In the 10th National Symposium on Pancreatic Surgery held in 2004, the additions and revisions of the draft were discussed and renamed as “Guidelines for the diagnosis and treatment of severe acute pancreatitis” in 2006, which was discussed and approved by all members of the Pancreatic Surgery Group of the Chinese Medical Association in November of the same year. In November of the same year, the guidelines were discussed and approved by all members of the Pancreatic Surgery Group of the Chinese Medical Association, and published in 2007.
Since the release of the guidelines, the standardized diagnosis and treatment of acute pancreatitis has achieved very good results. In recent years, there have been significant changes in the method of grading the severity of acute pancreatitis, the definition of local complications, and the timing and manner of surgical interventions, etc. Therefore, it is necessary to update and revise the Guidelines for the diagnosis and treatment of severe acute pancreatitis to further standardize the diagnosis and treatment of acute pancreatitis.
The revised guideline was renamed as “Guidelines for the diagnosis and treatment of acute pancreatitis (2014)”, and the clinical characteristics and treatment of moderately severe and severe acute pancreatitis were discussed according to the new classification criteria of acute pancreatitis.
I. Clinical diagnosis
(I) Definition
Acute pancreatitis (acute pancreatitis, AP) refers to the activation of pancreatic enzymes caused by multiple etiologies, followed by local inflammatory response of the pancreas as the main feature, and in severe cases, systemic inflammatory response syndrome (SIRS) can occur and can be accompanied by organ dysfunction.
(B) Clinical manifestations
The main symptom of AP is an acute onset of persistent severe pain in the upper abdomen, often radiating to the back, often accompanied by abdominal distension and nausea and vomiting. In mild cases, the clinical signs are only light pressure pain, while in severe cases, signs of peritoneal irritation, ascites, and occasionally subcutaneous bruising in the lumbar ribs (Grey-Turner’s sign) and periumbilical bruising (Cullen’s sign) may be seen. A mass may be palpable in the abdomen due to fluid accumulation or pseudocyst formation. It can be complicated by dysfunction of one or more organs, and can also be associated with severe metabolic dysfunction.
Enhanced CT is an effective test for the diagnosis of AP, and Balthazar CT rating (Table 1) and modified CTseverity index (MCTSI) (Table 2) are commonly used to determine the degree of inflammatory response and necrosis. ultrasound and laparotomy are helpful in the diagnosis of AP.
(iii) Diagnostic criteria
The diagnosis is made when 2 of the following 3 features are clinically met.
(1) Abdominal pain compatible with AP;
(2) Serum amylase and/or lipase activity at least 3 times higher than the upper limit of normal;
(3) abdominal imaging consistent with AP imaging changes.
II. AP pathological classification and severity grading
(A) Pathological typing
1, interstitial edematous pancreatitis: Most patients with AP have diffuse/limited pancreatic enlargement due to inflammatory edema, and CT shows uniform enhancement of pancreatic parenchyma, but the peripancreatic fat gap is blurred and may be accompanied by peripancreatic fluid.
2. necrotizing pancreatitis: some patients with AP have pancreatic parenchyma and/or peripancreatic tissue necrosis. The evolution of pancreatic perfusion injury and peripancreatic necrosis takes several days. Early enhancement CT may underestimate the extent of pancreatic and peripancreatic necrosis, and enhancement CT after 1 week of disease onset is more valuable.
(B) Severity grading
1, mild acute pancreatitis ( mild acute pancreatitis, MAP): accounts for the majority of AP, not accompanied by organ failure and local or systemic complications, usually recovering within 1-2 weeks, with a very low mortality rate.
2, moderately severe acute pancreatitis ( moderately severe acute pancreatitis, MSAP): accompanied by transient (<48 h) organ dysfunction. The mortality rate is low in the early stage and increases in the later stage if the necrotic tissue is combined with infection.
3, severe acute pancreatitis (severe acute pancreatitis, SAP): about 5% to lO% of AP, accompanied by continuous (>48 h) organ failure. early SAP mortality rate is high, such as late combined with infection, the mortality rate is higher. The diagnostic criteria of organ failure are based on the modified Marshall scoring system, and the presence of organ failure can be defined by any organ score ≥2.
Stage of disease
(I) Early stage (acute stage)
The onset of the disease to 2 weeks, the main manifestation of SIRS and organ failure in this period, this period constitutes the first peak of death, the focus of treatment is to strengthen intensive care, stabilization of the internal environment and organ function protection treatment.
(II) Middle stage (evolutionary stage)
2 weeks to 4 weeks after the onset of the disease, with peripancreatic fluid accumulation or post-necrotic fluid accumulation as the main manifestation. Most of the necrotic foci in this stage are aseptic and may be co-infected. The focus of treatment in this period is the comprehensive prevention and treatment of infection.
(C) late stage (infection stage)
After 4 weeks of onset, combined infection of the pancreas and peripancreatic necrotic tissue, systemic bacterial infection and deep fungal infection may occur, which may then cause complications such as infectious bleeding and gastrointestinal fistula. This period constitutes the second peak of death in critically ill patients, and the treatment focuses on the control of infection and surgical management of complications.
Systemic and local complications
(I) Systemic complications
Systemic complications can occur during the progression of AP, including SIRS, sepsis, multiple organ dysfunction syndrome (MODS), multiple organ failure (MOF) and abdominal septal compartment syndrome.
(B) Local complications
1, acute peripancreatic fluidcollection ( acute peripancreatic fluidcollection, APFC): occurs early in the course of the disease, manifested as peripancreatic or distal pancreatic interstitial fluid accumulation, and the lack of complete envelope, can be single or multiple.
2, acute necrotic collection ( acute necrotic collection, ANC): occurs in the early stage of the disease, manifested as a mixture of fluid and necrotic tissue accumulation, necrotic material including pancreatic parenchyma or peripancreatic tissue necrosis.
3, walled-off necrosis (WON): a cystic structure containing pancreatic and (or) peripancreatic necrotic tissue with clearly defined inflammatory envelope, mostly occurring 4 weeks after the onset of AP.
4. pancreatic pseudocyst: a fluid accumulation with an intact non-epithelial envelope, and the envelope of the pseudocyst gradually forms 4 weeks after the onset of the disease.
Each of the above local complications exists in both aseptic and infectious conditions. Among them, ANC and WON secondary infection is called infectious necrosis.
V. Treatment
(A) Treatment for the cause
1, biliary source acute pancreatitis: gallstone disease is currently the main causative factor of acute pancreatitis in China. Anyone with biliary stone obstruction needs to be promptly relieved of the obstruction, and the treatment modalities include transendoscopic or surgical treatment. Patients with mild acute pancreatitis with gallbladder stones should undergo cholecystectomy as soon as possible after disease control; while patients with necrotizing pancreatitis can be treated together with necrotic tissue removal at a later stage or elective treatment after disease control.
2, hyperlipidemic acute pancreatitis: acute pancreatitis and venous celiac blood or blood triglycerides > 11, 3 mmol/L can be clearly diagnosed, need to reduce triglyceride levels for a short time, as far as possible to 5, 65 mmol/L or less. These patients should limit the use of fat emulsions and avoid medications that may elevate lipids. Treatment can be low-dose low molecular heparin and insulin, or lipid adsorption and plasma replacement for rapid lipid lowering.
3, other causes: hypercalcemic pancreatitis is mostly related to hyperparathyroidism, which requires calcium-lowering therapy. The anatomical and physiological abnormalities of the pancreas, drugs, pancreatic tumors and other causes should be treated accordingly.
(B) Non-surgical treatment
1, general treatment: including fasting, gastrointestinal decompression, drug therapy including antispasmodic, analgesic, acid suppression and pancreatic enzyme inhibition therapy, such as growth inhibitors and their analogues or protease inhibitors.
2, fluid resuscitation and intensive care treatment: fluid resuscitation, maintenance of water-electrolyte balance and strengthening of monitoring treatment are the focus of early treatment, as SIRS causes capillary leak syndrome (CLS), resulting in massive leakage of blood components, resulting in blood volume loss and hematoconcentration.
Resuscitation fluid is preferred to lactated Ringer’s solution, and plasma substitute can be used in appropriate amounts for patients who need rapid resuscitation. Volume expansion therapy needs to avoid insufficient or excessive fluid resuscitation, which can be guided by dynamic monitoring of central venous pressure or pulmonary capillary wedge pressure, heart rate, blood pressure, urine volume, erythrocyte volume and mixed venous oxygen saturation.
3. Maintenance treatment of organ function.
(1) For the treatment of respiratory failure: give nasal catheter or face mask oxygen, maintain oxygen saturation above 95%, dynamically monitor blood gas analysis results, and apply mechanical ventilation if necessary.
(2) Treatment of acute renal failure: early prevention of acute renal failure is mainly volume resuscitation and other supportive therapy to stabilize hemodynamics; treatment of acute renal failure is mainly continuous renal replacement therapy (CRRT).
(3) support of other organ functions: liver function abnormalities such as the presence of liver-protective drugs, acute gastric mucosal injury requires the application of proton pump inhibitors or H2 receptor antagonists.
4) Nutritional support: 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 as soon as possible. Use nasojejunal tube or nasogastric tube infusion method, pay attention to the formula, temperature, concentration and infusion speed of nutritional preparation, and adjust according to the tolerance situation.
5.Antibiotic application: Intravenous antibiotics are not recommended for AP patients to prevent infection. For some susceptible people (such as biliary obstruction, advanced age, immunocompromised, etc.) may occur intestinal-derived bacterial translocation, quinolones, cephalosporins, carbapenems and metronidazole can be selected for infection prevention treatment.
6, Chinese medicine treatment: Chinese medicine treatment can be used to promote the recovery of gastrointestinal function and the absorption of pancreatic inflammation, including the internal administration of Chinese medicine, external application or enema for the management of Qi attack.
(C) Treatment of abdominal septal compartment syndrome
MSAP or SAP patients are often combined with abdominal compartment syndrome (ACS), when intra-abdominal pressure (IAP) >20 mmHg is often accompanied by new organ failure, thus becoming one of the important causes of death in MSAP or SAP. After emptying the bladder, 50 ml of saline is added to the bladder through the catheter, and the height of the water column at equilibrium is measured as IAP.
The principle of treatment for ACS is to relieve intra-abdominal pressure with timely and effective measures, including gastrointestinal decompression and catheterization, analgesia and sedation, use of inotropes and bedside hemofiltration to reduce tissue edema, and ultrasound or CT-guided intra-abdominal and retroperitoneal drainage to reduce abdominal pressure. ACS is not recommended as an indication for open surgery in early AP.
(IV) Surgical treatment
Surgical treatment is mainly aimed at local complications of the pancreas secondary to infection or producing compression symptoms, such as gastrointestinal obstruction and biliary obstruction, as well as other complications such as pancreatic fistula, gastrointestinal fistula and ruptured bleeding pseudoaneurysm. Asymptomatic aseptic necrotic effusion of the pancreas and peri-pancreatic does not require surgical treatment.
1. Indications and timing of surgery for pancreatic/peripancreatic infected necrosis.
Those with clinical sepsis, bubble sign on CT examination, fine needle aspiration aspirate smear or culture to find bacteria or fungi can be diagnosed as infected necrosis and need to consider surgical treatment. Surgical treatment should follow the principle of postponement. Once the necrotic infection is judged, targeted antibiotic treatment can be performed immediately, and the efficacy of anti-infection can be closely observed, and surgery can be postponed in stable cases.
Ultrasound or CT-guided percutaneous catheter drainage (PCD) drains the pus from the pancreatic/peripancreatic infection and relieves toxic symptoms, and can be used as a transitional treatment before surgery. Studies have shown that early surgical treatment significantly increases the number of operations, the incidence of postoperative complications and the morbidity and mortality rate.
2. Surgical modalities for infected necrosis of the pancreas/peripancreatic.
Surgical modalities for infected necrosis of the pancreas can be divided into PCD, endoscopic, minimally invasive surgery and open surgery. Minimally invasive surgery mainly includes small incision surgery, video-assisted surgery (laparoscopy, nephroscopy, etc.). Open surgery includes transabdominal or retroperitoneal route of pancreatic necrotic tissue removal and duct drainage.
For patients with biliary stones, additional cholecystectomy or choledochotomy for stone extraction may be considered, and intraoperative placement of jejunal nutrition tube is recommended. Infected necrosis of the pancreas is a complex and diverse condition, and various surgical procedures must be applied individually or in combination.
3. Principles of treatment of local complications.
APFC and ANC: asymptomatic people do not need surgical treatment. Those with obvious symptoms, gastrointestinal compression symptoms, affecting enteral nutrition or feeding, or secondary infection, can be treated with PCD under the guidance of ultrasound or CT, and further surgical treatment is required if the infection or compression symptoms are not relieved.
WON: Aseptic WON, in principle, is not treated surgically, and is observed on follow-up visits. In case of infection, PCD or surgical treatment is feasible. Pancreatic pseudocyst: secondary to infection, treatment is the same as WON, no symptoms, no treatment, follow-up observation; if the volume increases and pressure symptoms appear, surgical treatment is required. Surgical treatment is based on internal drainage surgery, and internal drainage surgery can be performed under laparoscopy or open surgery.
4. Treatment of other complications.
Pancreatic fistula is mostly caused by inflammation, necrosis and infection of the pancreas leading to rupture of the pancreatic duct. The treatment of pancreatic fistula includes patulous drainage and suppression of pancreatic secretion as well as endoscopic and surgical treatment. In the case of abdominal hemorrhage, angiography is preferred to identify the site of bleeding if available, and embolization is performed if the bleeding is arterial (pseudoaneurysm). If the bleeding site is not clear or embolization fails, active surgical hemostasis or tamponade can be considered. Monitor and correct the coagulation mechanism at the same time.
GI fistulas can originate from the AP itself, but may also be related to surgical manipulation, with colonic fistulas being the most common. Treatment is based on the same principles as for enterocutaneous fistulas and includes patency drainage and stoma diversion surgery.