Quiet belly

Introduction Acute pancreatitis is a common disease in abdominal surgery. In recent years, the incidence of severe pancreatitis has gradually increased. The mortality rate of severe pancreatitis is 20%, and those with complications can be as high as 50%. Clinical pathology often divides acute pancreatitis into two types: edema type and hemorrhagic necrosis. Although this classification can explain the pathological condition, the development of pancreatitis is not static. With the degree of obstruction of the pancreatic duct and the changes of interstitial blood vessels (arteries, veins and lymphatic vessels), the pathological changes are Dynamic development. Therefore, the method of classification of acute mild pancreatitis and severe pancreatitis is more suitable for clinical application. Serious pancreatitis (such as hemorrhagic necrosis) clinicians often attach great importance, but mild pancreatitis (such as edema type) can not be ignored, it can develop into severe pancreatitis.

Cause

Etiology

The etiology of this disease is still not very clear so far, mainly due to the large difference between animal models and clinical. From the current data, the cause of pancreatitis is related to the following factors.

Obstructive factor

Bile reflux occurs due to biliary mites, incarceration of ampullary calculi, and duodenal papilla narrowing. However, this phenomenon cannot explain: 130% of the cases of bile and pancreatic ducts without common channels; 2 no abnormal changes in the biliary tract at the autopsy, and no acute pancreatitis occurred in the history of no alcoholism; 3 chronic pancreas usually occurs after ligation of the pancreatic duct Inflammation, and few people with acute pancreatitis. Therefore, it is believed that under normal circumstances, bile reflux into the pancreatic duct does not occur pancreatitis, it must cause a high pressure environment in the pancreatic duct, such as obvious obstruction at the lower end of the bile duct, high pressure in the biliary tract, high pressure bile countercurrent to the pancreatic duct, causing pancreatic acinar rupture Pancreatic inflammation occurs when pancreatic enzyme enters the pancreatic stroma. Animal experiments have shown that there is no acute pancreatitis in the hypotensive perfusion pancreatic duct, and acute pancreatitis occurs when the pressure is too high. Clinically, it can be seen that when ERCP is performed, acute pancreatitis occurs if the perfusion pressure is too high. After perfusion of the pancreatic duct by electron microscopy, the ruptured site is observed at the junction of the pancreatic duct and the pancreatic vesicle, and then penetrates between the cytoplasmic membrane and the basement membrane of the cell, and finally destroys the basement membrane and infiltrates into the connective tissue. in. If the biliary tract has stones without causing obstruction of the ampulla and does not cause the bile fluid to flow back into the pancreatic duct, it should not be called biliary acute pancreatitis.

Some people have analyzed a large number of intraoperative cholangiography cases, and found that the history of pancreatitis has some features of the local anatomy of the biliary and pancreatic ducts: for example, the pancreatic duct is thicker, the angle between the biliary and pancreatic ducts is larger, the common channel is longer, and the cystic duct is longer. The common bile duct is also thicker, and the gallstones are many and small, and the shape is irregular. All of the above features are beneficial to the small stones in the gallbladder to migrate to the common bile duct, and temporarily stay and block in the ampulla, causing pancreatitis. Sometimes when the stone passes through the Oddi sphincter (especially irregularly shaped), causing a sphincter spasm, high pressure bile flows back into the pancreatic duct and induces pancreatitis. When the biliary tract infection, the bacteria flow back into the pancreas through the common lymphatic vessels of the gallbladder and the pancreas, and the Oddi sphincter has different degrees of stenosis, which causes pancreatitis. Is there a presence of bacteria in the pancreas to develop pancreatitis? Widdison et al. performed animal experiments as follows: he induced experimental pancreatitis by perfusion of pancreatic enzyme through the main pancreatic duct. The animals were divided into 5 groups. Group I received tracer E. coli. Groups II-V injected a certain amount of E. coli through the gallbladder, main pancreatic duct, obstructed renal pelvis or colon, and pancreas cultured 24 hours later. Colon group only. After 72 hours of culture, E. coli was grown in each group of pancreas. Compared with the group with frequent bacterial growth, in addition to the colon group, the growth rate of pancreatic sputum bacteria, pancreatic bacteria are often found, but not necessarily developed into pancreatitis infection.

2. Alcohol factors

Long-term drinkers are prone to pancreatitis, a common phenomenon in the West, accounting for 70%. The pathogenesis of alcoholic pancreatitis: 1 alcohol stimulates the parietal cells of the stomach to produce a large amount of gastric acid, gastric acid to the duodenum stimulates the S cells of the intestinal wall and the I cells of the small intestinal wall, and produces CCK-PZ, which is in the pancreatic duct in a short time. Form a high-pressure environment; 2 because alcohol often stimulates the duodenal wall, the intestinal wall is congested and edema, and spread to the duodenal papilla, resulting in obstruction of the bile duct opening; 3 long-term drinking, the secretion of protein in the pancreatic duct increased, The "Intraductal Protein Plug" formed in the pancreatic duct causes pancreatic duct obstruction. On the basis of this, when a large amount of drinking and binge eating, the secretion of pancreatic enzyme is promoted, causing the pressure in the pancreas to rise suddenly, causing the pancreatic vesicle to rupture, and the pancreatic enzyme enters the interstitial space between the acinus to promote acute pancreatitis. Alcohol and high-protein high-fat meal intake at the same time, not only increased secretion of pancreatic enzymes, but also can cause hyperlipoproteinemia. At this time, pancreatic lipase decomposes triglyceride to release free fatty acids and damage the pancreas.

3. Vascular factors

The phenomenon of acute pancreatitis caused by pancreatic acute venous circulation and acute pancreatitis caused by small arteries and veins of the pancreas has been confirmed. Some people use a microsome with a diameter of 8 ~ 20m for pancreatic artery injection, which causes large experimental pancreatitis. In the autopsy of pancreatitis, Popper found atherosclerotic thrombosis in the pancreatic vessels. Another vascular factor is based on the obstruction of the pancreatic duct. When the pancreatic duct is obstructed, the pancreatic duct is under high pressure, and the pancreatic enzyme passively "infiltrates" into the interstitial. The stimulation of pancreatic enzyme causes lymph in the interstitial. Tubes, veins, arterial embolization, and subsequent ischemic necrosis of the pancreas, the process of which occurs as shown in Figure 2. It can be seen from the figure that there is no obvious boundary between edema type and hemorrhagic necrotic pancreatitis. The former can develop into the latter if not handled properly. Reily experimented with the underlying hemodynamic mechanism of pancreatic ischemia in cardiogenic shock, induced pericardial occlusion induced by cardiogenic shock in pigs, observed hemodynamics of the pancreas, and found that pancreatic blood flow was unevenly reduced compared to The cardiac output of shock animals is significantly reduced, and the increase in pancreatic ischemia is caused by selective pancreatic vasoconstriction and decreased perfusion pressure. Pancreatic ischemia that occurs during cardiogenic shock is primarily due to selective pancreatic vasoconstriction. Castillo et al studied 300 patients undergoing cardiopulmonary bypass surgery to observe whether the pancreas had any damage to the pancreas. Blood amylase, pancreatic isoenzyme and lipase were measured at 1, 2, 3, 7 and 10 days after surgery. Of the 80 cases, 23 had abdominal findings, 3 had severe pancreatitis, and 11% died of secondary pancreatitis.

4. Trauma and iatrogenic factors

Pancreatic trauma causes pancreatic duct rupture, pancreatic fluid spillover and insufficient blood supply after trauma, resulting in acute severe pancreatitis. There are two conditions in iatrogenic pancreatitis: pancreatitis occurs in one case: one is done during gastric resection, especially in the antrum of the antrum or the posterior wall of the duodenum, penetrating into the pancreas, when the stomach is removed, The ulcer surface on the pancreas is scraped to form a pancreatic leak, and the pancreatic juice leaks out to self-digest the pancreas. In another case, the operation did not affect the pancreas, and pancreatitis occurred after surgery. This was mainly due to surgery in the adjacent organs of the pancreas. It may be due to Oddi sphincter edema, poor pancreatic drainage, and impaired pancreatic blood flow. Stimulate the vagus nerve, so that the secretion of pancreatic juice is excessive.

5. Infectious factors

Acute pancreatitis can cause various bacterial infections and viral infections, such as mumps virus, adenovirus, hepatitis A virus, and bacterial pneumonia. A virus or a bacterium causes pancreatitis by entering the pancreatic tissue through blood or lymph. Under normal circumstances, this infection is simple edematous pancreatitis, and there are fewer patients with hemorrhagic necrotizing pancreatitis.

6. Metabolic disease

(1) Hypercalcemia: Pancreatitis caused by hypercalcemia may be related to the following factors: calcium salt deposition forms pancreatic duct calcification, obstructs the pancreatic duct to cause pancreatic juice to enter the stroma and pancreatitis occurs; promotes pancreatic juice secretion; pancreas The proproteinase is converted to trypsin.

(2) Hyperlipidemia: About one-fourth of patients with acute pancreatitis have hyperlipidemia. It may be because the small blood vessels of the pancreas are embolized by the condensed serum lipid particles, and the high concentration of pancreatic lipase decomposes the serum triglyceride, releasing a large amount of free fatty acids, causing damage to the small blood vessels of the pancreas and embolization. Pancreatitis can occur when the blood triglyceride reaches 5-12 mmol/L.

7. Other factors

Such as drug allergy, drug poisoning, hemochromatosis, adrenocortical hormone, heredity and so on.

[Pathogenesis]

The pathogenesis of acute pancreatitis (AP) is mainly due to the self-digestion of pancreatic enzymes to the pancreas, the digestion of its surrounding tissues, and thus a series of organ dysfunction. The pancreas contains very rich digestive enzymes: proteases, lipases, amylases, and the like. The enzymes secreted by the pancreatic acinus are mainly trypsin, chymotrypsin, carboxypeptidase, elastase, phospholipase A2, hard protease, lipase, amylase, ribozyme and the like. Normally, except lipase, amylase, and nucleoprotein are present in an active form, others are present in an inactive state. Under pathological conditions, these enzymes can cause pancreatitis after being activated in pancreatic ducts and cells.

Pancreatic enzyme activation in the pancreatic duct: due to various factors, bile, duodenal juice, intestinal enzyme, emulsified fat, lysolecithin, etc. are returned to the pancreatic duct, then various zymogens in the pancreatic duct are activated, and the activated enzyme pair Pancreatic tissue occurs when the pancreatic tissue self-digests. Pancreatic enzyme activation in cells: zymogen particles in pancreatic vesicle cells prevent activation of intracellular enzymes by containing protease inhibitors (PSTI) secreted by the pancreas itself. A lysosomal enzyme formed in a cell, which is normally separated from the enzyme granule. Under the action of pathogenic factors, the enzyme granules and lysosomes are fused by a phagocytosis phenomenon, which causes the zymogen to activate in the cells at a low pH, thereby damaging the cells themselves. If pancreatic enzymes flow into the tissues, the pancreatic lesions will be further aggravated and cause damage to adjacent organs. Multiple lesions may occur when the lesions continue to develop. In addition to the above-mentioned self-digestion, acute pancreatitis has further intensive research in recent years, and found that trypsin and antitrypsin system, phospholipase A and thromboxane A2, pancreatic blood circulation disorder, oxygen free radicals, and cell membrane Stability and endotoxin play an important role in the pathogenesis of acute pancreatitis.

Trypsin-antitrypsin system

The pancreas secretes a variety of antitrypsin factors that prevent trypsin self-activation and self-digestion. In the case of severe pancreatitis, local antitrypsin consumption leads to unrestricted activation and self-digestion of pancreatic enzyme. Trypsin (MT), which is not inhibited by antitrypsin, is less than 10% of trypsin in pancreatic juice, but is 3 times more active than trypsin and has an antagonistic effect on trypsin inhibitor. Therefore, it The integrity of the pancreas and damage to the extra-pancreatic tissue is a serious punishment.

Experiments have shown that the efficacy of antitrypsin in the treatment of acute pancreatitis is obvious. The dry frozen plasma contains a large amount of antitrypsin, so the use of dry frozen plasma in acute pancreatic inflammation, not only supplemented with colloids, but also supplemented with antitrypsin.

2. Phospholipase A and thromboxane A2

Phospholipase A (PLA) is known as the "key enzyme" of the pathogenesis of acute pancreatitis. The self-digestion of pancreatic acinar cells is directly related to PLA. At the onset of acute pancreatitis, PLA zymogen is activated by bile salts, trypsin, calcium ions and intestinal peptides, and then PLA hydrolyzes the lecithin of the acinar cell membrane to produce free lipase (FFA) and lysolecithin. When the cell membrane collapses, various digestive enzymes in the cell are released, causing pancreatic hemorrhage and necrosis and damage to various organs of the body. There are two different types of PLA in the plasma of patients with acute pancreatitis.

When PLA decomposes FFA and lysolecithin from membrane phospholipids, it produces a thromboxane A2 which strongly contracts blood vessels. When the thrombosis A2 (TXA2) is pathologically increased, and the imbalance of TXA2/PGI2 can cause the blood supply of the pancreas to be impaired, the intracellular lysosomal membrane is destroyed and the intracellular calcium ions are increased. When the increase in TXA2 is prevented and the balance of TXA2/PGI2 is maintained, the development of acute pancreatitis can be effectively controlled.

3. Lysosomal enzyme

It has been thought that the activation of pancreatic enzyme in acute pancreatitis is outside the cells of acinar cells. In recent years, activation of zymogen has been found to occur in the cells of acinar cells by the action of lysosomal hydrolase. It has a low pH and inactivates trypsin inhibitors in an enzymatic environment, resulting in activation of pancreatic enzymes in cells. It has been suggested that trypsinogen activation by lysosomes in the acinar is an important step in pancreatic enzyme digestion and pancreatic hemorrhage. Wilson's research suggests that lysosomal involvement is an important cause of alcoholic acute pancreatitis.

4. Pancreatic blood circulation disorder

In pancreatitis, the blood flow to the pancreas is reduced, which is quite different from other tissues, and pancreatic tissue is also sensitive to changes in blood flow. In acute severe pancreatitis (acute hemorrhagic pancreatitis), pancreatic blood flow is significantly reduced. In acute edematous pancreatitis, acute hemorrhagic pancreatitis is caused by progressive ischemia if the pancreatic tissue is progressively ischemic. The reason is that the blood vessels between the pancreatic acinar embolism and even obstruction, the pancreas is ischemic and necrosis and the lesion is progressively aggravated. Another factor in pancreatic blood circulation disorder is that inflammation induces capillary vessels, especially small veins are embolized to further cause reflux obstruction, which is another cause of worsening lesions. According to research, the incidence of alcoholic pancreatitis, blood circulation disorders play an important role. Ssafey et al believe that increased capillary permeability is an important pathophysiological phenomenon in the early stage of acute pancreatitis. Therefore, if the permeability of capillaries can be improved, it is particularly beneficial for the treatment of acute pancreatitis. Capillary permeability is closely related to oxygen free radicals. Ven Ooijen's experiment pointed out that the increase of TXA2 is a key factor of acute pancreatitis caused by ischemia. When ischemia and hypoxia activate platelets, platelet aggregation combined with TXA2 aggravates ischemia of pancreatic tissue.

5. Oxygen derived free radicals

Recent studies suggest that oxygen free radicals are involved in the pathophysiological process of acute pancreatitis. Oxygen free radicals can be eliminated by the body's oxide dismutase (SOD) and catalase (CAT). Oxide deuterase (SOD): present in cell fluids and mitochondria, is a specific enzyme that scavenges reactive oxygen species in the body, accelerates the rate of reactive oxygenation, and renders reactive oxygen species produced by normal metabolism harmless. Catalase (CAT): It catalyzes the reduction of H2O2 to form H2O, an important oxygen free radical scavenger for cells. Glutathione peroxidase: It is present in the cytosol and mitochondria and is involved in the reduction of various peroxides. Under normal physiological conditions, the oxygen radicals are in equilibrium with the scavenging system. When the function of oxygen free radicals and scavenging system declines, it causes damage to the pancreas by reactive oxygen species. Oxygen free radicals can damage macromolecules such as proteins, nucleic acids, lipids, and polysaccharides, and the capillary permeability of the pancreas increases, leading to pancreatic edema, hemorrhage, and tissue degeneration and necrosis. In acute pancreatitis, the SOD of pancreatic tissue is reduced, and the activity of SOD in the blood is enhanced, which is caused by an increase in lipid peroxide caused by oxygen free radicals. Oxygen free radicals can also reduce the stability of the membrane, release lysosomal release of pancreatic gland cells and activation of various trypsin; oxygen free radicals can activate phospholipase A, thereby decomposing lecithin on the pancreatic cell membrane, further causing Damage to pancreatic tissue. Some people use SOD, CAT intravenous injection, see its activity time is very short, only a few minutes. Therefore, the combination of these two enzymes with the macromolecular polymer ethylene glycol (PGE) can maintain activity in plasma for 30 to 40 hours, which significantly reduces pancreatitis in rats.

6. Other

Endotoxemia is also involved in the development of acute pancreatitis. It is endotoxemia caused by acute pancreatitis, which in turn increases the damage of the pancreas. Some endotoxin damage mitochondrial structure, affect the ATPase and oxidative phosphorylation coupling process, cause energy metabolism disorders; change the body's immune function; directly destroy the lysosomal membrane in the mononuclear phagocytic system cells, thereby causing cell damage; And can cause a series of pathological changes in the body: vasomotor function, thrombocytopenia and leukopenia.

In short, the pathogenesis of acute pancreatitis is complex, and the action of various enzymes can cause positive and negative effects on the cell membrane and organelles of pancreatic cells. It is currently in the in-depth research stage. It is believed that the onset of acute pancreatitis is often not a single mechanism, and often multiple factors promote each other to form a vicious cycle chain. How to cut off this chain better, there will be a leap in the treatment of acute pancreatitis.

an examination

Patients with acute upper abdominal pain, nausea, vomiting, and fever should think of acute pancreatitis, timely blood and urine amylase test, and if necessary, ascites amylase test. If the amylase rises to the diagnostic criteria, the diagnosis can be confirmed. For example, an empty stomach can be used as an abdominal B-assisted diagnosis. Hemorrhagic necrotic pancreatic disease is dangerous, sometimes due to atypical symptoms and amylase is not easy to diagnose, the following signs are conducive to the diagnosis of hemorrhagic necrotic pancreatitis: shock, peritonitis, pleurisy and atelectasis, gastrointestinal bleeding and skin purpura, sowing Disseminated intravascular coagulation, decreased blood calcium and elevated blood glucose, acute renal failure.

Differential diagnosis

Acute gastroenteritis

Acute gastroenteritis has a history of eating unclean diet, upper abdominal pain is paroxysmal, may be associated with nausea, vomiting and diarrhea, abdominal pain relief after vomiting. Acute pancreatitis has severe abdominal pain and radiates to the lower back. The abdominal pain does not relieve after vomiting. Acute gastroenteritis blood and urine amylase were normal.

2. Acute perforation of digestive ulcer

There is a history of ulcers, often due to improper eating and sudden pain in the upper abdomen knife, abdominal pain, rebound tenderness and muscle tension, can be plate-shaped abdomen. The dullness of the liver is reduced or disappeared. The X-ray shows the free gas under the armpit. Although the serum amylase is elevated, it does not exceed 500U.

3. Cholecystitis and cholelithiasis

Pain in the right upper abdomen or colic, radiating to the right shoulder and back, may be accompanied by jaundice. Check the Morphy sign positive, B-ultrasound can be diagnosed. Serum amylase can be elevated, but not more than twice the normal value.

4. Acute intestinal obstruction

Mechanical ileal obstruction such as volvulus has umbilical colic, which is aggravated by paroxysmal. The bowel sounds are hyperactive, stopping the exhaust or defecation. X silk shows liquid air level, serum amylase is slightly elevated, no more than 500U. Hemorrhagic necrotic pancreatitis may have paralytic ileus, abdominal distension, bowel sounds weakened or disappeared, X-ray can also show liquid-gas plane, However, serum amylase is significantly elevated.

5. Acute myocardial infarction

Have a history of coronary heart disease, sudden pain in the precordial area. If the inferior wall infarction can cause upper abdominal pain. However, the pathological Q wave can appear in the electrocardiogram, and the serum amylase is normal.

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