Since the implementation of the “Draft of Diagnosis and Treatment of Severe Acute Pancreatitis” (hereinafter referred to as “the draft”) in China in 2000, the Pancreatic Surgery Group of the Chinese Medical Association’s Surgery Branch has received good results. In recent years, due to the rapid development of medical science and technology, new concepts and new treatment measures have been introduced, some of which have been relatively mature and effective. For this reason, the 10th National Symposium on Pancreatic Surgery held in 2004 focused on the additions and revisions of the “draft”, followed by several discussions in Beijing, Nanjing, Wuhan and Shanghai. Since the “draft” has been clinically applied for 5 years, it has got positive effect and has a guiding effect on clinical work, so the revised “draft” was renamed as “Guidelines for the diagnosis and treatment of severe acute pancreatitis”. The revised “draft” was renamed “Guidelines for the diagnosis and treatment of severe acute pancreatitis”, and was read out at the 11th National Symposium on Pancreatic Surgery in September 2006 to solicit opinions, and was adopted by all members of the Pancreatic Surgery Group of the Chinese Medical Association in November of the same year.
I. Clinical diagnosis
1.Severe acute pancreatitis
Acute pancreatitis with organ dysfunction, or local complications such as necrosis, abscess or pseudocyst, or both. Common abdominal signs include obvious pressure pain in the upper abdomen, rebound pain, muscle tension, abdominal distension, and diminished or absent bowel sounds. Abdominal masses may be present, and subcutaneous bruising of the lumbar ribs (Grey-Turner sign) and periumbilical bruising (cullen sign) are occasionally seen. It can be complicated by dysfunction of one or more organs and can also be associated with severe metabolic dysfunction, including hypocalcemia (blood calcium <1.87 mmoFL). Enhanced CT is the most effective method for the diagnosis of pancreatic necrosis, and ultrasound and laparotomy are helpful for diagnosis.
APACHE II score ≥ 8. Balthazar CT grading system ≥ grade II.
2.Fulminant acute pancreatitis
In patients with severe acute pancreatitis, fulminant acute pancreatitis can be diagnosed in those who develop organ dysfunction despite regular non-surgical treatment (including adequate fluid resuscitation) within 72 h of the onset of the disease. Fulminant acute pancreatitis is a dangerous condition, non-operative treatment is often ineffective and often secondary to abdominal septal compartment syndrome.
Second, the severity of grading
Severe acute pancreatitis without organ dysfunction is grade 1, with organ dysfunction is grade 1, which within 72 h after adequate fluid resuscitation, but still appearing organ crying dysfunction of patients with grade 1 severe acute pancreatitis is fulminant acute pancreatitis.
Third, the course of the disease stage
The whole course of the disease can be roughly divided into three stages, but not all patients have three stages of the disease, some have only the first stage, some have two stages, and some have three stages.
(1) Acute reaction phase: from onset to 2 weeks, there may be complications such as shock, respiratory dysfunction, renal dysfunction and encephalopathy.
(2) Systemic infection phase: 2 weeks to 2 months from onset, with systemic bacterial infection, deep fungal infection or dual infection as its main clinical manifestations.
(3) Residual infection period: 2 to 3 months after onset, with systemic malnutrition, presence of retroperitoneal or intra-abdominal residual cavity, often with poor drainage and long-lasting sinus tracts, accompanied by gastrointestinal rash as the main clinical manifestations.
IV. Local complications
1, acute fluid accumulation
Occurs early in the course of pancreatitis, located in the pancreas or peri-pancreatic, without the accumulation of fluid encapsulated by the cystic wall. It is usually detected by imaging. On imaging, it is a fluid accumulation without obvious cystic wall encapsulation. Acute fluid accumulation will mostly absorb on its own, but a few may develop into acute pseudocysts or pancreatic abscesses.
2. Necrosis of the pancreas and peripancreatic tissue
It refers to diffuse or focal necrosis of the pancreatic parenchyma, accompanied by peripancreatic fat necrosis. According to infection or not, it is divided into infected pancreatic necrosis and aseptic pancreatic necrosis. Enhanced CT is currently the best method to diagnose pancreatic necrosis. The enhancement of the necrotic area does not exceed 50 Hu after intravenous injection of enhancer (the enhancement of the normal area is 50-150 Hu). Necrotic infection is characterized by the clinical presence of septic syndrome, and enhanced CT confirms the presence of necrotic lesions, sometimes visible as bubble signs. The clinical manifestations of encapsulated necrotic infection are varying degrees of fever, weakness, gastrointestinal dysfunction, catabolic and organ function involvement, mostly without signs of peritoneal irritation, and sometimes abdominal or lumbar masses can be palpated, and CT scan mainly shows encapsulated hypodense lesions in the pancreas or peripancreatic area.
3. Acute pancreatic pseudocysts
It refers to the accumulation of pancreatic fluid wrapped by fibrous tissue or fleshy tooth cyst wall formed after acute pancreatitis. A few pseudocysts in patients with acute pancreatitis can be detected by palpation, and most of them are diagnosed by imaging examination. It is often round or oval with a clear cyst wall.
4.Pancreatic abscess
Occurs as an encapsulated accumulation of pus around the pancreas in acute pancreatitis, with or without pancreatic necrotic tissue. The sepsis syndrome is its most common clinical manifestation. It occurs in the later stages of severe pancreatitis, often 4 weeks after the onset of the disease or 4 weeks later. The presence of pus with positive bacterial or fungal cultures containing little or no pancreatic necrotic tissue is the characteristic that distinguishes it from infected necrosis. Pancreatic abscesses are in most cases formed by focal necrotic liquefaction secondary to infection.
V. Treatment
Select the treatment plan according to the stage of the disease
1.Treatment of acute reaction period
(1) Treatment for etiology
(1) Biliary acute pancreatitis: first of all, identify the presence or absence of biliary obstruction lesions. Where there is biliary obstruction, the obstruction must be removed in a timely manner. The first choice is to perform a trans-fiber duodenoscopic oddi sphincterotomy for stone extraction and nasobiliary drainage, or combined laparoscopic cholecystectomy, or open surgery, including cholecystectomy and exploration of the common bile duct to clarify whether there is obstruction of the lower end of the common bile duct. If the pancreatic gland is obviously involved, small omental sac pancreatic drainage can be added. If there is no biliary obstruction, non-surgical treatment should be performed first, and further diagnosis and treatment should be performed as soon as possible when the disease is in remission. The cause of biliary origin is sometimes hidden, such as bile mud obstruction, which needs to be identified through close clinical observation, liver function tests and imaging examinations, and ERCP can be done to clarify the cause of biliary tract if non-surgical treatment is not effective and biliary obstruction is suspected, and drainage can be placed at the same time.
② hyperlipidemic acute pancreatitis: In recent years, there has been a significant increase in the number of cases. Therefore, it is important to ask about the history of hyperlipidemia, fatty liver and familial hyperlipidemia, as well as the use of medications that may elevate lipids. Triacylglycerol >11.3 mmol/L is prone to acute pancreatitis and needs to be reduced to below 5.65 mmol/L within a short period of time. These patients should limit the use of fat emulsions and avoid drugs that may raise blood lipids. Pharmacological treatment can use small doses of low molecular heparin and insulin, mainly to increase the activity of lipoproteinase and accelerate the degradation of celiac particles; rapid lipid-lowering techniques include lipid adsorption and plasma replacement.
③Alcoholic acute pancreatitis: for the possible pathogenic mechanism of alcoholic acute pancreatitis, emphasis is placed on reducing pancreatic juice secretion, gastric acid secretion, and improving the acidified state of duodenum; emphasis is placed on relieving the spasm of Oddi sphincter and improving the drainage state of pancreatic juice.
④ Other etiologies: For other etiologies that can be found, timely treatment should also be directed at the etiology, such as hypercalcemic acute pancreatitis mostly related to hyperparathyroidism, which requires calcium-lowering therapy and corresponding parathyroid surgery. For those with unknown etiology, while choosing the appropriate treatment according to the stage of the disease, we should carefully observe the presence of hidden causes.
(2) Non-surgical treatment
(1) Fluid resuscitation, maintenance of water-electrolyte balance and intensive monitoring treatment. Due to the large amount of peripancreatic and retroperitoneal exudate, resulting in blood volume loss and hemoconcentration, and due to the presence of capillary leakage, dynamic monitoring of CvP or PWCP and I-ICT is needed as a guide for volume expansion, and attention should be paid to the crystalloid ratio to reduce tissue interstitial fluid storage. Changes in urine output and intra-abdominal pressure should be observed.
Attention should also be paid to maintaining the oxygen supply of the organism and monitoring of visceral function.
② Pancreatic rest therapy, such as fasting, gastrointestinal decompression, acid and enzyme suppression therapy.
Prophylactic antibiotic application: mainly for intestinal-derived Gram-negative bacilli translocation, antibiotics that can pass the hemopancreatic barrier should be used, such as chlortetracycline, cephalothiazide, hydrocarbon enzymes and metronidazole.
④ Sedation, antispasmodic and analgesic treatment.
⑤Chinese medicine: raw rhubarb 15 g, instillation in the gastric tube or rectal drip, twice a day. Chinese herbal medicine skin nitrate is applied externally to the whole abdomen, 500 g, twice a day.
(6) Prevention of fungal infection: fluconazole can be used.
(7) Nutritional support: after the correction of the disorder of the internal environment and before the recovery of intestinal function, parenteral nutrition can be used as appropriate; once the recovery of intestinal function, enteral nutrition should be carried out at an early stage, and the nasojejunal tube infusion method must be used, and according to the strong condition of intestinal function, the appropriate formula, concentration and speed should be selected, and the amount must be gradually increased, while the tolerance reaction should be closely observed.
(3) Early recognition of fulminant acute pancreatitis and abdominal septal compartment syndrome
In the early stage of regular non-surgical treatment including adequate fluid resuscitation and treatment to remove the cause, while closely observing the changes in organ function, if the organ dysfunction is progressively aggravated, it can be promptly judged as fulminant acute pancreatitis, and it is necessary to strive for early surgical drainage, and the surgical approach should be as simple as possible to overcome the difficulties. If the patient does not have surgical conditions, it is necessary to actively create, including the application of mechanical ventilation to improve the body’s oxygen supply, the application of hemofiltration to correct the crisis of internal environmental disorders, etc.
Intra-abdominal pressure (IAP) increases to a certain level, generally speaking, when IAP ≥ 25 cm H2O (1 cm H O = 0.098 kPa), it will trigger organ dysfunction and abdominal compartment syndrome (ACS) will appear. This syndrome is often an important complication of fulminant acute pancreatitis and one of the causes of death. A simple and practical method to determine intra-abdominal pressure is the transcatheter cystometry method, in which the patient is lying down with the pubic symphysis as the 0 point, and after emptying the bladder, 100 ml of saline is injected into the bladder through the catheter, and the height of the water column at equilibrium is measured as the IAP. the principle of treatment for ACS is to use timely and effective measures to relieve intra-abdominal pressure, including intra-abdominal drainage, retroperitoneal drainage, and intestinal decompression. need to be selected as appropriate.
(4) Treatment of necrotic infections should be referred to surgery
In the course of regular non-surgical treatment, if infection is suspected, a CT scan should be performed, and in case of difficulty in judgment, CT-guided fine-needle aspiration can be performed to determine whether pancreatic necrosis and extra-pancreatic invasion are already infected. For those with clinically significant sepsis syndrome or peritoneal irritation sign, or those with bubble sign on CT, and those who can find bacteria or fungi on smear of fine needle aspiration, they can be judged as necrotic infection and should be referred to surgery immediately. The surgical method is pancreatic infection necrotic tissue removal and small omental cavity drainage plus irrigation, and for those with extra-pancreatic retroperitoneal cavity invasion, the corresponding retroperitoneal necrotic tissue removal and drainage should be done. For those who have biliary tract infection, common bile duct drainage should be added. A jejunostomy is required. If necessary, the incision should be partially open.
2.Treatment of systemic infection
(1) According to the bacterial culture and drug sensitivity test, select sensitive antibiotics.
(2) Combine with clinical signs for dynamic CT monitoring to clarify the site of infection. After the acute inflammatory response period, the body temperature rises again, or the hyperthermia does not decrease, to suspect the appearance of necrotic infection or pancreatic abscess, CT scan should be done. Patients with obvious sepsis syndrome, excluding factors such as ductal infection, and the presence of necrotic lesions or encapsulated fluidic lesions in the pancreas or peripancreatic as seen on CT scan, can make a clinical judgment of necrotic infection or pancreatic abscess without relying on the CT bubble sign, or fine needle aspiration aspirate smear to find bacteria or fungi. Aggressive surgical management of infected lesions is one of the keys to controlling the infection. For necrotic infection, including encapsulated necrotic infection, necrotic tissue removal and drainage is required, and postoperative continuous irrigation and sometimes re-invasive debridement is needed; for pancreatic abscess, surgical drainage or percutaneous puncture drainage can be used, but close attention should be paid to drainage, and if drainage is unsatisfactory, surgical drainage should be performed in a timely manner; for those with extra-pancreatic retroperitoneal cavity invasion, corresponding retroperitoneal necrotic tissue removal and drainage should be performed, or retroperitoneal drainage should be performed via the lumbar side. The patient should be drained. A jejunostomy is required.
(3) Be alert to deep fungal infections and use antifungal drugs such as fluconazole or amphotericin B according to the strain.
(4) Pay attention to the presence of catheter-associated infections.
(5) Continue to strengthen systemic support therapy to maintain organ function and internal environment stability.
(6) Continue jejunal nutritional support while the disease is still in remission; diet restoration must be done gradually after remission.
(7) If a GI fistula develops, appropriate management measures need to be applied according to the type of fistula. A duodenal fistula can be drained by low negative pressure continuous irrigation with a three-lumen tube, which has the possibility of self-healing; a colonic fistula should be treated with a proximal dysfunctional fistula to reduce the infection of the peripancreatic lesion, and a colostomy should be performed at a later stage to return the fistula.
(8) If postoperative bleeding from the wound occurs, it is important to distinguish whether it is vascular bleeding, necrotic infected bleeding, or granulation bleeding. For vascular bleeding, surgical hemostasis is required. Since tissues and blood vessels are often brittle, hemostasis can be achieved by using a small circular needle with 1/2 arc or 4-6 “0” sutures for damaged blood vessels; for necrotic infection bleeding, hemostasis is required while removing necrotic tissues; granulation bleeding does not require surgical treatment. At the same time do a good job of monitoring and correction of coagulation mechanism.
3.Treatment of residual infection period
(1) To clarify the site, scope and adjacent relationship of the infected residual cavity by imaging, and to pay attention to the presence of pancreatic fistula, biliary fistula and gastrointestinal fistula.
(2) Continue intensive systemic support therapy.
(2) Continue to intensify systemic support therapy, strengthen nutritional support and improve nutritional status. If there is upper gastrointestinal insufficiency or duodenal fistula, jejunal nutrition is required.
(3) Promptly drain the residual cavity and treat different gastrointestinal fistulas accordingly.
Principles of treatment of local complications
(1) Acute fluid accumulation: most of it will be absorbed on its own without surgery or puncture, and the absorption can be accelerated by using external application of Chinese herbal medicine, 500 g of skin nitrate in a cotton bag as a large external application on the abdomen, which is changed twice a day.
(2) Pancreatic and peripancreatic tissue necrosis: necrotic infection, necrotic tissue removal plus local irrigation and drainage; in principle, aseptic necrosis is not treated surgically, but those with obvious symptoms and ineffective intensive treatment should be treated surgically; for encapsulated necrotic infection, necrotic tissue removal plus local irrigation and drainage is required.
(3) Acute pancreatic pseudocyst: if the cyst is <6 cm in length and asymptomatic, it should not be treated and should be observed with prevention; if symptoms appear, or if the volume increases or if secondary infection occurs, surgical drainage or percutaneous percutaneous drainage is required, and if the percutaneous drainage is poor, surgical drainage should be performed instead; if the cyst is larger than 6 cm and is not absorbed after 3 months, internal drainage should be performed, and ERCP examination is feasible before surgery to clarify the relationship between the pseudocyst and the main pancreatic duct. The relationship between the pseudocyst and the main pancreatic duct can be clarified. For patients who cannot be observed for 3 months due to the appearance of symptoms or increase in size, when making surgical treatment, it can be decided whether to make internal drainage according to the intraoperative situation; if the cyst wall is mature and there is no infection or necrotic tissue inside the cyst, then internal drainage is feasible; otherwise, external drainage is made.
(4) Pancreatic abscess: If the pancreatic gland and extra-pancreatic invasion area are clinically and CT confirmed to have abscess formation, surgical drainage should be performed immediately, or percutaneous puncture drainage should be performed first, but if the drainage effect is not obvious, surgical drainage should be performed immediately.