Acute pancreatitis management guide
Common knowledge
1. Non-imaging clinical staging criteria: Ranson’s criteria
1.1 Evaluation indicators on admission (5 items).
Age 55 years or older; white blood cell 16×109/L; blood glucose greater than 11.2mmol/L; serum LDH greater than 350IU/L; GOT greater than 250IU/L.
1.2 Evaluation indexes within 48 hours after admission (6 items).
Erythrocyte pressure volume decreased more than 10%; BUN elevated more than 1.79mmol/L; serum calcium less than 2mmol/L; arterial blood PO2 less than 8kPa; base deficiency more than 4mmol/L; estimated body fluid loss more than 6000ml.
2. Clinical diagnostic terms
2.1 Acute pancreatitis (AP)
Clinical manifestations are acute, persistent abdominal pain (occasionally without abdominal pain), increased serum amylase activity greater than/equal to 3 times the upper limit of normal values, and imaging suggesting morphological changes in the pancreas with/without other diseases excluded. Other organ dysfunction may be present/absent. In a few cases, the serum amylase activity is normal or mildly increased.
2.2 Mild acute pancreatitis (MAP)
Ranson score 2.0 mg/dL); respiratory failure (PaO2 ≤ 60 mmHg); shock (systolic blood pressure ≤ 80 mmHg for 15 min); coagulation dysfunction (PT < 70%, and/or APTT > 45 sec); sepsis (T > 38.5°C, WBC > 38.5°C); and septicemia (T > 38.5°C). 38.5℃, WBC > 16.0×109/L, BE ≤ 4 mmol/L for 48 h, positive bacterial culture of blood/extracts); systemic inflammatory response syndrome (SIRS) (T > 38.5℃, WBC > 12.0×109/L, BE ≤ 2.5 mmol/L for 48 h, negative bacterial culture of blood/extracts).
3. Standard clinical diagnosis writing format
Standard clinical diagnosis includes etiological diagnosis, graded diagnosis, and complication diagnosis, such as: acute pancreatitis (biliary, heavy, ARDS), acute pancreatitis (biliary, light).
4.Other terms
4.1 Acute fluid collection (acute fluid collection)
Occurs early in the course of the disease, fluid accumulation in the pancreas or peripancreatic or distal pancreatic space, and lack of complete envelope.
4.2 pancreatic necrosis
Enhanced CT examination suggests lifeless pancreatic tissue or peripancreatic adipose tissue.
4.3 Pseudocyst (pseudocyst)
A fluid accumulation with intact non-epithelial envelope, containing pancreatic secretions, granulation tissue, fibrous tissue and so on. It mostly occurs after 4 weeks of acute pancreatitis onset.
4.4 Pancreatic abscess (pancreatic abscess)
An accumulation of pus in or around the pancreas, surrounded by a fibrous cystic wall.
4.5 Biliary-derived transient pancreatic hypertension (this description is not recognized)
The symptoms of biliary tract infection with typical gallstones, but no acute pancreatitis, elevated blood and urine amylase in laboratory tests, normal pancreatic exploration during surgery, and rapid recovery after surgical treatment of biliary tract disease may cause transient pancreatic ductal hypertension or biliopancreatic reflux due to transient obstruction of the common channel by gallstones, and the obstruction of the common channel is quickly removed by stone removal or stone uplifting, and pancreatic hypertension is relieved before pancreatitis occurs.
Medical treatment
1.General examination
Blood routine, urine routine, fecal occult blood; renal function, liver function, blood sugar, lipids, serum electrolytes (calcium); blood and urine amylase; blood gas analysis; C-reactive protein (CRP), 72 hours after the onset of CRP > 150 mg/L indicates pancreatic tissue necrosis; ECG.
2.Imaging examinations
2.1 Standard imaging examinations: CT plain scan (enhanced if necessary)
Grade A: normal pancreas; Grade B: pancreatic parenchymal changes. including local or diffuse glandular enlargement; Grade C: inflammatory changes in and around the pancreatic parenchyma, mild peripancreatic exudation; Grade D: significant peripancreatic exudation in addition to Grade C, single fluid accumulation in or around the pancreatic parenchyma; Grade E: extensive intra- and extra-pancreatic fluid accumulation, including pancreatic and fat necrosis, pancreatic abscess.
2.2 Other imaging examinations.
Ultrasound examination in the early 24-48h of the onset of disease can initially determine the histomorphological changes of the pancreas and the presence of biliary tract disease. The finding of pulmonary atelectasis and pleural effusion on chest radiograph suggests poor prognosis.
3.Dietary management
Routine fasting; with severe abdominal distension, paralytic intestinal obstruction should be gastrointestinal decompression; conditions for open diet: in patients with abdominal pain reduction/ disappearance, abdominal distension reduction/ disappearance, intestinal dynamics restored/ or partially restored. Start carbohydrate-based diet and transition to low-fat diet; serum amylase is not a necessary condition for open diet.
4. Clinical monitoring
Dynamic observation of abdominal signs and bowel sound changes; cardiac and blood pressure monitoring; central venous pressure measurement; recording 24h urine output and changes in volume of intake and output. Choose according to the condition.
5.Analgesia
Dulcolax can be injected under close observation of the condition. Morphine (Oddi’s sphincter contraction) or 654-2 (induce or aggravate intestinal paralysis) is not recommended.
6. Nutritional support and prevention of intestinal failure
6.1 Principles
Mild acute pancreatitis requires only short-term fasting, and resume diet as soon as the condition allows; in severe acute pancreatitis, administer parenteral nutrition for 7-10 d first, and change to enteral nutrition in remission, paying attention to changes in symptoms and signs.
6.2 Energy requirements
Total energy 8000～10000kJ/d, 50%～60% from sugar (250g), 15%～20% from protein (8.5% amino acid 750-1000ml), 20%～30% from lipid (10% fat emulsion 500ml). The supplementation of fatty substances should be reduced in hyperlipidemia.
6.3 Prokinetic drugs
Early to give intestinal prokinetic drugs, such as raw rhubarb, magnesium sulfate, lactulose, etc., but also can be used in Chinese medicine skin nitrate external application.
6.4 Micro-ecological agents
Regulate intestinal flora, such as pefikon 420mg tid
6.5 Protection of intestinal mucosal barrier
Apply glutamine preparations to protect the intestinal mucosal barrier: ginseng enteramine, 2-4 capsules, tid.
7. Inhibition of pancreatic exocrine secretion and pancreatic enzyme activity
7.1 Growth inhibitors and analogues
Direct inhibition of pancreatic exocrine secretion, such as octreotide: the first dose of 0.1 mg push, followed by 25 μg to 50 μg/h; or Stanozolam: the first dose of 250 μg, followed by 250 μg /h maintenance. Indications for discontinuation: Improvement of clinical symptoms, disappearance of abdominal pain, and/or reduction of serum amylase activity to normal.
7.2 H2 receptor antagonists and proton pump inhibitors (PPIs)
Inhibit gastric acid secretion and indirectly inhibit pancreatic secretion to prevent stress ulcers.
7.3 Protease inhibitors
Apply early and in adequate doses. Such as gabexate: starting dose 300mg/d, change to 100mg/d after 3 d, total course 6-10 d, the rate of static drip is 1mg/kg.h, there may be allergic reactions; ustekin: 100,000 units diluted static drip, 1-3 times/day, there may be allergic reactions.
8.Antibiotics
Antibiotics are used as appropriate for mild non-biliary acute pancreatitis, and antibiotics are routinely used for acute pancreatitis (biliary, mild) and acute pancreatitis (heavy). Fever and other manifestations that cannot be explained by bacterial infection should be considered fungal infections, and fungal cultures of blood or body fluids should be performed along with empirical application of antifungal drugs.
8.1 Nitroimidazoles: Metronidazole
8.2 Quinolones.
8.3 Imipenem or a course of 7 to 14 d depending on the drug sensitivity results
9 Vasoactive drugs
Improve microcirculatory disorders in the pancreas and other organs. Such as prostaglandin E1 preparation: 100-200mg/d, diluted IV, use with caution or not for pregnancy and glaucoma; Salvia preparation.
Key points of medical record writing
1.Common etiology
Cholelithiasis (including biliary microstones), alcohol, hyperlipidemia, hypercalcemia, jugular papillary sphincter dysplasia, paraduodenal papillary diverticulum, pancreatic split, drugs and toxins, post-ERCP, post-abdominal surgery, traumatic, peripotent cancer, pancreatic cancer, vasculitis, infectious (coxsackievirus, mumps virus, HIV, ascariasis), autoimmune (systemic lupus erythematosus Dry syndrome), α1-antitrypsin deficiency, etc.
2.Symptom characteristics
Abdominal pain is the main symptom, located in the upper abdomen, often radiating to the back, mostly acute and persistent, but a few do not have abdominal pain. It may be accompanied by nausea and vomiting. Fever often originates from acute inflammation, secondary infection of necrotic pancreatic tissue, or secondary fungal infection. Fever and jaundice are most often seen in biliary pancreatitis. It can also be accompanied by the following systemic complications: tachycardia and hypotension, or shock; pulmonary atelectasis, pleural effusion and respiratory failure, oliguria and acute renal failure; tinnitus, diplopia, delirium, speech disorders and limb stiffness, coma and other signs of pancreatic encephalopathy.
3.Features of physical signs
In mild cases, only light pressure pain, in severe cases, peritoneal irritation sign, ascites, Grey-Turner sign, Cullen sign may appear. Portal hypertension and splenomegaly may occur due to splenic vein embolism. A mass may be palpable in the abdomen due to fluid accumulation or pseudocyst formation. Other signs of corresponding complications may also be present.
4. Differential diagnosis strategy
4.1 When the primary diagnosis is unclear (abdominal pain pending investigation)
4.1.1 Acute cholecystitis, cholelithiasis
There may be right upper abdominal distension and pain, radiating to the right chest and back and right shoulder, with normal or slightly high blood and urine amylase, accompanied by chills, fever and jaundice, which can be identified by B ultrasound.
4.1.2 Biliary tract ascariasis
Mostly in children and young adults. Sudden onset of severe paroxysmal colic under the right side of the subxiphoid process, upward drilling-like pain, the patient tossing and turning, cold sweat, as normal after the pain, the general symptoms are heavy but the signs are light, and the eggs of worms can be detected in the fecal routine.
4.1.3 Gastroduodenal perforation
Most of them have a history of peptic ulcer, sudden onset of severe epigastric knife-like pain, which soon spreads to the whole abdomen, with plate-like tonicity of the abdominal wall, disappearance of intestinal sounds, and free gas under the diaphragm seen on abdominal fluoroscopy can be clearly diagnosed.
4.1.4 Acute renal colic
Paroxysmal renal colic in the lumbar region, radiating to the inter-abdominal region, with interstitial distension, often accompanied by hematuria.
4.1.5 Coronary artery disease, myocardial infarction
There is often a history of coronary heart disease. There is pressure in the anterior thoracic region, and abdominal signs are not obvious. Note the EKG changes (compared with previous).
4.1.6 Intestinal obstruction
History of abdominal surgery or history of abdominal wall hernia. There is abdominal distension, vomiting, cessation of defecation, high-pitched bowel sounds and gas-over-water sounds, and distended intestinal cavity with fluid-gas planes seen on abdominal fluoroscopy.
4.2 Acute pancreatitis with clear diagnosis
4.2.1 Discussion of etiology
In addition to the common biliary and alcoholic factors, the following special types of pancreatitis should be noted: family hereditary pancreatitis (family hereditary pancreatitis), the onset of early childhood, recurrent episodes of abdominal pain with nausea and vomiting, with age, the number of episodes decreases; Pancreatitis of drugs (Pancreatitis of drugs), azathioprine, dihydrochlorhexidine The pancreatitis of drugs (Pancreatitis of drugs), caused by azathioprine, dihydrocortizone, estrogen, steroid hormones, tetracycline, calcium, Ara-c, etc.; metabolic pancreatitis (Metabolic pancreatitis), caused by hyperlipidemia, hyperparathyroidism, etc.; malnutrition pancreatitis (tropical pancreatitis), with long-term protein malnutrition as the main cause; geriatric pancreatitis (gerontal pancreatitis), caused by hyperlipidemia, atherosclerosis, hypertension, etc.
4.2.2 Grading discussion
4.2.3 Complications discussion
Treatment measures for special cases
1. Endoscopic treatment of acute pancreatitis (biliary origin)
Heavy cases with cholangitis, jaundice, dilated common bile duct, or those initially judged to be mild but deteriorating during treatment may be considered for nasobiliary drainage or EST under ERCP.
2. Indications for surgical treatment
Severe diffuse peritonitis with severe systemic infection; early occurrence of MOF; SAP caused by stone in the lower biliary tract or stone obstruction in the pancreatic duct; pancreatic abscess and partial pancreatic pseudocyst
3. Principles of complications management
ARDS: mechanical ventilation and high-dose, short-course glucocorticoid application; acute renal failure: supportive therapy is the main focus, if necessary, dialysis; hypotension: hemodynamic monitoring, intravenous rehydration, if necessary, the use of vasoactive drugs; diffuse intravascular coagulation (DIC): the use of heparin; pseudocyst: part of it will be self-absorption, if the pseudocyst diameter > 6 cm, and there are compression phenomena and clinical manifestations If the pseudocyst is >6 cm in diameter and has compression and clinical manifestations, puncture drainage or surgical drainage is feasible; pancreatic abscess: an absolute indication for surgical intervention.