Pathophysiology of systemic inflammatory response syndrome and multiorgan dysfunction syndrome in acute pancreatitis

Abstract

This chapter focuses on the pathophysiology of the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) in acute pancreatitis (AP). Severe systemic inflammation is associated with dysfunction of vital end organs, including the cardiovascular, respiratory, and renal systems. While the inflammatory and immune responses to acute disease can be protective, in the setting of severe AP, there is an out of proportion and dysregulated immune response and hyperinflammation, which can result in end‐organ dysfunction and failure. The innate immune system is activated by foreign antigens particularly microbe‐related peptides. Cells involved in innate immunity possess pattern recognition receptors (PRRs), which recognize what are termed as ‘pathogen‐associated molecular patterns’ (PAMPs) present on the microbes. After activation, immune cells secrete many proinflammatory cytokines, including TNF‐a and IL‐1. The initial inflammatory response by itself does not have significant clinical consequences, but it leads to the adherence, migration, and activation of leukocytes.