Acute pancreatitis (AP) is a disease caused by activation of pancreatic enzymes from multiple etiologies, followed by a local inflammatory response in the pancreas, with or without functional changes in other organs. Clinically, the course of the disease is self-limiting in most patients; 20% to 30% of patients have an aggressive clinical course. The overall mortality rate is 5% to -10%.
I. Terms and definitions
According to the classification system of acute pancreatitis developed by the International Symposium on Acute Pancreatitis (1992, Atlanta, USA) and the guidelines for the management of acute pancreatitis issued by the World Congress of Gastroenterology (2002, Bangkok, Thailand), combined with the specific situation in China, the terminology and definitions of acute pancreatitis, in order to play a guiding role in clinical and scientific research, and to regulate the academic terminology in this field.
(I) Clinical terminology
Acute pancreatitis (AP) is clinically manifested by acute, persistent abdominal pain (occasionally without abdominal pain), increased serum amylase activity greater than/equal to 3 times the upper limit of normal value, imaging suggests that the pancreas has/does not have morphological changes, excluding other diseases. Other organ dysfunction may be present/absent. In a few cases, serum amylase activity is normal or mildly elevated.
Mild acute pancreatitis (MAP) has the clinical manifestations and biochemical changes of acute pancreatitis without organ dysfunction or local complications, and responds well to fluid replacement therapy. ranson score < 3, or APACHE-II score < 8, or CT classification of A, B, C.
Severe acute pancreatitis (SAP) has clinical manifestations and biochemical changes of acute pancreatitis with one of the following: local complications (pancreatic necrosis, pseudocyst, pancreatic abscess); organ failure; Ranson score ≥ 3; APACHE-II score ≥ 8; CT classification of D, E.
(II) Other terms
Acute fluid collection occurs early in the course of the disease, with fluid accumulation in the pancreas or peripancreatic or distal pancreatic compartment, and lack of an intact envelope.
Pancreatic necrosis is an enhanced CT examination that shows lifeless pancreatic tissue or peripancreatic fatty tissue.
Pseudocyst is a fluid accumulation with intact non-epithelial envelope containing pancreatic secretions, granulation tissue, and fibrous tissue. It mostly occurs after 4 weeks of acute pancreatitis onset.
The pancreatic abscess is an accumulation of pus in or around the pancreas, surrounded by a fibrous cyst wall.
Causes of acute pancreatitis
There are many causes of acute pancreatitis, and there are regional differences. Based on the diagnosis of acute pancreatitis, the etiology should be clarified as much as possible, and efforts should be made to remove the causes to prevent recurrence.
(A) Common causes
Gallstone disease (including biliary microstones), alcohol, hyperlipidemia.
(II) Other etiologies
Jugular papillary sphincter dyskinesia, drugs and toxins, post-ERCP, paraduodenal papillary diverticulum, traumatic, hypercalcemia, post-abdominal surgery, pancreatic split, peripotent cancer, pancreatic cancer, vasculitis, infectious (coxsackievirus, mumps virus, HIV, ascariasis), autoimmune (systemic lupus erythematosus, dry syndrome), α1-antitrypsin deficiency, etc.
(c) Those who cannot determine the cause by clinical and imaging, biochemical and other examinations are called idiopathic.
Three, the etiology of acute pancreatitis investigation
Detailed medical history: including family history, past medical history, history of alcohol intake, history of drug intake, etc. Calculate the body mass index (BMI).
Basic examination: serum amylase measurement, liver function test, lipid measurement, blood glucose measurement, blood calcium measurement; abdominal ultrasound.
In-depth examination: viral assay, autoimmune marker assay, tumor marker assay (CEA, CA19-9) assay; CT scan (enhanced CT if necessary), ERCP/MRCP, ultrasound endoscopy (EUS), potbelly papillary sphincter manometry (if necessary), pancreatic exocrine function test, etc.
IV. Diagnostic process of acute pancreatitis
(A) Clinical manifestations of acute pancreatitis
Abdominal pain is the main symptom of acute pancreatitis, located in the upper abdomen, often radiating to the back, mostly acute onset, persistent, and a few without abdominal pain. It can 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 mostly seen in biliary pancreatitis.
In addition, acute pancreatitis can be accompanied by 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 acute pancreatitis and suggests a poor prognosis; oliguria and acute renal failure; tinnitus, diplopia, delirium, speech disorders and limb rigidity, coma and other signs of pancreatic encephalopathy, which can occur after the onset of the disease The symptoms of pancreatic encephalopathy can occur early after the onset of the disease, or during the recovery period.
In mild cases, there is only light pressure pain, but in severe cases, there may be 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. Persistently high serum amylase should be noted for: recurrent disease, complications of pseudocysts or abscesses, suspected stones or tumors, renal insufficiency, macroamylasemia, etc. Care should be taken to identify other acute abdominal conditions causing increased serum amylase. Measurement of serum lipase activity has important clinical significance, especially when serum amylase activity has decreased to normal, or when serum amylase activity is increased due to other causes, 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 at 72 hours after onset suggests possible pancreatic tissue necrosis. Increased serum interleukin-6 (IL-6) levels are dynamically measured to indicate poor prognosis.
3. Diagnostic imaging: Ultrasound examination at 24 to 48 hours after the onset of the disease can initially determine the morphological changes of the pancreatic tissue and help to determine the presence of biliary tract diseases, but the influence of gas accumulation in the gastrointestinal tract during acute pancreatitis often prevents accurate judgment of acute pancreatitis.
CT scan is recommended as the standard imaging method for the diagnosis of acute pancreatitis. Enhanced CT (CE-CT) or dynamic enhanced CT examination is performed when necessary.?
Grading is A-E according to the severity of inflammation.
Grade A: normal pancreas.
Grade B: parenchymal changes of the pancreas. This includes local or diffuse enlargement of the gland.
Grade C: parenchymal and peripheral inflammatory changes of the pancreas with mild peripancreatic exudation.
Grade D: Significant peripancreatic exudate in addition to grade C, with a single fluid accumulation in the pancreatic parenchyma or in the peripancreatic area.
Grade E: Extensive intra- and extra-pancreatic fluid accumulation, including pancreatic and fat necrosis, and pancreatic abscess.
Grade A – C: clinically mild acute pancreatitis; Grade D? Grade E: clinically severe acute pancreatitis.
Recommendations.
(1) The importance of clinical manifestations in the diagnosis of acute pancreatitis must be emphasized. Persistent upper middle abdominal pain, increased serum amylase, and imaging changes, excluding other diseases, can diagnose the disease.
(2) The clinical term “moderate acute pancreatitis” or “tendency to severe acute pancreatitis” should no longer be used.
(3) Clinical attention should be paid to the possibility that some patients with acute pancreatitis are transformed from “mild acute pancreatitis” to “severe acute pancreatitis”. Therefore, it is necessary to make dynamic observation of the disease. In addition to the Ranson index and APACHE-II index, other valuable discriminatory indicators are: body mass index over 28 kg/m2; pleural exudate, especially bilateral pleural effusion; CRP > 150 mg/L after 72 h and continues to increase, etc. are valuable clinical indicators for severity assessment.
V. Principles of management of acute pancreatitis
(A) 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 measurement, routine urine measurement, fecal occult blood measurement, renal function measurement, 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 24-h urine output and volume changes were recorded. The above indicators can be selected according to the patient’s specific condition. Routine fasting, gastrointestinal decompression should be performed for those with severe abdominal distension and paralytic intestinal obstruction. The open diet can be considered when the patient’s abdominal pain is reduced/disappeared, abdominal distension is reduced/disappeared, and intestinal motility is restored/or partially restored, starting with carbohydrate-based diet and gradually transitioning to low-fat diet, without the high or low serum amylase activity as a necessary condition for the open diet.
(II) Fluid rehydration
The amount of rehydration fluid includes the basal requirement 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.
(iii)Analgesia
Consider analgesic treatment when the pain is severe. Under close observation of the condition, quatidine hydrochloride (dulcolax) may be injected. Morphine or cholinergic receptor antagonists, such as atropine, 654-2, etc., are not recommended because the former will contract the sphincter of Oddi, and the latter will induce or aggravate intestinal paralysis.?
(iv) Inhibition of pancreatic exocrine secretion and pancreatic enzyme inhibitor application
Growth inhibitors and their analogs (octreotide) can act by directly inhibiting pancreatic exocrine secretion and are advocated for use in the treatment of severe acute pancreatitis. Octreotide usage: The first dose is 0.1 mg by push, followed by 25 μg to 50 μg/h maintenance therapy. H2 receptor antagonists and proton pump inhibitors (PPI) can indirectly inhibit pancreatic secretion by suppressing gastric acid secretion, in addition to preventing the development of stress ulcers, and are therefore recommended in the treatment of severe acute pancreatitis. acute pancreatitis. Early and adequate application of protease inhibitors is advocated, and preparations such as gabester can be used.
(E) Application of vasoactive substances
Since microcirculatory disorders play an important role in the development of acute pancreatitis, especially severe acute pancreatitis, it is recommended to apply drugs that improve microcirculation in the pancreas and other organs, such as prostaglandin E1 preparations, platelet-activating factor antagonist preparations, salvia preparations, etc.
(F) Antibiotic application
The routine use of antibiotics is not recommended for mild non-biliary acute pancreatitis. For mild acute pancreatitis of biliary origin, or severe acute pancreatitis, 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, strong lipid solubility, and effective passage through the blood-pancreatic barrier. Therefore, metronidazole combined with quinolones is recommended as the first-line drug, and in case of poor efficacy, it should be replaced by Imipenem or a course of 7 to 14 d according to the drug sensitivity results, which can be extended in special cases. The diagnosis of secondary bacterial infections in extra-pancreatic organs should be noted, and antibiotics should be selected according to the drug sensitivity. The diagnosis of fungal infection should be paid attention to. If 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.
(VII) Nutritional support
In patients with mild acute pancreatitis, only short-term fasting is required, so enteral or parenteral nutrition is not needed. In patients with severe acute pancreatitis, parenteral nutrition is often administered first, usually for 7 to 10 days, and enteral nutrition is considered when the disease tends to remit. Place the nasal feeding tube below the Treitz ligament to start enteral nutrition with an energy density of 4.187 J/ml, and gradually increase the amount if it is tolerated. Supplementation with glutamine preparations should be noted. In general, patients with SAP require 8,000-10,000 kJ/d of calories, 50%-60% from sugar, 15%-20% from protein, 20%-30% from lipids, and for hyperlipidemic patients, the supplementation of fatty substances should be reduced. When enteral nutrition is carried out, attention should be paid to whether the patient’s abdominal pain, intestinal paralysis, abdominal pressure and other signs and symptoms of pancreatitis are aggravated, and electrolytes, lipids, blood glucose, total bilirubin, serum leukocytes, etc. should be reviewed regularly. (H) Prevention and treatment
(H) Prevention and treatment of intestinal failure
For patients with SAP, abdominal signs and bowel movements 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. As soon as possible, the resumption of diet or enteral nutrition is important for the prevention of intestinal failure as soon as the disease condition allows.
(ix) Traditional Chinese medicine
Single herbs, such as raw rhubarb, and compound preparations, such as Qing Pancreatic Tang and Da Cheng Qi Tang with addition and subtraction are proven to be effective in clinical practice.
(J) Endoscopic treatment of acute pancreatitis (bile-derived ABP)
It is recommended that in units where available, nasobiliary drainage or EST under ERCP should be performed for suspected or confirmed ABP that meets the index of severe disease and/or has cholangitis, jaundice, dilated common bile duct, or is initially judged to be simple type pancreatitis but deteriorates during conservative treatment.
(XI) Management of complications
ARDS is a serious complication of acute pancreatitis. Management 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, if necessary, dialysis. Hypotension is associated with hyperdynamic circulation, and management includes close hemodynamic monitoring, intravenous rehydration, and vasoactive drugs if necessary. Heparin should be used in cases of disseminated intravascular coagulation (DIC). In acute pancreatitis with pancreatic fluid accumulation, some will develop into pseudocysts. If the pancreatic pseudocyst is > 6 cm in diameter and has 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 blockers and proton pump inhibitors, can be applied.
(XII) Surgical treatment
Surgical intervention is considered under close observation in cases of secondary infection of necrotic pancreatic tissue. In severe cases, it is advocated that on the basis of intensive care and intensive conservative treatment, the patient’s condition remains unstable or deteriorates further, which is an indication for surgical treatment, or laparotomy.