#千IP创科学普# Things about acute pancreatitis

#千IP创科学普# Things about acute pancreatitis

The pancreas is located in the upper abdomen, behind the stomach, and is an important secretory organ in the human body. In addition to secreting insulin to regulate blood sugar levels, the pancreas can also secrete a variety of digestive enzymes , especially trypsin, which plays an important role in protein digestion.

What is pancreatitis?

Pancreatic tissue damage is caused by various reasons, resulting in the premature activation of various enzymes originally used to digest food. Instead of digesting food, the pancreas itself is digested . This "self-destructive" behavior causes a series of consequences, namely pancreatitis. Many patients with acute pancreatitis are hospitalized for repeated attacks, so they are also "old acquaintances" of the gastroenterology department. Most patients have mild acute pancreatitis. After appropriate fluid replacement, analgesia, anti-vomiting, and oral feeding as soon as possible, the symptoms can be quickly improved. However, 20% to 30% of patients still have severe acute pancreatitis, which is a fatal disease with an in-hospital mortality rate of about 15%.

What are the typical symptoms of pancreatitis?

(1) Acute pancreatitis: ① Abdominal pain , mainly in the upper abdomen, which occurs suddenly and feels like a knife cutting; ② Fever ; ③ Nausea and vomiting ; ④ Sometimes symptoms such as yellowing of the skin and itching may occur.

(2) Severe acute pancreatitis (SAP): In addition to the above symptoms, there may also be clinical manifestations such as shock, dyspnea, central nervous system symptoms, gastrointestinal bleeding, and DIC .

What is the pathogenesis of SAP?

Its pathogenesis is similar to that of sepsis, in which cytokines play a key role. They mediate systemic inflammatory responses. Once out of control, they are amplified step by step into a cascade reaction, leading to MODS . Another point that we all need to pay attention to is the aggravation mechanism of SAP in the later stage, that is, the second blow. SAP causes pancreatic self-digestion and shock in the early stage; the complex aggravation mechanism is pancreatic necrosis followed by systemic sepsis, bidirectional preexcitation, and cascade reactions, which lead to the emergence of multiple complications such as SIRS MODS and MOF.

How should severe acute pancreatitis be treated?

As society develops and the times progress, the treatment of pancreatitis has also experienced a step-by-step development stage, from early surgery to the current multidisciplinary comprehensive treatment with non-surgical treatment as the main treatment and surgical treatment as the auxiliary treatment. The international consensus guidelines for the management of severe acute pancreatitis published in the World Journal of Emergency Surgery in June 2019 proposed that due to the large amount of peripancreatic and retroperitoneal exudation, blood volume loss and hemoconcentration are caused, and due to the existence of capillary leakage, it is necessary to use dynamic monitoring of CVP or PWCP and HCT as a guide to expand the volume, and pay attention to the crystalloid colloid ratio to reduce interstitial fluid retention . Attention should be paid to changes in urine volume and intra-abdominal pressure, while paying attention to maintaining the body's oxygen supply and visceral function monitoring. Supportive treatment, especially preventing hypoxemia and ensuring adequate rehydration, is the key to the treatment of patients with acute pancreatitis. The second aspect is to give the pancreas adequate rest through fasting, gastrointestinal decompression, acid suppression, etc. The prophylactic use of antibiotics in patients with acute pancreatitis cannot reduce mortality or improve the condition, so routine prophylactic use of antibiotics is not recommended for all patients with acute pancreatitis. It is recommended to perform an enhanced CT scan within 3 days of the disease course to determine the area of ​​pancreatic necrosis and whether there are concurrent gallstones as early as possible. If the area of ​​pancreatic necrosis is ≥30% or biliary pancreatitis occurs, preventive antibiotic intervention should be given immediately. The best time to prevent antibiotics is within 1-3 weeks of SAP onset. It is reasonable to use antibiotics for 10-14 days. Generally, it should not exceed 21 days.

What types of antibiotics are available?

Urea penicillins and third-generation cephalosporins are effective against gram-negative bacteria. Piperacillin-tazobactam is effective against gram-positive bacteria and anaerobes. Quinolones (ciprofloxacin and moxifloxacin) and carbapenems have shown good pancreatic penetration and can cover anaerobic bacteria.

Nutritional support therapy for severe pancreatitis

Nutritional support for SAP runs through the entire course of the disease. In the 1980s, it was one month after the onset of SAP. In the mid-to-late 1990s, it was gradually advanced to 2 weeks after the patient was admitted to the hospital. Recently, it was proposed to start 5-7 days after the patient was admitted to the hospital, or even as early as 2-3 days after admission. SAP patients need nutritional support, which should be carried out under the premise that their vital signs, hemodynamics and internal environment are stable. Once gastrointestinal function is restored, enteral nutrition ( EN ) should be given in time, and every effort should be made to establish an EN pathway. Although there is no difference between EN and parenteral nutrition (PN) in mortality and pain scores, it can improve prognosis and reduce the incidence of infection-related complications and treatment costs.

It is well known that nutrition delivered through the stomach and duodenum can significantly increase the secretion of pancreatic juice, but nutrition infusion into the jejunum does not increase the secretion of pancreatic juice. Enteral nutrition (TPN) has many adverse effects (such as damage to the intestinal mucosal barrier leading to infection, etc.), and enteral nutrition is increasingly valued. Studies have shown that in the acute phase of pancreatitis, placing a jejunal nutrition tube under the guidance of an endoscope below the Treitz ligament and infusing enteral nutrition can effectively overcome gastroduodenal motility disorders caused by pancreatic inflammation and necrosis. Within 48 hours after the onset of the disease, enteral nutrition can be infused through a nasojejunal tube, and patients can also tolerate it well, and no adverse clinical reactions have been found compared with TPN. Early enteral nutrition significantly reduces complications such as infection. Whether in terms of effectiveness, patient tolerance, clinical outcomes, and costs, it is suggested that the jejunal route of enteral nutrition is more conducive to severe acute pancreatitis.


Difficulties in nutritional support for severe acute pancreatitis

Early nutritional support is very important, but the heart and lung functions often cannot tolerate a large amount of fluid load. At the same time, due to glucose metabolism disorders and insulin resistance, nutritional support can only be based on the principle of providing necessary nutritional substrates and not increasing organ load. It is impossible to insist on sufficient calories in the early stage. There is a consensus on advocating early enteral nutrition, but SAP is often accompanied by gastric and duodenal dysfunction in the early stage, making it difficult to implement and the timing of implementation is still controversial.

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