Acute pancreatitis (AP) is an inflammatory condition of the pancreas that constitutes one of the most common and clinically challenging gastrointestinal emergencies encountered in clinical practice. The global incidence of acute pancreatitis has been steadily increasing, with an estimated annual incidence of 34 per 100,000 population, placing considerable burden on healthcare systems worldwide [1, 2]. While the majority of cases (approximately 80%) follow a mild, self-limiting course with interstitial edema and minimal organ dysfunction, the remaining 20% progress to severe necrotizing pancreatitis characterized by local and systemic complications carrying a mortality rate of 15-30% [3, 4]. The early and accurate assessment of disease severity is paramount for appropriate clinical triage, as patients with severe disease require intensive monitoring, aggressive fluid resuscitation, nutritional support, and timely intervention for complications such as infected necrosis, pseudocyst formation, and multiorgan failure.5,6 Several clinical scoring systems have been developed for prognostication, including the Ranson criteria, the Acute Physiology and Chronic Health Evaluation II (APACHE II) score, and the Bedside Index for Severity in Acute Pancreatitis (BISAP). However, these systems rely on clinical and biochemical parameters that may not fully capture the extent of pancreatic parenchymal damage and peripancreatic involvement [7, 8]. Imaging plays a central role in the evaluation of acute pancreatitis. Conventional radiography can identify sentinel loop sign, colon cut-off sign, or pleural effusions but lacks sensitivity for pancreatic pathology. Transabdominal ultrasonography (USG), while valuable for identifying gallstone etiology, is frequently limited by overlying bowel gas, body habitus, and operator dependence, particularly in acutely ill patients [9, 10]. Magnetic resonance imaging (MRI) offers superior soft-tissue contrast and is particularly useful for evaluating pancreatic ductal anatomy and distinguishing fluid from necrosis, but its limited availability, longer acquisition times, and the difficulty of performing MRI in critically ill patients constrain its use in the acute setting [11]. Contrast-enhanced computed tomography (CECT) has established itself as the gold standard imaging modality for the evaluation of acute pancreatitis [12, 13]. CECT provides rapid, highly sensitive, and reproducible assessment of the pancreatic parenchyma, peripancreatic tissues, and vascular structures. The CT Severity Index (CTSI), originally described by Balthazar et al. in 1990, combines morphological CT grading with the extent of pancreatic necrosis to provide a composite severity score of 0-10.14 Multiple large-scale studies have validated the CTSI as a reliable predictor of morbidity and mortality in AP, demonstrating a strong correlation between higher CTSI scores and adverse clinical outcomes including increased complication rates, longer hospital stays, need for surgical or percutaneous intervention and death [15, 16]. It must be noted that this study applies only to cases of acute pancreatitis, not to chronic pancreatitis, flare-ups of chronic pancreatitis (i.e., acute-on-chronic pancreatitis), groove pancreatitis, autoimmune pancreatitis, and other forms of pancreatitis (e.g., tuberculous, hereditary pancreatitis), which differ considerably in clinical presentation, imaging findings, prognosis, therapy, and clinical outcome. The present study was designed to evaluate the role of CECT in the assessment of acute pancreatitis and to determine the prognostic correlation between the CT Severity Index and clinical outcomes in a cohort of 50 patients presenting to a tertiary care teaching hospital in southern India.

Study Design And Setting This prospective observational study was conducted in the Department of Radiodiagnosis at BRIMS Teaching Hospital, Bidar, Karnataka, India, over a period of six months following approval from the Institutional Ethics Committee. Written informed consent was obtained from all participants prior to enrollment. Study Population Fifty consecutive patients who presented with clinical features suggestive of acute pancreatitis and were referred for cross-sectional imaging were enrolled. Acute pancreatitis was diagnosed according to the revised Atlanta classification when at least two of the following three criteria were present: 1) Characteristic abdominal pain. 2) Serum amylase and/or lipase levels at least three times the upper limit of normal. 3) Characteristic imaging findings [17]. Inclusion Criteria Patients ≥18 years of age with a clinical diagnosis of acute pancreatitis who were not adequately evaluable by ultrasonography due to body habitus (large or obese patients), overlying bowel gas, or other technical limitations. Exclusion Criteria Were 1) Patients in whom acute pancreatitis was adequately diagnosed and evaluated by ultrasonography and who therefore did not undergo CT. 2) Patients who declined participation. Ct Imaging Protocol All patients underwent CECT of the abdomen on a multidetector CT scanner (128-slice MDCT). The imaging protocol consisted of an initial non-contrast phase followed by a portal venous phase acquired 60-70 seconds after intravenous administration of 80-100 mL of non-ionic iodinated contrast medium (Iohexol 350 mg I/mL) at a rate of 3-4 mL/sec via an 18-gauge peripheral intravenous catheter in the antecubital fossa. Scanning parameters included: tube voltage 120 kVp, automatic tube current modulation (150-350 mA), slice thickness 5 mm with 3 mm reconstructions, pitch 1.0, and a field of view extending from the dome of the diaphragm to the iliac crests. Multiplanar reformations in coronal and sagittal planes were generated from the axial dataset. Image Analysis And Ct Severity Index All CT examinations were independently reviewed by two radiologists (one senior consultant and one post-graduate trainee) blinded to the clinical outcome. Discrepancies were resolved by consensus. The CT Severity Index was calculated as the sum of the Balthazar CT grade points and the necrosis score, as shown in Table 1. Table 1: CT Severity Index scoring system (Balthazar et al., 1990)-CT Grade (Morphological Score) Grade CT Findings Points A Normal pancreas 0 B Focal or diffuse pancreatic enlargement 1 C Pancreatic gland abnormalities with peripancreatic inflammatory changes 2 D Single peripancreatic fluid collection 3 E Two or more fluid collections and/or retroperitoneal gas 4 Table 1: (Continued). Necrosis Score Degree of Necrosis Additional Points No necrosis 0 ≤30% necrosis 2 30-50% necrosis 4 >50% necrosis 6 Based on the composite CTSI score (range 0-10), patients were stratified into three severity categories: Mild (CTSI 0-3), Moderate (CTSI 4-6), and Severe (CTSI 7-10). Clinical Outcome Parameters Clinical and imaging outcomes recorded for each patient included pancreatic/peripancreatic complications, extrapancreatic findings, organ failure, sepsis, need for surgical or percutaneous intervention, duration of hospitalization, and mortality. Patients were followed until discharge or death. Statistical Analysis Data were analyzed using SPSS version 25.0 (IBM Corp., Armonk, NY). Continuous variables were expressed as mean ± standard deviation or median (interquartile range), as appropriate. Categorical variables were expressed as frequencies and percentages. Comparisons among CTSI severity categories were performed using one-way ANOVA or Kruskal-Wallis test for continuous variables, and chi-square or Fisher's exact test for categorical variables, as appropriate. The association between CTSI and duration of hospital stay was assessed using correlation analysis. A two-sided p-value <0.05 was considered statistically significant. Sensitivity, specificity, positive predictive value, and negative predictive value of CTSI ≥7 for mortality were calculated with 95% confidence intervals.

Demographic And Etiological Profile The study cohort comprised 50 patients, with a mean age of 42.3 ± 12.8 years (range 21-68 years). Males predominated (n=38, 76%) with a male-to-female ratio of 3.17:1. The peak age incidence was in the 31-40 year age group (32%), followed by the 41-50 year group (26%). Table 2: Demographic characteristics of study population (N=50) Variable n % Sex Male 38 76.0 Female 12 24.0 Age Group (years) 21-30 8 16.0 31-40 16 32.0 41-50 13 26.0 51-60 9 18.0 61-70 4 8.0 Etiology Alcohol 25 50.0 Gallstones 15 30.0 Idiopathic 5 10.0 Post-ERCP 2 4.0 Hypertriglyceridemia 2 4.0 Drug-induced 1 2.0 Ct Morphological Findings Balthazar CT grading revealed Grade A in 5 patients (10%), Grade B in 10 (20%), Grade C in 12 (24%), Grade D in 13 (26%), and Grade E in 10 (20%). The distribution of grades is presented in Figure 3. Extent Of Pancreatic Necrosis No necrosis was identified in 28 patients (56%). Among the 22 patients with necrosis, the extent was ≤30% in 10 (20%), 30-50% in 7 (14%), and >50% in 5 (10%). The presence and degree of necrosis correlated significantly with Balthazar CT grade (p<0.001). Ct Severity Index Distribution The CTSI scores ranged from 0 to 10, with a mean of 4.5 ± 2.9. Based on the composite CTSI, 18 patients (36%) were classified as mild (CTSI 0-3), 20 patients (40%) as moderate (CTSI 4-6), and 12 patients (24%) as severe (CTSI 7-10). Association Of Ctsi Severity Category With Clinical Outcomes The correlation between CTSI severity category and clinical outcomes is summarized in Table 4. There were statistically significant differences in clinical outcomes across CTSI severity categories, with higher CTSI categories associated with longer hospitalization, higher complication rates, increased organ failure and ICU admission, greater need for intervention, and higher mortality. Table 4: Association of CTSI severity category with clinical outcomes Outcome Parameter Mild (CTSI 0-3) n=18 Moderate (CTSI 4-6) n=20 Severe (CTSI 7-10) n=12 p-value Mean hospital stay (days ± SD) 8.2 ± 3.1 14.6 ± 4.2 22.4 ± 6.8 <0.001* Complications, n (%) 2 (11.1) 7 (35.0) 11 (91.7) <0.001* Organ failure, n (%) 0 (0) 3 (15.0) 7 (58.3) <0.001* Intervention required, n (%) 0 (0) 4 (20.0) 8 (66.7) <0.001* ICU admission, n (%) 1 (5.6) 6 (30.0) 10 (83.3) <0.001* Mortality, n (%) 0 (0) 1 (5.0) 2 (16.7) 0.048* *Statistically significant (p<0.05). ANOVA for continuous variables, Chi-square/Fisher's exact test for categorical variables. Pancreatic/Peripancreatic And Extrapancreatic Complications/Findings Among the 50 patients, 20 (40%) developed one or more pancreatic/peripancreatic or extrapancreatic complications/findings. The most frequent was acute peripancreatic fluid collection (15 patients, 30%), followed by pleural effusion (12, 24%), ascites (10, 20%), pseudocyst (8, 16%), pancreatic abscess (4, 8%), and vascular complications (3, 6%). The distribution is presented in Table 5. Table 5: Pancreatic/peripancreatic and extrapancreatic complications/findings by CTSI category Complication Overall n (%) Mild (0-3) Moderate (4-6) Severe (7-10) Acute peripancreatic fluid collection 15 (30) 1 5 9 Pleural effusion 12 (24) 1 4 7 Ascites 10 (20) 0 3 7 Pseudocyst 8 (16) 0 3 5 Pancreatic abscess 4 (8) 0 1 3 Vascular complications 3 (6) 0 0 3 Correlation Of Ctsi With Hospital Stay Pearson's correlation analysis demonstrated a strong positive correlation between CTSI score and duration of hospital stay (r = 0.84, p<0.001). The scatter plot with regression line is presented in Figure 7. Diagnostic Performance Of Ctsi For Predicting Mortality Using a CTSI threshold of ≥7, sensitivity for mortality was 66.7% and specificity was 78.7%. The positive predictive value was 16.7% and the negative predictive value was 97.4%. Given the small number of deaths (3/50), these estimates should be interpreted cautiously. The overall mortality rate was 6% (3/50). All three deaths occurred in patients with CTSI scores of ≥5, and two of the three were in the severe category (CTSI 7-10). Table 6: Diagnostic performance of CTSI ≥7 for predicting mortality Parameter Value (%) 95% CI Sensitivity 66.7 22.3-95.7 Specificity 78.7 64.3-89.3 Positive Predictive Value 16.7 4.2-44.8 Negative Predictive Value 97.4 86.2-99.6 Overall Accuracy 78.0 64.0-88.5

The present study demonstrated a significant association between higher CT Severity Index scores and adverse clinical outcomes in acute pancreatitis. These findings are consistent with previous studies evaluating the prognostic value of CT-based severity assessment. In our cohort, the male predominance (76%) and the peak incidence in the 31-40 year age group reflect the strong etiological association with alcohol consumption, which accounted for 50% of cases. This demographic profile is consistent with data from other Indian studies, where alcohol has been reported as the leading cause in 40-60% of cases, in contrast to Western populations where gallstone pancreatitis predominates [18, 19]. Gallstones were the second most common etiology (30%) in our study, predominantly affecting female patients and the older age group, consistent with the established gender-specific risk profile for biliary disease. The distribution of Balthazar CT grades in our study, with Grade D being the most common (26%), followed by Grade C (24%) and Grade E (20%), suggests that the majority of patients who underwent CECT had moderate to severe morphological changes at the time of imaging. This finding likely reflects an inherent selection bias, as patients with milder disease were more likely to have been adequately evaluated by ultrasonography alone and thus excluded from our study cohort. A critical finding of this study was the progressive and significant increase in complication rates with escalating CTSI severity. Only 11.1% of patients in the mild group (CTSI 0-3) developed complications, compared with 35% in the moderate group (CTSI 4-6) and 91.7% in the severe group (CTSI 7-10). This stepwise increase mirrors the findings of Balthazar et al., [14] who reported complication rates of 0% for CTSI 0-1, 8% for CTSI 2-3, 35% for CTSI 4-6, and 92% for CTSI 7-10. Raghuwanshi et al. similarly demonstrated a significant correlation between CTSI severity and complication rates in an Indian population [15] The mean duration of hospital stay increased significantly across severity categories (8.2 days for mild, 14.6 days for moderate, and 22.4 days for severe disease; p<0.001), with a strong linear correlation (r=0.84) between CTSI and hospital stay. This positive correlation has been consistently reported across multiple studies and underscores the clinical utility of CTSI in predicting resource utilization and guiding early management decisions [20, 21]. Mortality in our study was 6% (3/50), with deaths occurring exclusively in the moderate and severe categories. Two of the three deaths occurred in patients with CTSI ≥7, yielding a sensitivity of 66.7% and NPV of 97.4% for CTSI ≥7 in predicting mortality. While the modest PPV (16.7%) reflects the overall low mortality rate in our cohort, A CTSI <7 was associated with a high negative predictive value for mortality in this cohort. However, the small number of deaths limits the precision and generalizability of this estimate, and the finding should be considered hypothesis-generating rather than definitive. These findings are concordant with Block et al. [22] and Melkundi and Anand [23] who reported similar predictive performance of the CTSI for mortality in AP. Pancreatic necrosis, identified as non-enhancing pancreatic parenchyma on CECT, was present in 22 patients (44%). The extent of necrosis increased with higher Balthazar grades and CTSI categories. Among patients with extensive (>50%) necrosis, the observed rates of infected necrosis, intervention, and mortality were high; however, these findings should be interpreted cautiously because of the small subgroup size [24, 25]. The spectrum of local complications in our study, dominated by acute peripancreatic fluid collections (30%), pleural effusion (24%), and ascites (20%), is consistent with the natural history of severe AP as described in the revised Atlanta classification.17 Vascular complications, while less frequent (6%), were observed exclusively in the severe CTSI category and included splenic vein thrombosis (n=2) and pseudoaneurysm of the gastroduodenal artery (n=1), both of which required intervention. These findings reinforce the importance of dedicated vascular evaluation during CECT interpretation in severe AP. Limitations This study has several limitations. The sample size was small (n=50), and only three deaths occurred, limiting the precision of mortality-related estimates. The single-center design limits generalizability. Exclusion of patients adequately evaluated by ultrasonography introduced selection bias and may have enriched the cohort for more severe or diagnostically challenging cases. CT timing was not standardized relative to symptom onset, which may influence assessment of pancreatic necrosis. Follow-up was limited to the index hospitalization, and long-term outcomes were not assessed. The study also did not simultaneously compare CTSI with the modified CTSI or established clinical severity scores such as BISAP or APACHE II.

In this prospective single-center cohort, higher CT Severity Index scores were significantly associated with increased complication rates, prolonged hospitalization, organ failure, ICU admission, need for intervention, and mortality. CECT provided useful morphological and prognostic information in patients with acute pancreatitis who underwent CT for clinical indications. Because of the small sample size, selected study population, non-standardized CT timing, and limited number of mortality events, these findings should be interpreted cautiously. Larger multicenter studies with standardized imaging timing and comparison with clinical severity scores are warranted.

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