What is acute pancreatitis?

Acute pancreatitis is an acute inflammation of the pancreas caused by various reasons, such as pancreatic duct obstruction, pancreatic duct hypertension and insufficient blood supply to the pancreas.

There are many causes of acute pancreatitis (Table 1), but the mechanism of these diseases triggering pancreatic inflammation has not been determined. Gallstones continue to be the main cause of acute pancreatitis in most cases (3%-6%). Alcohol is the second most common cause of disease in the United States, accounting for 15%-3%. The incidence of pancreatitis among alcoholics is surprisingly low (5/1,), which indicates that there are unknown factors affecting the individual's susceptibility to pancreatic damage besides the amount of alcohol intake. The mechanism of injury is not very clear. Hypertriglyceridemia is the cause of acute pancreatitis, accounting for 1.3%-3.8% of cases; The serum triglyceride level is usually > 11.3 mmol/L (> 1 mg/DL). Subsequent examination of most hypertriglyceridemia patients shows that there is a basic disorder of lipid metabolism, which may not be related to pancreatitis. Diabetic patients with ketoacidosis or taking certain drugs can also have hypertriglyceridemia. After endoscopic retrograde cholangiopancreatography (ERCP), 5%-2% patients developed acute pancreatitis. About 2%-5% of acute pancreatitis cases are related to drugs. Drugs cause pancreatitis through allergic reactions or through the production of toxic metabolites, although in some cases it is not clear which of these mechanisms plays a role (Table 1).

Autodigestion is a pathogenic theory. According to this theory, pancreatitis occurs when proteolytic enzymes (e.g., trypsinogen, chymotrypsin, elastase, phospholipase A) are activated in the pancreas instead of in the small intestine. Many factors (such as endotoxin, exotoxin, virus infection, ischemia, hypoxia and direct trauma) are thought to activate these prozymes. Activated proteolytic enzymes, especially trypsin, can not only digest pancreas and peripancreatic tissues, but also activate other enzymes such as elastase and phospholipase.

table 1 causes of acute pancreatitis

common causes

gallstones (including minor lithiasis)

alcohol (acute and chronic alcoholism)

hypertriglyceridemia

endoscopic retrograde cholangiopancreatography (ERCP), Especially after biliary tract manometry

trauma (especially blunt abdominal trauma)

postoperative (abdominal and non-abdominal surgery)

drugs (azathioprine, 6- mercaptopurine, sulfonamides, estrogen, tetracycline, valproic acid, Anti-AIDS drugs

Oddi's sphincter dysfunction

uncommon causes

vascular causes and vasculitis (ischemic hypoperfusion after heart surgery)

connective tissue diseases and thrombotic thrombocytopenic purpura (TTP)

pancreatic cancer

hypercalcemia

periampullary diverticulum

pancreatic division. , Coxsackie virus, cytomegalovirus, echo virus, parasite)

Autoimmunity (such as Sjogren's syndrome)

Etiology that should be considered in patients with acute pancreatitis with no obvious cause

Hidden diseases of biliary system or pancreatic duct, especially mini-lithiasis, bile sludge

drugs

hypertriglyceridemia

pancreatic division

. Any severe acute abdomen or back pain should think of acute pancreatitis. The diagnosis of acute pancreatitis should usually be considered when patients with the constitution that may be prone to pancreatitis present with severe and persistent abdominal pain, nausea, vomiting, fever, tachycardia and abnormal findings in abdominal examination. Laboratory tests often show leukocytosis, hypocalcemia and hyperglycemia. The diagnosis is usually made by a positive finding that serum amylase and/or lipase are increased by more than three times. Not all the above characteristics are necessary for diagnosis.

In most patients with acute pancreatitis (85%-9%), pancreatitis is self-limited and usually subsides spontaneously within 3-7 days after starting treatment. Conventional treatment includes (1) painkillers, (2) intravenous fluids and colloids to maintain normal blood volume, and (3) fasting. Controlled trials have shown that gastrointestinal decompression does not provide any clear advantages for the treatment of mild to moderate acute pancreatitis. Therefore, its application must be selective rather than compulsory.

It has been proved that pancreatic secretion stimulated by CCK is almost cancelled in four different experimental models of acute pancreatitis. This finding may explain why drugs blocking pancreatic secretion in acute pancreatitis have no effect. For this and other reasons, anticholinergic drugs are not indicated for acute pancreatitis. Besides gastrointestinal decompression and anticholinergic drugs, other treatments aimed at "resting the pancreas" by inhibiting pancreatic secretion cannot change the course of pancreatitis.

patients with mild to moderate pancreatitis usually need intravenous infusion and fasting treatment. A total liquid diet usually begins on the 3rd to 6th day, while a normal diet begins on the 5th to 7th day. The decision to resume oral diet is usually based on the following criteria: (1) abdominal pain is relieved or eliminated; (2) The patient is hungry; (3) Organ dysfunction, if it exists, has been eliminated. Elevated serum amylase/lipase or persistent inflammatory changes in CT scan should not prevent asymptomatic and hungry patients from eating. At this point, the persistent inflammatory changes or the continuous increase of serum amylase/lipase on CT scan may not be resolved for weeks or months. Patients with persistent fulminant pancreatitis usually need a lot of fluids, and they need to pay close attention to complications such as cardiovascular failure, respiratory insufficiency and pancreatic infection. The latter should be combined with radiology and surgical methods. Although early non-controlled studies showed that peritoneal lavage through percutaneous dialysis catheter was beneficial to severe pancreatitis, subsequent studies showed that this treatment did not affect the outcome of this attack. Active surgical pancreatic debridement (resection of necrotic tissue) should be performed shortly after infectious necrosis is confirmed, and may require multiple operations. Because the mortality rate of aseptic acute necrotizing pancreatitis is ~1%, if routine treatment can't stop the deterioration of patients, laparotomy with adequate drainage and removal of necrotic tissue should be considered. Total parenteral nutrition (TPN) makes it possible for severe acute or persistent pancreatitis patients who can't eat normally to be given nutritional support. It has been shown that enteral feeding with nasojejunal tube may be preferred over TPN because of reducing infection. Cheap enteral feeding only meets about 5% of nutritional needs, while TPN meets 9% of such needs. At present, there is no large-scale normal controlled trial comparing enteral feeding with TPN in patients with severe acute pancreatitis. Only a small proportion of patients with acute pancreatitis need high nutrition therapy.

If papillotomy is performed within the first 36-72 hours, the patients with severe gallstone pancreatitis can be significantly improved. Studies have shown that only patients with very severe gallstone pancreatitis should consider emergency ERCP. Finally, the treatment of patients with pancreatitis related to hypertriglyceridemia includes (1) losing weight to an ideal weight, (2) limiting lipid diet, (3) exercising, (4) avoiding alcohol and drugs that can increase serum triglycerides (namely estrogen, vitamin A, thiazides and propranolol), and (5) controlling diabetes.

according to the condition, the treatment also includes the treatment of severe pancreatitis, operation, rational use of antibiotics, treatment of infectious pancreatic necrosis or abscess and pancreatic pseudocyst, treatment of pancreatic ascites and pancreatic pleural effusion, and so on.