Novel strategies for the treatment of acute pancreatitis based on the determinants of severity

Abstract

Acute pancreatitis (AP) is a common disease for which a specific treatment remains elusive. The key determinants of the outcome from AP are persistent organ failure and infected pancreatic necrosis. The prevention and treatment of these determinants provides a framework for the development of specific treatment strategies. The gut-lymph concept provides a common mechanism for systemic inflammation and organ dysfunction. Acute and critical illness, including AP, is associated with intestinal ischemia and drastic changes in the composition of gut lymph, which bypasses the liver to drain into the systemic circulation immediately proximal to the major organ systems which fail. The external diversion of gut lymph and the targeting of treatments to counter the toxic elements in gut lymph offers novel approaches to the prevention and treatment of persistent organ failure. Infected pancreatic necrosis is increasingly treated with less invasive techniques, the mainstay of which is drainage, both endoscopic and percutaneous. Further improvements will occur with the strategies to accelerate liquefaction and through a fundamental redesign of drains, both of which will increase drainage efficacy. The determinants of severity and outcome in patients admitted with AP provide the basis for innovative treatment strategies. The priorities are to translate the gut-lymph concept to clinical practice and to improve the design and active use of drains for infected complications of AP.

Cardiac depression in severe acute pancreatitis: development mechanisms and possible treatment approaches. Review

“…Обычно исследователи рассматривали передачу гуморальных факторов, вызывающих депрессию миокарда, только через системный кровоток. Однако гуморальные факторы, выделяющиеся при ОП из поджелудочной железы, могут попадать в системный кровоток не напрямую, а через лимфатическую систему, тем самым минуя инактивацию в печени, о чем постулирует гипотеза «кишечник-лимфа» [49,50]. Одной из тканей, которые должны быть подвержены влиянию такой лимфы, является миокард: он первым встречается на пути оттока лимфы в системный кровоток.…”

“…Путь передачи веществ, вызывающих МД, через лимфу имеет клиническое значение: существует метод экстракорпоральной детоксикации, воздействующий на лимфу, -лимфосорбция [52]. Применение этого способа детоксикации представляется патофизиологически обоснованным, однако высокая травматичность доступа к грудному лимфатическому протоку и слабая доказательная база препятствуют внедрению метода в практику [50].…”

Dynamic Nomogram for Predicting Thrombocytopenia in Adults with Acute Pancreatitis

“…Acute pancreatitis (AP) is an inflammatory disease triggered by acinar cells with various clinical manifestations, and most patients can recover with conservative treatment. [1][2][3][4] The activation of inflammatory cells triggers the cascade release of a large number of inflammatory factors, leading to the disorder of pro-inflammatory and anti-inflammatory states, which can induce lethal severe acute pancreatitis (SAP) characterized by systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). [5][6][7][8][9] The coagulopathy associated with SIRS is a manifestation of host immune dysfunction stimulated by severe abdominal infection in AP.…”

The effect of respiration and body position on terminal thoracic duct diameter and the lymphovenous junction: An exploratory ultrasound study

“…Impaired lymph drainage can perpetuate chronic illnesses, worsening congestive heart failure and cirrhosis (Dumont & Mulholland, 1962; Haider et al, 1987; Laine et al, 1987), and lead to nutritional deficiency and immunosuppression (Nair et al, 2007). The TD, via its intestinal lymphatic tributaries, also provides an unfiltered and non‐detoxified route for pathogens and inflammatory substrates to enter the systemic circulation, promoting critical illness, multiple organ failure, and death (Deitch, 2001, 2010, 2012; Fanous et al, 2007; Shanbhag et al, 2018; Windsor et al, 2017).…”