Pancreatic Diseases Group of the Chinese Medical Association, Gastroenterology Branch
Acute pancreatitis (AP) is a disease caused by activation of pancreatic enzymes from multiple etiologies, followed by local inflammatory response of the pancreas with or without functional changes in other organs. Clinically, the course of the disease is self-limiting in most patients, and 20%-30% of patients have an aggressive clinical course. The overall morbidity and mortality rate is 5-10%.
I. Terminology and definitions
According to the AP grading and classification system developed by the International AP Symposium (Atlanta, USA, 1992) and the AP management guidelines issued by the World Congress of Gastroenterology (Bangkok, Thailand, 2002), and taking into account the specific situation in China, the terminology and definitions of AP are stipulated to guide clinical and scientific work and to standardize the academic terminology in this field.
(A) clinical use of terminology
1, AP: clinically manifested as acute, persistent abdominal pain (occasionally without abdominal pain), increased serum amylase activity ≥ 3 times the upper limit of normal value, imaging suggests the pancreas with or without morphological changes, excluding other diseases. Other organ dysfunction may or may not be present. In a few cases, serum amylase activity is normal or mildly elevated.
2, Mild AP (MAP): with clinical manifestations and biochemical changes of AP without organ dysfunction or local complications, responding well to fluid supplementation therapy. ranson score <3, or APACHE-II score <8, or CT classification of A, B, C.
3. Severe AP (SAP): those with clinical manifestations and biochemical changes of AP with one of the following: local complications (pancreatic necrosis, pseudocyst, pancreatic abscess); organ failure.
(B) Other terms
1. Acute fluid accumulation: Occurs early in the course of the disease, with fluid accumulation in the pancreas or peripancreatic or distal pancreatic space, and lack of complete envelope.
2, pancreatic necrosis: enhanced CT examination suggests lifeless pancreatic tissue or peripancreatic adipose tissue.
3. Pseudocyst: fluid accumulation with intact non-epithelial envelope, containing pancreatic secretions, granulation tissue, fibrous tissue, etc. It mostly occurs 4 weeks after the onset of AP.
4. Pancreatic abscess: an accumulation of pus in the pancreas or the peri-pancreatic area, surrounded by a fibrous cyst wall.
AP etiology
There are many causes of AP, and there are regional differences. Based on the diagnosis of AP, the etiology should be clarified as much as possible, and efforts should be made to remove the etiology to prevent recurrence.
1. Common causes: cholelithiasis (including biliary microstones), alcohol, hyperlipidemia.
2. Other etiologies: malfunction of the papillary sphincter of the jugular abdomen, drugs and toxins, post retrograde cholangiopancreatography (ERCP), paraduodenal papillary diverticulum, traumatic, hypercalcemia, post-abdominal surgery, pancreatic splitting, peripotent cancer, pancreatic cancer, vasculitis, infectious (coxsackievirus, mumps virus, acquired immunodeficiency virus, ascariasis), autoimmune (systemic lupus erythematosus The disease can be caused by the following factors
3, by clinical and imaging, biochemical and other examinations, can not determine the cause of the disease is called idiopathic.
AP etiological investigation
1.Detailed medical history: including family history, history of both resident diseases, history of alcohol intake, history of drug intake, etc. Calculate body mass index.
2.Basic examination: serum amylase measurement, liver function test, lipid measurement, blood glucose measurement, blood calcium measurement; abdominal ultrasound.
3.In-depth examination: viral assay, autoimmune marker assay, tumor marker assay (carcinoembryonic antigen, CAl9-9) assay; CT scan (enhanced CT if necessary), ERCP/magnetic resonance cholangiopancreatography, ultrasound endoscopy, potbelly papillary sphincter manometry (if necessary), pancreatic exocrine function test, etc.
IV. Diagnostic process of AP
(I) Clinical manifestations of AP
Abdominal pain is the main symptom of AP, located in the upper abdomen, often radiating to the back, mostly acute, persistent, and a few without abdominal pain. It may be accompanied by nausea and vomiting. Fever often arises from acute inflammation, secondary infection of necrotic pancreatic tissue, or secondary fungal infection. Fever and jaundice are usually seen in biliary pancreatitis.
In addition, AP can be associated with the following systemic complications: tachycardia and hypotension or shock; pulmonary atelectasis, pleural effusion and respiratory failure, and some studies have shown that the presence of pleural effusion is closely related to the severity of AP and suggests a poor prognosis; oliguria and acute renal failure; tinnitus, diplopia, delirium, speech disorders and rigidity of the limbs, coma and other signs of pancreatic irritability, which can occur early after the onset of the disease or in the It can occur in the early stage of disease onset or in the recovery period.
In mild cases, there is only light pressure pain, but in severe cases, there are signs of peritoneal irritation, ascites, Grey-Turner sign and Cullen sign. A few patients present with portal hypertension and splenomegaly due to splenic vein embolism. Rarely, there is transverse colon necrosis. A mass may be palpable in the abdomen due to fluid accumulation or pseudocyst formation. Other signs may be present that are characteristic of the corresponding complications.
(II) Ancillary tests
1.Serum enzymatic examination: The clinical significance of serum amylase measurement is emphasized, and the change of urinary amylase is only for reference. High or low serum amylase activity does not correlate with the disease. The judgment of whether the patient is open to diet or the degree of the disease cannot simply rely on whether the serum amylase is reduced to normal, but should be a comprehensive judgment. Persistent increase in serum amylase should be noted for recurrent disease, complication of pseudocyst or abscess, suspected stone or tumor, renal insufficiency, macroamylasemia, etc. Attention should be paid to identify other acute abdominal conditions causing increased serum amylase. Measurement of serum lipase activity is clinically important, especially when serum amylase activity has decreased to normal, or when other causes of increased serum amylase activity are present, serum lipase activity measurement has a complementary effect. Similarly, serum lipase activity is not positively correlated with disease severity.
2. Serum markers: c-reactive protein (cRP) is recommended. CRP >150 mg/L after 72 h of onset suggests pancreatic tissue necrosis. Dynamic measurement of increased serum interleukin-6 level suggests poor prognosis.
3. Imaging diagnosis: ultrasound examination performed at 24-48h after the initial onset of the disease can initially determine the morphological changes of pancreatic tissue, and also help to determine the presence of biliary tract disease, but the influence of gas accumulation in the gastrointestinal tract at the time of AP cannot make an accurate judgment of AP. CT scan is recommended as the standard imaging method to diagnose AP. Enhanced CT or dynamic enhanced CT examination is performed if necessary. Grade A: normal pancreas according to the severity of inflammation. grade B: pancreatic parenchymal changes, including local or diffuse glandular enlargement. grade c: pancreatic parenchymal and peripheral inflammatory changes with mild peripancreatic exudation. grade D: significant peripancreatic exudation in addition to grade c, with a single fluid accumulation in or around the pancreatic parenchyma. grade E: extensive intra- and extra-pancreatic fluid accumulation, including pancreatic and fat necrosis, and pancreatic abscess. grade A Grade -c: clinically MAP; Grade D-E: clinically SAP.
4. Recommendations.
(1) The importance of clinical manifestations in the diagnosis of AP must be emphasized. Persistent mid-upper abdominal pain, increased serum amylase, and imaging changes, excluding other diseases, can diagnose this disease.
(2) The clinical term “moderate AP” or “severe AP tendency” is no longer applied.
(3) Clinical attention should be paid to the possibility of conversion from MAP to SAP in some AP patients. Therefore, dynamic observation of the disease is necessary. In addition to Ranson index and APACHE-II index, other valuable differentiating indexes are: body mass index over 28kg/m2; pleural exudate, especially bilateral pleural effusion: CRP>150mg/L after 72h and continues to increase, etc. are all valuable clinical severity assessment indexes.
V. Principles of AP management
1. Treatment and monitoring at the early stage of the disease: the purpose is to correct water and electrolyte disorders, support treatment, and prevent local and systemic complications. Contents include: routine blood and urine measurement, fecal occult blood, renal function, liver function measurement; blood glucose measurement; cardiac monitoring; blood pressure monitoring; blood gas analysis; serum electrolyte measurement; chest X-ray; central venous pressure measurement. Dynamic observation of abdominal signs and bowel sound changes. The 24h urine output and volume changes were recorded. The above indicators can be selected according to the patient’s specific condition. Routine fasting should be performed for gastrointestinal decompression in patients with severe abdominal distension and paralytic intestinal obstruction. Open diet can be considered when abdominal pain is reduced or disappeared, abdominal distension is reduced or disappeared, and intestinal dynamics is restored or partially restored, starting with sugar-based diet, gradually transitioning to low-fat diet, and not taking high or low serum amylase activity as a necessary condition for open diet.
2. Fluid rehydration: The amount of fluid rehydration includes the amount of basic needs and the amount of fluid flowing into the tissue interstitial space. Attention should be paid to infusion of colloidal substances and supplementation of trace elements and vitamins.
3.Analgesia: Consider analgesic treatment when the pain is severe. Pethidine hydrochloride (Dulcolax) can be injected under close observation of the condition. It is not recommended to apply morphine or cholinergic receptor antagonists, such as atropine, 654-2, etc., because the former will contract the sphincter of Oddi, and the latter will induce or aggravate intestinal paralysis.
4, inhibition of pancreatic exocrine secretion and pancreatic enzyme inhibitor application: growth inhibitor and its analogue octreotide can play a role by directly inhibiting pancreatic exocrine secretion, which is advocated in the treatment of heavy acute pancreatitis. H2 receptor antagonists and proton pump inhibitors can indirectly inhibit pancreatic secretion by inhibiting gastric acid secretion, in addition to preventing the occurrence of stress ulcers, which is advocated for use in SAP. Protease inhibitors are advocated to be applied early and in sufficient quantity.
5. Application of vasoactive substances: Since microcirculatory disorders play an important role in the pathogenesis of AP, especially SAP, it is recommended to apply drugs that improve microcirculation in the pancreas and other organs, such as prostaglandin E1 preparations, platelet-activating factor antagonists, salvia preparations, etc.
6, antibiotic application: for non-biliary MAP is not recommended for the routine use of antibiotics. For biliary MAP, or SAP, antibiotics should be used routinely. The causative agents of pancreatic infection are mainly gram-negative bacteria and anaerobic bacteria and other intestinal resident bacteria. The application of antibiotics should follow three major principles: antibacterial spectrum for gram-negative and anaerobic bacteria mainly, strong lipid solubility, and effective passage through the blood-pancreatic barrier. Metronidazole combined with quinolones is recommended as the first-line drug, with a switch to other broad-spectrum antibiotics in case of poor efficacy, for a course of 7-14 d, with extended application in special cases. It is important to pay attention to the diagnosis of fungal infection. When fever and other manifestations cannot be clinically explained by bacterial infection, the possibility of fungal infection should be considered, and antifungal drugs can be applied empirically, and fungal cultures of blood or body fluids can be performed at the same time.
7.Nutritional support: MAP patients only need short-term fasting, so they do not need enteral or parenteral nutrition; SAP patients often implement parenteral nutrition first, and then consider implementing enteral nutrition when their condition tends to be in remission. The implementation of enteral nutrition means placing the nasal feeding tube at the distal end of Treitz ligament and infusing the elemental nutrients with energy density of 4,187 J/ml. If the energy is insufficient, parenteral nutrition can be supplemented and the patient’s response can be observed, and if it is tolerated, the dose will be gradually increased. Attention should be paid to the supplementation of glutamine preparations. For patients with hyperlipidemia, the supplementation of fatty substances should be reduced. When performing enteral nutrition, attention should be paid to whether the patient’s abdominal pain, intestinal paralysis, abdominal pressure and other symptoms and signs of pancreatitis are aggravated, and electrolytes, blood lipids, blood sugar, total bilirubin, serum albumin level, blood routine and renal function should be reviewed regularly to evaluate the metabolic status of the body and adjust the dose of enteral nutrition.
8.Immune-enhancing agent application: For severe cases, immune-enhancing agents can be selectively applied.
9.Prevention and treatment of intestinal failure: For SAP patients, abdominal signs and defecation should be closely observed, and changes in bowel sounds should be monitored. Give early pro-intestinal motility drugs, including raw rhubarb, magnesium sulfate, lactulose, etc.; give microecological preparations to regulate intestinal bacterial flora; apply glutamine preparations to protect the intestinal mucosal barrier. At the same time, traditional Chinese medicine, such as skin nitrate, can be applied externally. If the disease condition allows, early resumption of diet or implementation of enteral nutrition is important to prevent intestinal failure.
10. Chinese herbal medicine: single herbal medicine, such as raw rhubarb, and compound preparations, such as Qing Pancreatic Tang and Chai Shao Cheng Qi Tang, have been proven effective in clinical practice. Chinese herbal preparations achieve therapeutic efficacy by reducing vascular permeability, inhibiting macrophage and neutrophil activation, and removing endotoxin.
11.Endoscopic treatment of AP (biliary origin type): It is recommended that in conditional units, nasobiliary drainage or endoscopic sphincterotomy should be performed for suspected or confirmed AP (biliary origin type) if it meets the index of severe disease, and/or if there is cholangitis, jaundice, dilatation of the common bile duct, or if it is initially judged to be MAP, but the condition worsens during treatment.
Management of complications: Acute respiratory distress syndrome is a serious complication of AP. Treatment includes mechanical ventilation and high-dose, short-course glucocorticoid application, such as methylprednisolone, and bronchoscopic alveolar lavage if necessary. Acute renal failure is treated primarily with supportive therapy, stabilization of hemodynamic parameters, and dialysis if necessary. Hypotension is associated with hyperdynamic circulation, and management includes close hemodynamic monitoring, intravenous rehydration, and vasoactive drugs if necessary. Heparin should be administered in cases of disseminated intravascular coagulation.AP with pancreatic fluid accumulation will in part develop into pseudocysts. For pancreatic pseudocysts should be closely observed, some of them will absorb on their own, and for bitter pseudocysts >6 cm in diameter with compression and clinical manifestations, puncture drainage or surgical drainage is feasible. Pancreatic abscess is an absolute indication for surgical intervention. For upper gastrointestinal bleeding, acid-control agents such as H2 receptor antagonists and proton pump inhibitors can be applied.
13, surgical treatment: surgical intervention is considered under close observation in cases of secondary infection of necrotic pancreatic tissue. For severe cases, it is advocated that on the basis of intensive care and intensive conservative treatment, after 72h, the patient’s condition is still not stabilized or further deteriorated, which is an indication for surgical treatment, or abdominal irrigation.