Acute biliary pancreatitis

Introduction to acute biliary pancreatitis Biliary stones, inflammation, etc. can cause pancreatic duct obstruction, pancreatic mucosal barrier damage, pancreatic juice spillover, pancreatic tissue self-digestion, the formation of acute biliary pancreatitis (acutebiliary pancreatitis, ABP). basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: pancreatic abscess acute cholangitis pancreatic pseudocyst ascites intestinal obstruction respiratory failure pleural effusion acute renal failure gastrointestinal bleeding sepsis diabetes diffuse intravascular coagulation

Causes of acute biliary pancreatitis

(1) Causes of the disease

More than 80% of the causes of acute pancreatitis are related to biliary diseases and alcohol intake. It is generally believed that 10% of patients with gallstones develop acute pancreatitis. In recent years, it has been recognized that biliary microlithiasis is acute pancreatitis, especially acute recurrence. One of the causes of pancreatitis is that 20% to 30% of patients with cholelithiasis develop pancreatitis during the course of the disease. Therefore, the proportion of biliary pancreatitis in pancreatitis is estimated to exceed 2/3 of the total. China is a country with frequent cholelithiasis. The cause of acute and acute recurrent pancreatitis is mainly biliary diseases. According to the latest theory, the proportion of biliary pancreatitis in China is more than 60%-80%, so the age is 50-60 years old. Patients with obese women with pancreatitis should pay special attention to the cause of biliary causes.

(two) pathogenesis

The exact pathogenesis of acute biliary pancreatitis is unclear. In 1901, Opie first proposed the Common Channel Hypothesis. Until today, this theory is still the most respected, but the concept of the common channel has a new Recognizing, Opie's common channel theory anatomically proposes that the pancreatic duct and bile duct merge into a common channel before entering the duodenum, the common channel is blocked, causing bile to flow back into the pancreatic duct, causing pancreatitis, and there is an anatomical common channel in ABP patients. 2/3, the rest are open, so the pathogenesis of biliary pancreatitis can not be completely explained by the common channel theory, but the researchers collected bile tests on ABP patients with indwelling T tube and found that pancreatic enzymes were refluxed to In bile, and in the same condition, non-ABP patients with cholelithiasis have no pancreatic enzymes. Therefore, some scholars have proposed the existence of a functional common channel to explain its pathogenesis. The current debate is focused on gallstone-induced pancreatitis. Mechanism, there are the following hypotheses.

1. The abdomen incarceration This is the earliest proposed viewpoint, including gallstone incarceration, mites occlusion, Oddi sphincter spasm caused by common bile duct and biliary tract infection, causing bile drainage disorder, and pressure in the biliary tract exceeds the pressure inside the pancreatic duct (normal pancreatic duct pressure) In the bile duct pressure), causing bile to flow back into the pancreatic duct and causing pancreatitis. Intraoperative angiography and animal research support this view. The literature reports that 63% to 78% of acute biliary pancreatitis emergency surgery found common bile duct stones, during elective surgery 3% to 33% have common bile duct stones. However, the current view is that true incarceration is rare. In most cases, gallstones do not form incarceration in the ampulla.

2. Gallstones through the doctrine This is the most popular view at present, that the gallstones roll from the biliary tract into the duodenum, stimulate the Oddi sphincter, causing congestion, edema, spasm, leading to Oddi sphincter dysfunction, and even reverse contraction, formation Temporary or functional obstruction, causing bile reflux, or reflux of duodenal contents, causing pancreatitis, 85% to 95% of patients with biliary pancreatitis find stones in the stool without acute Only 10% of patients with cholelithiasis of pancreatitis have stones in the stool. The theory of micro-calculus-induced pancreatitis, which is currently under study, supports this view. The theory can also explain the occurrence of mild and severe ABP, ie single or Less stones lead to mild ABP, and multiple stones pass through it, leading to severe ABP. Recent studies have found that some ABP patients are too small (<3mm) because of stones, routine examinations are not found, and diagnosed as special hair In fact, more than 50 years ago, microlithiasis was reported to be associated with pancreatitis. Recent research has further confirmed this view. Microscopic stones refer to the naked eye and existing images. Small stones that can not be found in the examination, including: 1 stone with diameter <2mm or 3mm; 2 biliary sand; 3 biliary pigment calcium particles, cholesterol crystal and calcium carbonate particles, Ros et al reported by duodenoscopic or surgical resection The bile of 51 patients with acute idiopathic pancreatitis underwent microscopic examination. It was found that 34/51 (67%) had microlithiasis, the ultrasonographic positive rate of micro stones was extremely low, and ERCP acquired bile or CCK stimulation. Microscopic examination of the duodenal drainage fluid can be used for diagnosis. The sensitivity and specificity of ERCP for bile microscopy are 83% and 100%, respectively.

3. Oddi sphincter dysfunction Oddi sphincter relaxation, gallstones migrate into the duodenum, can cause temporary Oddi sphincter dysfunction, duodenal contents rich in enterokinase flow back into the pancreatic duct, activate pancreatic enzyme, this theory There is not much support.

4. Biliary tract inflammation and its toxin free cholic acid, unconjugated bilirubin, lysolecithin, etc. can also diffuse into the pancreas through the common lymphatic system with the pancreas, or bile duct inflammation spreads to the pancreatic duct, which may be caused by obstructive bile duct inflammation Play a role.

5. Common bile duct and main pancreatic duct dilatation It has been reported that the average diameter of Common Bile Duct (CBD) in patients with biliary pancreatitis is 9.2 mm. The average diameter of CBD in other pancreatitis is 5.0 mm, and there are stones in CBD. The average diameter is 12.5mm, the main pancreatic Duct (MPD) is 4.02mm, and the CBD has no stones, but the CBD and MPD of the gallbladder stones are 7.1mm and 3.5mm, respectively. Therefore, the larger the biliary diameter, the more likely it is. The stone causes temporary obstruction of the ampulla during the migration process.

Acute biliary pancreatitis prevention

This disease is caused by biliary tract diseases. Therefore, active treatment of biliary tract diseases can effectively prevent the occurrence of this disease.

Complications of acute biliary pancreatitis Complications Pancreatic abscess Acute cholangitis Pancreatic pseudocyst ascites Intestinal obstruction Respiratory failure Pleural effusion Acute renal failure Digestive tract hemorrhage Diabetes Diabetic disseminated intravascular coagulation

Biliary pancreatitis has more complications than pancreatitis caused by other causes.

1. Local complications include acute cholangitis, pancreatic abscess, pseudocyst, pancreatic necrosis, massive ascites, portal vein embolization, and duodenal obstruction.

2. Systemic complications Severe pancreatitis can occur in a variety of serious systemic complications within a few days after the disease, such as respiratory failure, pleural effusion, acute renal failure, circulatory failure, gastrointestinal bleeding, pancreatic encephalopathy, sepsis, diabetes , disseminated intravascular coagulation and so on.

Acute biliary pancreatitis symptoms Common symptoms Abdominal pain, bloating, nausea and vomiting, pale jaundice, shock, abdominal muscle tension, mobile voiced, acute abdominal pain, indifferent expression

Symptom

(1) Abdominal pain: It is the main symptom of this disease. It starts in the upper abdomen and appears early. The typical person often feels pain on the left side of the umbilicus. It is persistent and has a paroxysmal aggravation. It is cut into the knife and often radiates to the shoulder. Department, flank and lower back, with the spread of inflammation, the range of abdominal pain can be banded, or spread to the whole abdomen.

(2) nausea and vomiting: It is an early symptom of this disease, which occurs almost at the same time as abdominal pain. The initial episodes are frequent, often sprayed, with food and bile, and intestinal paralysis in the late stage, which can vomit fecal samples.

(3) bloating: It is a common symptom of this disease. The degree of bloating has a certain relationship with the degree of pancreatitis. The lighter lasts for 2 to 3 days, and the severe one can last for more than 7 days, often accompanied by venting and defecation.

(4) Astragalus: generally lighter, mostly obstructive, but a small number of patients with hemorrhagic necrosis, jaundice is a manifestation of liver function damage caused by severe intra-abdominal infection.

(5) Others: fever, gastrointestinal bleeding, shock, etc. may occur in some patients.

2. Signs

(1) Abdominal tenderness and abdominal muscle tension: Most patients have abdominal tenderness, mainly above the abdomen, and the abdominal muscles are more tense, but the degree is not as good as gastrointestinal perforation or gallbladder perforation, and some patients have diffuse peritonitis.

(2) Shock: Some patients have faster pulse, lower blood pressure, faster breathing, pale face, cold limbs, indifferent expression or irritability.

(3) signs of bleeding: the overflowing pancreatic juice reaches the subcutaneous fat along the interstitial space, causing the capillary to rupture and hemorrhage, so the local skin is blue-purple, which can be seen in the waist, anterior lower abdominal wall or umbilical cord.

(4) intestinal obstruction and mobile dullness: intestinal obstruction is often paralyzed, intra-abdominal hemorrhage, when there is more exudation, can move out of mobile dullness.

Examination of acute biliary pancreatitis

1. This disease often has hypovolemic shock and co-infection. Therefore, white blood cell count is mostly increased, hemoglobin and hematocrit are increased, carbon dioxide binding is decreased, blood glucose is increased in the early stage of attack, lasting for several hours to several days, acute necrosis type Blood calcium begins to decline in 2 to 5 days. If it is below 1.75mmol, it indicates that the disease is severe, and the increase of blood urease amylase is one of the important basis for the diagnosis of pancreatitis. About 70% to 95% of patients with acute pancreatitis have serum amylase. Increased, reached the peak at 24h, returned to normal within 5 days, and continued to increase for more than 12 days, indicating that there are complications, urinary amylase increased slightly and lasted for a long time, serum lipase increased to 1.5 Kang 24 hours after onset More than unit.

2. Abdominal puncture acute necrotizing pancreatitis, abdominal puncture can often draw turbid liquid, and may see fat droplets, may be purulent when infected, peritoneal fluid amylase often increased, often higher than serum amylase, and The duration is also 2 to 4 days longer than serum amylase.

3. Abdominal plain film patients with acute pancreatitis can show abnormalities in 2/3, including: pancreatic shadow, unclear margin, increased density, localized intestinal paralysis, transverse colon truncation (the liver of the colon can be seen in the supine position) The song, the spleen is inflated, and the middle part of the transverse colon is airless.

4. Thoracic fluoroscopy showed elevated left diaphragm, moderate left pleural effusion, or left lower atelectasis.

5. B-mode ultrasonography can find diffuse swelling of the pancreas, increase, the outline is slightly curved, the positive rate can reach 45% to 90%, and biliary tract disease can be found.

6. CT examination is a modern and sensitive non-invasive diagnosis method, 70% to 90% of patients have abnormal performance: focal or diffuse pancreas enlargement, uneven density, irregular shape, pancreatic or pancreatic fluid accumulation Wait.

Diagnosis and diagnosis of acute biliary pancreatitis

Diagnostic points

The diagnosis of acute pancreatitis still lacks a unified standard. It is often combined with clinical, biochemical and imaging findings to make a comprehensive judgment. The criteria established by Japan in 1988 are as follows:

1. Acute abdominal pain is accompanied by upper abdominal tenderness or peritoneal irritation.

2. Increased trypsin in blood, urine or ascites.

3. Imaging examination, surgery and biopsy found abnormalities in the pancreas.

If you have more than 2 criteria including the first item and exclude other acute abdomen, you can diagnose it as acute pancreatitis.

Differential diagnosis

Early or edematous pancreatitis should be differentiated from gastroduodenal ulcer, acute biliary tract disease, intestinal obstruction and appendicitis. Hemorrhagic necrotic pancreatitis should be perforated with gastroduodenal ulcer, strangulated intestinal obstruction, mesenteric vessel The identification of embolism, myocardial infarction, etc., can not be identified by some special examinations, should be laparotomy, the identification of this disease and non-biliary pancreatitis is sometimes difficult, but because the two treatments are basically the same, therefore, is not identified Focus.

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