, especially due to improper care of the catheter.

　　(Six) Peritoneal lavage

　　1. The method of abdominal lavage: under local anesthesia, a small incision is made along the midline of the umbilicus, a soft and not easily broken silicone tube is inserted, and then the surrounding area of the silicone tube is sealed. The lavage fluid is isotonic, including dextran and glucose 15g/L, potassium 4mmol/L, heparin 100IU/L, and ampicillin 125-250mg/L. 2L is infused every 15 minutes, retained for 30 minutes, and then drained out through the drainage tube (which takes another 15 minutes), with a cycle time of 1 hour. This is done for 48 hours or longer (depending on the patient's condition), usually for 2 to 7 days.

　　Since 1965, Wall first applied it to the treatment of acute pancreatitis, and Ranson also used it in clinical practice. He implemented peritoneal lavage for 24 out of 103 severe cases of pancreatitis within 24 hours after diagnosis; 24 cases were implemented within 48 hours after diagnosis, and the rest were the control group. The clinical symptoms of peritoneal lavage improved rapidly, and there was no death in the lavage group in the first 10 days of treatment, while 45% of the patients who did not undergo lavage died, but there was no significant difference in the total mortality rate between the two groups, and the lavage group mostly died later from secondary pancreatic abscesses. The conclusion is that lavage therapy is effective in preventing early systemic complications, but ineffective in preventing late pancreatic abscesses, so the total mortality rate has not decreased.

　　The purpose of lavage is to remove various toxic and harmful substances contained in the pancreatic effusion of pancreatitis, such as amylase, lipase, phospholipase A, trypsinogen, prostaglandin-like active enzymes, and kallikrein, to expel them from the body and reduce poisoning, and to expel the continuing necrotic pancreatic tissue from the body. When performing peritoneal lavage, attention should be paid to: do not damage the highly distended intestinal tract when inserting the catheter; the infusion fluid, as per routine, is about 2L per time, but due to the frequent concurrent respiratory failure in acute pancreatitis, if the abdominal volume is increased again in a short period of time, it will aggravate respiratory failure, therefore, the infusion volume must be reduced and the infusion time extended. At the same time, intensive monitoring should be strengthened, such as regular measurement of blood gas changes; if glucose is used to maintain osmotic pressure, the patient's blood sugar changes should be closely monitored, as the tolerance of sugar in severe pancreatitis patients is often reduced, and insulin can be used simultaneously if there is a reduction.

　　Peritoneal lavage played a good role in the early stage due to the reduction of the absorption of toxic substances, the reduction of complications of heart and lung, and the reduction of complications of heart and lung. However, its drainage effect is still not ideal, and some necrotic or liquefied pancreatic material cannot be drained out of the body. The late drainage lavage effect is not as good as the drainage effect after laparotomy through the peritoneal cavity around the pancreas and posterior abdominal pancreas.

　　3. We have adopted a compromise method: for acute severe pancreatitis with inflammatory exudate, a small incision is made at the right lower abdomen and left lower abdomen respectively to release a large amount of inflammatory fluid, and the drainage tube is sent to the lowest position below both diaphragms and both lower abdomens with a circular clamp. This is a small incision drainage under local anesthesia, which has little disturbance to the body and a good effect.

　　Our experience is that, whether it is peritoneal lavage or bilateral lower abdominal small incision drainage, it is necessary to understand the pathological changes of the pancreas before surgery, that is, if the pancreas has necrotic changes after B-ultrasound and CT examination, it cannot be used. And during the lavage process, B-ultrasound and CT should still be used for dynamic observation. When pancreatic necrosis and infection occur, abdominal exploration should be performed and the focus should be cleared and thoroughly drained according to the principles of surgical treatment.

　　(Seven) Enhanced monitoring

　　Enhanced monitoring should be conducted during the perioperative period of acute severe pancreatitis.

　　Focus of monitoring: lung, kidney, heart, and others.

　　Indications for monitoring: PaO2 1.8 mmol/L; blood glucose > 11.0 mmol/L; CT grading as grade III and IV; abdominal puncture of hemorrhagic ascites, etc.

　　Monitoring and support for Acute Respiratory Distress Syndrome (ARDS): The incidence of ARDS in acute severe pancreatitis is 30-45%, which is much higher than the incidence of general acute abdominal diseases (19%). In acute pancreatitis, the highest mortality is also due to ARDS, while renal failure and other complications such as stress ulcer gastrointestinal bleeding, hemorrhagic rupture of abdominal great vessels due to pancreatic juice digestion, etc., are lower than ARDS. And because ARDS accounts for 60% of the deaths from acute pancreatitis, if ARDS can be recognized early in clinical practice and treated reasonably, the mortality can be greatly reduced. However, it is often found in clinical practice that ARDS is often in the late stage, and the opportunity for rescue is lost.

　　According to the report of 85 cases of acute pancreatitis by Ranson, 38% of the cases had PaO2 below 8.78 kPa (the critical level is 9.31 kPa) within 48 hours of starting treatment, but the clinical signs were not obvious, and about 10% had frosted glass shadows on chest X-rays. If not corrected at this time, the condition may continue to develop into irreversible changes. Therefore, in cases of acute severe pancreatitis, routine blood gas analysis should be performed for monitoring. Severe cases should have blood gas measured every 8 hours. When PaO2

　　急性肾功能衰竭：急性胰腺炎时并发肾功能衰竭并不少见，各家报道不一，约发生10～15％，主要病理改变为急性肾小管坏死。其原因可概括为：低血容 量血压下降肾脏灌血不足;胰腺坏死后释出的血管活性物质，通过血流入肾导致肾血管通透增加，肾间质水肿而使肾小管坏死;一些脱落的碎屑形成管型堵塞肾小管 等。这些诸多因素使肾小球滤过率下降，则少尿或无尿。处理的方法：首先扩充血容量，并给以强效利尿剂。为鉴别少尿或无尿是肾前性抑或肾脏的损害，可采用 “快速利尿”法进行试验，使用甘露醇、速尿、多巴胺静脉推注，观察注射后1小时的尿量，若尿量达60～100ml，系血容量不足，如未达到上述标准可再重 复1次，若仍未达到上述指标，则进一步证实为肾衰。则应彩腹腔(膜)透析以及相应方法治疗。

　　(八)间接降温疗法

　　急性胰腺炎的间接降温方法可分为开放式间接降温和封闭式间接降温疗法两种。前者是应用冷溶液行胃灌洗，但并发症较多，而改用封闭式间接降温。

　　封闭式的间接降温，是应用含有冷液的封闭式管道系统，在胃内循环用以降低胰腺的温度。动物实验证明可降低淀粉酶100％，脂肪酶可降低40％，动物 的生存率提高。1964年临床应用，也被许多人所承认。它虽然没有开放式间接降温的并发症，如冷溶液返流或吸入呼吸道、严重腹泻、电解质紊乱、低氯性碱中 毒、手足抽搐等，但封闭式间接降温也有一些并发症，如期外收缩、呼吸抑制和代谢紊乱等。相继有人用冷液循环在体外进行腰部和腹部降温：用1～5℃奴夫卡因 200～500ml腹膜后注射进行渗透降温;用1～4℃液体以9～10mg/kg?min的速度进行腹腔动脉灌注。但由于急性胰腺炎时胰腺微循环遭到破坏 而使局部降温的效果不佳，未能广泛使用。

　　二.手术治疗

　　急性出血坏死性胰腺炎内科治疗往往无效，死亡率甚高，幸存者很少。外科治疗的作用已被充分肯定。手术的目的、手术原则已基本上取得较为一致的意见。 但对手术的时机，手术的方式意见不一，甚至有明显的分岐。问题主要是集中在早期施行规则的胰腺切除，抑或延期施行局限性坏死胰腺病灶清除等，相信通过临床 不断的实践，将会得到一个较为合理而统一的论点。

　　The current surgical methods for acute hemorrhagic necrotic pancreatitis include: pancreatic capsule incision decompression; debridement of necrotic pancreatic tissue; regular pancreatic resection; abdominal open blockage; abdominal zipper installation, etc. How do these surgical methods work? When to use them? If they are mastered properly, not only will the patient suffer less pain, but the mortality rate can also be reduced.

　　(One) Indications and timing of surgery

　　1. The timing of surgery directly affects the effectiveness of treatment. There are many controversies about early surgery and delayed surgery. Early surgery refers to within 2 weeks after onset, while surgery after 2 weeks is delayed surgery. Early or delayed surgery must start from the changes of the disease: such as systemic toxic infection, abdominal signs, shock, degree of pancreatic destruction, and the existence of MOF. Therefore, the timing of surgery for acute hemorrhagic necrotic pancreatitis, early or delayed, is generally determined according to the progress of pancreatic pathological changes. It appears during the treatment process.

　　① The manifestations of surgical acute abdomen

　　② If other life-threatening acute abdominal conditions cannot be ruled out, they should be actively prepared for surgery exploration.

　　Disadvantages of early (or premature) surgery: The necrotic pancreas and non-necrotic pancreas, due to the short time, the pathological changes have not been clearly divided, it is difficult to judge the range and depth of necrosis during surgery, and it is often very difficult to fully clear necrotic tissue. If it is cleared (or excised) too little, the lesion continues, and sometimes a second operation is needed, and excessive excision increases trauma. Therefore, many scholars support delayed surgery. Becker et al. pointed out that the lesions of acute hemorrhagic necrotic pancreatitis can be localized 3-6 weeks after onset, and the systemic response ends. If the surgery can be postponed to 2 weeks later, the cure rate can reach 85%. For those who undergo early surgery (within 2 weeks), due to the frequent need for repeated surgery, the mortality rate reaches 40%. It has been recognized from practice that it is impossible to block the course of self-digestion and necrosis of the pancreas, and the residual pancreas continues to necrose and develop secondary infection after surgery. It has basically reached a consensus that early surgery exploration is not advisable. Before surgery, the patient should be given vigorous supportive therapy, including anti-infection, TPN, prevention and treatment of cardiovascular and pulmonary complications, correction of water and electrolyte balance, as well as acid-base balance, to get through the severe period of systemic response.

　　Advantages of delayed surgery: The boundary between necrotic and non-necrotic areas is clear, which reduces the difficulty and risk of surgery; the lesion is localized, the surgical range is reduced, it is targeted, and the trauma is small; the surgical method is simple and reasonable, and it can clear necrotic tissue according to the method of debridement, so as to avoid the need for reoperation; the surgical effect is significantly improved, and the complications and mortality after surgery are greatly reduced.

　　The issues that need to be paid attention to are the delay in surgery, which cannot be unlimited, as the waiting time is too long, and the liquefaction of the necrotic area of the pancreas and secondary infection may spread to the whole body, resulting in sepsis, toxicosis, and infectious shock. Therefore, in addition to observing the systemic response in patients with acute hemorrhagic necrotic pancreatitis, ultrasound, CT, and enhanced CT should be used to observe the development of pancreatic lesions. The delay in surgery is not immutable in time, and individual differences can be very large, and it is necessary to make the correct choice and reasonable changes according to the specific situation.

　　(Two) Pancreatic Capsule Incision

　　Pancreatic capsule incision refers to incising or stripping the pancreatic capsule appropriately, loosening the pancreas bed, and placing drainage tubes around the pancreas and retroperitoneally. In cases of pancreatic edema, hemorrhage, and necrosis, the tension of the actual tissue of the pancreas increases, while the pancreatic capsule is inelastic, tightly wrapping around it like a 'straitjacket', with no room for retreat, causing ischemia of the actual pancreas tissue due to pressure, and the necrosis will progress further. Cutting the pancreatic capsule or partially stripping it off can achieve decompression, improve blood circulation, and thus prevent the further progression and aggravation of necrosis.

　　(Three) Regular Pancreatic Resection

　　Regular pancreatic resection is based on the extent of necrosis, resecting different parts of the pancreas, such as the tail, body, subtotal, and total resection. The resection boundary should reach the normal tissue of the pancreas. Sometimes, the resection should be combined with the removal of extrapancreatic tissues invaded by the pancreas, and corresponding additional surgery should be performed.

　　Since Watts first reported the successful experience of treating fulminant pancreatitis with total pancreatectomy in 1963, a wave of enthusiasm has swept across Europe. Hollender and Alexandre, among others, actively promote the regular practice of pancreatic resection, even to the extent of performing typical total abdominal resection, as well as resection of the stomach and duodenum. They believe that if the necrosis exceeds 50%, partial pancreatectomy should be performed, and if it exceeds 75%, total pancreatectomy should be performed. The surgical results of Hollender et al. show that due to the high invasiveness of the surgery, the mortality rate of partial pancreatectomy is 35%, and the mortality rate of pancreaticoduodenectomy is as high as 67%. Alexandre performed 20 total pancreatectomies with a mortality rate of 60%. In addition to the dysfunction of the endocrine and exocrine secretion of the pancreas, there are also other complications in a few surviving cases. Aldridge's experience with 15 pancreatic resections includes 14 subtotal resections and 1 total resection, of which 5 (33%) died, and 40% of the survivors developed insulin-dependent diabetes. A total of 44 complications occurred sequentially in 15 patients after pancreatectomy. The vast majority of patients require repeated or multiple surgical treatments. From the collected literature, regular pancreatic resection for the treatment of acute hemorrhagic necrotic pancreatitis has a very high mortality rate, reaching 40~

　　Through some experiences of death, it is summarized that surgery overly emphasizes thoroughness, which is not as simple as cholecystectomy, gastrectomy, or appendectomy. The reason is that pathological changes are progressive hemorrhage, necrosis, digestion, and infection, with unclear boundaries and intermingling; the residual lesions of the pancreas after partial resection can still develop; the etiology of hemorrhagic necrotic pancreatitis has not been removed, and the toxic substances entering the blood circulation have not been removed; surgery on a critically ill patient, especially within an infected focus, is not only traumatic but also more toxic substances enter the blood circulation due to the operation, resulting in a high mortality rate.

　　(Four) Pancreatic necrotic tissue removal surgery

　　The removal of pancreatic necrotic tissue is performed using钝性钳夹法 or with a suction apparatus to remove the necrotic tissue, and tubes are placed for drainage in the pancreatic bed, lesser omentum sac, subdiaphragmatic space, and even both pelvic cavities. After dynamic CT and CT enhancement scanning, the diagnosis is confirmed and the surgery is performed. Beger has advocated this procedure since 1982, and reported on the treatment status of 205 cases of necrotic pancreatitis in 1985, of which 79 cases were limited necrosis and 126 cases were extensive necrosis. In this group, 40.4% were confirmed to have infection by bacterial examination. The overall mortality rate was 24.4%, among which the mortality rate was 6.0% for 50 cases who underwent necrotic tissue removal and lavage drainage of the lesser omentum sac and retroperitoneal space. Larvin et al. used this method to treat patients, with a mortality rate of 21%. Attention should be paid to the removal of pancreatic necrotic tissue: whether there are blood vessels passing through the necrotic tissue. If there are blood vessels, they should be carefully dissected to avoid massive hemorrhage during surgery and the vessels should be dealt with; otherwise, due to soaking in the necrotic tissue, massive hemorrhage may occur uncontrollably. It is not necessary to strive for complete removal of necrotic tissue; some residual necrotic matter can be removed through the drainage tube. If forced separation or tearing is performed during surgery, bleeding at the断面 is more likely to occur; necrotic tissue at the root of the mesentery (at the junction of the head and body of the pancreas) should never be forcibly separated or dissected. Drains should be placed nearby, allowing the necrotic tissue to decompose and be naturally expelled.

　　From the above clinical data and the pathological basis of pancreatic necrosis, the surgical procedure for the removal of pancreatic necrotic tissue has the advantages of being reasonable, simple, easy to perform, minimally invasive, with fewer complications, and a low mortality rate. If supplemented with continuous local lavage, it can continuously extract activated pancreatic enzymes, vasoactive substances, pus, necrotic tissue, and toxins from the body, further increasing the efficacy of the surgery and is worthy of promotion and application.

　　(Five) Open abdominal packing and zip closure technique

　　Given that the pathological changes of acute hemorrhagic necrotic pancreatitis are progressive, there is no single surgical procedure that can completely treat this condition in one go. Therefore, an open abdominal packing technique is advocated. The method involves opening the lesser omentum sac, fully freeing the pancreas, and clearing the necrotic tissue. Non-adhesive porous gauze is used to cover the exposed mesentery of the transverse colon, major blood vessels, and the posterior wall of the stomach for protection, and then saline gauze is used to pack. The abdominal wall can be loosely sutured; or the 'sandwich' technique can be used, where a polypropylene (Marlx) mesh is covered over the exposed viscera or omentum and sutured to the edges of the incision on both sides of the fascia, with a transparent surgical adhesive drape covering the outside; the adhesive drape is removed during each debridement, the omental flap is cut into the abdomen, and the mesh is sutured at the end of the surgery, covered with a transparent adhesive drape, thus restoring the 'sandwich' structure. Both methods have their own advantages and disadvantages. Some people have also proposed various methods for closing the abdomen, the principle being to make it simple, convenient for repeated debridement, and to prevent mixed infection.

　　1. Debridement (reoperation): Performed under sterile conditions in the operating room, debridement is carried out every 48 hours, and the necrotic foci are cleared each time. Bradley reported that 28 cases of hemorrhagic necrotic pancreatitis were treated with this method, with a mortality rate of 10.7%, and Pemberton's mortality rate was 18%.

　　2. The application of the zipper technique is roughly the same as abdominal open occlusion, but the difference is that a nylon zipper is installed on the abdominal wall to close the peritoneal cavity (a polyethylene film is placed below to isolate the viscera). This makes the change of dressings simple and easy, as the zipper can be opened to change the dressing. However, it requires good control of the indications in order to use it, and not every case of hemorrhagic and necrotic pancreatitis can use it.

　　3. Trilocular stoma (stomach, jejunum, gallbladder), in the past, it was considered a routine additional surgery for patients with hemorrhagic and necrotic pancreatitis. Due to the use of TPN and understanding of the biliary tract condition, it should be considered according to different conditions whether to apply it or not.

　　(Six) Low temperature and cryosurgical treatment for acute severe pancreatitis

　　The pathogenesis of acute pancreatitis is the progressive necrosis of pancreatic cells and enzymatic self-digestion. Low temperature can reduce metabolic rate and enzymatic catalytic ability. When the temperature of the pancreas drops to 8～10℃, the secretion of enzymes (exocrine) can be suppressed, and irreversible suppression occurs when it drops to 0～4℃. Cryosurgical treatment of acute pancreatitis has been applied in clinical practice and has achieved certain efficacy. By contacting the cold probe (-160～-196℃), it can destroy the inflammatory tissue and pancreatic enzymes produced by acute pancreatitis, suppress self-digestion, and achieve the therapeutic effect. It is different from cryotherapy for tumors, as it does not require the destruction of all tissue cells, but only needs to suppress the production of enzymes by most pancreatic cells, acting to inactivate them and block self-digestion.

　　1. Direct cooling therapy for acute pancreatitis: Initially, this involved placing a ball bag with a cold fluid circulation system within the omental bursa through surgery, with the ball bag directly contacting the pancreas for cooling. Subsequently, it emerged that the ball bag could be placed directly in the pancreas through laparoscopy for pancreas cooling. Soviet scholars used a cryotherapy machine to test the normal pancreas of dogs at different temperatures from 100～37℃, observing the effect of cryotherapy on pancreatic exocrine secretion. At 35℃, 25℃, and 15℃, there was no significant change in the structure of the pancreas and islet function, but the exocrine secretion of the pancreas was suppressed. At 5～15℃, the acinar tissue was destroyed, later replaced by connective tissue containing islet structures. At -20℃, acute pancreatitis with edema, interstitial hemorrhagic necrosis, and destruction of both exocrine and endocrine functions occurred. The effect is better when the pancreas temperature is maintained at 31℃.

　　2. Cryosurgical treatment for severe acute pancreatitis: This method uses a super-low temperature probe (-140℃ or below) to directly freeze the hemorrhagic and necrotic pancreatic tissue. Some people have caused dogs to have hemorrhagic and necrotic pancreatitis for cryogenic tests, using a -195.8℃ cold probe for total pancreatic cryotherapy, forming a 5×3cm2 destruction area within 10～15 seconds. Only one out of ten dogs treated died. In 1989, Soviet scholars reported the results of cryotherapy in 15 patients: hemorrhagic pancreatitis in 2 cases; fatty pancreatitis in 12 cases; purulent pancreatitis in 1 case. Corresponding to the necrotic focus, cryotherapy is performed at 3～5 points, with a probe temperature of -195℃ and a duration of 1～2 minutes. In cases with pancreas head edema and jaundice, cholecystostomy can be added according to the need of the disease. Only one patient out of the 15 died.

　　On the contrary, some experiments have shown the opposite, with the activity of pancreatic enzymes actually increasing after freezing. The reason may be that the edge of the frozen area contains some cells whose cell membranes rupture and release the enzymes into the blood, without denaturation of the enzyme protein. However, the increase in serum enzyme activity caused by freezing in acute pancreatitis is minor compared to its inhibitory effect on enzyme activity.

　　3. Localized Pancreatic Necrosis and Peripancreatic Exudation: Severe pancreatitis not only has varying degrees of necrosis in the pancreas itself, but also has a large amount of inflammatory exudation around the pancreas, accompanied by muscle tightness, tenderness, elevated body temperature, and increased white blood cells in the upper abdomen. B-ultrasound or CT examination shows that the pancreas image is enlarged, with scattered or localized necrotic areas, and there is a lot of exudation around the pancreas. However, whether the necrotic pancreas and surrounding exudation have infection has different opinions on treatment. If there is no infection, palliative treatment can be adopted, and the exudate can gradually absorb, and the small necrotic area of the pancreas can also be absorbed. If there is infection, appropriate surgical treatment should be given.

　　Therefore, it is very important to differentiate whether there is infection or not. CT-guided puncture of the pancreas can be performed to differentiate between necrotic tissue and fluid. By determining the characteristics, concentration, smear, and bacterial culture of the aspirate, it can be decided whether there is infection in the regional necrosis and exudative fluid. However, it is impossible to obtain immediate positive or negative results from bacterial culture. At this time, the nature of the puncture fluid, the severity of peritonitis, such as whether peritonitis is limited to the upper abdomen or the entire abdomen, as well as changes in body temperature and blood count, should be judged to determine whether there is infection. Sometimes it is difficult to judge the aspirate, and for more caution, multiple punctures of the pancreas (CT-guided) can be performed under strong systemic support and rational use of antibiotics to determine whether there is infection in the regional pancreatic necrosis and surrounding inflammatory exudation.

　　In summary, although there is limited regional pancreatic necrosis and exudation, if there is no infection and the systemic toxic symptoms are not very serious, there is no need to rush for surgery. If there is infection, appropriate surgical treatment should be given. This view is different from immediate surgery once the diagnosis of acute hemorrhagic necrotic pancreatitis is established. However, it is necessary to strengthen clinical observation carefully and meticulously.