Acute Pancreatitis: Current Perspectives on Diagnosis and Management

Acute pancreatitis (AP) is one of the most common gastrointestinal emergencies, with more than 275,000 hospital admissions annually in the United States [2]. While most cases are mild, 15–20% progress to moderately severe or severe disease characterized by systemic inflammation, organ failure, and local complications [1,3]. Overall mortality remains 3–5%, but increases to 20–35% in patients with persistent organ failure requiring intensive care [7].Early assessment remains challenging. Traditional scoring systems (APACHE II, BISAP, Ranson, mCTSI) demonstrate modest accuracy within the first 24 hours [4,11]. Consequently, emerging biomarkers—including IL-6, IL-8, IL-10 [16–17], pentraxin-3 [8], sCD163 [7], NGAL [10], and presepsin—are critical for identifying early severity. Endothelial dysfunction markers including angiopoietin-2 [19], proADM, endocan, and VEGF provide additional predictive value by reflecting microcirculatory failure and shock. Oxidative stress markers such as MDA and GSH depletion correlate with necrosis and multi-organ dysfunction. ICU physiological predictors—vasopressor requirement, rising lactate, Horowitz-index deterioration, and early AKI—remain the strongest bedside indicators of poor outcome [18]. Modern management emphasizes goal-directed fluid therapy, controlled resuscitation with balanced crystalloids, and selective use of CRRT, although no multicenter RCT has yet confirmed its mortality benefit [20]. This review synthesizes classical and novel biomarkers, endothelial and oxidative markers, and ICU predictors to support a modern, precision-based approach to early risk assessment and managementin acute pancreatitis.