The dissertation is dedicated to the study and coverage of surgical treatment of patients with infected necrotizing pancreatitis through a personalized approach and the use of advanced surgical technologies of sequestrant necrotectomy.
Acute pancreatitis is one of the most common diseases of the abdominal cavity, which leads to hospitalization in most countries of the world. The incidence of acute pancreatitis in different countries of the world ranges from 4.9 to 73.4 cases per 100 thousand population. In Ukraine, the incidence is 67–69.5 per 100 thousand population.
Acute necrotizing pancreatitis is a life-threatening complication of acute pancreatitis, characterized by the development of necrosis of pancreatic and parapancreatic tissue, and occupies one of the leading positions in the structure of overall surgical mortality. Acute necrotizing pancreatitis develops in 15% to 20% of patients with acute pancreatitis. Infection of pancreatic necrosis occurs in 16–47% of patients. Mortality in the development of infectious complications of acute necrotizing pancreatitis reaches 30%.
Among all patients with GP, according to various data, in 80-85% of cases, the edematous form of GP is diagnosed, the course of which is favorable, and in 15-20% of patients it has a necrotic nature with a severe and very severe course, which requires long-term and difficult treatment. At the same time, at the early stage, the mortality rate is 30-50% of patients from endogenous intoxication, the extreme manifestation of which is pancreatogenic shock. In the late period, it is 50% or more from complicated purulent-necrotic forms. Therefore, the main factors that worsen the course of GP and mortality are infection of the foci of pancreatic necrosis and the occurrence of multiple organ failure. Infection of the foci of pancreatic necrosis occurs in 16-47% of cases.
Etiological factors that predispose to the occurrence of acute necrotizing pancreatitis include cholelithiasis, chronic alcohol consumption, hypertriglyceridemia, and certain medications. The pathophysiology of acute necrotizing pancreatitis is characterized by premature activation of pancreatic enzymes, leading to pancreatic tissue autodigestion, inflammation, and necrosis. This process can lead to the development of systemic inflammatory response syndrome (SIRS), multiple organ failure, and sepsis, which complicates clinical management and is a factor leading to high mortality among patients [1–9].
Modern studies have proven that the high mortality rate in acute necrotizing pancreatitis is due to both direct damage to the gland parenchyma and extrapancreatic lesions, primarily parapancreatitis and peritonitis. It has been established that it is extrapancreatic factors that cause the development of a malignant intravascular inflammatory reaction, which causes endothelial damage, a generalized increase in microvascular permeability, a decrease in circulating blood volume and a decrease in visceral microcirculation. The above-mentioned changes constitute the pathogenetic basis of multiple organ failure [3, 5, 9–15].
