Acute pancreatitis is an inflammatory reaction in which pancreatic enzymes are activated in the pancreas due to multiple etiologies causing self-digestion, edema, hemorrhage and even necrosis of the pancreatic tissue. It is characterized by acute epigastric pain, nausea, vomiting, fever and increased blood pancreatic enzymes. The degree of lesion varies, the milder ones are mainly pancreatic edema, which is clinically common, and the condition is often self-limiting with good prognosis, also known as mild acute pancreatitis. In a small number of severe cases, the pancreas is hemorrhagic and necrotic, often followed by a variety of complications such as infection, peritonitis and shock, with a high mortality rate, which is called severe acute pancreatitis.
Disease description.
Acute pancreatitis is a relatively common type of acute abdominal disease, and its incidence accounts for the 3rd to 5th place of acute abdominal diseases. More than 80% of patients with mild disease, namely acute edematous pancreatitis, can be cured by non-surgical treatment, basically a medical disease. 10% of patients belong to severe pancreatitis, namely acute hemorrhagic necrotizing pancreatitis, the inflammation of the pancreas is not reversible or self-limiting, often requiring surgical treatment, should be considered a surgical disease.
Due to the deeper understanding of acute pancreatitis, the diagnostic techniques and treatment methods have been more developed and have become of great interest to surgeons, while the death rate remains high at 30% to 60% and prone to various serious comorbidities, which is also a serious challenge to surgeons.
Many reports indicate that the disease has a tendency to increase year by year, related to factors such as increased incidence of biliary tract diseases and increased awareness among clinicians. Acute pancreatitis is more common in women than in men, with a male to female ratio of 1:1.7. It can be seen at all ages, but is more common in people between 20 and 50 years of age. However, the age of onset is also somewhat related to the etiology, for example, pancreatitis caused by roundworms is more common in children, and as human life expectancy increases and the incidence of gallstone disease increases, the age of onset will also increase.
Disease classification.
The pathological changes of acute pancreatitis are generally divided into two types.
1. Acute edema type.
Grossly, the pancreas is seen to be enlarged, edematous, lobulated and blurred, brittle, with lesions involving part or the entire pancreas and a small amount of fat necrosis around the pancreas. Histological examination showed interstitial edema, congestion and inflammatory cell infiltration, and scattered punctate fat necrosis, without obvious pancreatic parenchymal necrosis and hemorrhage.
2. Acute necrotic type.
The gross presentation was reddish-brown or grayish-brown with fresh hemorrhagic areas and loss of lobulated structures. There are larger foci of fat necrosis scattered in the pancreas and peripancreatic tissues such as the greater omentum, called calcium soap spots. Longer disease may be complicated by abscess, pseudocyst or fistula formation. Microscopically, the necrosis of pancreatic tissue is mainly coagulative necrosis with loss of cellular structures. The necrotic foci are surrounded by inflammatory cell infiltration. Phlebitis, lymphangitis, thrombosis and hemorrhagic necrosis are common.
Due to pancreatic fluid spillage and vascular damage, some cases may have chemical ascites, pleural fluid and pericardial effusion, and are prone to secondary bacterial infection. Pulmonary edema, pulmonary hemorrhage and pulmonary hyaline membrane formation may occur in the presence of acute respiratory distress syndrome, and pathological changes such as glomerular lesions, tubular necrosis, fat embolism and diffuse intravascular coagulation may also be seen.
Pathogenesis.
There are many causes of acute pancreatitis. The common causes are gallstone disease, heavy alcohol consumption and overeating.
1. Cholelithiasis and biliary tract diseases.
Gallstone disease, biliary tract infection or biliary tract roundworm can cause acute pancreatitis, of which gallstone disease is the most common. Acute pancreatitis and gallstones are closely related, because anatomically about 70% to 80% of the pancreatic duct and common bile duct converge into a common channel opening in the duodenal jug abdomen, once the stone is embedded in the jug abdomen, will lead to pancreatitis and upstream cholangitis, that is, the “common channel theory”.
In addition to the “common channel”, there are other mechanisms, which can be summarized as follows
(1) obstruction: due to the above-mentioned causes of jugular stenosis or (and) spasm of the sphincter of Oddi, the pressure in the bile duct exceeds the pressure in the pancreatic duct (the normal intrapancreatic pressure is higher than the intrapancreatic pressure), resulting in bile reflux into the pancreatic duct, causing acute pancreatitis.
(2) Insufficiency of the sphincter of Oddi: damage to the common bile duct, jugular abdomen in the migration of gallstones, etc. or inflammation of the biliary tract causes temporary relaxation of the sphincter of Oddi, which causes regurgitation of duodenal fluid rich in enterokinase into the pancreatic duct and damage to the pancreatic duct.
(3) Bacterial toxins, free bile acids, non-conjugated bilirubin, lysophosphatidylcholine, etc. during biliary inflammation may also diffuse into the pancreas through the traffic branches of the biliopancreatic interstitial lymphatics, activating pancreatic enzymes and causing acute pancreatitis.
2. Heavy alcohol consumption and overeating.
The mechanism of acute pancreatitis caused by heavy drinking.
① ethanol induces an increase in pancreatic exocrine secretion by stimulating gastric acid secretion and causing the secretion of pancreatin and cholecystokinin (CCK).
(ii) Stimulation of spasm of the sphincter of Oddi and edema of the duodenal papilla, and obstruction of pancreatic juice drainage, resulting in increased intrapancreatic ductal pressure.
(3) Long-term alcoholics often have increased protein content in the pancreatic juice, which can easily precipitate and form protein plugs, resulting in poor pancreatic juice drainage.
Overeating makes a large amount of chyme enter the duodenum in a short period of time, causing papilledema and spasm of the sphincter of Oddi, and stimulating a large amount of pancreatic juice and bile secretion, which causes acute pancreatitis due to poor excretion of pancreatic juice and bile.
3, pancreatic duct obstruction.
Pancreatic duct stones or roundworms, pancreatic duct stenosis, tumors, etc. can cause pancreatic duct obstruction, and when the pancreatic fluid secretion is high, the internal pressure in the pancreatic duct increases, so that the small branches of the pancreatic duct and pancreatic vesicles rupture, and pancreatic fluid and digestive enzymes seep into the interstitium, causing acute pancreatitis. In pancreatic schizophrenia, when the embryonic development of the pancreas is abnormal, it is mostly due to poor drainage of pancreatic fluid from most of the pancreas by the parapancreatic duct through the narrow parapapillary head due to its relative narrowing.
4.Surgery and trauma.
Abdominal surgery, especially pancreaticobiliary or gastric surgery, abdominal blunt contusions, etc. can directly or indirectly damage the pancreatic tissue and blood supply to the pancreas causing pancreatitis. after ERCP examination, pancreatitis can occur in a few cases due to repeated injection of contrast agent or high injection pressure.
5. Endocrine and metabolic disorders.
Any cause of hypercalcemia, such as parathyroid tumor and excessive vitamin D, can cause pancreatic duct calcification, intraductal stones leading to poor pancreatic drainage and even pancreatic duct rupture, and hypercalcemia can also stimulate, increase pancreatic fluid secretion and promote trypsinogen activation. Hyperlipidemia of any cause, such as familial hyperlipidemia, is complicated by pancreatitis due to lipid deposition in the pancreatic fluid or from extra-pancreatic fat embolism. Acute pancreatitis can also occasionally occur in pregnancy, diabetic coma and uremia; pancreatitis in pregnancy occurs mostly in the middle and late stages, but 90% of combined gallstone disease.
6, infection.
Acute pancreatitis secondary to acute infectious diseases are mostly mild and subside on their own as the infection heals, such as acute mumps, infectious mononucleosis, coxsackie virus, Echo virus and Chlamydia pneumoniae infection. It may often be accompanied by elevated concentrations of specific antibodies. Pancreatitis may occur in cases of salmonella or streptococcal sepsis.
7. Drugs.
It is known that the application of certain drugs such as thiazide diuretics, azathioprine, glucocorticoids, tetracycline, sulfonamides, etc. can directly damage the pancreatic tissue, which can increase the secretion or viscosity of pancreatic fluid and cause acute pancreatitis, which mostly occurs in the first 2 months of taking the drug and is not necessarily related to the dose.
8, other:
Rare factors include penetrating ulcers behind the duodenal bulb, duodenal diverticulitis adjacent to the papilla, input collaterals syndrome after gastric surgery, post-renal or cardiac transplantation, vascular diseases and genetic factors. Although there are many causes of pancreatitis and most causative factors can be found, there are still 5% to 25% of acute pancreatitis of unknown etiology, which is called idiopathic pancreatitis.
Pathogenesis:
The pathogenesis of acute pancreatitis has not been fully elucidated. There is a consensus that although the pathogenic pathways are different, there is a common pathogenic process, namely the theory of pancreatic self-digestion. There are two forms of digestive enzymes secreted by the normal pancreas: one is biologically active enzymes such as amylase, lipase and ribonuclease; the other is inactive enzymes in the form of precursors or zymogens, such as trypsinogen, chymotrypsinogen, prephospholipase, preelastase, kinin-releasing zymogens and prehydroxypeptidase.
Under normal conditions, the vast majority of synthesized pancreatic enzymes are inactive zymogens, the zymogen granules are isolated from the cytoplasm, and the pancreatic ducts of the pancreatic vesicles contain trypsin-inhibiting substances that inactivate small amounts of biologically active or prematurely activated enzymes. This is a physiological defense barrier of the pancreas to avoid self-digestion. Normally, when pancreatic juice enters the duodenum, it first activates trypsinogen under the action of intestinal kinase to form trypsin, which causes various pancreatic digestive enzymes to be activated into biologically active digestive enzymes for digestion of food under the action of trypsin.
Mechanisms associated with the theory of auto-digestion.
(i) Various etiologies lead to activation of enzymogen in its alveoli and a chain reaction of pancreatic self-digestion occurs;
(ii) increased permeability in the pancreatic ducts, which allows the leakage of active pancreatic enzymes into the pancreatic tissue and aggravates pancreatic inflammation. The two may act sequentially in the development of acute pancreatitis.
Once various digestive zymogens are activated, among the activating enzymes that play a major role are phospholipase A2, kinin release enzyme or pancreatic diastase, elastase and lipase. Phospholipase Az breaks down phospholipids of cell membranes with the participation of small amounts of bile acids, producing lysophosphatidylcholine and lysophosphatidic brain phospholipids, whose cytotoxic effects cause coagulative necrosis of pancreatic parenchyma, adipose tissue necrosis and hemolysis.
Kinin releasing enzyme can change kininogen to bradykinin and pancreatic kinin, which increases vasodilation and permeability, causing edema and shock. Elastase can dissolve vascular elastic fibers causing bleeding and thrombosis. Lipase is involved in the necrosis and liquefaction of fat in and around the pancreas. These digestive enzymes act together to cause lesions in the pancreatic parenchyma and adjacent tissues, and cell damage and necrosis in turn promote the release of digestive enzymes, forming a vicious circle.
Recent studies have revealed that in acute pancreatitis, a series of inflammatory mediators are produced during the damage of pancreatic tissue, such as oxygen free radicals, platelet activating factor, prostaglandins, leukotrienes, etc. play an important mediating role, and these inflammatory mediators and vasoactive substances such as nitric oxide (No), thromboxane (TXAz), etc. also lead to impaired circulation in the pancreas, which in turn can be transported to the whole body through the blood circulation and lymphatic channels. transported to the whole body, causing multi-organ damage and becoming a variety of complications and causes of death in acute pancreatitis.
Clinical manifestations
Acute pancreatitis often occurs after a full meal, fatty meal or alcohol consumption. Some patients have no causative factors to detect. Its clinical manifestations and the severity of the disease depend on the etiology, the type of pathology and whether the diagnosis and treatment are timely.
Symptoms
1, abdominal pain is the main manifestation and the first symptom of the disease, sudden onset, varying degrees of severity, can be dull pain, knife-like pain, drilling pain or colic, persistent, may have paroxysmal intensification, can not be relieved by general gastrointestinal antispasmodics, eating can be intensified. The pain site is mostly in the middle and upper abdomen, and can be radiated to the waist and back in a band, and the pain can be relieved by taking a bent knee position. Edema type abdominal pain is relieved in 3 to 5 days. The necrotic type develops faster and the severe abdominal pain continues for a longer period of time, which can cause total abdominal pain due to the spread of exudate. Very few elderly and frail patients may have no abdominal pain or mild abdominal pain.
The mechanisms of abdominal pain are mainly.
(i) acute edema of the pancreas, inflammation stimulates and strains the nerve endings on its envelope;
(2) Inflammatory exudate and pancreatic fluid spillage from the pancreas irritate the peritoneum and retroperitoneal tissues;
(iii) Inflammation of the pancreas involving the intestine, resulting in intestinal distention and intestinal paralysis;
④Pancreatic duct obstruction or pain caused by cholecystitis or cholelithiasis.
2, nausea, vomiting and abdominal distension mostly appear after the onset of the disease, sometimes quite frequently, vomiting food and bile, and abdominal pain does not decrease after vomiting. At the same time there is abdominal distension, and even paralytic intestinal obstruction.
3, fever Most patients have moderate fever or more, lasting 3 to 5 days. Those with fever that does not subside for more than a week or increases day by day and elevated white blood cells should be suspected of having secondary infection, such as pancreatic abscess or biliary tract infection.
4. Hypotension or shock often occurs in severe pancreatitis. Patients are irritable, pale skin, wet and cold, etc.; there are very few shock can occur suddenly, and even sudden death occurs. The main reason is the lack of effective blood volume, bradykinin substances cause peripheral vasodilation, complicated by gastrointestinal bleeding.
5, water, electrolytes, acid-base balance and metabolic disorders, there are many mild and severe dehydration, hypokalemia, frequent vomiting may have metabolic alkalosis. In severe cases, there is also obvious dehydration and metabolic acidosis, hypocalcemia (<2retool/L), partly accompanied by increased blood sugar, occasionally diabetic ketoacidosis or hyperosmolar coma may occur.
Physical signs
The abdominal signs of patients with mild acute pancreatitis are mild and often do not correspond well to the degree of abdominal pain complained of, there may be abdominal distention and reduced bowel sounds, no muscle tension and rebound pain.
2, patients with severe acute pancreatitis have significant epigastric or total abdominal pressure pain, and abdominal muscle tension, rebound pain, diminished or absent bowel sounds, mobile turbid sounds may appear, and abdominal masses with significant pressure pain can be found when the abscess is complicated. With paralytic intestinal obstruction and obvious abdominal distension, ascites is mostly bloody, in which amylase is significantly elevated. In a few patients, pancreatic enzymes, necrotic tissues and hemorrhage infiltrate into the abdominal wall along the peritoneal space and muscle layer, resulting in dark gray-blue skin on both sides of the abdomen, which is called Gre旷Turnet’s sign;
The skin around the umbilicus can be bruised, which is called Cullen’s sign. Gangrene may occur when the common bile duct is compressed by stones in the common bile duct or jugular abdomen or inflammatory edema of the pancreatic head. The later appearance of gangrene should be considered as a complication of pancreatic abscess or pseudocysts compressing the common bile duct or due to hepatocellular damage. Patients with hypocalcemia causing hand and foot twitching is a poor prognosis, which is caused by the combination of fatty acids from necrotic decomposition of large amounts of adipose tissue with calcium to form fatty acid calcium, resulting in a large consumption of calcium, and is also related to the stimulation of calcitonin secretion by the thyroid gland during pancreatitis.
Diagnosis and differentiation
The diagnosis can often be made based on the typical clinical manifestations and laboratory tests. In mild cases, patients with severe and persistent epigastric pain, nausea, vomiting, mild fever, epigastric tenderness without abdominal muscle tension, along with significant elevation of serum amylase and/or urinary amylase, and exclusion of other acute abdominal conditions, can be diagnosed.
Severe cases have the diagnostic criteria of mild acute pancreatitis in addition to local complications (pancreatic necrosis, pseudocysts, abscesses) and/or organ failure. Since the course of severe pancreatitis is sinister and complex, various scoring systems have been proposed at home and abroad to predict the severity and prognosis of the disease, the key of which is to closely monitor the changes in the disease and laboratory tests within 48 or 72 hours of onset and make a comprehensive assessment.
It is important to distinguish between mild and severe pancreatitis, because the clinical prognosis of the two is very different.
The following manifestations should be treated as severe pancreatitis.
① clinical symptoms: irritability, cold extremities, blotchy skin and other signs of shock;
②Signs: abdominal muscle tonicity, peritoneal irritation sign, Grey_Turner sign or Cullen sign;
③laboratory tests: significant drop in blood calcium below 2 mmol/L, blood glucose >11.2 mmol/L (no history of diabetes), sudden drop in blood and urine amylase;
(iv) diagnostic abdominal puncture with ascites with high amylase activity.
Acute pancreatitis should be differentiated from the following diseases.
(a) acute perforation of peptic ulcer
A more typical history of ulcer, sudden increase in abdominal pain, abdominal muscle tension, disappearance of hepatic turbinates, and free gas under the diaphragm seen on x-ray can be differentiated.
(B) Cholelithiasis and acute cholecystitis
Ultrasound and x-ray cholangiography can make a clear diagnosis.
(C) Acute intestinal obstruction
Abdominal pain is paroxysmal, abdominal distension, vomiting, hyperactive bowel sounds, with air over water sound, no exhaust, and visible intestinal pattern. The abdominal x-ray is visible as a liquid-gas plane.
(IV) Myocardial infarction
There is a history of coronary artery disease with sudden onset, sometimes with pain limited to the upper abdomen. Electrocardiogram shows myocardial infarction images, and serum cardiac enzymes are elevated. Blood and urine amylase are normal.
Disease treatment
Most acute pancreatitis is a mild acute pancreatitis and can mostly be cured with 3 to 5 days of active treatment.
Treatment measures.
① fasting ;
②Gastrointestinal decompression: if necessary, place a nasogastric tube to continuously attract gastrointestinal decompression, which is suitable for those with severe abdominal pain, abdominal distension and vomiting;
③Intravenous infusion, actively replenish blood volume, maintain water-electrolyte and acid-base balance, and pay attention to maintaining heat supply;
④Anti-pain: pethidine can be given to those with severe abdominal pain;
⑤ Antibiotics: Since acute pancreatitis is a chemical inflammation, antibiotics are not necessary; however, the occurrence of acute pancreatitis in China is often related to biliary tract diseases, so it is clinically customary to apply; if combined infection is suspected, it must be used;
(6) acid suppression therapy: the clinical habit of applying Hz receptor antagonists or proton pump inhibitors administered intravenously is believed to inhibit pancreatic juice secretion by inhibiting gastric acid, and also has the effect of preventing stress ulcers.
Severe pancreatitis must take comprehensive measures, active rescue treatment, in addition to the above treatment measures should also be.
Internal medicine treatment
1, monitoring if conditions should be transferred to the intensive care unit (ICU). Take appropriate measures for organ failure and metabolic disorders.
2, maintain water, electrolyte balance, maintain blood volume should be actively supplemented with fluids and electrolytes (potassium, sodium, calcium, magnesium plasma) to maintain effective blood volume. Severely ill patients often have shock and should be given albumin, fresh blood or plasma substitutes.
3, nutritional support is especially important for patients with severe pancreatitis. In the early stage, total parenteral nutrition (TPN) is generally used; if there is no intestinal obstruction, jejunal intubation should be performed as early as possible to transition to enteral nutrition (EN). Nutritional support can enhance the intestinal mucosal barrier and prevent intestinal bacterial translocation causing pancreatic necrosis combined with infection. Glutamine preparation has the effect of protecting the intestinal mucosal barrier and can be added.
4, antibacterial drugs severe pancreatitis routine use of antibiotics, there is a role in the prevention of pancreatic necrosis combined with infection. Antibiotic selection should be considered: antibiotics that are sensitive to intestinal translocation bacteria (Escherichia coli, Pseudomonas, Staphylococcus aureus, etc.) and have good permeability to the pancreas. Quinolones or imipenem are preferred, and drugs effective against anaerobic bacteria such as metronidazole are applied in combination.
Later in the course of the disease, close attention should be paid to fungal infections, empirical antifungal treatment if necessary, and fungal culture of blood and body fluid specimens.
5, reduce pancreatic fluid secretion growth inhibitor has the effect of inhibiting the secretion of pancreatic fluid and pancreatic enzymes and inhibiting the synthesis of pancreatic enzymes. Although the efficacy has not been finally determined, but currently domestic scholars recommend the early use. Growth inhibitor (somatostatin) dose of 250/~g/h; growth inhibitor analogs of oxytetracycline for 25-50 “g/h, continuous intravenous infusion, the course of treatment 3-7 days.
6, inhibition of pancreatic enzyme activity is only used in the early stage of severe pancreatitis, but the efficacy has yet to be confirmed. Peptidase (aprotinin) can be anti-pancreatic vasoprotein, so that bradykininogen can not be changed into bradykinin, but also inhibit protease, chymotrypsin and serotonin, 200,000 ~ 500,000 U / d, in 2 times dissolved in glucose solution intravenous drip; gabexate (FoY, gabexate) can inhibit protease, vasoprotein, prothrombin, elastase, etc., according to the condition, start daily 100-300mg dissolved in 500-1500ml of glucose saline at a rate of 2.5mg/(kg?h). 2-3 days after the condition improves, the dosage can be gradually reduced.
It is suitable for biliary pancreatitis combined with bile duct obstruction or biliary tract infection. Dedi sphincterotomy and/or placement of nasobiliary duct for drainage should be performed.
Traditional Chinese medicine
The pancreas belongs to the spleen and is connected to the stomach, with the ducts of jin connected to the bile and intestine. Chinese medicine believes that the main causes of pancreatitis are: over-eating cold, greasy, fatty and sweet, alcohol and wine, resulting in damage to the spleen and stomach; or emotional discomfort, liver depression and qi stagnation, coupled with the accumulation of bile and pancreatic stones, roundworm disturbance, blocking the ducts, resulting in liver and gallbladder stagnation, transverse to the spleen and stomach; or due to heat, heat poison, damp heat and other evil invasion, resulting in the internal organs of the lower and middle jiao dysfunction, eventually leading to pancreatitis. It prevents the rebellion of stomach qi, internal qi not descending, liver qi stagnation, followed by nausea and vomiting, abdominal distension and constipation, etc.; it strongly prevents the entry of heat into the interior, internal heat, stagnation of qi and blood stasis, so that stagnation can be unblocked and qi and blood can be tonified.
Surgical treatment
1, abdominal lavage can remove bacteria, endotoxin, pancreatic enzymes, inflammatory factors, etc. in the abdominal cavity through abdominal lavage to reduce the damage to the systemic organs after these substances enter the blood circulation.
2.Surgical indications for surgery are.
① Pancreatic necrosis combined with infection: consider surgical treatment under close monitoring and perform necrotic tissue removal and drainage.
② Pancreatic abscess: surgical drainage or percutaneous puncture drainage can be chosen.
③Pancreatic pseudocyst: surgical treatment, percutaneous puncture and drainage or endoscopic treatment can be chosen depending on the situation.
④Biliary tract obstruction or infection: surgical release of obstruction if EST is not available.
(⑤) If the diagnosis is not clear and perforation of abdominal organs or intestinal necrosis is suspected, dissection is performed.
Disease prognosis
The course and prognosis of acute pancreatitis depends on the extent of the lesion and the presence of complications. Mild cases often recover within a week and do not leave sequelae. In severe cases, the prognosis is poor, with a death rate of 20% to 40%. After active resuscitation, most of the deceased are left with varying degrees of pancreatic insufficiency, and very few evolve into chronic pancreatitis. Factors affecting the prognosis include: old age, hypotension, hypoalbumin, hypoxemia, hypocalcemia and various complications.
Disease prevention
Active treatment of biliary tract disease, abstinence from alcohol and avoidance of overeating.
Complications
Local complications
① Pancreatic abscess: 2-3 weeks after the onset of severe pancreatitis, abscess is formed due to secondary infection of the pancreas and peripancreatic necrosis. At this time, high fever, abdominal pain, epigastric masses and toxic symptoms appear;
②Pseudocysts: often formed 3 to 4 weeks after the disease, caused by pancreatic fluid and liquefied necrotic tissue wrapped in or around the pancreas. Most of them are located in the tail of the pancreatic body and are a few millimeters to tens of centimeters in size, which can compress the adjacent tissues and cause corresponding symptoms. There is no epithelium in the wall of the cyst, only necrotic granulation and fibrous tissue are seen, and penetration of the cyst can lead to pancreatic-derived ascites.
Systemic complications
Severe pancreatitis is often complicated by different degrees of multi-organ failure (MoF).
①Acute respiratory failure: that is, acute respiratory distress syndrome, sudden onset, progressive respiratory distress, cyanosis, etc., which cannot be relieved by conventional oxygen therapy;
②Acute renal failure: manifested as oliguria, proteinuria and progressive blood urea nitrogen, creatinine increase, etc.;
③Heart failure and arrhythmia: pericardial effusion, arrhythmia and heart failure;
④Gastrointestinal bleeding: upper gastrointestinal bleeding is mostly due to stress ulcers or mucosal erosion, and lower gastrointestinal bleeding can be caused by pancreatic necrosis penetrating the transverse colon;
⑤ Pancreatic encephalopathy: manifested by mental abnormalities (fantasy, hallucination, manic state) and disorientation, etc;
⑥Sepsis and fungal infection: Gram-negative bacilli predominate in the early stage, and the later stage is often a mixture of bacteria, and sepsis often coexists with pancreatic abscess; in severe cases, the body’s resistance is extremely low, and with the extensive use of antibiotics, fungal infection is very easy to produce;
(7) Hyperglycemia: mostly temporary;
(viii) chronic pancreatitis: a few evolve into chronic pancreatitis.
Disease examination
(I) White blood cell count
There is mostly leukocytosis and left shift of neutrophil nuclei.
(B) Blood and urine amylase measurement
Serum (pancreatic) amylase starts to rise 6 to 12 hours after the onset of the disease, and starts to fall at 48 hours and lasts for 3 to 5 days. The diagnosis of the disease can be confirmed if the serum amylase exceeds 3 times the normal value. The amylase level does not necessarily reflect the severity of the disease, and the amylase value can be normal or below normal in hemorrhagic necrotizing pancreatitis. Other acute abdominal conditions such as peptic ulcer perforation, cholelithiasis, cholecystitis, intestinal obstruction, etc. can have elevated serum amylase, but generally do not exceed two times the normal value.
Urinary amylase is elevated later, starting to rise 12-14 hours after the onset of the disease and decreasing slowly for 1 to 2 weeks, but the urinary amylase value is affected by the patient’s urine volume. Amylase values in pancreatic-derived ascites and pleural fluid are also significantly higher.
(C) Serum lipase measurement
Serum lipase often starts to rise 24 to 72 hours after the onset of the disease and lasts for 7 to 10 days. It is of diagnostic value for patients with acute pancreatitis who present late after the disease and has a high specificity.
(iv) C-reactive protein (CRP)
CRP is a non-specific marker of tissue damage and inflammation. It helps to assess and monitor the severity of acute pancreatitis, and CRP is significantly elevated in the presence of pancreatic necrosis.
(E) Biochemical tests
Transient elevation of blood glucose is common and may be associated with decreased insulin release and increased glucagon release. Persistent fasting glucose higher than 10 mmol/L reflects pancreatic necrosis and suggests poor prognosis. Hyperbilirubinemia is seen in a small number of patients and mostly returns to normal 4 to 7 days after onset. Serum AsT and LDH may increase.
Transient hypocalcemia (<2mmol/L) is commonly seen in severe acute pancreatitis, the degree of hypocalcemia parallels the clinical severity, and if the calcium is below 1.5mmol/L it suggests a poor prognosis. Hypertriglyceridemia can occur in acute pancreatitis, and this condition may be the cause or the consequence, the latter can return to normal after the acute phase.
(F) Imaging tests
1. Abdominal plain films can exclude other acute abdominal conditions, such as visceral perforation. “Sentinel collaterals” and “colonic cut sign” are indirect indications of pancreatitis. Diffuse blurred shadow and indistinct lumbar muscle margins suggest the presence of ascites. Intestinal paralysis or paralytic intestinal obstruction signs can be found.
2. Ultrasound of the abdomen should be used as a routine primary screening test. Acute pancreatitis ultrasound can see enlarged pancreas, abnormal echogenicity in and around the pancreas; it can also understand the situation of gallbladder and bile duct; later it has diagnostic significance for abscesses and pseudocysts. However, the patient’s abdominal distension often affects its observation.
3, CT imaging CT is graded according to the imaging changes of pancreatic tissue, which is of great value for the diagnosis and differential diagnosis of acute pancreatitis and assessment of its severity, especially for the differentiation of mild and severe pancreatitis, and whether nearby organs are involved. In mild cases, non-specific enlargement and thickening of the pancreas with irregular peripancreatic margins are seen; in severe cases, disappearance of the peripancreatic area; omental capsule and omental fatty degeneration with increased density; and pleuroperitoneal cavity effusion. Enhanced CT is the best method to diagnose pancreatic necrosis, and CT-guided puncture is feasible for suspected necrosis and co-infection.