Clinical diagnosis
I. Severe acute pancreatitis
Acute pancreatitis with organ dysfunction, or those with local complications such as necrosis, abscesses or pseudocysts, 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. There may be abdominal masses and occasionally subcutaneous bruising in the lumbar ribs and subcutaneous bruising around the umbilicus. It can be complicated by one or more organ dysfunction, and can also be accompanied by severe metabolic dysfunction, including hypocalcemia, enhanced CT is the most effective method to diagnose pancreatic necrosis, and B ultrasound and laparotomy are helpful for diagnosis.
Second, fulminant acute pancreatitis
In patients with severe acute pancreatitis, where organ dysfunction still occurs within 72 hours of onset by regular non-surgical treatment, fulminant acute pancreatitis can be diagnosed. Fulminant acute pancreatitis is dangerous, non-surgical treatment is often ineffective, often secondary to abdominal septal compartment syndrome.
Severity grading
Severe acute pancreatitis without organ dysfunction is grade I, and with organ dysfunction is grade II, of which patients with grade II severe acute pancreatitis with organ dysfunction despite adequate fluid resuscitation within 72 hours belong to fulminant acute pancreatitis.
Stage of disease
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 stage: from onset to 2 weeks, there may be complications such as shock, respiratory dysfunction, renal dysfunction and encephalopathy.
2, systemic infection period: 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, the main clinical manifestations are systemic malnutrition, the presence of retroperitoneal or intra-abdominal residual cavity, often poor drainage, long-lasting sinus tracts, accompanied by gastrointestinal fistula.
Local complications
Acute fluid accumulation
Occurs early in the course of pancreatitis and is located in the pancreas or peri-pancreatic, without fluid accumulation encapsulated by a cystic wall. It is usually detected by imaging. On imaging, it is an accumulation of fluid without a distinct cystic wall. Acute fluid accumulations tend to resolve on their own, while a few may develop into acute pseudocysts or pancreatic abscesses.
Necrosis of the pancreas and peripancreatic tissue
This refers to diffuse or focal necrosis of the pancreatic parenchyma, accompanied by peripancreatic fat necrosis. It is further divided into infected pancreatic necrosis and aseptic pancreatic necrosis depending on whether it is infected or not. 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. In encapsulated necrotic infection, clinical manifestations include varying degrees of fever, weakness, gastrointestinal dysfunction, catabolic and organ function involvement, mostly without signs of peritoneal irritation, sometimes a mass in the upper abdomen or lumbar region can be palpated, and CT scan mainly shows encapsulated hypodense lesions in the pancreas or peripancreatic area.
Acute pancreatic pseudocysts
It refers to the accumulation of pancreatic fluid encapsulated 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 the diagnosis is mostly established by imaging. It is often round or oval in shape with a clear cyst wall.
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 a characteristic that distinguishes it from infected necrosis. Pancreatic abscesses are in most cases formed by focal necrotic liquefaction secondary to infection.
Treatment
1. Treatment for etiology.
(1) Cholestatic acute pancreatitis: first of all, we must identify the lesions with metabolic biliary obstruction. Where there is biliary obstruction, it is important to remove the obstruction in a timely manner. The first choice is to perform a trans-fiberoduodenoscopic 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 the lower end of the common bile duct has metabolic obstruction. 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 early 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: There has been a significant increase in recent years, so it is important to ask about a history of hyperlipidemia, fatty liver and familial hyperlipidemia upon admission, as well as whether drugs that may elevate blood lipids are used, and to pay attention to whether plasma has become celiac when phlebotomy is performed. Triacylglycerol >11.3mmol/L is prone to acute pancreatitis and needs to be reduced to below 5.65mmol/L within a short period of time. Such patients should limit the use of fat emulsions and avoid the application of drugs that may elevate 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.
(3) Alcoholic acute pancreatitis: for the possible pathogenic mechanism of alcoholic acute pancreatitis, emphasis is placed on reducing pancreatic fluid secretion, gastric acid secretion, and improving the acidified state of duodenum; strong apoptosis relieves 0ddi sphincter spasm and improves the drainage state of pancreatic fluid.
(4) Other etiologies: For other etiologies that can be found, it is also important to treat the etiology in a timely manner, for example, hypercalcemic acute. Most of the descending pancreatitis is 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, 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 HCT is needed as a guide for volume expansion, and attention should be paid to the crystalloid ratio to reduce interstitial fluid retention in tissues. Changes in urine volume and intra-abdominal pressure should be observed, and attention should be paid to maintaining the body’s oxygen supply and monitoring of visceral function.
(2) Pancreatic rest therapy, such as fasting, gastrointestinal decompression, acid and enzyme suppression therapy.
(3) Prophylactic antibiotic application: mainly for enterogenic gram-negative bacilli translocation, antibiotics that can pass the blood-pancreatic barrier should be used, such as quinolones, ceftazidime, carbapenems and metronidazole.
(4) Sedation, antispasmodic and analgesic treatment.
(5) Chinese herbal medicine raw rhubarb 15g, instillation in the gastric tube or rectal drip, twice a day. Chinese herbal medicine skin nitrate applied externally to the whole abdomen, 500g, twice daily.
(6) Prevention of fungal infection: Fluconazole can be used.
(7) Nutritional support: after the correction of the disorder of the internal environment, before the recovery of intestinal function, parenteral nutrition can be used as appropriate; once the recovery of intestinal function, early enteral nutrition should be carried out, and the nasojejunal tube infusion method must be used, according to the status of intestinal function, choose the appropriate formula, concentration and speed, and be sure to gradually increase the amount, while closely observing the tolerance reaction.
3. Early identification of fulminant acute pancreatitis and abdominal septal compartment syndrome.
In early regular non-operative treatment including adequate fluid resuscitation and removal of etiology treatment, while closely observing changes in organ function, if organ dysfunction is progressively aggravated, the drama can be promptly judged as fulminant acute pancreatitis, the need to strive for early surgical drainage, the surgical approach as simple as possible to tide over 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 critical signs of internal environmental disorders.
4. Those who develop necrotic infection during treatment should be referred to surgical treatment.
In the course of regular non-surgical treatment, if infection is suspected, a CT scan should be performed, and when judgment is difficult, a fine-needle aspiration can be performed under CT guidance to discern whether pancreatic necrosis and extra-pancreatic invasion have been infected. For those who have obvious clinical sepsis syndrome or peritoneal irritation sign, or those who have 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, with extra-pancreatic retroperitoneal cavity invasion, the corresponding retroperitoneal necrotic tissue removal and drainage should be made. For those who have biliary tract infection, common bile duct drainage should be added. A jejunostomy is required. The incision should be partially opened if necessary.
5.Treatment of systemic infection period
(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, if the body temperature rises again or if the hyperthermia does not decrease, the appearance of necrotic infection or pancreatic abscess should be suspected and CT scan should be performed. Patients with obvious sepsis syndrome, excluding factors such as ductal infection, and the presence of necrotic lesions or encapsulated fluid 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 necessary to distinguish between vascular bleeding, necrotic infected bleeding, and granulomatous 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.
6.Treatment of residual infection period
(1) Clarify the site, scope and adjacent relationship of the infected residual cavity by imaging, and pay attention to the presence of pancreatic fistula, biliary fistula and gastrointestinal fistula.
(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 perform residual cavity dilation and drainage, and treat different GI fistulas accordingly.
III. Principles of treatment of local complications
1. Acute fluid accumulation.
Most of them will be absorbed by themselves without surgery or puncture, and the absorption can be accelerated by using external application of Chinese herbal medicine, 500g of skin nitrate in a cotton bag as a large external application on the abdomen, which is changed twice a day.
2. Necrosis of the pancreas and peripancreatic tissue.
For necrotic infection, necrotic tissue removal plus local irrigation and drainage is required; for aseptic necrosis, no surgical treatment is required in principle, but those with obvious symptoms and ineffective strengthening treatment should be treated surgically; for encapsulated necrotic infection, necrotic tissue removal plus local irrigation and drainage is required.
3. Acute pancreatic pseudocysts.
If the cyst is <6cm 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 not good, surgical drainage should be performed instead; if the cyst is >6cm 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. 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 can be performed; 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, it should be established immediately for surgical drainage, or first for percutaneous puncture drainage, but if the drainage effect is not obvious, it should be immediately for surgical drainage.