Abstract
The syndrome of intestinal insufficiency (SII) in patients with acute obstructive pancreatitis (ADP) leads to the formation of intra-abdominal hypertension (IAH), and then to the development of abdominal compartment syndrome (ACS) with all its inherent symptoms: acute heart, lung and kidney failure. Objective: to determine the role of SII in the development of abdominal compartment syndrome in patients with ADP. Materials and methods. Clinical studies were conducted in 71 patients with sterile pancreatic necrosis. Pathoanatomical studies of the small intestine were performed in 20 patients who died due to sterile pancreatic necrosis, of which 10 (50 %) died without SII and 10 (50 %) with SII. Results and discussion. SII developed in 57 (80 %) patients. Absolute quantitative and chronological relationships between SII and IAH and subsequent development were found in 11 (15 %) patients with ACS. SII was ahead of the formation of IAH by an average of 24 hours. IAH and, accordingly, ACS were not formed in patients without SII. The data of enterometry in the deceased with and without SII fully confirmed the results of clinical studies on the leading role of intestinal insufficiency in the development of IAH. Conclusions. SII is the initial and main link in the pathogenesis of the formation of IAH and the subsequent development of ACS in patients with ADP.
Highlights
The syndrome of intestinal insufficiency (SII) in patients with acute obstructive pancreatitis (ADP) leads to the formation of intra-abdominal hypertension (IAH), and to the development of abdominal compartment syndrome (ACS) with all its inherent symptoms: acute heart, lung and kidney failure
Clinical studies were conducted in 71 patients with sterile pancreatic necrosis
Pathoanatomical studies of the small intestine were performed in 20 patients
Summary
Выборка пациентов исключительно со стерильным панкреонекрозом объяснялась тем, что эти больные не требовали в течение первых 7 суток от начала заболевания оперативного лечения по основному заболеванию, связанному с диссолюцией поджелудочной железы (ПЖ) и забрюшинной клетчатки. Критериями исключения из клинического исследования служили: «отечный панкреатит», так как у этих больных оборвать острый приступ нам удавалось в течение 2–3 дней, и СКН не успевал развиться; «инфицированный панкреонекроз», который вне зависимости от наличия СКН и ВБГ требовал оперативного лечения с целью санации ПЖ, забрюшинной клетчатки и/или брюшной полости. Для определения объема газа и жидкости сцеживали их поочередно в резиновые круглые шары (в нашем случае в презервативы) и вычисляли по формуле V = πD3/6, где V – объем шара, π – 3,14, D – диаметр шара. Различие в показателях считали статистически значимыми при p < 0,05
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