Search

Background and Objectives: Patients undergoing open necrosectomy (ON) for acute pancreatitis (AP) often face high morbidity and mortality rates. This study aims to identify risk factors associated with adverse outcomes by comparing survivors and non-survivors of ON. Materials and Methods: A retrospective analysis was conducted on 74 patients who underwent ON for AP. Patients were divided into two groups: survivors (n = 52) and non-survivors (n = 22). Preoperative and postoperative variables were compared, and p-values were calculated to identify significant differences. Results: The mortality rate was 29.73%. Significant risk factors for mortality included age over 60 (p = 0.008), multiple organ failure (p = 0.001), early necrosectomy before 28 days (p = 0.001), higher neutrophil-to-lymphocyte ratio (NLR) (p = 0.045), and postoperative complications such as bleeding (p = 0.005) and intestinal fistula (p = 0.038). Delayed ON after 28 days showed a significantly lower mortality rate (12.5%) compared to early ON (50%). Conclusions: Age, severity of AP, timing of ON, and postoperative complications significantly influence mortality rates in patients undergoing ON. Delaying surgery beyond 28 days and optimizing surgical techniques may improve patient outcomes. [ABSTRACT FROM AUTHOR]

Acute pancreatitis is a complex inflammatory disorder with significant morbidity and mortality. This review aims to integrate the current knowledge of pancreatic morphology and immunology with the pathogenesis of acute pancreatitis, providing a comprehensive understanding of this critical condition. We conducted an extensive literature review, synthesizing data from recent studies and authoritative sources on pancreatic anatomy, histology, immunology, and the pathophysiology of acute pancreatitis. We also incorporated epidemiological data, clinical features, diagnostic criteria, and prognostic factors. The pancreas exhibits a complex morphology with intricate interactions between its exocrine and endocrine components. Its unique immunological landscape plays a crucial role in maintaining homeostasis and orchestrating responses to pathological conditions. In acute pancreatitis, the disruption of intracellular calcium signaling leads to premature enzyme activation, triggering a cascade of events including mitochondrial dysfunction, ATP depletion, and the release of proinflammatory mediators. This process can escalate from localized inflammation to systemic complications. The interplay between pancreatic morphology, immune responses, and pathophysiological mechanisms contributes to the varied clinical presentations and outcomes observed in acute pancreatitis. Understanding the intricate relationships between pancreatic morphology, immunology, and the pathogenesis of acute pancreatitis is crucial for developing more effective diagnostic and therapeutic strategies. This integrated approach provides new insights into the complex nature of acute pancreatitis and may guide future research directions in pancreatic disorders. [ABSTRACT FROM AUTHOR]