Severe acute pancreatitis occurs in approximately 20 % of patients with acute pancreatitis and progresses rapidly, posing a high risk of mortality [1]. Inflammatory cytokines, produced by trypsinogen activation, are active in patients [2], [3] and clinically manifested as intestinal obstruction, dyssynergic defecation, vomiting, and infections [4], [5], [6], [7]. According to a study [8], parenteral nutrition-associated liver disease (PNALD) is a complication of gastrointestinal diseases. Long-term parenteral nutrition in the treatment of patients with acute pancreatitis in vivo may lead to hepatocyte infiltration and other phenomena [9], [10], thus causing continuous hepatic injury. To address PNALD, it is essential to clarify its influencing factors first, an area that has been relatively underexplored to date. In this study, a risk model of PNALD in patients with severe acute pancreatitis was constructed to explore the related risk factors.