Septic Complications In Acute Pancreatitis Research Articles

The use of ridge regression for estimating the severity of acute pancreatitis

Purpose. Increasing of treatment efficiency for patients with acute pancreatitis by improving objective means of determining the severity of acute pancreatitis.Materials and method. The study was based on a retrospective analysis of 130 cases of acute pancreatitis: 47 cases from «Krasnoyarsk Regional Clinical Hospital» and 83 cases from «Regional Interdistrict Clinical Hospital No 20 named after I.S. Berzon» in the period from 2015 to 2017. The raw data was pre-processed. In particular, different methods (median, linear regression) were used to fill the missing values in the observation matrix. The initial dataset contained features measured in various quantitative and categorical scales. For some features with a pronounced asymmetric distribution, a quantile transformation was applied to initial values. The quantile transformation allows features to be brought to a uniform distribution in order to reduce the risk of excluding significant features. Ridge regression was used in combination with an algorithm for sequential reduction of attribute space.Results. The classifier of three degrees of acute pancreatitis severity was developed. This classifier can help to determine better treatment tactics. During validation, the method of determining the severity of acute pancreatitis classification has proven to be effective. The average accuracy was 92% compared to the experts’ decisions. This procedure for constructing a classifier can be used as part of the basis to the medical decision support system.Conclusion. The results of this study will help to make the choice of a necessary starting therapy, assess the need for surgical intervention and in severe cases, prescribe enhanced antibacterial and detoxification therapy. This will predictably reduce the percentage of septic complications of acute pancreatitis, and consequently will reduce the frequency of fatal outcomes.

Tumor necrosis factor–α and interleukin-10 contribute to immunoparalysis in patients with acute pancreatitis

Immunoparalysis, defined as downregulation of human leukocyte antigen–DR (HLA-DR) expression on monocytes, is strongly associated with septic complications of acute pancreatitis. However, the possible causes of this immunoparalysis have been largely unknown. A prospective case control study was performed in 54 patients with acute pancreatitis and 24 normal volunteers. HLA-DR expression on monocytes and serum cytokine levels were measured. In addition, monocytes from normal volunteers treated with tumor necrosis factor (TNF)–α in vitro were evaluated for HLA-DR expression and cytokine release. HLA-DR expression was significantly lower in patients with severe pancreatitis than in those with mild acute pancreatitis and healthy volunteers (42.28% ± 11.49% vs. 86.85% ± 14.56% vs. 93.92% ± 7.40%, p < 0.0001). Pearson correlation analysis showed that serum TNF-α and serum interleukin-10 levels were both correlated with HLA-DR expression. In addition, exogenous TNF-α could enhance IL-10 secretion from normal monocytes in a dose–response manner. In addition, TNF-α could downregulate the HLA-DR expression on monocytes even in the presence of anti-IL-10 antibodies. Therefore, both TNF-α and IL-10 contributed to the development of immunoparalysis in patients with acute pancreatitis.

Alterations in intestinal function in acute pancreatitis in an experimental model.

Gastrointestinal tract failure may be involved in the development of systemic septic complications in acute pancreatitis. Systemic and intestinal circulation, intestinal permeability and absorptive function were evaluated in the early course of acute pancreatitis induced in rats by retrograde intraductal injection of 0.2 ml of 5 per cent sodium taurodeoxycholate and 0.4 nmol trypsin. A decrease in systemic arterial pressure and intestinal blood flow and an increase in intestinal permeability as measured by the leakage of 125I-labelled human serum albumin from blood to lumen were noted in the distal ileum and colon, reaching statistically significant differences 6 h after induction of pancreatitis. The transport of small molecular markers (sodium fluorescein and 51Cr-labelled ethylenediamine tetra-acetic acid) through the distal ileum and colon in vitro from the mucosal to the serosal site in Ussing chambers significantly increased in the early periodic (20-60 min) of incubation, while the passage of a macromolecular marker (ovalbumin) demonstrated a definite increase at 60-120 min of incubation. D-Xylose absorption from the gut lumen to the portal vein was significantly less in acute pancreatitis than after sham operation. Intravenous administration of the hydroxyl radical scavenger dimethylsulphoxide prevented the compromised intestinal permeability and gut absorptive capacity induced by acute pancreatitis, but did not affect the reduced arterial pressure and intestinal microcirculation. Cytotoxic oxygen-derived free radicals may contribute to the development of alterations in intestinal permeability and absorptive function found in the early stage of acute pancreatitis in the rat.

Surgical strategies in the treatment of pancreatic necrosis and infection

Controversy still surrounds the management of necrotic and septic complications of acute pancreatitis. A review of the literature of the past decade dealing with the surgical treatment of pancreatic necrosis, pancreatic abscess and infected pancreatic necrosis has been undertaken. Three main patterns of management could be identified: (1) 'conventional treatment', consisting of pancreatic resection or necrosectomy with drainage; (2) 'local lavage', consisting of necrosectomy followed by regional lavage; and (3) 'open management', with resection or necrosectomy followed by planned multiple re-explorations. From this review it appears that local lavage and open management offer better survival prospects than conventional treatment. Open abdomen techniques, however, are associated with an increased risk of complications, such as colonic necrosis, intestinal fistula, and intra-abdominal bleeding. Excellent results can be achieved in specialized centres with any of the three methods, provided adequate debridement and prompt reoperations are undertaken if the septic state persists.

Pancreatitis and nutrition. Significance of the gastrointestinal tract and nutrition for septic complications

Septic complications are an important factor for the morbidity and mortality of acute pancreatitis. The gut has been identified as a source of infection early in the course of the disease allowing intestinal bacteria to translocate into pancreatic necrosis and other organs. Bacterial translocation is promoted by an impaired intestinal mucosal barrier which can be attributed to the reduced oxygen and substrate supply of the intestine during the early systemic response to the pancreatic injury. A rat model of severe acute pancreatitis has been used to confirm the hypothesis that an impaired mucosal barrier can be stabilized by supplying certain nutritients, vitamins and trace elements. Following a discussion of the many aspects of bacterial translocation and gut derived sepsis, the role of the gut and nutrition for the development of septic complications in acute pancreatitis is summarized as follows: Early in the course of acute pancreatitis the gut is a target organ of the primary systemic inflammatory response (SIRS) to pancreatic injury. SIRS-induced gut barrier dysfunction promoting bacterial translocation makes the gut the motor for secondary (septic) complications. As a septic focus the gut becomes a target for therapeutic measures aimed at stabilizing the impaired gut barrier. Nutritive factors demonstrated to improve impaired gut barrier function include early enteral feeding and specific factors like glutamine which are essential for enterocytes and colonocytes in stress. Experimental data are presented to underline the significance of these nutritive factors and subsequent randomized multicenter trials performed to verify the positive experimental results are introduced. The effect of other nutritive factors (e.g. omega-3-fatty acids) has not yet been systemically investigated. Thus, experimental and clinical studies need to be performed for evaluating their effect on bacterial translocation and the disease course in acute pancreatitis.

The effect of interleukin-6 on bacterial translocation in acute canine pancreatitis.

Bacterial translocation from the gut to mesenteric lymph nodes and other extraintestinal sites is an important source of infection in acute pancreatitis. Impaired host immunity is known to promote bacterial translocation. Interleukin-6 (IL-6) is a multifunctional cytokine that regulates the immune response, acute phase reaction, and hematopoiesis. Twenty-four mongrel dogs (18-29 kg) were studied in four equal groups. In Groups I and II, acute pancreatitis was induced by direct pressure injection of 4% taurocholate and trypsin into the pancreatic duct at laparotomy. Groups III and IV had only laparotomy. Group I and III dogs were given IL-6 (50 microg/kg/d, sq) daily starting 24 h after operation and Group II and IV dogs received an equal volume of saline administered at similar time. All animals had blood drawn for culture, complete blood count (CBC), platelets, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and amylase on d 0, 1, 4, and 7. On d 7, mesenteric lymph nodes (MLN), spleen, liver, pancreas, and cecum were harvested for pathology study and for cultures of aerobic and anaerobic bacteria. Quantitative cecal cultures of aerobic and anaerobic bacteria were obtained. All Group I and Group II dogs had severe pancreatitis. The increase of plasma CRP in Group I was sustained throughout treatment (1.3+/-0.3 on d 0 vs 3.1+/-0.3*, 3.0+/-0.3*, and 2.9+/-0.3* on d 1,4, and 7, respectively). Plasma CRP was increased in Group II on d 1 and d 4 (1.3+/-0.3 mg/dL on d 0 vs 3.6+/-0.3* mg/dL on d 1, and 3.1+/-0.3* on d 4, *p < 0.05). There were no differences in white blood cell (WBC) count, differential, platelets, and ESR between Groups I and II. Bacterial translocation to MLN was lower in Group I (1/6) than in Group II (6/6) (p < 0.05). All 6 dogs in Group II had bacterial spread to distant sites compared to 2 of 6 dogs in Group I (p = 0.066). Both MLN and other distant organ cultures were negative in Group III and only 1 of 6 MLN cultures was positive in Group IV. IL-6 treatment decreases bacterial translocation to MLN and may be beneficial in reducing septic complications in acute pancreatitis.

Does large-bowel enema reduce septic complications in acute pancreatitis?

BACKGROUND: The source of septic complications in acute pancreatitis was unknown until recent years. The pathogenesis of bacterial translocation from the gut has been accepted as the main source of pancreatic or peripancreatic infection. This study was designed to investigate the role of large bowel enema during acute pancreatitis in preventing bacterial translocation. MATERIALS AND METHODS: Twenty-four Spraque-Dawley rats were used in this study. The rats were divided into two groups. Group I animals received biliopancreatic duct ligation plus colon cleansing by rectal enemas; group II animals received only biliopancreatic duct ligation. Rectal enemas were applied to the first group of animals three times, at 6, 24, and 48 hours after the operation using 10 cc sodium hydrogen phosphate solutions. All animals were sacrificed 72 hours later, and tissue samples were taken from mesenteric lymph nodes, pancreas, spleen, and liver for bacteriologic cultures via a midline laparatomy. Blood and cecum cultures were also prepared. RESULTS: Positive mesenteric lymph node cultures were found in all 12 animals in group II but in only 3 of 11 animals of group I ( P <0.05). Distant organ cultures were positive in 9 of group II, but the only infected distant organ culture found in group I was the positive liver culture ( P <0.05). CONCLUSION: As a result of this study, we believe that large bowel enema can reduce the frequency of septic complications in acute pancreatitis by reducing bacterial translocation.

Monoclonal antibodies against ICAM-1 reduce septic complications in acute pancreatitis

Monoclonal antibodies against ICAM-1 reduce septic complications in acute pancreatitis

The Effect of Epidermal Growth Factor on the Septic Complications of Acute Pancreatitis

Bacterial translocation (BT) from the gastrointestinal tract to mesenteric lymph nodes (MLN) and other extraintestinal organs is an important source of infection in acute pancreatitis (AP). Epidermal growth factor (EGF), a peptide hormone with trophic effects on gut mucosa, has decreased intestinal mucosal injury in septic rats and decreased burn-induced BT in mice. The purpose of this study is to examine whether EGF could affect BT in acute necrotizing pancreatitis. Forty-eight male Sprague–;Dawley rats (250–;350 g) were studied. AP was induced in Group I and Group II by pressure injection of 3% taurocholate and trypsin into the biliopancreatic duct (1 ml/kg of body weight). Group III and Group IV underwent laparotomy without induction of acute pancreatitis. Group I rats received human recombinant EGF (100 μg/kg, subcutaneously twice daily) and Group II rats received a similar volume of 0.1% bovine serum albumin as a placebo postoperatively. Group III and Group IV received EGF and placebo, respectively. At 48 hr postoperatively, blood was drawn for culture and amylase determinations. Jejunum and ileum were obtained to measure mucosal protein content, mucosal thickness, villus height, and crypt depth. Specimens from MLN, spleen, liver, pancreas, and cecum were harvested for pathology and culture of gram positive (G+), gram negative (G−), and anaerobic bacteria. Ileal mucosal protein levels were increased significantly in Group I (1.96 ± 0.14 mg/cm) compared to Group II (0.95 ± 0.15 mg/cm intestinal segment) (P< 0.01). Jejunal and ileal mucosal thickness, villus height, and crypt depth in Group I were significantly increased when compared to Group II (P< 0.05). All 12 rats in Group II had BT to MLN compared to 58% (7 of 12 rats) in Group I (P< 0.05). Thirty-three percent (4 of 12 rats) had BT to distant sites such as pancreas, spleen, liver, and/or blood in Group I vs 83% (10 of 12 rats) in Group II (P< 0.05). EGF treatment minimizes intestinal damage, decreases BT to MLN and bacterial spread to distant sites, and may be beneficial in preventing septic complications in AP.

Effect of early jejunal feeding on the septic complications in acute pancreatitis. A prospective randomized study

Effect of early jejunal feeding on the septic complications in acute pancreatitis. A prospective randomized study

Classification and treatment of local septic complications in acute pancreatitis

Background: An international symposium on acute pancreatitis recently developed a clinical classification system for severe acute pancreatitis that classifies all local septic complications into three groups: infected necrosis (IN), sterile necrosis (SN), and pancreatic abscess (PA). Despite the appeal of having three distinct, well-defined labels for this complex process, the clinical utility of this schema has yet to be determined. The purpose of this study was to investigate the prognostic and therapeutic utility of applying this clinical classification system to a large group of surgical patients with local septic complication from acute pancreatitis. Patients and methods: We reviewed the cases of 62 patients with complicated pancreatitis, classifying them into IN (n = 20), SN (n = 14), or PA (n = 28) groups. Ranson's score, APACHE II score, and computed tomography grading were calculated within the first 48 hours of admission. Information on patient demographics, etiology of pancreatitis, operative procedures, timing of intervention, bacteriology, blood loss, intensive care unit days, ventilator days, and morbidity and mortality were also accrued and analyzed. Results: Despite similar demographics and etiology of pancreatitis, patients with necrosis, both IN and SN, were more critically ill than were patients with PA (APACHE II score >15, 21% versus 0%, respectively), required earlier operative intervention (mean 14 days versus 29 days, P = 0.02), required necrosectomy with drainage (65% versus 4%, P <0.001) rather than simple drainage (3% versus 86%, P <0.001), more reoperations (2.3 versus 1.1, P <0.05), and had a significantly higher mortality rate (35% versus 4%, P <0.05). In addition, patients with IN required significantly more hospital days, ventilator days, and blood transfusions than elther patients with SN or PA ( P <0.05). Conclusions: We conclude that this classification system allows for the stratification of patients into three distinct groups—infected necrosis, sterile necrosis, and pancreatic abscess— and has both therapeutic and prognostic usefulness.

Improved zipper closure of the abdominal wall in patients requiring multiple intra-abdominal operations

Optimal management of pancreatic abscess and septic complications of acute pancreatitis remains controversial. With the "open packing" approach, repeated closure of the midline fascia is complicated by loss of tissue integrity and suture strength. An improved zipper closure of the abdominal wall in six patients with pancreatic abscess is presented. Improvements included: (1) using a separating jacket-type zipper to allow maximal intraoperative exposure; (2) employing a removable tuck for expansion of the patch covering the wound; (3) substituting a nonmeshed polytetrafluoroethylene material for the polypropylene mesh to prevent adherence to the underlying viscera; and (4) creating a flap underneath the zipper teeth to protect the underlying tissue from injury. Satisfactory results were achieved with the improved zipper technique.

Pancreatic abscess and infected pancreatic necrosis. Different local septic complications in acute pancreatitis.

Local septic complications in acute pancreatitis need to be exactly characterized and defined in order to develop improved concepts for their prevention, early diagnosis, and therapy. While up to now all local septic complications have been termed abscesses, the present study for the first time delineates the morphologic, clinical, and laboratory criteria needed to distinguish between two separate clinical entities: the infected necrosis (IN) and the pancreatic abscess (PA). IN is defined as a diffuse bacterial inflammation of necrotic pancreatic and peripancreatic tissue, but without any significant pus collections. On the other hand, the morphologic substrate of PA is a localized collection of pus surrounded by a more or less distinct capsula. IN becomes clinically evident during the early phase of acute pancreatitis (AP). The patients with IN present both the signs of sepsis and the laboratory findings of AP. Thus in these patients the most fulminant course of AP is observed; 51.8% and 35.7% of them have pulmonary or renal insufficiency, respectively. The mortality of the patients with IN is high and amounts to 32.1%. Pancreatic abscess, on the other hand, does not develop before the fifth week after onset of symptoms and after subsidence of the acute phase of pancreatitis. In these patients laboratory signs of AP-like amylasemia, hypocalcemia, hyperglycemia, and rise of LDH are rarely observed. Corresponding to the lack of pathophysiologic effects of AP per se, pulmonary and renal insufficiencies occur in only 33.3% and 16.7%, respectively, and mortality in these patients is 22.2%. While an abscess may readily be identified by computed tomography, the differentiation between IN and non-IN can be very difficult.(ABSTRACT TRUNCATED AT 250 WORDS)