The incidence of infectious complications after pancreatic diseases and their surgical procedures has a tendency to increase, so it should attract the surgeons’ high attention. I. Etiology The occurrence of infection is the result of an imbalance between the number of pathogens, virulence and the immunity of the body. 1, the pathogenic factors of pathogenic bacteria Experimental studies have shown that, in addition to the more virulent Streptococcus haemolyticus, when the number of germs per 1 gram of tissue reaches 100,000 (105/g), is the number of germs necessary for wound infection or the spread of infection. However, when there is local necrotic tissue, hematoma or foreign body, the ability to resist infection is greatly weakened and infection can occur when there are 100 (102/g) pathogens per 1 gram of tissue. The average number of germs per gram of tissue in a contaminated open wound can reach 100,000 (105/g) after 6 hours of injury. This concept of the number of germs in the tissue at the time of infection has important implications for surgical management. To prevent postoperative infections, clinicians must emphasize: early debridement of wounds; flushing with large amounts of fluid in case of peritonitis or abdominal contamination; laminar flow filtration devices for operating room air; and aseptic operation during surgery, all with the aim of reducing the number of contaminating pathogens. The pathogenic effect of germs is related to the virulence of germs or toxins such as extracellular enzymes, exotoxins, endotoxins, etc. In addition, pathogens have adhesion factors that attach to tissue cells in the body; podocytes or micro-podocytes resist phagocytosis or bactericidal components. Fungi can be phagocytosed by phagocytes can be multiplied in the cell, resulting in tissue cell lesions. 2, the human body is vulnerable to infection factors (1) local conditions: human skin or mucous membrane injury, such as surgical trauma, preoperative puncture, etc.; pipe obstruction; local tissue blood circulation disorders, tissue loss of antibacterial and repair capabilities, can be secondary to infection. Pre-existing lesions of the skin or mucosa such as ringworm and oral ulcers can also be secondary to infection. The pancreatic head and duodenum resection involves many tissues and organs, the surgical trauma is large, and the standardized radical pancreatic head cancer surgery often requires extensive lymphatic and retroperitoneal contouring, and there are different degrees of exudation in the postoperative surgical field, so it is necessary to place drains in appropriate areas and keep the drains open to drain the exudate in a timely manner. However, some areas often fail to be adequately drained, which, together with the possible existence of different degrees of bile-intestinal anastomosis and pancreatic-intestinal anastomotic leak, leads to accumulation of fluid in the abdominal cavity, which may lead to secondary infection and subsequent formation of abdominal abscess. The incidence of intra-abdominal abscesses after pancreatic head duodenectomy is reported in the literature to be about 4% to 10%. Poor drainage of the abdominal drainage tube after pancreatic surgery can lead to the occurrence of intra-abdominal infection and even the formation of abdominal abscesses. (2) Reduced systemic resistance to infection, such as: ① Severe injury, shock, diabetes, uremia, hepatic insufficiency, etc. (② In the process of treating other co-morbidities, the massive use of hormones or immunosuppressants, anticancer chemotherapy and radiation therapy can increase the chance of intra-abdominal infection. ③Severe malnutrition, hypoproteinemia, leukemia or low white blood cell count, etc. ④AIDS. (⑤Irrational use of high-dose broad-spectrum antibacterial drugs increases the chance of secondary infection and can also increase the incidence of abdominal cavity infection. (3) Potential infection pathways: ①Intravenous catheter infection: postoperative patients with pancreatitis or pancreatic cancer are often left with central venous placement due to long fasting time and need for intravenous nutritional support, and if the intravenous catheter is carelessly or left for too long, intravenous catheter-derived infection is very likely to occur. (2) Enteric-derived infection: the intestine is the largest reservoir of bacteria and endotoxin in the human body. In patients with pancreatitis or pancreatic cancer, fasting and parenteral nutrition support are often required, and when the intestinal mucosal barrier function is impaired or failed, intestinal pathogens and endotoxins can be translocated (bacterial translocation) and lead to intestinal-derived infection. 3, the role of inflammatory mediators and cytokines systemic surgical infections are often germs, mycotoxins and their mediated damage to the body of a variety of inflammatory mediators and cytokines. Bacterial toxins can stimulate the body to produce a variety of inflammatory mediators, such as tumor necrosis factor (TNF), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8) and oxygen free radicals, nitric oxide, etc.. The right amount of inflammatory mediators can play a defensive role, but in excess can cause tissue damage. If the infection is not controlled in time, the release of inflammatory mediators and cytokines can be mediated by each other, resulting in a cascade or network reaction, leading to a systemic inflammatory response syndrome, which in severe cases can lead to infectious shock and multi-organ insufficiency (dysfunction) syndrome. Clinical manifestations and diagnosis Pancreatic diseases and their post-surgical infections can be divided into local and systemic infections according to the site of occurrence, and into bacterial and fungal infections according to pathogenesis. The most common one is localized bacterial infection in the postoperative abdominal cavity. The clinical types include peritonitis, abdominal abscess and pancreatic abscess, which are not described here. Systemic surgical infections occurring after pancreatic diseases and their surgical procedures are serious and have a high morbidity and mortality rate. Systemic infections include sepsis and bacteraemia. Bacteremia differs from the previous concept of transient bacteraemia, which now mostly refers to bacteraemia with clinically significant signs of infection and is a type of sepsis with positive blood cultures. Sepsis is a collective term for surgical infections with manifestations of systemic inflammatory response (marked changes in body temperature, circulation, and respiration). Sepsis has an acute onset, is severe and develops rapidly. It often manifests as follows: 1, sudden chills, high fever, body temperature 40-41℃ or low temperature; 2, headache, dizziness, nausea, vomiting, abdominal distension, pale or flushed face, cold sweat, indifference or irritability, delirium and coma; 3, rapid heart rate, rapid pulse, rapid or difficult breathing; 4, liver and spleen may be enlarged, jaundice or subcutaneous bleeding petechiae in severe cases; 5, infectious shock or MODS, MOF. 6, laboratory tests: leukocyte elevation 20 Laboratory tests: elevated white blood cells 20-30×109/L or decreased, nuclear left shift, increased naive type, toxic particles; acidosis, azotemia, hemolysis, protein in urine, leukocytes, ketone bodies, etc.; blood culture + drug sensitivity before chills and fever, pus culture + drug sensitivity, because the culture is often negative after antibiotic treatment, so should emphasize the need to do multiple blood cultures; multiple culture is still negative, anaerobic culture should be done. or for urine and blood fungal examination and culture. Common clinical types of systemic infections: 1. Gram-positive bacterial sepsis There are three common pathogenic bacteria: (1) Staphylococcus aureus (S. aureus): multi-drug resistant strains have emerged, such as β-lactam-resistant, aminoglycosides, etc., have a tendency to disseminate blood, and can form metastatic abscesses in the body. Some local infections can also cause high fever, rash, and even shock. (2) Staphylococcus epidermidis (Staphylococcus epidermidis): It is one of the normal flora settled on human skin and mucous membrane, which was considered non-pathogenic in the past, but the infection has increased significantly in recent years. Easy to adhere to medical plastic products, bacteria embedded in the mucus can escape the body’s defense and antibiotic effect. (3) enterococci: is the intestinal resident bacteria, can participate in multi-bacterial infection, some enterococcal sepsis is not easy to find the primary focus. Toxins produced by Staphylococcus aureus can cause peripheral vasodilation and decreased resistance. May or may not have chills, high fever in the form of retention fever or chill fever, flushed face, warm, dry extremities, much delirium and coma. There is often a rash, diarrhea, vomiting, metastatic abscesses, and myocarditis. Shock occurs late and blood pressure falls slowly. G. cepacia produces only -toxin, an N-terminal formylated -helix polypeptide, which causes erythrocyte lysis and participates in the formation of an inflammatory polypeptide complex in G. cepacia, thereby regulating cytokines and promoting cell differentiation. Most infections caused by D. epimedium are preceded by biofilm formation, which is closely related to foreign body implantation. The mucus layer of the biofilm is composed mainly of lipoproteins and lipopolysaccharides, which will absorb the positively charged amino side chains, thus forming a natural barrier that prevents hydrophilic antibiotics from penetrating into the organism to exert their bactericidal effect. Infections caused by P. aeruginosa are mostly intra-hospital infections and are often associated with foreign body implantation in addition to autoimmune deficiencies. The main route of invasion is through the injured skin (e.g. trauma, surgical wounds, etc.). The clinical presentation lacks characterization and most of them develop in the context of an underlying disease. In patients with fever, especially irregular fever, retention fever and flaccid fever due to skin or respiratory infections, blood cultures should be performed and the diagnosis can be confirmed by the presence of S. epimedium growth. G. oxysporum produces more than 80% of β-lactamase, so the resistance rate to penicillin and enzyme-intolerant penicillins and erythromycin is high, but the resistance to vancomycin is less. The mechanism of resistance to β-lactam antibiotics in Gluconobacter cepacia are: ① Inactivation of antibiotics by β-lactamase; ② Action target penicillin binding protein, change and inherent resistance, which can be produced by the mecA gene encoded on the chromosome of Gluconobacter cepacia; ③ Tolerance to the bactericidal effect of β-lactam antibiotics, as shown by the bacteria are not resistant to β-lactam antibiotics, but still not killed, the reason may be related to its The reason may be related to its lack of autolysis enzymes. Blood culture is an important basis for the diagnosis of S. cepacia sepsis. However, because of the potential for contamination at all stages from blood collection to culture, multiple cultures are generally necessary. If blood is collected from multiple venous sites, the diagnosis can be made only if the bacteria cultured are the same and combined with the clinical situation. 2, gram-negative bacillus sepsis currently has more than gram-positive cocci, common for Escherichia coli, anthropoid bacteria, Pseudomonas aeruginosa, Proteus, followed by Klebsiella, Enterobacter, etc., is the resident bacteria in the intestine, necrotic tissue to facilitate its growth, mainly endotoxin production. Some antibiotics can kill bacteria, but they are powerless against endotoxin and its mediated inflammatory mediators, therefore, the sepsis caused by them is more serious, often manifested as “three low and one more” phenomenon: low body temperature, low white blood cells, low blood pressure, and more infectious shock. The toxins produced by E. coli, P. aeruginosa and P. aeruginosa can cause peripheral vasoconstriction, increased permeability, microcirculatory stagnation and microthrombosis, resulting in cellular ischemia and hypoxia. The manifestations are sudden chills, intermittent fever, in severe cases the body temperature does not rise or is below normal, the extremities are cold, cyanosis, little or no urine. The increase of white blood cells is not obvious or even reduced, and shock appears early and lasts long. 3, fungal sepsis Deep fungal infection is a very difficult problem in the treatment of acute pancreatitis, and it is reported in the literature that deep fungal infection is increasing year by year and is one of the main causes of death in the late stage of pancreatitis. Therefore, attention should be paid to the prevention and treatment of deep fungal infections. According to the relevant research, deep fungal infections are mainly caused by pathogenic fungi of intestinal origin, of which Candida spp. account for more than 90%, and the rest are mainly Trichoderma spp. and Cryptococcus spp. In the Candida spectrum, Candida albicans accounts for more than half, and non-Candida albicans is Candida tropicalis, Candida subsmoothis, Candida smoothis, as well as Candida gory, Candida stellaris, Candida pseudo-tropica and Candida keru, in order of conditioned infection. There has been an increasing trend of non-Candida albicans infections in the last decade. Commonly found in: ① in the continuous application of antibiotics (especially broad-spectrum antibiotics), fungal overgrowth caused by secondary infection; ② heavy underlying disease, and the application of immunosuppressive drugs, hormones, etc.; ③ long-term indwelling intravenous catheter, the fungus can be disseminated through the bloodstream, general blood culture is not easy to find, can form granulomas or necrotic foci in multiple organs, especially Aspergillus, Trichoderma has hemophilic, easy to cause vascular embolism, tissue progressive necrosis. Deep fungal infection is often secondary to bacterial infection, or mixed with bacterial infection, not easy to distinguish, easy to miss, misdiagnosis. Clinical manifestations are similar to gram-negative bacillary sepsis: sudden chills and high fever, 39.5 to 40℃. The disease may deteriorate rapidly with apathy, drowsiness, decreased blood pressure, and shock. A few have gastrointestinal bleeding. The peripheral blood picture may show a leukemia-like reaction, with late and intermediate granulocytes and a leukocyte count of up to 25×109/L. The definitive diagnosis of deep fungal infection is extremely difficult due to its insidious onset and lack of characteristic clinical manifestations, as well as the fact that definitive diagnosis must rely on biopsy and fungal search from the diseased tissue. If treatment is carried out after definitive diagnosis, most patients will not survive due to loss of time for resuscitation. Therefore, clinicians should make a preliminary clinical diagnosis based on the diagnostic clues, combined with the pathogenetic examination of body fluids. For respiratory and urinary tract infections that may be combined after surgery, it is sufficient to refer to the prevention and treatment measures for respiratory and urinary tract infections after other major surgeries. It is worth mentioning that some patients with pancreatic cancer, especially those of advanced age, severe obstructive jaundice and malnutrition, are prone to chronic hepatic insufficiency after pancreatic head and duodenum resection, manifesting as unremitting or deepening jaundice, abdominal distention, ascites, delayed recovery of gastrointestinal function and bleeding from stress ulcers. The immunity of these patients is extremely low, and they are prone to intra-abdominal and systemic infections, which can be complicated by long-term fasting, application of broad-spectrum antibiotics, etc., resulting in dysbiosis and fungal infections. Effective hepatic function support and nutritional support, selection of antibiotics based on pathogenesis and drug sensitivity tests, and combined application of antifungal drugs are required along with the management of intra-abdominal infectious foci. Treatment of sepsis is divided into empirical dosing and selection of targeted antibiotics based on bacterial culture and drug sensitivity testing. Patients suspected of fungal infection should be treated immediately empirically, and only then can the cure rate be improved. Since the disease is mostly infected by Candida spp. and predominantly by Candida albicans, fluconazole can often cover it, therefore, the first-line antifungal drug is fluconazole; the second-line antifungal drug is amphotericin B. The indications for treatment with amphotericin B are: (1) evidence of hematogenous infection and hemodynamic instability; (2) non-Candida albicans infections: because Candida klebsiella is naturally resistant to fluconazole Candida tropicalis is partially resistant to fluconazole; (3) Trichophyton infection; (4) Those who are ineffective with fluconazole therapy should be switched to amphotericin therapy. The side effects of amphotericin B are mainly fever, which is countered by the addition of hydrocortisone, in addition to hypokalemia and rising blood creatinine, which should be closely observed and corrected promptly. While antifungal treatment, removal of the lesion is crucial. Once deep fungal infection is suspected, all indwelling catheters should be removed or replaced, and the pancreatic abscess should be surgically drained or the necrotic infected foci removed. If there is conclusive evidence of simple fungal infection, antibiotics should be discontinued. In addition, nutrition should be strengthened and cellular immune therapy should be enhanced. For those with mixed fungal and bacterial infections, effective antibiotic therapy should be applied in combination, usually early, adequate and combined application of antibiotics according to the primary foci of infection first, and then timely adjustment of antibiotics according to bacterial culture and drug sensitivity test results. 2, local treatment Strictly follow the basic principles of surgery, strengthen the aseptic operation, fully flush the surgical field and reasonably place the abdominal drainage tube is an effective measure to prevent postoperative abdominal cavity infection. Therefore, the smooth drainage of postoperative abdominal drains and the reasonable use of antibacterial drugs are effective measures for the prevention of postoperative abdominal infection. Abscess puncture and drainage can be performed under ultrasound guidance for those who have already developed abdominal infection, and in a few cases, multiple drainage procedures are required. Local residual abscesses can be located according to abdominal CT or local imaging and surgical drainage can be done as early as possible. Removal of necrotic tissue and foreign bodies, elimination of dead space, drainage of abscess, etc. Special attention should be paid to potential sources and routes of infection, e.g. in case of intravenous catheter infection, the first measure is to remove the catheter. In case of intestinal origin infection, shock should be corrected, intestinal mucosal perfusion should be restored, early enteral nutrition should be done to promote intestinal mucosal repair, and oral intestinal ecological preparations should be given to maintain normal flora, etc.