Bacterial overgrowth syndrome of upper parts of gastrointestinal tract in acute necrotizing pancreatitis

Aim: to study the changes in the microflora of the upper part of digestive tract during acute necrotizing pancreatitis. Material and methods. Acute necrotizing pancreatitis was induced in 42 white rats; changes in the mucous microflora of the upper part of digestive tract were studied. Bacteriological examination of the contents of the proximal small intestine was performed in 42 patients with acute necrotic pancreatitis during gastrofibroscopy. Results and discussion. Induction of acute necrotic pancreatitis was accompanied by impaired colonization resistance of the intestinal mucosa due to the elimination of bifidobacteria and lactobacilli: the frequency of their growth from the mucosa decreased threefold (p<0.01), and the population level, respectively, by 25% (p<0.05) and by 36% (p<0.02). The mucosa was actively colonized by gram-negative pathogenic and conditionally pathogenic enterobacteria at high population level (3.07‒5.39 lg CFU/g), which allowed this microflora to overcome the damaged intestinal barrier and translocate. Pathogenic Escherichia spp. and Proteus spp. were cultivated from the mesenteric lymph nodes in 24 hours; Enterobacteria spp. and Staphylococci spp. were isolated from portal blood, pancreatic tissue, and peritoneal cavity 48 hours after induction of acute pancreatitis. Eight strains of gram-negative microorganisms were identified in small intestine in 69% of patients before surgery. Similar microflora was cultivated from pathological foci in 57.4% of patients after surgery. Conclusion. Severe deficiency of autochthonous anaerobic microflora occurred in the upper parts of the digestive tract in acute necrotizing pancreatitis, causing excessive colonization by pathogenic and conditionally pathogenic microorganisms and promoting bacterial translocation.

Download Full-text

ARROSIVE BLEEDING WITH PANCREATIC NECROSIS — TACTICAL APPROACHES

Kharkiv Surgical School ◽

10.37699/2308-7005.1.2020.12 ◽

2020 ◽

pp. 85-88 ◽

Cited By ~ 1

Author(s):

V. V. Mishchenko ◽

P. I. Pustovoit ◽

R. Yu. Vododyuk ◽

V. V. Velichko ◽

V. V. Goryachy

Keyword(s):

Minimally Invasive ◽

Pancreatic Necrosis ◽

Necrotizing Pancreatitis ◽

Acute Necrotizing Pancreatitis ◽

Stent Grafts ◽

Invasive Treatment ◽

Results Of Treatment ◽

Hemorrhagic Complications ◽

Necrotic Pancreatitis ◽

Acute Necrotizing

Summary. The problem of hemorrhagic complications of destructive pancreatitis is relevant. The aim of the study was to study the frequency and sources of hemorrhagic complications in patients with pancreatic necrosis, to evaluate the tactics of diagnosis and the effectiveness of methods to stop bleeding. Materials and methods. A study of the results of treatment of 40 patients with acute necrotizing pancreatitis was conducted. Results and its discussion. In 67.5 % of patients with acute necrotizing pancreatitis, hemorrhagic complications in the form of arrosive bleeding were observed. A method of endovascular occlusion of vessels using Gianturco spirals or stent grafts to stop arrosive bleeding in acute necrotizing pancreatitis has been introduced in the clinic. In 37.0 % of cases, repeated signs of arrosive bleeding were observed. In acute necrotizing pancreatitis complicated by arrosive bleeding, mortality was 44.4 %. Conclusions. The main cause of hemorrhagic complications in acute necrotic pancreatitis is acute necrotic changes, during infection of which arrosia of adjacent vessels occurs. The predominant tactic in case of bleeding from the retroperitoneal space against the background of minimally invasive treatment is clamping of drains, endovascular hemostasis using Gianturco spirals or stent grafts and the use of hemostatic soluble gauze (hemostop). Mortality in the development of arrosive bleeding in acute necrotic pancreatitis is 44.4 %.

Download Full-text

MORPHOLOGICAL AND FUNCTIONAL CHANGES OF INTESTINAL MUCOSA AT ACUTE NECROTIZING PANCREATITIS

Clinical anatomy and operative surgery ◽

10.24061/1727-0847.17.2.2018.7 ◽

2018 ◽

Vol 17 (2) ◽

pp. 37-41

Author(s):

O V. Rotar

Keyword(s):

Intestinal Mucosa ◽

Necrotizing Pancreatitis ◽

Intestinal Barrier ◽

Acute Necrotizing Pancreatitis ◽

Triple P ◽

Protective Function ◽

Functional Changes ◽

Necrotic Pancreatitis ◽

Mucosal Layer ◽

Acute Necrotizing

The purpose - to investigate the morphological and functional changes of the intestinal mucosa during acute necrotic pancreatitis and their effect on the translocation of bacteria and endotoxin. Material and methods. The conditions of the intestinal barrier were studied at 74 patients in clinics and 60 white rats in experiment during acute necrotic pancreatitis. The morphological and histological changes of the mucosal layer of the intestine, its enzyme activity, the microflora and its permeability for the endotoxin were studied. Results and discussion. During the early phase of acute necrotic pancreatitis barrier function of the intestine has been disturbed by increasing the activity of lysosomal enzymes (β-galactosidase double and N-acetyl-β-glucosaminidase triple, p <0.05), which caused the qualitative and quantitative changes of composition of glycoproteins in the epithelial layer of the mucosa shells. Disorders of the intestinal barrier were accompanied by bacterial translocation to the internal organs in 57.4% of patients who were operated early (up to 4 weeks) of the disease and in 90% of the animals after 72 hours of the experiment. High concentrations of endotoxin (over than 0.30EO/ml) delivered from the intestine have activated a specific proinflammatory cascade through the membrane receptor of monocytes/macrophages CD14, which was accompanied by the development of a systemic inflammatory response syndrome and multiple organ failure. Conclusions. During acute necrotizing pancreatitis the structure and protective function of the pre-epithelial mucosal layer are disordered, colonization of intestine by pathogenic and conditionally pathogenic gram-negative microflora is occurred which promoted migration of bacteria and transport of endotoxin into systemic blood circulation.

Download Full-text