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.

Background and Objectives: Severe acute pancreatitis carries a substantial risk of complications and death. Prompt identification of prognostic factors is crucial to optimize management and reduce mortality. This study aims to compare inflammatory scores, laboratory markers, and clinical outcomes between survivors and non-survivors with severe acute pancreatitis, drawing on data from 179 patients admitted between 2017 and 2024. Methods: We conducted a retrospective cohort study of 179 patients diagnosed with severe acute pancreatitis. Of these, 55 patient records were extracted from an existing database, and an additional 124 were included from hospital archives (2017–2024). We divided participants into survivors (n = 121) and non-survivors (n = 58). Clinical data were obtained from medical records, including demographic information, comorbidities, laboratory markers (neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR)), and severity scores (Acute Physiology and Chronic Health Evaluation (APACHE), Computed Tomography Severity Index (CTSI), and Ranson). Results: Non-survivors had significantly higher ages (mean of 66.4 vs. 52.7 years, p = 0.002), elevated inflammatory markers (median NLR of 14.2 vs. 10.3, p = 0.031), and more frequent multiorgan failure (75.9% vs. 31.4%, p < 0.001). The timing of intervention before 28 days was associated with higher mortality (p = 0.004). Chronic kidney disease and advanced cardiovascular comorbidities independently predicted worse survival (p = 0.009). The mortality rate in this cohort was 32.4%. Logistic regression identified age >60 years with an odds ratio (OR = 2.9), multiple organ failure (OR = 4.1), and high severity scores as primary contributors to mortality. Conclusions: Advanced age, comorbidities, elevated inflammatory markers, and multiple organ failure significantly impact mortality in severe acute pancreatitis. Delaying major interventions when feasible, optimizing perioperative care, and early recognition of high-risk patients may improve outcomes. Further research should explore targeted management strategies for high-risk groups and refine the role of delayed or minimally invasive approaches in severe acute pancreatitis management.

Acute pancreatitis is an unpredictable disease affecting the pancreas and it is characterized by a wide range of symptoms and modified lab tests, thus there is a continuing struggle to classify this disease and to find risk factors associated with a worse outcome. The main objective of this study was to identify the risk factors associated with the fatal outcome of the intensive care unit’s patients diagnosed and admitted for severe acute pancreatitis, the secondary objective was to investigate the prediction value for the death of different inflammatory markers at the time of their admission to the hospital. This retrospective study included all the patients with a diagnosis of acute pancreatitis admitted to the Intensive Care Unit of the Emergency County Hospital Timisoara between 1 January 2016 and 31 May 2021. The study included 53 patients diagnosed with severe acute pancreatitis, out of which 21 (39.6%) survived and 32 (60.4%) died. For the neutrophils/lymphocytes ratio, a cut-off value of 12.4 was found. When analyzing age, we found out that age above 52 years old can predict mortality, and for the platelets/lymphocytes ratio, a cut-off value of 127 was found. Combining the three factors we get a new model for predicting mortality, with an increased performance, AUROC = 0.95, p < 0.001. Multiple persistent organ failure, age over 50, higher values of C reactive protein, and surgery were risk factors for death in the patients with severe acute pancreatitis admitted to the intensive care unit. The model design from the neutrophils/lymphocytes ratio, platelets/lymphocytes ratio, and age proved to be the best in predicting mortality in severe acute pancreatitis.

Although inguinal hernia repair is one of the most common surgical procedures, finding a retroperitoneal structure, such as the ureter, is a rather rare occurrence. Ureteroinguinal hernias may arise in the presence or absence of obstructive uropathy, the latter raising difficulties in diagnosis for the general surgeon performing a regular inguinal hernia surgery. This study aims to collect the relevant literature describing the diagnosis and management of ureteroinguinal hernias and update it with a case encountered in our clinic. The following study was reported following the SCARE guidelines. The relevant literature describes less than 150 cases of ureteroinguinal hernias overall, considering the 1.7% prevalence of inguinal hernias in the general population. With only 20% of these hernias being described as extraperitoneal, such an encounter becomes an extremely rare finding. Our clinical experience brings a case of a 75-year-old male with frequent urinary tract infections and a large irreducible inguinoscrotal hernia of about 20/12 cm located at the right scrotum. The patient underwent an open inguinal hernia repair technique under general anesthesia, incidentally finding an extraperitoneal ureteral herniation. Segmental ureterectomy was performed with uneventful recovery. Intraoperatively, finding an incidental ureteroinguinal hernia raises concerns about probable urinary tract complications during regular hernia repair surgery and whether the diagnosis is likely to happen prior to surgical intervention. Although imaging is rarely indicated in inguinal hernias, the case reports show that a pelvic CT scan with urography in symptomatic patients with urinary symptoms will provide accurate confirmation of the diagnosis. The relevant literature is limited due to the rarity of respective cases, thus making standardized management of such cases unlikely.

Acute pancreatitis is a complex inflammatory disorder with significant morbidity and mortality. This review aims to integrate 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, disruption of intracellular calcium signaling leads to premature enzyme activation, triggering a cascade of events including mitochondrial dysfunction, ATP depletion, and release of pro-inflammatory 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.

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.