Overview
Biliary acute pancreatitis refers to the formation of acute biliary pancreatitis due to biliary stones, inflammation and other causes of pancreatic duct obstruction, pancreatic mucosal barrier damage, pancreatic fluid spillage, pancreatic tissue self-digestion. It has a high clinical incidence, second only to acute appendicitis, acute intestinal obstruction, acute biliary tract infection and gastroduodenal ulcer.
Causes
Acute pancreatitis can be caused by various diseases of the biliary tract, such as stones, roundworms, infections, scarring and stenosis, tumors, and inflammatory edema, among which stones and infections are the most common causes. The “common pathway” is the anatomical basis for its occurrence.
1. Stones
Stones in the biliary system not only cause stenosis of the jugular abdomen, but also cause damage to the mucous membrane, resulting in secondary edema or infection, aggravating the stenosis. Stenosis of the jugular abdomen, increased pressure in the bile duct, bile backflow into the pancreas, pancreatic enzymes are activated, causing pancreatic auto-digestion.
2.Infection
When the biliary system is infected by bacteria, the bile contains a large number of bacteria and their metabolites, and some components such as bacterial amidase can activate pancreatic enzymes, resulting in auto-digestion and acute inflammation of the pancreas; inflammation of the common bile duct can directly involve the pancreatic duct, resulting in the development of the disease due to poor pancreatic drainage and reflux into the pancreatic tissues.
3.Other
Biliary tract parasites, scar stenosis, tumor and sphincter of Oddi insufficiency can cause pancreatic duct obstruction, poor pancreatic juice drainage, bile reflux and other occurrences of the disease.
Pathogenesis
1. The stone is embedded in the jugular abdomen, the bile flows back into the pancreatic duct through the common duct, and the infection is brought into the pancreatic duct.
2. During the excretion of gallstones, the sphincter of Oddi undergoes paralytic relaxation, and the intestinal contents flow back into the pancreatic duct, leading to pancreatitis.
3. Damage to pancreatic tissue by toxic substances. Including free bile acids, bacterial unconjugated bilirubin and hemolyzed lecithin. Free bile acid is toxic and can damage the mucosal barrier of the pancreatic duct; bacteria can secrete glucuronidase, which can decompose bound bilirubin into unconjugated bilirubin, and unconjugated bilirubin has toxicity to the pancreas; there is hemolysed lecithin in the bile of patients with acute cholecystitis, which can directly damage the pancreatic tissues.
Symptoms
1. Symptoms
(1) Abdominal pain begins in the upper abdomen, appears early, and is the main clinical manifestation of the disease. Typical clinical symptoms are sudden pain to the left above the umbilicus, cut-like, persistent pain with paroxysmal aggravation, which can be radiated to the shoulder, coercion and lumbar back. With the spread of inflammation, the range of abdominal pain can be banded or spread to the whole abdomen.
(2) Nausea and vomiting: Initial episodes are more frequent, often in the form of jets, containing food and bile. In the late stage of intestinal paralysis, fecal matter can be vomited. This symptom appears together with abdominal pain, which is the early manifestation of the disease.
(3) Abdominal distension The degree of abdominal distension is related to the degree of pancreatitis, lasting 2-3 days in mild cases and more than 7 days in severe cases, often accompanied by the anus stopping defecation. It is a common symptom of this disease.
(4) Jaundice Mostly obstructive jaundice with mild symptoms in general, but a few hemorrhagic necrotic jaundice is a manifestation of liver function impairment caused by severe intra-abdominal infection.
(5) Others A few patients may have fever, gastrointestinal bleeding, shock signs and other symptoms.
2. Physical signs
(1) Abdominal pressure and abdominal muscle tension Most patients have pressure and pain in the upper abdomen and abdominal muscle tension, but the degree is not as high as gastrointestinal perforation or gallbladder perforation, and some patients have diffuse peritonitis.
(2) Shock Some patients may have accelerated pulse, decreased blood pressure, accelerated respiration, pallor, cold extremities, apathetic expression or irritability.
(3) Bleeding signs The spilled pancreatic fluid reaches the subcutaneous fat along the tissue gap, causing the capillaries to rupture and bleed, and the local skin around the umbilicus or the anterior and inferior abdominal wall of the waist is blue-purple.
(4) Intestinal obstruction and mobile turbid sounds Often paralytic intestinal obstruction. When there is more bleeding and exudation in the abdominal cavity, mobile turbid sounds can be detected.
Examination
1. Laboratory tests
(1) Blood tests There is often an increase in white blood cell count, an increase in hemoglobin and hematocrit, and a decrease in carbon dioxide binding capacity. Blood glucose increases early in the attack and lasts for hours to days. Blood calcium begins to fall in patients with the acute necrotizing form in 2 to 5 days, and if it is below 1.75 mmol, it indicates severe disease. Increased blood amylase is one of the most important bases for the diagnosis of pancreatitis. Acute pancreatitis patients 70% ~ 95% have increased serum amylase. 24h to reach the peak within 5 days to return to normal, continued to increase for more than 12 days, indicating the existence of complications. Serum lipase increases to more than 1.5 Con’s units 24h after the onset of the disease.
(2) Peritoneal puncture In acute necrotizing pancreatitis, peritoneal puncture often draws turbid fluid, and may see fat droplets, and when complicated by infection, it may show purulent turbid fluid in the abdominal cavity, and amylase is often increased, higher than serum amylase, and its duration is also longer than that of serum amylase by 2 to 4 days.
2. Other auxiliary examinations
(1) Abdominal plain film: Acute pancreatitis patient’s pancreas has enlarged shadow, unclear edge, increased density, limited intestinal paralysis, transverse colon truncation sign (when supine position, the liver and spleen curvature of the colon can be seen to be inflated, while the middle part of the transverse colon is not inflated).
(2) Chest fluoroscopy Elevated left diaphragm, moderate amount of left pleural effusion, or left lower lung atelectasis may be seen.
(3) B-mode ultrasonography Diffuse swelling and enlargement of the pancreas with a slightly curved bulge in the contour line may be detected.
(4) CT examination Focal or diffuse enlargement of the pancreas with uneven density, irregular shape, accumulation of fluid in the pancreas or around the pancreas.
Diagnosis
The diagnosis of acute pancreatitis should be made by combining clinical, biochemical indexes and imaging findings to make a comprehensive judgment.
Differential diagnosis
Early or edematous pancreatitis should be differentiated from gastroduodenal ulcer, acute biliary tract disease, intestinal obstruction and appendicitis. Hemorrhagic necrotizing pancreatitis should be differentiated from gastroduodenal ulcer perforation, strangulated intestinal obstruction, mesenteric vascular embolism and myocardial infarction.
Treatment
This disease often requires a combination of traditional Chinese and Western medicine, especially for acute hemorrhagic necrotizing pancreatitis, it should be combined with anti-shock, anti-infection, symptomatic support, surgery and other measures.
1. Diet control and gastrointestinal decompression
If the symptoms are mild, eat a small amount of light fluid, nausea, vomiting, abdominal distension is obvious, gastrointestinal decompression is needed, Chinese medicine can be injected from the gastric tube.
2.Supportive therapy
Intravenous electrolyte supplementation, maintenance of adequate circulating blood volume, supplementation of adequate and comprehensive nutrition is very important to improve the efficacy of this disease.
3. Application of antibiotics
The main purpose is to inhibit the growth of intestinal bacteria, and broad-spectrum antibiotics are often used to prevent and control secondary infections.
4. Antipancreatic enzyme therapy
Inhibit pancreatic secretion and other measures can be applied.
5.Surgical treatment
The current trend is based on active symptomatic and supportive therapies, after the patient’s acute symptoms have been relieved, and then take the postponed surgery, mostly in about 7 days after the acute attack. However, for those whose diagnosis is uncertain and whose condition is still deteriorating after various supportive therapies, timely surgery should be performed. The surgical approach should be chosen according to the biliary tract lesions. For the management of the pancreas itself, pancreatic drainage and pancreatectomy can be used.
Questions you may be concerned about
How to treat biliary acute pancreatitis
The treatment of biliary acute pancreatitis includes a variety of methods such as surgical treatment, nutritional support, anti-infective treatment and negative pressure suction.
1. Acute pancreatitis of biliary origin should be promptly relieved of obstruction through surgical methods to relieve the pain caused by obstruction and to ensure smooth secretion of pancreatic fluid and bile, such as endoscopic retrograde pancreaticobiliary lithotripsy and biliary stenting.
2. At the same time, during the acute attack period, certain nutritional support and anti-infection treatment such as cefoperazone and moxifloxacin should be given to maintain the stability of the internal environment.
3. The source of most biliary pancreatitis is the gallbladder, and removal of the gallbladder should be considered to prevent recurrence of pancreatitis.
When pancreatitis occurs, it is necessary to consult a doctor promptly for a series of tests such as pancreatic amylase, CT and ultrasound, etc. After comprehensive analysis, the doctor will issue a targeted treatment plan.
Prognosis
Acute edema type has a good prognosis, but if the biliary tract lesions are not treated thoroughly, one attack is often followed by frequent attacks. The prognosis for the hemorrhagic necrosis type is still more serious and multiple complications can occur.
Prevention
Aggressive treatment of biliary tract disease can effectively prevent the development of this disease.