Year 2021 Vol. 29 No 5




Vitebsk State Medical University 1,Vitebsk,
Belarusian Medical Academy of Postgraduate Education 2, Minsk
The Republic of Belarus

Acute necrotizing pancreatitis (ANP) is associated with significantly higher morbidity and mortality. It is still difficult for the surgeon to choose and schedule the most appropriate treatment. In the early phase of the disease, surgical activity is considered to be ineffective and is associated with high risks. The only chance to save the patient is to conduct the intensive therapy in the intensive care unit, based on current pathogenetic approaches. The present review analyzed the current understanding of the pathogenesis of multiple organ dysfunction syndrome (MODS) in acute necrotizing pancreatitis. he role of inflammatory mediators, cytokines, biogenic amines, bradykinins, and lipid peroxidation products in the development of organ hypoperfusion is reflected. It is shown that the violation of the intestinal barrier function with the translocation of microorganisms exacerbates endogenous intoxication and contributes to the development of MODS. The endothelial dysfunction that develops in acute necrotizing pancreatitis has a significant effect on hemostasis. The literature analysis revealed the contradictory data on the functional activity of the coagulation and anticoagulation systems at different stages of the disease. The mechanisms of development of intra-abdominal hypertension and its multisystem negative impact are reflected. There are still controversial question of appropriate timing and indications for surgical decompression.
The analysis of the available literature data showed the need for further study of the mechanisms of multiple organ dysfunction development in acute necrotizing pancreatitis to work out new pathogenetically justified methods of its intensive therapy with an assessment of their effectiveness.

Keywords: acute necrotizing pancreatitis, multiple organ failure, endogenous intoxication, systemic inflammatory reaction, intra-abdominal hypertension, changes in hemostasis
p. 598-606 of the original issue
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Address for correspondence:
210023, Republic of Belarus,
Vitebsk, Frunze Avenue, 27,
Vitebsk State Medical University,
the Department of Anesthesiology and Resuscitation with the Course of Advanced Training and Retraining
tel. mobilr: +375 (33) 316-10-25,
Nikitina Ekaterina V.
Information about the authors:
Nikitsina Katsiaryna V., PhD, Associate Professor, Head of the Department of Anesthesiology and Resuscitation with the Course of Advanced Training and Retraining, Vitebsk State Medical University, Vitebsk, Republic of Belarus.
Ilukevich Georgy V., MD, Professor, Head of the Department of Anesthesiology and Resuscitation, Belarusian Medical Academy of Postgraduate Education, Minsk, Republic of Belarus.
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