Childhood acute pancreatitis

　　1. Etiology

　　The causes of childhood pancreatitis are significantly different from those of adults. The main causes of adult acute pancreatitis are gallstones, chronic infections, tumors, and alcoholism. The common causes of children are viral infections, trauma, multisystem diseases, and congenital malformations of the pancreaticobiliary system, among which viral infections are the most important cause that can lead to childhood pancreatitis. However, there are still about 30% of children whose causes are unknown.

　　1, Infection

　　Secondary infections caused by bacteria or viruses from other parts of the body.

　　(1) Virus: Acute epidemic parotitis virus, measles virus, rubella virus, Coxsackievirus, Echovirus, hepatitis A and B viruses, and cytomegalovirus can all cause acute pancreatitis. Among them, pancreatitis caused by epidemic parotitis virus is relatively common. When children have epidemic parotitis, about 50% of the patients have varying degrees of impact on their pancreas. According to statistics from Xinhua Hospital in Shanghai, among 662 cases of epidemic parotitis, 2 cases were complicated with pancreatitis. In recent years, interstitial pancreatitis has been reported as another manifestation of rubella virus infection, and it has been confirmed by post-mortem examination. Rubella virus has also been confirmed by pancreatic tissue culture.

　　(2) Parasitic infection: In the Asian region, parasitic infection is also a common cause, such as ascending infection and obstruction caused by Ascaris lumbricoides and liver flukes can lead to the occurrence of acute pancreatitis.

　　(3) Bacterial infection: Infections caused by Salmonella, Shigella, Campylobacter, and Leptospira can be accompanied by acute pancreatitis, which is clinically seen in pneumonia, bacillary dysentery, tonsillitis, etc., but it is mostly due to their toxins. There are reports in China of children with typhoid fever complicated with acute pancreatitis.

　　(4) Mycoplasma infection: In addition, mycoplasma infection can also cause acute pancreatitis, and pancreatitis can be the initial manifestation of mycoplasma infection.

　　2, Gastrointestinal diseases

　　Upper gastrointestinal tract diseases or malformations at the bileo-pancreatic junction, where bile refluxes into the pancreas, causing pancreatitis. Only 10% to 16% of pediatric pancreatitis is caused by congenital pancreaticobiliary abnormalities. The commonly associated conditions such as choledochal cysts, duodenal atresia, and pancreatoduodenal divisum often lead to recurrent pancreatitis. The patient's body and tail of the pancreas and part of the head are drained by smaller accessory pancreatic ducts, which are relatively narrow and can cause poor excretion of pancreatic juice.

　　Gallstones are a common cause of acute pancreatitis in adults, but they are rare in children. The common obstructive cause in children is biliary ascariasis. The ascaris worm gets stuck in the common channel, blocking the excretion of pancreatic juice and causing pancreatitis.

　　3, Drugs and toxins

　　This etiology is less common in children than in adults. According to a statistics from Xinhua Hospital affiliated with the Second Military Medical University of Shanghai, during the treatment of 230 children with acute lymphoblastic leukemia and stage IV lymphoma with asparaginase (L-ASP), 6 cases of acute necrotizing pancreatitis (ANP) occurred (2.6%). Abroad, Joseph et al. reported that valproic acid treatment after 10 years can cause 1 case of necrotizing pancreatitis. The use of large amounts of adrenal corticosteroids, immunosuppressants, morphine, and other drugs can cause acute pancreatitis.

　　4, Systemic diseases

　　It can be concurrent with systemic diseases, such as systemic lupus erythematosus, allergic purpura, hyperparathyroidism, skin and mucous membrane lymph node syndrome, hemolytic uremic syndrome, and inflammatory bowel disease, which can all be accompanied by pancreatitis. These diseases cause necrotizing pancreatitis due to vasculitis involving the blood vessels of the pancreas and other organs, leading to inflammation, necrosis, and thrombosis of the vascular wall.

　　5, Trauma

　　Acute pancreatitis can be caused by various abdominal blunt injuries, commonly seen in bicycle collisions, traffic accidents, and other situations. In the statistics of etiology of pediatric pancreatitis, trauma accounts for 13% to 30%. The middle segment of the pancreatic duct crosses the spine, making it particularly prone to injury and fracture. The mild form may only be a hematoma without substantial injury; the severe form may have pancreatic duct rupture, leakage of pancreatic juice, and factors such as impaired blood supply and infection, which can lead to acute hemorrhagic necrotic pancreatitis.

　　6, Endocrine and metabolic diseases

　　This type of etiology is rare in children.

　　(1) Hypercalcemia: It can stimulate the secretion of pancreatic enzymes, activate trypsin, and form pancreatic duct stones, thereby causing acute pancreatitis. Hypercalcemia can occasionally occur during total parenteral nutrition (TPN), leading to pancreatitis.

　　(2) Hyperlipidemia: The earliest injury caused by hyperlipidemia in pancreatitis occurs in the small blood vessels of the pancreas. Triglycerides are hydrolyzed by lipases, releasing free fatty acids, which act on the endothelium of the small blood vessels in the pancreas, causing vascular injury and thrombosis.

　　(3) Malnutrition: Low-protein diet can lead to pancreas atrophy, fibrosis, and stone formation.

　　(4) Metabolic diseases: such as lactic acidemia, propionic acidemia, glycogen storage disease type I, homocystinuria, and others. The pathogenesis is unclear, and some patients with the primary disease have not been diagnosed and are often diagnosed with idiopathic pancreatitis during an attack.

　　(5) Diabetes: In children with type 1 diabetes and diabetic ketoacidosis, amylaseemia may occur due to increased salivary amylase. However, it is rare to be accompanied by acute pancreatitis.

　　7. Hereditary pancreatitis

　　Hereditary pancreatitis is an autosomal recessive genetic disorder that often affects multiple family members. There is no gender difference among patients, and it is more common in white people. Patients often develop typical acute pancreatitis in childhood, which later turns into chronic recurrent episodes, gradually leading to pancreatic calcification, diabetes, and steatorrhea.

　　Second, pathogenesis

　　The pathophysiology of acute pancreatitis is the premature activation of zymogens within the pancreas into active digestive enzymes, accompanied by the obstruction of pancreatic enzymes from being secreted into the intestinal lumen. Under normal physiological conditions, the pancreas has a series of protective mechanisms to prevent the parenchyma from being damaged by proteolytic enzymes, with the main factor being the existence of zymogens in the acinar cells in a non-activated form. All enzymes in the pancreas are synthesized in the endoplasmic reticulum and then transported to the Golgi apparatus for assembly. These enzymes are stored in non-active form in membrane-bound zymogen granules. These granules and the cytoplasm of pancreatic cells contain trypsin inhibitors, and active enzymes are not released into the cytoplasm of the adenocytes but directly enter the lumen after fusion of the enzyme granule membrane with the adenocyte membrane. Zymogens are activated in the intestinal lumen by the brush border of intestinal kinases, first activating trypsinogen to form trypsin.

　　1. Activation of various pancreatic enzymes

　　The pathogenesis of acute pancreatitis is very complex. Common pathogenic factors can cause an increase in the secretion of acinar cells, an increase in intraductal pressure, and lead to the rupture of pancreatic ductules and acinar cells, causing extrusion of pancreatic juice and contact with pancreatic parenchyma and extrapancreatic tissues. At this time, various pancreatic enzymes in the pancreatic juice are activated and produce autodigestion, causing edema, hemorrhage, or necrosis of the pancreatic tissue. The first step in the pathogenesis of acute pancreatitis is the premature activation of trypsinogen within the acinar cells into trypsin. Trypsinogen is activated into trypsin by an lysosomal hydrolase called cathepsin B. Then, trypsin converts various zymogens into active enzymes, including phospholipase A2, elastase, and carboxypeptidase, etc., which are then released into the cytoplasm and leak into the interstitial tissue to initiate the autodigestion process. Trypsin can also activate the complement and kinin systems. In experimental pancreatitis, the most toxic enzyme activated is lipase, followed by elastase and phospholipase A2, with trypsin being the least toxic. Lipase causes necrosis of peripancreatic fat, and damaged fat cells can produce harmful factors, further exacerbating the injury to surrounding acinar cells. Elastase can dissolve elastic fibers in the vascular wall, leading to pancreatic vascular rupture, hemorrhage, and necrosis. Pancreatic kallikrein can catalyze kininogen into bradykinin, both of which cause vasodilation, increased vascular wall permeability, leukocyte exudation, and pain. Trypsin and chymotrypsin can cause tissue edema, hemorrhage, and necrosis. Phospholipase A2 converts lecithin into hemolytic lecithin with cytotoxicity, causing necrosis of the pancreatic tissue and potentially damaging pulmonary alveolar lecithin, leading to lung injury. Various enzymes may be involved in acute pancreatitis, and the pathophysiological mechanisms of the main enzyme classes are as follows:

　　(1) Phospholipase A: In a normal human body, phospholipase A (PLA) is distributed in the pancreas in an inactive enzyme precursor form. During acute pancreatitis, the activated PLA has two functions:

　　① Hydrolyzing lecithin within acinar cells to produce free fatty acids (FFA) and lysophosphatidylcholine, lysophosphatidylcholine can cause cell membrane lysis, releasing various digestive enzymes within the cell, causing hemorrhagic necrosis of the pancreas and systemic multi-organ damage.

　　② The activation of PLA leads to the damage of lysosomal membranes and the release of lysosomal enzymes, further causing the activation of pancreatic enzymes and self-digestion.

　　(2) Thromboxane A2 (TXA2): During the process of PLA being decomposed from membrane phospholipids into free fatty acids and lysophosphatidylcholine, a strong vasoconstrictor substance - thromboxane A2 (TXA2) - is produced, leading to impaired blood supply to pancreatic tissue, lysosomal membrane damage in the cytoplasm, and an increase in calcium ions in the cytoplasm.

　　(3) Trypsin: Trypsinogen can self-activate to become trypsin, and trypsin can activate various zymogens, making them active. The third variant of trypsin - mesotrypsin (MT) - is three times more active than trypsin and almost resistant to all trypsin inhibitors.

　　(4) Elastase: In addition to its general proteolytic enzyme activity, its specific action is mainly the digestion of elastic fibers, especially the dissolution of elastic fibers in blood vessel walls, leading to necrosis, rupture, and hemorrhage of pancreatic blood vessels.

　　(5) Kallikrein: After being activated by trypsin, kallikreinogen is converted into kallikrein, which degrades kallikreinogen in the blood into substances with vascular activity. These pancreatic vascular active substances can strongly dilate blood vessels and increase capillary permeability, reducing the effective circulating blood volume and leading to a decrease in blood pressure or shock; kallikrein is also a pain-inducing substance, causing severe visceral pain; in addition, kallikrein can cause histamine release and leukocyte aggregation.

　　(6) Lysosomal enzymes: Lysosomes are intracellular granules containing high concentrations of acidic hydrolytic enzymes and have potential enzyme reactions, known as the 'intracellular digestive system'. During acute pancreatitis, the activation of zymogens can occur within acinar cells through the action of lysosomal hydrolases. The activation of trypsinogen by lysosomal enzymes is a key step in the self-digestion of pancreatic enzymes and the hemorrhagic necrosis of pancreatic tissue. Large vacuoles containing trypsin and lysosomal enzymes can be observed in acinar cells in the early stages of acute pancreatitis.

　　Under normal circumstances, the pancreas can secrete various antiprotease factors to prevent the self-activation and self-digestion of trypsin. During acute pancreatitis, this function is weakened, exacerbating the activity of trypsin complexes and causing damage to the body. In addition, during acute pancreatitis, oxygen free radicals can cause damage to macromolecules such as proteins, nucleic acids, lipids, and polysaccharides, leading to increased permeability of the capillary walls in the pancreas, exacerbating pancreatitis, hemorrhage, and tissue变性 and necrosis, but it does not affect enzyme activation.

　　2. Endotoxemia

　　The incidence of endotoxemia during acute pancreatitis is very high, with endotoxins mainly coming from the intestines and being the main cause of multi-organ failure and death. Endotoxins are lipopolysaccharides in the cell wall of Gram-negative bacteria, and they may be involved in the pathogenesis of pancreatitis in the following aspects:

　　(1) It binds non-specifically to the cell membrane, interfering with the normal function of the cell membrane.

　　(2) It binds non-specifically to the cell membrane, interfering with the normal function of the cell membrane.

　　(3) It directly destroys the lysosomal membrane in the cells of the mononuclear phagocytic system, causing cell damage.

　　(4) It alters the body's immune function.

　　(5) It causes a series of pathological changes in the body, mainly affecting vascular contraction and relaxation function, activating vasoactive substances, causing a decrease in platelets and white blood cells, lowering blood pressure, and leading to disseminated intravascular coagulation (DIC) and multi-organ failure.

　　During acute pancreatitis, various enzymatic toxic substances produced and secreted by the pancreas can cause tissue edema, hemorrhage, and necrosis in the pancreas and peripancreatic area. The toxins produced by enzymatic toxic substances and necrotic tissue can be transported to the whole body through the blood circulation and/or lymphatic system, causing complications of systemic organs and becoming the main cause of damage to extrapancreatic organs.

　　3. It can be divided into 2 types according to its pathological changes

　　During the onset of pediatric acute pancreatitis, the activation of white blood cells also plays a very important role in systemic lesions. After neutrophils are activated, elastase and superoxide anions are produced, causing endothelial damage. In addition, macrophages, monocytes, and lymphocytes release various inflammatory mediators in the pancreas and other tissues, such as platelet-activating factor, oxygen-reactive substances, and cytokines. They can be divided into acute edematous type and acute necrotic type:

　　(1) Edematous pancreatitis (interstitial type): This type is the most common, accounting for 85% to 95%. The pancreas is swollen or locally edematous and congested, with increased volume. The excretion of pancreatic juice is obstructed, leading to increased amylase levels in blood and urine. There may be a small amount of fat necrosis around the pancreatic tissue. Histological examination shows interstitial edema, congestion, and infiltration of inflammatory cells, but no acinar necrosis, and vascular changes are not obvious.

　　(2) Hemorrhagic-necrotic pancreatitis (acute necrotic type): The condition is severe, accounting for about 10% of pediatric acute pancreatitis. Necrosis of acinar and adipose tissue, with vascular necrosis and hemorrhage as the characteristics of this type. Pancreatic duct dilation, arterial thrombosis, and a large amount of necrotic exudate are present. The pancreas appears deep red or purple-black, with fresh hemorrhage also visible. The surrounding tissues of the pancreas, such as omentum, mesentery, and retroperitoneal tissue, are involved, which easily leads to secondary infection. A large amount of exudate containing pancreatic juice flows into the peritoneal cavity, causing diffuse peritonitis. The digestive enzymes in the pancreatic juice seep out and act on the rich omentum, mesentery, and intestinal wall, causing widespread fat necrosis foci. The fat is decomposed into glycerol and fatty acids. The latter absorbs calcium from the blood to form calcification foci. Blood calcium can significantly decrease, leading to cramps and shock, with a very high mortality rate. When the pancreatic parenchyma is inflamed, islet cells are also damaged, affecting glucose metabolism, and diabetes may occur as a complication. After recovery, fibrous tissue hyperplasia, pseudocyst formation, and calcification may occur.

　　1. Local complications

　　1. Pancreatic abscess

　　It usually forms 2 to 3 weeks after the onset due to secondary bacterial infection after the necrosis of the pancreas and peripancreatic tissue. At this time, the patient may have persistent high fever, persistent abdominal pain, and palpable mass in the upper abdomen.

　　2. Pseudocyst

　　It usually forms 3 to 4 weeks after the onset, caused by liquefaction or excretion of the contents of the pancreatic pseudocysts communicating with the pancreatic duct due to the digestion of pancreatic enzymes by the pancreas. It is usually located in the body and tail of the pancreas, with the cyst wall consisting of necrotic, granulation, and fibrous tissue without epithelial covering. Rupture or fissure of the cyst wall is a major cause of pancreatic pseudocysts.

　　3. Portal hypertension

　　A few cases may develop segmental portal hypertension due to compression of the splenic vein by pancreatic fibrosis or pseudocysts, leading to symptoms such as portal hypertension.

　　2. Systemic complications

　　In addition to local hemorrhage and necrosis of the pancreatic tissue, acute hemorrhagic necrotic pancreatitis can also cause dysfunction of multiple organs, such as adult respiratory distress syndrome (ARDS), renal failure, arrhythmia or heart failure, sepsis, pneumonia, diabetes, thrombophlebitis, and disseminated intravascular coagulation, with extremely high mortality.

　　The main symptoms are upper abdominal pain, which is often persistent and accompanied by nausea and vomiting. The vomit contains food and secretions from the stomach and duodenum. In severe cases, in addition to the acute and serious appearance, there may be dehydration and early symptoms of shock, and abdominal distension due to intestinal paralysis. Due to the swelling of the pancreatic head compressing the distal end of the common bile duct, jaundice may occur, but it is rare in children.

　　1. Prevent the occurrence of infectious diseases such as biliary ascariasis, viral infection, sepsis, mycoplasma pneumonia, and other diseases;

　　2. Prevent overeating and malnutrition to avoid gastrointestinal dysfunction, which may hinder the normal activity and emptying of the intestines, obstructing the normal drainage of bile and pancreatic juice, and causing pancreatitis.

　　3. Avoid or eliminate biliary tract diseases: timely treatment of biliary tract stones, and prevention of intestinal ascaris.

　　4. Avoid abdominal damage, such as surgery? Endoscopic retrograde cholangiopancreatography, and others.

　　5. Prevention of metabolic disorders such as hypercalcemia, hyperlipidemia, diabetes, and others

　　6. Other factors such as the prevention of alcohol intoxication, trauma, emotions, and medication.

　　1. Laboratory examination

　　1. Routine blood test

　　）Before massive fluid resuscitation, blood cell volume increases.

　　(2) White blood cell count and neutrophil classification increase, and nuclear left shift may occur.

　　2. Amylase measurement

　　Elevated levels of blood and urine amylase can be seen. They are often the main diagnostic criteria, but not the decisive factor

　　(1) Precautions:

　　① The degree of amylase elevation is often not proportional to the severity of inflammation.

　　② An elevated serum amylase level does not necessarily indicate acute pancreatitis. Normal serum amylase levels do not exclude acute pancreatitis.

　　③ Salivary amylase:

　　A. Salivary glands: Trauma, surgery, anorexia nervosa, mumps, salivary duct obstruction, diabetic ketoacidosis, bulimia.

　　B. Ovary: Cysts, malignant lesions, malignant tumors.

　　③ Urinary amylase is not as accurate as serum amylase.

　　④ The significantly elevated amylase levels in pleural and peritoneal effusions can be used as a diagnostic criterion, but it needs to be differentiated from pleural effusions and increased amylase levels in ascites caused by gastrointestinal perforation and other conditions.

　　3. Electrolyte and acid-base balance determination

　　(1) Hypocalcemia: The normal value of blood calcium is 2.25～2.75mmo1/L(9～11mg/dl), ≤1.87mmol/L(7.5mg/dl) can cause tetany of the hands and feet.

　　(2) Other:

　　There are often metabolic acidosis, respiratory acidosis, and mixed acid-base imbalance, with hypokalemia.

　　4. Amylase and creatinine clearance ratio

　　The normal ratio is 1％～4％，>6％ suggests acute pancreatitis. The formula is: urine amylase/serum amylase × blood creatinine/urine creatinine × 100％

　　5. Coagulation mechanism

　　When disseminated intravascular coagulation occurs, various coagulation tests are abnormal. In extremely severe cases, positive DIC indicators may appear, with significantly lower platelet counts, significantly prolonged prothrombin time (PT), Fbg below 2g/L, and fibrinolysis indicators such as a positive 3P test and shortened clot lysis time. The thrombin time (TT) is prolonged to more than 3 seconds, or the plasma elution time (ELT) is shortened (

　　6. Serum methemalbumin determination

　　Non-specific, any cause of intra-abdominal hemorrhage results in the release of hemoglobin from hemolysis, which is acted upon by fatty acids and elastase to form methemoglobin. Methemoglobin combines with albumin to form methemalbumin. In hemorrhagic necrotizing pancreatitis, serum methemalbumin often appears 12 hours after onset, while it is negative in edematous pancreatitis.

　　7. Serum lipase determination

　　Serum lipase levels are elevated. Due to conditions such as intestinal obstruction, ulcer perforation, common bile duct stones, and acute cholecystitis, blood lipase levels can also rise, making an increase of more than 3 times more specific. The normal value is 0.5～1U(comfort). It starts to rise after 24 hours of onset and can last for 8～14 days. It is of diagnostic significance for patients who seek medical attention late after onset, but not very significant for early diagnosis.

　　8. Blood biochemistry examination

　　In severe cases, hyperglycemia and hyperglycosuria may occur. Blood tests such as blood urea nitrogen, C-reactive protein, blood gas analysis, α2'-microglobulin, liver function, and others can reflect the severity of pancreatitis.

　　9. Abdominal puncture

　　In severe cases with peritonitis, if there is a lot of peritoneal effusion, peritoneal puncture can be performed. The nature of peritoneal effusion (hemorrhagic, mixed with fat necrosis) and amylase measurement can help with diagnosis.

　　Second, imaging examination

　　1. B-ultrasound examination

　　It is valuable for the diagnosis of edematous pancreatitis and late complications such as pancreatic pseudocysts, as well as for the diagnosis of whether pancreatitis is complicated with biliary calculi and biliary obstruction.

　　(1) Edematous acute pancreatitis: The pancreas is significantly diffusely enlarged, with exudation around the pancreas, regular edges, clear, and uniform hyperechoic;

　　(2) Hemorrhagic necrotic type: Severe enlargement of the pancreas with irregular and blurred edges, uneven and irregular hyperechoic and mixed echoes.

　　(3) Complicated pseudocyst: Smoothly rounded or oval hyperechoic areas with cystic masses, often located outside the pancreatic contour, with enhanced posterior wall echo and unclear boundary with the pancreas.

　　In addition, some patients may have unclear pancreas imaging due to the influence of intestinal gas, and the examination cannot be performed.

　　2. X-ray examination

　　The manifestations are not specific to pancreatitis, so the abdominal X-ray lacks specificity.

　　3. Computed tomography (CT)

　　It has certain value in judging whether the pancreas has necrosis and the range and size of the necrosis when the diagnosis of acute pancreatitis is uncertain using B-ultrasound. However, more than 20% of acute pancreatitis patients have normal CT results, so normal CT cannot exclude the diagnosis of pancreatitis.

　　4. Chest X-ray examination

　　During acute pancreatitis, there are often pulmonary complications, often manifested as elevated diaphragm, restricted movement, pleural reaction or effusion, patchy infiltration at the base of the lung, or atelectasis. Changes in the chest during acute pancreatitis are not specific.

　　5. Endoscopic retrograde cholangiopancreatography (ERCP)

　　ERCP is particularly useful for diagnosing recurrent pancreatitis with suspected pancreatic duct abnormalities and pancreatolithiasis.

　　6. Electrocardiogram examination

　　Severe cases may show signs of myocardial ischemia or injury.

　　1. Acute pancreatitis patients should temporarily abstain from food completely to avoid food and acidic gastric juice entering the duodenum, causing stimulation to the pancreas and continuing destruction of the pancreas. During this stage, nutrition is mainly supplied through parenteral nutrition. After the patient's symptoms gradually subside, they can consume fat-free and low-protein liquid foods such as fruit juice, rice gruel, tomato juice, and thin noodle soup. When the condition improves, low-fat liquid foods such as liver soup, soy milk, egg broth, and kidney soup can be consumed, and then gradually changed to low-fat semi-liquid foods, with 5-6 meals per day.

　　2. If hyperglycemia occurs in the lesion, the intake of sugar and fat should be controlled accordingly. If the patient experiences pain, it indicates that they are intolerant to fat digestion and absorption, and it is even more important to choose low-fat, low-protein foods.

　　3. During the period of abstinence from food, attention should be paid to maintaining electrolyte balance. If the levels of potassium, magnesium, sodium, and calcium decrease, they should be supplemented in a timely manner, and at the same time, drink more fresh mushroom soup, vegetable juice, and fruit juice.

　　4. Avoid greasy foods. Greasy foods are difficult to digest and can promote the secretion of bile, which can activate digestive enzymes in the pancreas, worsening the condition. Therefore, foods high in fat, such as fatty meat, peanuts, sesame seeds, fried snacks, and fried foods, should be prohibited from consumption.

　　5. Abstain from smoking, alcohol, and spicy foods.

　　6. As the condition improves, gradually increase the amount and variety of food intake, but do not overeat to avoid recurrence of the condition.

　　1. Non-surgical treatment
　　Prevention and treatment of shock, improvement of microcirculation, antispasmodic, analgesic, inhibition of pancreatic enzyme secretion, anti-infection, nutritional support, prevention of complications, and strengthening of intensive care measures.
　　(1) Prevention and treatment of shock Improvement of microcirculation should be actively supplemented with fluids, electrolytes, and calories to maintain circulatory stability and electrolyte balance.
　　(2) Inhibition of pancreatic secretion ①H2 receptor antagonist; ②Trypsin inhibitor; ③5-Fluorouracil; ④Fasting and gastric decompression.
　　(3) Antispasmodic analgesia Analgesics should be administered regularly. The traditional method is intravenous infusion of 0.1% procaine for venous closure. It is also possible to use pethidine and atropine in combination at regular intervals, which can relieve pain and relax the Oddi sphincter spasm. Morphine should be avoided to prevent the spasm of the Oddi sphincter. In addition, isosorbide dinitrate, isosorbide mononitrate, and other substances can be used in severe pain, especially in elderly patients, which can relieve the spasm of the Oddi sphincter to some extent and is also very beneficial to the coronary blood supply.
　　(4) Nutritional support In cases of acute severe pancreatitis, the body's catabolism is high, there is inflammatory exudation, long-term fasting, high fever, and patients are in negative nitrogen balance and hypoproteinemia, so nutritional support is needed, while at the same time, the pancreas should not secrete or secrete less.
　　(5) Application of antibiotics Antibiotics are an indispensable part of comprehensive treatment for acute pancreatitis. The use of antibiotics in acute hemorrhagic necrotic pancreatitis is uncontroversial. In acute edematous pancreatitis, as a preventive measure against secondary infection, a reasonable amount of antibiotics should be used.
　　(6) Peritoneal lavage for patients with a large amount of exudation in the peritoneal cavity, peritoneal lavage can be performed to dilute and excrete the liquid containing a large amount of pancreatic enzymes and toxic substances in the peritoneal cavity.
　　(7) Enhanced monitoring.
　　(8) Indirect hypothermia therapy.
　　2. Surgical Treatment
　　For patients with limited regional pancreatic necrosis and exudation, without infection and not severe systemic toxic symptoms, there is no need to rush for surgery. If there is infection, appropriate surgical treatment should be provided.