Guidelines for diagnosis and treatment of severe acute pancreatitis
1. Clinical diagnosis
Acute pancreatitis with organ dysfunction, or local complications such as necrosis, abscess or pseudocyst, or both. The abdominal signs include obvious pressure pain, rebound pain, muscle tension, abdominal distension, and diminished or absent bowel sounds. Abdominal masses may be present, and subcutaneous bruising of the lumbar region (Grey-Turner sign) and periumbilical bruising (Cullen sign) may occasionally be seen. It can be complicated by one or more organ dysfunctions, and can also be associated with severe metabolic dysfunction, including hypocalcemia, with calcium below 1.87 mmol/L (7.5 mg/dl). Enhanced CT is the most effective method to diagnose pancreatic necrosis, and B-ultrasound and laparotomy are helpful for diagnosis. The APACHE II score of severe acute pancreatitis is 8 or more, and the Balthazar CT grading system is grade II or more. In patients with severe acute pancreatitis, those with organ dysfunction despite adequate fluid resuscitation within 72 hours of onset are considered fulminant acute pancreatitis.
2.Severity classification
Severe acute pancreatitis without organ dysfunction is grade I, with organ dysfunction is grade II, where within 72 hours after adequate fluid resuscitation, but still organ dysfunction in patients with grade II severe acute pancreatitis is fulminant
acute pancreatitis.
3. Stage of disease
The whole course of the disease can be 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.
3.1 Acute reaction period: From the onset of the disease to about two weeks, there are often shock, respiratory failure, renal failure, encephalopathy and other major complications.
3.2 Systemic infection period: 2 weeks to 2 months, with systemic bacterial infection, deep fungal infection (later stage) or dual infection as the main clinical manifestations.
3.3 Residual infection period: after 2-3 months, the main clinical manifestations are systemic malnutrition, presence of retroperitoneal or intra-abdominal residual cavity, often with poor drainage, long-lasting sinus tracts, and associated with gastrointestinal fistula.
4.Local complications
4.1 Acute fluid accumulation: It occurs early in the course of pancreatitis and is located in the pancreas or peri-pancreatic area, with no fluid accumulation encapsulated by the cystic wall. It is usually detected by imaging. On imaging, it is an acute fluid accumulation without obvious cystic wall encapsulation. Acute fluid accumulation will mostly resolve on its own, while a few may develop into acute pseudocysts or pancreatic abscesses.
4.2 Pancreatic and peripancreatic tissue necrosis: Diffuse or focal necrosis of the pancreatic parenchyma, accompanied by peripancreatic fat necrosis. Pancreatic necrosis is divided into infected pancreatic necrosis and aseptic pancreatic necrosis according to whether it is infected or not. Enhanced CT is currently the best method to diagnose pancreatic necrosis. After intravenous injection of enhancement agent, the enhancement density of necrotic area does not exceed 50 Hu (the enhancement of normal area is 50-150 Hu).
4.3 Encapsulated necrotic infection, mainly manifested by different degrees of fever, weakness, gastrointestinal dysfunction, catabolic and organ function involvement, mostly without peritoneal irritation signs, sometimes a mass in the upper abdomen or lumbar region can be palpated, some cases have insidious symptoms and signs, and CT scan mainly shows encapsulated low density lesions in the pancreas or peri-pancreas.
4.4 Acute pancreatic pseudocyst: It refers to the accumulation of pancreatic fluid surrounded by fibrous tissue or granulocyst wall after acute pancreatitis. A few pseudocysts in patients with acute pancreatitis can be detected by palpation, and most of them are diagnosed by imaging. They are often round or oval in shape and have clear walls.
4.5 Pancreatic abscess: An encapsulated accumulation of pus around the pancreas in acute pancreatitis with or without pancreatic necrotic tissue. Infection signs are 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, positive bacterial or fungal cultures, with little or no pancreatic necrotic tissue, is a characteristic that distinguishes it from infected necrosis. In most cases, pancreatic abscesses are formed by focal necrotic liquefaction secondary to infection.
5.Treatment
5.1 Selecting the treatment plan according to the stage of the disease
5.1.1 Treatment of acute reaction stage
5.1.1.1 Treatment for etiology
(1) Biliary acute pancreatitis: The first thing to do is to identify the presence of biliary obstruction, and if there is biliary obstruction, it should be removed in time. It can be done either by fibreoptic duodenoscopy with 0ddi sphincter extraction and nasobiliary drainage, or by open surgery, including cholecystectomy and exploration of the common bile duct to determine whether there is obstruction of the lower end of the common bile duct, with additional drainage of the small omental pancreatic area as needed. If there is no biliary obstruction, non-surgical treatment will be performed first, and the disease will be treated later when it is in remission. The cause of biliary origin is sometimes hidden and needs to be identified by close clinical observation, liver function tests and imaging examinations, and ERCP can be done to identify 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: The number of hyperlipidemic acute pancreatitis has increased in recent years, so we must ask about the history of hyperlipidemia, fatty liver and familial hyperlipidemia, and the use of drugs that may elevate lipids, and pay attention to whether the plasma has become celiac during intravenous blood sampling. Triacylglycerol >11.3 mmo1/L is prone to acute pancreatitis and needs to be reduced to below 5.65-6.8 mmol/L within a short period of time. The drugs can be low-dose low molecular heparin and insulin, mainly to increase the activity of lipoproteinase and accelerate the degradation of celiac particles, and rapid lipid-lowering techniques include lipid adsorption and plasma replacement.
(3) Other etiologies: For example, patients with hyperparathyroidism need calcium-lowering therapy or parathyroid tumor removal. For patients with no current treatment, such as those with alcoholic etiology, or those with unknown etiology, treatment should be chosen according to the stage of the disease and observed clinically for occult etiology.
5.1.1.2 Non-surgical treatment
(1) Anti-shock treatment, maintenance of water-electrolyte balance and intensive monitoring treatment. In resuscitation, due to massive peripancreatic and retroperitoneal exudation, blood volume loss and hematoconcentration, and due to the presence of capillary leakage. The CVP or PWCP test should be used as a guide for volume expansion, and the crystalloid ratio should be paid attention to reduce interstitial fluid retention.
(2) Pancreatic rest therapy, such as fasting, gastrointestinal decompression, acid and enzyme suppression therapy.
(3) Prophylactic antibiotic application: mainly for intestinal-derived Gram-negative bacilli translocation, antibiotics that can pass the blood-pancreatic barrier should be used, such as quinolones, ceftazidime, imipenem, metronidazole, etc.
(4) Sedation, antispasmodic and analgesic treatment.
(5) 15 grams of raw Chinese rhubarb should be instilled into the stomach tube or injected into the rectum twice a day. Chinese herbal medicine, dermal nitrate, 500 grams, applied externally to the whole abdomen twice a day.
(6) Prevention of fungal infection, fluconazole can be used.
(7) Nutritional support, before intestinal function is restored, parenteral nutrition can be used as appropriate after the correction of internal environmental disorder.
5.1.1.3 Early recognition of fulminant acute pancreatitis and abdominal septal compartment syndrome
In addition to early fluid resuscitation, regular non-surgical treatment and treatment to remove the cause of the disease, close observation of organ function changes, if organ dysfunction is progressively aggravated, it can be promptly determined as fulminant acute pancreatitis, and it is necessary to create conditions for early surgical drainage, and the surgical approach should be as simple as possible to overcome the difficulties.
Intra-abdominal pressure (IAP) increases to a certain level, generally speaking, when IAP ≥ 25 cmHz0, it will lead to organ dysfunction and Abdominal Compartment Syndrome (ACS). This syndrome is often an important comorbidity of fulminant acute pancreatitis and one of the causes of death. The treatment of ACS is based on timely and effective measures to relieve intra-abdominal pressure, including intraperitoneal drainage, retroperitoneal drainage and intestinal decompression.
5.1.1.4 In case of necrotic infection during treatment, the patient should be referred to surgery. In the course of non-operative treatment, if infection is suspected, CT scan should be performed. If the clinical temperature is ≥ 38°C, WBC ≥ 20×109/L and peritoneal irritation sign is ≥ 2 quadrants, or if bubble sign appears on CT, or if bacteria are found in the aspirate smear of fine needle aspiration, necrotizing infection can be judged. If the patient’s past non-surgical treatment is not reasonable and comprehensive, the treatment should be intensified for 24 hours and surgical treatment should be performed if the disease continues to deteriorate. If there is extra-pancreatic retroperitoneal cavity invasion, the corresponding retroperitoneal necrotic tissue removal and drainage should be performed, or retroperitoneal drainage should be performed through the lumbar side. If there is biliary tract infection, common bile duct drainage should be added. If the necrotic infection is extensive and severe, gastrostomy and jejunostomy should be performed. If necessary, the incision should be partially opened.
5.1.2 Treatment of systemic infection
5.1.2.1 Select sensitive antibiotics such as quinolones, ceftazidime or imipenem that can cross the blood-pancreatic barrier.
5.1.2.2 Perform dynamic CT monitoring with clinical signs to identify the site of infection and perform aggressive surgical treatment on the infected lesion.
5.1.2.3 Be alert to deep fungal infections and use fluconazole or amphotericin B according to the strain.
5.1.2.4 Pay attention to the presence of catheter-associated infections.
5.1.2.5 Continue to strengthen systemic support therapy to maintain organ function and internal environment stability.
5.1.2.6 Nutritional support: use parenteral nutrition for a short period of time until gastrointestinal function is restored; after gastric emptying function is restored and abdominal distension is relieved, discontinue gastrointestinal decompression and gradually start enteral nutrition.
5.1.3 Treatment of retroperitoneal residual infection
5.1.3.1 Define the site, extent and adjacent relationship of the infected residual cavity by imaging, and pay attention to the presence of pancreatic fistula, biliary fistula, and gastrointestinal fistula.
5.1.3.2 Intensify systemic support therapy, strengthen enteral nutrition support, and improve nutritional status.
5.1.3.3 Drainage of the residual cavity should be performed in a timely manner, and different gastrointestinal fistulas should be treated accordingly.
5.2 Principles of treatment of local complications
5.2.1 Acute fluid accumulation
Most of them will be absorbed by themselves without surgery or puncture, and the absorption can be accelerated by external application of Chinese herbal medicine, such as 500 grams of skin nitrate in a cotton bag for a large area of the abdomen, which should be changed twice a day.
5.2.2 Necrosis of the pancreas and peripancreatic tissue
For necrotic infection, if the response is not good after 24 hours of intensive treatment and the general condition continues to deteriorate, surgery is required, which is necrotic tissue removal plus local irrigation and drainage; for aseptic necrosis without clinical symptoms, close observation should be made and no hasty puncture or surgery should be performed; for encapsulated necrotic infection, necrotic tissue removal plus local irrigation and drainage should be performed.
5.2.3 Acute pancreatic pseudocysts
If the cyst is smaller than 6 cm and asymptomatic, it should be left untreated and observed; if symptoms appear or the size increases, percutaneous puncture and drainage can be performed first; if secondary infection occurs, external drainage is required; if the cyst is larger than 6 cm, B ultrasound, CT or MRI examination confirms that there is no infected necrotic tissue mass, percutaneous puncture and drainage can be performed. If the cyst is not absorbed after three months, internal drainage should be performed, and FRCP examination should be performed before surgery to determine the relationship between the pseudocyst and the main pancreatic duct.
5.2.4 Pancreatic abscess
If the pancreatic gland and extra-pancreatic invasion area are clinically and CT confirmed to have abscess formation, immediate surgical drainage should be performed.
5.2.5 Extra-intestinal fistula
Duodenal or jejunal fistulas can be treated with continuous low-pressure negative suction flow through a double-lumen tube, with the possibility of self-healing. For colonic fistula, proximal fistula is recommended to reduce the infection of peripancreatic lesions, and later colostomy is performed to return the fistula.