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 this guideline, the standardized diagnosis and treatment of acute pancreatitis (AP) has achieved very good results. In recent years, the method of grading the severity of AP, the definition of local-related complications, and the timing and manner of surgical intervention have changed significantly, so it is necessary to add to and revise the Guidelines for the diagnosis and treatment of severe acute pancreatitis to further standardize the process of AP diagnosis and treatment. 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 in accordance with the new classification criteria of AP.
I. Clinical diagnosis of AP
(I) Definition
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) may occur, and may 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 sign) and periumbilical bruising (Cullen 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.
The Balthazar CT rating (Table 1) and the modified CT severity 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.
Table 1
Balthazar CT ratings
Table 2
Modified CT severity index score (MCTSI) criteria
(III) Diagnostic criteria
AP is diagnosed when 2 of the following 3 features are clinically present.
(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 (IEP).
Most patients with AP have diffuse or limited pancreatic enlargement due to inflammatory edema, and CT shows uniform enhancement of pancreatic parenchyma, but the peripancreatic fat gap is blurred, which may be accompanied by peripancreatic fluid accumulation.
2, necrotizing pancreatitis (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, and early enhancement CT may underestimate the extent of pancreatic and peripancreatic necrosis, and enhancement CT 1 week after the onset of disease is more valuable.
(II) Severity grading
1, Mild acute pancreatitis (MAP).
It accounts for the majority of AP, is not associated with organ failure and local or systemic complications, usually recovers within 1 to 2 weeks, and has a very low morbidity and mortality rate.
2. Moderately severe acute pancreatitis (MSAP).
Accompanied by transient (≤48 h) organ dysfunction. The morbidity and mortality rate is low in the early stage, but increases in the later stage if the necrotic tissue is combined with infection.
3, severe acute pancreatitis (severe acute pancreatitis, SAP).
SAP has a high mortality rate in the early stages and a higher mortality rate in the later stages if infection is combined. The diagnostic criteria for organ failure are based on the modified Marshall scoring system, and the presence of organ failure is defined by a score of ≥2 for any organ (Table 3).
Table 3
Modified Marshall scoring system
III. Disease stage
(I) Early stage (acute stage)
Onset to 2 weeks, this period is dominated by SIRS and organ failure, which constitute the first peak of death. The focus of treatment is to strengthen intensive care, stabilize the internal environment and protect organ function.
(II) Middle stage (evolutionary stage)
The onset of the disease is 2 to 4 weeks, with peripancreatic fluid accumulation or necrotic fluid accumulation as the main manifestation. Most of the necrotic foci in this stage are aseptic and may also be combined with infection. The focus of treatment in this stage is the comprehensive prevention and treatment of infection.
(III) Late stage (infection stage)
After 4 weeks of onset, combined infection of the pancreas and peripancreatic necrotic tissue, systemic bacterial infection, deep fungal infection, etc. 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 (MDOS), multiple organ failure (MOF) and abdominal compartment syndrome (ACS). ACS), etc.
(B) Local complications
1, acute peripancreatic fluid collection (APFC).
It occurs early in the course of the disease and manifests as peripancreatic or distal pancreatic interstitial fluid collection, and lacks a complete envelope, and can be single or multiple.
2, acute necrotic collection (ANC).
It occurs early in the course of the disease and shows a mixture of liquid and necrotic tissue accumulation, and the necrotic material includes necrosis of the pancreatic parenchyma or peripancreatic tissue.
3, wrapped-off necrosis (WON).
It is a kind of cystic solid structure containing pancreatic and (or) peripancreatic necrotic tissues and with well-defined inflammatory envelope, mostly occurring 4 weeks after the onset of AP.
4. pancreatic pseudocyst.
There is an accumulation of fluid encapsulated by an intact non-epithelial envelope, and the envelope of the pseudocyst gradually forms 4 weeks after the onset of disease.
Each of the above local complications exists both aseptically and infectiously. Among them, ANC and WON secondary infection is called infected necrosis (infected necrosis).
V. Treatment
(a) Treatment for the cause
1. Biliary-derived 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. MAP patients 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.
AP combined with venous celiac disease or blood triglycerides >11.3 mmol/L can be clearly diagnosed, and triglyceride levels need to be lowered for a short time, as much as possible to below 5.65 mmol/L. Such patients should limit the use of fat emulsions and avoid the application of drugs 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 etiologies.
Hypercalcemic pancreatitis is mostly associated with hyperparathyroidism, which requires calcium-lowering therapy. The anatomical and physiological abnormalities of the pancreas, drugs, pancreatic tumors and other causes should be treated accordingly.
(II) Non-surgical treatment
1.General treatment.
Including fasting, gastrointestinal decompression, pharmacological treatment including antispasmodic, analgesic, protease inhibitors and pancreatic enzyme inhibition therapy, such as growth inhibitors and their analogues.
2, fluid resuscitation and intensive care treatment.
Fluid resuscitation, maintenance of water-electrolyte balance and intensive monitoring therapy are the focus of early treatment. As SIRS causes capillary leak syndrome (CLS), which leads to massive leakage of blood components, resulting in blood volume loss and hematoconcentration. Resuscitation fluid is preferred to lactated Ringer’s solution, and plasma substitute preparations can be used in appropriate amounts for patients requiring rapid resuscitation. The treatment of volume expansion needs to avoid insufficient or excessive fluid resuscitation, which can be guided by dynamic monitoring of central venous pressure (CVP) or pulmonary capillary wedge pressure (PWCP), heart rate, blood pressure, urine volume, erythrocyte specific volume (HCT) and mixed venous oxygen saturation (SvO2), etc.
3. Treatment for maintenance of organ function.
(1) For the treatment of respiratory failure: give nasal catheter or mask oxygen, maintain oxygen saturation above 95%, dynamically monitor the results of blood gas analysis, and apply mechanical ventilation if necessary.
(2) Treatment for 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 can be given hepatoprotective drugs, acute gastric mucosal injury requires the application of proton pump inhibitors or H2 receptor antagonists.
(4) Nutritional support.
Before intestinal function is restored, parenteral nutrition can be used as appropriate; once intestinal function is restored, enteral nutrition should be performed as soon as possible. Adopt nasojejunal tube or nasogastric tube infusion method, pay attention to the formula, temperature, concentration and infusion speed of nutrition preparation, and adjust according to the tolerance situation.
5.Antibiotic application.
Intravenous use of antibiotics to prevent infection is not recommended for patients with AP. For the possible intestinal-derived bacterial translocation in some susceptible groups (such as biliary obstruction, advanced age, immunocompromised, etc.), quinolones, cephalosporins, carbapenems and metronidazole can be chosen for infection prevention.
6.Chinese medicine treatment.
Chinese herbal medicine treatment can be used to promote the recovery of gastrointestinal function and the absorption of pancreatic inflammation, including internal administration, external application or enema of Chinese herbs that regulate and attack the qi.
(C) Treatment of ACS
Patients with MSAP or SAP can be combined with ACS when intra-abdominal pressure (IAP) is >20 mmHg (1 mmHg=0.133 kPa), which is often accompanied by new organ failure and thus becomes an important cause of death in MSAP or SAP. A simple and practical method to determine IAP is transcatheter cystometry, in which the patient is lying down with the pubic symphysis as the 0 point, and after emptying the bladder, 50 ml of saline is injected into the bladder through the catheter, and the height of the water column at equilibrium is measured as IAP. Ultrasound or CT-guided intraperitoneal and retroperitoneal drainage to reduce abdominal pressure. ACS is not recommended as an indication for open surgery in the early stages of AP.
(IV) Surgical treatment
Surgical treatment is mainly aimed at local complications of the pancreas secondary to infection or the production of pressure 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 infected necrosis of the pancreas and peripancreatic.
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. percutaneous catheter drainage (PCD) of pancreatic or peripancreatic infection under ultrasound or CT guidance can be used as a transitional treatment before surgery to relieve toxic symptoms. The results of some studies have shown that early surgical treatment significantly increases the number of operations, postoperative complication rate and morbidity and mortality rate.
2. Surgical modalities for infected necrosis of the pancreas and 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 complex and diverse, and various surgical procedures must follow individualized principles applied individually or in combination.
3. Principles of treatment of local complications.
(1) 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 ultrasound or CT guidance, and further surgical treatment is needed if infection or compression symptoms are not relieved.
(2) WON: aseptic WON, in principle, no surgical treatment, follow-up observation; when infection occurs, PCD or surgical treatment is feasible.
(3) pancreatic pseudocyst: secondary to infection, treatment is the same as WON, no symptoms, no treatment, follow-up observation; if the size of the increase in compression symptoms will require surgical treatment. 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.
In case of intra-abdominal hemorrhage, angiography is preferred to clarify the site of bleeding if the condition is 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.
Gastrointestinal 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.