Acute pancreatitis (AP) is one of the most common gastrointestinal emergencies, characterized by acute inflammation of the pancreas with variable involvement of surrounding tissues and remote organ systems. Its global incidence has risen steadily, with reported annual rates of 15 to 45 cases per 100,000 population depending on geography and etiology [1]. The disease spans a wide clinical spectrum, from mild self-limiting illness to severe necrotizing pancreatitis with substantial morbidity and mortality.

According to the revised Atlanta classification, the internationally accepted standard for defining and classifying AP, the disease is categorized on the basis of the presence or absence of necrosis into interstitial edematous pancreatitis and necrotizing pancreatitis [2]. Interstitial edematous pancreatitis accounts for the large majority of cases and is characterized by inflammatory enlargement of the pancreas, whereas necrotizing pancreatitis—seen in a minority of cases—leads to tissue death in the pancreatic parenchyma and/or peripancreatic tissues and is linked to much poorer outcomes [3]. Patients with the necrotizing form frequently experience persistent organ failure, infected necrosis, longer hospital stays, and a greater need for intervention, with mortality reaching 15% to 30% in severe cases, particularly when infection and multi-organ failure coexist [4].

Extrapancreatic necrosis (EXPN) is increasingly recognized as an important determinant of outcome. It refers to tissue death developing in the peripancreatic and retroperitoneal regions outside the pancreatic parenchyma. Because the pancreas lies within the retroperitoneum, activated enzymes and inflammatory exudate spread along fascial planes and anatomical pathways, producing necrosis in multiple surrounding spaces including the lesser sac, anterior and posterior pararenal spaces, paracolic gutters, mesentery, and omentum, and occasionally extending to the pelvis, mediastinum, or inguinoscrotal region [5].

Computed tomography is the principal imaging tool for evaluating AP, allowing detailed assessment of pancreatic and peripancreatic changes, detection of necrosis and complications, and prediction of severity. Contrast-enhanced CT (CECT) performed after 72-96 hours from symptom onset permits clear identification of both pancreatic and extrapancreatic necrosis, with non-enhancing areas below 30 Hounsfield units indicating necrotic tissue [6]. The Modified CT Severity Index (MCTSI), which grades pancreatic inflammation, necrosis, and extrapancreatic complications, has proved more effective than earlier scoring systems in predicting outcomes, the need for intervention, and mortality [7].

Numerous studies indicate that the presence, extent, location, and volume of EXPN are strongly associated with disease severity, organ failure, infectious complications, the need for intervention, hospitalization duration, and mortality [8]. Patients with isolated EXPN may have outcomes similar to those with isolated pancreatic parenchymal necrosis, whereas those with combined pancreatic and extrapancreatic necrosis usually experience the most severe course [9]. Despite this, the independent effect of EXPN and its distribution patterns remains incompletely defined, with most research focused on pancreatic parenchymal necrosis.

The present study was therefore undertaken to systematically evaluate the role of CT in detecting EXPN and to analyse the relationship between the presence, site, and size of extrapancreatic necrotic collections and clinical outcomes in patients with AP. The specific objectives were: (1) to compare the clinical outcome of patients with AP (acute interstitial pancreatitis plus pancreatic parenchymal necrosis) having EXPN versus those without EXPN; and (2) to evaluate the impact of the site and size of EXPN on clinical outcomes in acute necrotizing pancreatitis.

Study design and settingThis was a prospective cohort study conducted in the Department of Radiodiagnosis, Bangalore Medical College and Research Institute (BMCRI), Bengaluru, Karnataka, India, in collaboration with the Department of General Surgery. Patients diagnosed with acute pancreatitis in the inpatient and outpatient departments of General Surgery underwent CECT of the abdomen in the Department of Radiodiagnosis. The study period extended from March 2024 to August 2025. The diagnosis of AP was established using the revised Atlanta classification, requiring at least two of three features: characteristic abdominal pain; serum amylase or lipase elevated to three times or more the upper limit of normal; and characteristic cross-sectional imaging findings [2]. Participants Consecutive sampling was employed, enrolling all patients who met the criteria and gave written informed consent until the required sample was reached. Inclusion criteria were: age greater than 18 years; willingness to give informed consent; a diagnosis of AP by the revised Atlanta classification; and an initial CECT performed between 4 and 7 days after the onset of pain. Exclusion criteria were: contraindications to CECT such as pregnancy or deranged renal function; chronic calcific pancreatitis; and unwillingness to provide informed written consent. Sample size The sample size was calculated using the single-proportion formula with absolute precision, n = (Z² × p × (1 − p)) / d², where Z = 1.96 (95% confidence), p = 0.79 (expected proportion of patients with multiple extrapancreatic necroses, based on Gupta et al. [8]), and d = 0.09 (absolute precision). This yielded n = 79; after accounting for a potential 10% data loss, the total sample size was adjusted to 87 patients. CT technique and image analysis CECT scans were acquired using either a 128-slice scanner (Philips Ingenuity 128 Elite) or a 32-slice scanner (Siemens Somatom). Imaging was performed 65 seconds after intravenous injection of 80-100 mL of non-ionic contrast medium (Omnipaque 300 mg/mL). The abdomen was scanned from the domes of the diaphragm to the pubic symphysis in the craniocaudal direction with a slice thickness of 1 mm; field of view was 350 mm, tube voltage 120 kV, and tube current 300 mAs. Pancreatic necrosis was defined as a non-enhancing or hypoenhancing area with attenuation less than 30 HU within the pancreatic parenchyma on contrast-enhanced images. The MCTSI was calculated for all patients from the degree of pancreatic inflammation, the percentage of pancreatic necrosis, and the presence of extrapancreatic complications [7]. EXPN was defined as a collection of fluid with or without a solid component located outside the pancreatic parenchyma. Its location was documented according to anatomical sites including the lesser sac, perihepatic/subhepatic, gastrosplenic or perisplenic, anterior pararenal space, posterior pararenal space, paracolic gutters, pelvis, mesentery, omentum, anterior abdominal wall, paraduodenal region, inguinoscrotal region, and thoracic cavity. The craniocaudal, transverse, and anteroposterior dimensions of the largest extrapancreatic necrotic collection were measured, and its volume (mL) was estimated using the ellipsoid formula (Volume = Length × Width × Height × 0.52) [8]. Clinical outcomes were assessed by a general surgeon and comprised: length of hospital stay (days, from admission to discharge); need for intervention including percutaneous catheter drainage (PCD), endoscopic drainage, and necrosectomy (open, minimally invasive, or endoscopic); and death (mortality) recorded up to 12 weeks after discharge. Additional parameters recorded were development of organ failure, infectious complications of necrosis, and need for intensive care unit admission. Statistical analysis Data were entered in Microsoft Excel 2016 and analysed using IBM SPSS Statistics for Windows, Version 29.0. Categorical variables were summarized as frequencies and percentages and continuous variables as mean ± standard deviation (SD). The independent-samples t-test compared means between two groups, and the Mann-Whitney U test was used for non-normally distributed continuous variables; the Kruskal-Wallis test compared more than two groups. The chi-square test assessed associations in categorical data, with Fisher’s exact test applied where expected cell frequencies were below 5. Pearson and Spearman correlation coefficients assessed relationships between continuous variables, and multivariate logistic regression identified independent predictors of adverse outcomes. A p-value less than 0.05 was considered statistically significant. Participant flow: during the study period, patients with AP satisfying the revised Atlanta criteria who met the inclusion criteria and provided written informed consent were enrolled by consecutive sampling until the target of 87 patients was reached. All 87 enrolled patients underwent CECT of the abdomen between 4 and 7 days of symptom onset and were included in the analysis. EXPN was present in 29 patients and absent in 58 patients, forming the two comparison groups.

Table 1. Age distribution of study participants (mean ± SD).

Independent-samples t-test.

Table 2. Age-category distribution of study participants.

Chi-square = 2.326; p = 0.676.

Table 3. Gender distribution of study participants.

Chi-square test (χ² = 1.093).

Eighty-seven patients with acute pancreatitis were studied, of whom 29 (33.3%) had extrapancreatic necrosis (EXPN present) and 58 (66.7%) did not (EXPN absent). The mean age of the cohort was 43.31 ± 11.15 years; patients with EXPN were slightly older (45.83 ± 11.64 vs 42.05 ± 10.77 years) but the difference was not significant (p=0.137) (Table 1). Most patients in both groups were aged 41-50 years, with no significant difference in age-category distribution (χ²=2.326, p=0.676) (Table 2). Males predominated overall (66.7%) and in both groups, without a significant between-group difference (χ²=1.093, p=0.296) (Table 3).

Table 4. Distribution of etiology and socioeconomic status.

Chi-square test.

Table 5. Clinical characteristics of study participants.

†Mann-Whitney U test; *chi-square test.

Alcohol was the commonest etiology (44.8%), followed by gallstones (27.6%); neither etiology (p=0.263) nor socioeconomic status (p=0.637) differed significantly between groups (Table 4). The duration of symptoms before presentation was similar (3.21 ± 1.35 vs 3.10 ± 1.52 days, p=0.638), as was the presence of comorbidities (p=0.756). In contrast, clinical severity by the Atlanta classification differed markedly between groups (p<0.001): all 10 patients with severe AP had EXPN, whereas only 17.2% of EXPN-present patients had mild disease (Table 5).

On CT, pancreatic parenchymal necrosis was far more prevalent among EXPN-present patients (62.1% vs 6.9%, p<0.001) (Table 6). Among the 22 patients with parenchymal necrosis, the extent (<30%, 30-50%, >50%) did not differ significantly by EXPN status (p=0.315). The MCTSI was substantially higher in the EXPN-present group (7.45 ± 2.77 vs 1.55 ± 1.76, p<0.001). Representative CECT images of extrapancreatic necrotic collections at various anatomical sites are shown in Figures 1-6.

Figure 1                                    Figure 2.                                         Figure 3.

Figure 1. Axial contrast-enhanced CT of the abdomen (venous phase) showing well-defined, peripherally enhancing hypodense extrapancreatic necrotic collections in the lesser sac and perisplenic locations. Such extrapancreatic collections are scored within the extrapancreatic-complication component of the Modified CT Severity Index.

Figure 2. Axial contrast-enhanced CT of the abdomen (venous phase) showing well-defined, peripherally enhancing hypodense collections with internal septations in the lesser sac, gastrosplenic and subhepatic locations, reflecting multifocal extrapancreatic necrosis.

 Figure 4.                                                  Figure 5.                                         Figure 6.

Figure 3. Axial contrast-enhanced CT of the abdomen (venous phase) showing a well-defined, peripherally enhancing hypodense extrapancreatic necrotic collection with internal septations in the mesenteric location.

Figure 4. Axial contrast-enhanced CT of the abdomen (venous phase) showing a peripherally enhancing hypodense extrapancreatic necrotic collection with internal septations in the perihepatic location within the right subphrenic region.

Figure 5. Axial contrast-enhanced CT of the abdomen (venous phase) showing a non-enhancing hypodense extrapancreatic necrotic collection in the perihepatic and gastrosplenic locations.

Figure 6. Axial contrast-enhanced CT of the abdomen (venous phase) showing a peripherally enhancing hypodense collection with a few air foci and dependent isodense debris in the left paracolic gutter, extending into the left iliopsoas muscle; the intralesional air foci raise the possibility of infected extrapancreatic necrosis.

Table 6. CT imaging findings in study participants.

*Chi-square test; †Mann-Whitney U test.

Table 7. Comparison of clinical outcomes between EXPN-present and EXPN-absent groups.

†Mann-Whitney U test; *chi-square test; ‡Fisher’s exact test.

Table 8. Association of EXPN with clinical severity and outcomes.

Clinical outcomes were consistently worse with EXPN (Table 7). Hospital stay was longer (29.41 ± 13.44 vs 9.31 ± 3.69 days, p<0.001), intervention was required more often (51.7% vs 6.9%, p<0.001), and 12-week mortality was higher (17.2% vs 1.7%, p=0.015) (Figure 7). Of 19 patients who underwent intervention, PCD was the commonest procedure. Within each Atlanta severity stratum, EXPN was associated with a longer stay and higher intervention rate; among severe cases—all of which had EXPN—mortality was 40.0% (Table 8).

Table 9. Distribution of EXPN by anatomical location (n=29).

Total exceeds 29 as multiple sites were involved in some patients.

Table 10. Comparison of clinical outcomes based on number of EXPN sites (single versus multiple).

†Mann-Whitney U test; ‡Fisher’s exact test.

Table 11. Comparison of clinical outcomes based on EXPN volume categories.

†Kruskal-Wallis test; *chi-square test; ‡Fisher’s exact test.

Table 12. Correlation of EXPN dimensions and volume with hospital stay.

Spearman’s rank correlation coefficient.

EXPN most frequently involved the lesser sac (48.3%), anterior pararenal space (37.9%), mesentery (31.0%), and posterior pararenal space (24.1%); inguinoscrotal and thoracic extension were not observed, and multiple sites were involved in most patients (Table 9, Figure 8). Comparisons by number of sites (single vs multiple), EXPN volume category, and location (retroperitoneal vs non-retroperitoneal/combined) showed no statistically significant differences in outcome, although these subgroups were limited by small single-site (n=2) and retroperitoneal-only (n=2) samples (Tables 10, 11, 13). EXPN dimensions and volume showed only weak, non-significant positive correlations with hospital stay (Table 12).

The MCTSI category was strongly associated with all outcomes (Table 14): hospital stay rose progressively from mild (8.3 ± 2.9 days) to moderate (15.9 ± 7.0) to severe (36.7 ± 10.0) categories (p<0.001) (Figure 9), as did intervention (p<0.001) and mortality (p<0.001) (Figure 10). On multivariate logistic regression (Table 15), EXPN (OR 12.66, 95% CI 1.47-109.31, p=0.021) and clinical severity (OR 9.19, 95% CI 1.68-50.38, p=0.011) were independent predictors of intervention requirement (pseudo R² = 0.340) (Figure 11). No variable reached significance for mortality, likely owing to the small number of deaths (n=6), although clinical severity showed a trend (OR 8.48, p=0.080; pseudo R² = 0.358).

Figure 7.                                                                                                                  Figure 8.

Figure 7. Pancreatic parenchymal necrosis and adverse clinical outcomes (intervention required and 12-week mortality) in patients with versus without extrapancreatic necrosis (data from Tables 6 and 7).

Figure 8. Anatomical distribution of extrapancreatic necrosis across sites among the 29 EXPN-present patients; multiple sites were involved in most patients, so percentages sum to more than 100% (data from Table 9).

Figure 9.                                                                       Figure 10.

Figure 9. Mean length of hospital stay across Modified CT Severity Index categories (data from Table 14).

Figure 10. Intervention and 12-week mortality rates across Modified CT Severity Index categories (data from Table 14).

Figure 11. Adjusted odds ratios (95% CI) for independent predictors of intervention requirement on multivariate logistic regression; the vertical line marks the null value (OR = 1) and the x-axis is logarithmic (data from Table 15).

Table 13. Comparison of outcomes based on EXPN location (retroperitoneal versus non-retroperitoneal/both).

†Mann-Whitney U test; ‡Fisher’s exact test.

Table 14. Modified CTSI score and its association with clinical outcomes.

†Kruskal-Wallis test; *chi-square test; ‡Fisher’s exact test.

Table 15. Multivariate logistic regression analysis for predictors of adverse outcomes.

1. Predictors of intervention requirement (pseudo R² = 0.340)

1. Predictors of mortality (pseudo R² = 0.358)

CI = confidence interval; EXPN = extrapancreatic necrosis; CTSI = CT severity index; *statistically significant (p<0.05).

This prospective study evaluated the role of CT in detecting extrapancreatic necrosis and its effect on clinical outcomes in acute pancreatitis. EXPN emerged as a significant prognostic marker: its presence was strongly associated with greater clinical severity, longer hospitalization, a higher need for intervention, and increased mortality, and it independently predicted the requirement for intervention. These findings add to the growing evidence establishing EXPN as an independent determinant of disease course. EXPN was identified in 33.3% of our cohort, occurring predominantly in patients with more severe disease. This is consistent with existing literature: Gupta et al. documented EXPN in 79% of patients with acute necrotizing pancreatitis, and Dhaka et al. reported combined pancreatic and extrapancreatic necrosis in 84.7% and isolated EXPN in 11.8% of necrotizing cases [8,9]. The frequent occurrence of EXPN reflects the spread of activated enzymes and inflammatory exudate along fascial planes and anatomical spaces beyond the pancreas [10]. The commonest sites in our study—lesser sac, anterior pararenal space, and mesentery—accord with the multicenter series of Bollen et al., in which the lesser sac (62.4%), anterior pararenal space (58.1%), and posterior pararenal space (31.6%) predominated [11]. This distribution follows the retroperitoneal location of the pancreas and the natural pathways of exudate dissection along established fascial planes and potential spaces [12]. The presence of EXPN was closely linked to greater clinical severity, and all severe (Atlanta) cases in our cohort had EXPN. This relationship parallels the work of Petrov et al., who found persistent organ failure in 60.2% of patients with EXPN versus 32.8% without (p<0.001), with extensive EXPN independently associated with organ failure (adjusted OR 4.67, 95% CI 2.18-10.02, p<0.001) [13]. The pathophysiological basis lies in the systemic inflammatory response triggered by extensive necrosis, with capillary leak, third-space sequestration, hemodynamic instability, and multi-organ dysfunction [14]. Extensive tissue necrosis also predisposes to infection. Bollen et al. reported infected necrosis in 38.5% of patients with EXPN versus 22.1% with isolated parenchymal necrosis (p<0.001), and Wang et al. found infected necrosis in 45.8% of patients with combined necrosis versus 17.4% with isolated EXPN (p=0.012) [11,15]. The larger burden of devitalized tissue provides a favorable substrate for bacterial growth, while involvement of the mesentery or colon may facilitate bacterial translocation from the bowel [16]. Gupta et al. showed that both size and site modulate this risk, with collections exceeding 200 mL associated with higher infection rates (52.3% vs 28.6%, p=0.009) and mesenteric involvement independently linked to adverse outcomes (OR 3.24, 95% CI 1.48-7.11, p=0.003) [8]. Consistent with these mechanisms, patients with EXPN in our study required intervention far more often (51.7% vs 6.9%, p<0.001). Bollen et al. similarly reported intervention in 56.4% of patients with EXPN versus 35.7% without (p<0.001), and Wang et al. documented 56.3% versus 26.1% for combined versus isolated involvement (p=0.008) [11,15]. A dose-response relationship has been described, with Gupta et al. reporting intervention in 61.7% for multiple-site versus 32.0% for single-site involvement (p=0.007), and multiple-site involvement and volume greater than 200 mL emerging as independent predictors [8]. In our cohort, EXPN was itself an independent predictor of intervention on multivariate analysis (OR 12.66, p=0.021). The presence of EXPN was strongly associated with prolonged hospitalization (29.41 vs 9.31 days, p<0.001). This mirrors the landmark study of Lankisch et al., in which patients with extrapancreatic fluid collections had significantly longer stays (35.8 ± 23.4 vs 17.6 ± 14.2 days, p<0.001) [5]. Dhaka et al. reported median stays of 32 days for combined necrosis versus 18 days for isolated EXPN and 8 days for interstitial pancreatitis, and Thandassery et al. found markedly prolonged resolution of necrotic collections in extensive disease [9,17]. Prolonged hospitalization reflects higher complication rates, multiple interventions, and delayed recovery. Mortality was significantly higher with EXPN (17.2% vs 1.7%, p=0.015). Lankisch et al. reported mortality of 15.4% versus 2.2% for patients with versus without extrapancreatic collections (p<0.001) [5]. More recent studies confirm graded mortality by necrosis pattern: Dhaka et al. reported 2.4% in interstitial pancreatitis, rising to 23.7% in combined necrosis; Wang et al. found 12.5% for combined versus 0% for isolated EXPN (p=0.042); Gupta et al. reported 18.1% for multiple-site versus 4.0% for single-site involvement (p=0.037); and Thandassery et al. reported 20.6% versus 7.5% for extensive versus limited EXPN (p=0.049) [8,9,15,17]. Anatomic location also carried prognostic weight in prior series, with mesenteric involvement particularly associated with adverse outcomes through the risk of bowel ischemia, bacterial translocation, hemorrhage, and technical difficulty of drainage [18]. Beger et al. identified superior extension into the mediastinum as especially ominous (30.0% mortality vs 14.2% average) and multiple-pattern extension as a driver of postoperative complications [19]. In our smaller cohort, subgroup comparisons by site number, volume, and location did not reach significance, most likely because of limited subgroup sizes. The MCTSI performed robustly in our study, showing strong association with hospital stay, intervention, and mortality, consistent with validation data from Mortele et al. (area under the curve 0.78-0.85) [7]. Bollen et al. found CT-based indices comparable or superior to clinical scores such as APACHE II and Ranson in early severity prediction [20]. The Extrapancreatic Inflammation on CT (EPIC) score of De Waele et al. offers early prediction within 24 hours before necrosis becomes evident, with scores of 3-4 predicting severe AP in 77.8% versus 20.8% for lower scores (p<0.001) [21], and combined CT and clinical scoring further refines risk assessment before necrosis develops [22]. These findings have clear management implications. Early identification of EXPN by CECT at optimal timing (72-96 hours after onset) enables accurate risk stratification and informed decisions regarding monitoring intensity, nutritional support, and anticipatory planning for intervention [23], and the extent and distribution of EXPN should be documented systematically in radiology reports [24]. The optimal timing of intervention remains under study; Beger et al. found that delayed intervention beyond four weeks improved outcomes in extensive peripancreatic necrosis, supporting the conservative, minimally invasive step-up approach advocated by van Santvoort et al. rather than early aggressive surgery [3,19]. Extensive EXPN should therefore prompt close monitoring rather than automatic early intervention [25]. Strengths of this study include its prospective design, systematic CT evaluation using a standardized protocol, comprehensive documentation of EXPN location and extent, adherence to the revised Atlanta classification, use of the validated MCTSI, and assessment of multiple clinically relevant outcomes. Several limitations warrant acknowledgment. The single-center design may limit generalizability. Although the sample size was adequate for the primary objectives, statistical power was limited for certain subgroup analyses, particularly for single-site EXPN (n=2), isolated retroperitoneal involvement (n=2), and mortality (n=6 events), so that the effects of EXPN site, number, and volume could not be reliably demonstrated. Inter-observer variability in CT interpretation, though minimized by standardized protocols, is a potential source of measurement error. Outcomes beyond 12 weeks were not assessed; future research into long-term quality of life, pancreatic function, and recurrence in survivors with extensive EXPN would be valuable [26]. Prospective multicenter studies with larger samples, novel imaging biomarkers such as dual-energy CT and quantitative volumetric analysis [27], and comparative evaluation of interventional strategies in extensive EXPN [28] are needed to refine risk assessment and management.

Extrapancreatic necrosis is an important independent determinant of adverse outcomes in acute pancreatitis. Its presence was significantly associated with greater clinical severity, prolonged hospital stay, a higher need for intervention, and increased mortality, and it independently predicted the requirement for intervention. Contrast-enhanced CT performed at the optimal window of 72-96 hours after symptom onset reliably detects and characterizes EXPN, and the Modified CT Severity Index—incorporating both pancreatic and extrapancreatic findings—is a strong predictor of outcome. Systematic documentation of the presence, number of sites, location, and volume of extrapancreatic necrotic collections should be incorporated into routine radiological reporting to support risk stratification and multidisciplinary management, underscoring the need to evaluate not only the pancreas but also the surrounding tissues in acute pancreatitis.

1. Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med. 2016;375(20):1972-1981.
2. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, et al. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62(1):102-111.
3. van Santvoort HC, Bakker OJ, Bollen TL, Besselink MG, Ahmed Ali U, Schrijver AM, et al. A conservative and minimally invasive approach to necrotizing pancreatitis improves outcome. Gastroenterology. 2011;141(4):1254-1263.
4. Petrov MS, Shanbhag S, Chakraborty M, Phillips AR, Windsor JA. Organ failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology. 2010;139(3):813-820.
5. Lankisch PG, Struckmann K, Lehnick D. Presence and extent of extrapancreatic fluid collections are indicators of severe acute pancreatitis. Int J Pancreatol. 1999;26(3):131-136.
6. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990;174(2):331-336.
7. Mortele KJ, Wiesner W, Intriere L, Shankar S, Zou KH, Kalantari BN, et al. A modified CT severity index for evaluating acute pancreatitis: improved correlation with patient outcome. AJR Am J Roentgenol. 2004;183(5):1261-1265.
8. Gupta P, Rana P, Bellam BL, Samanta J, Mandavdhare H, Sharma V, et al. Site and size of extrapancreatic necrosis are associated with clinical outcomes in patients with acute necrotizing pancreatitis. Pancreatology. 2020;20(1):9-15.
9. Dhaka N, Sinha SK, Samanta J, Gupta V, Yadav TD, Gulati A, et al. Impact of the site of necrosis on outcome of acute pancreatitis: site of necrosis in acute pancreatitis. JGH Open. 2018;2(6):295-299.
10. Takeda K, Takada T, Kawarada Y, Hirata K, Mayumi T, Yoshida M, et al. JPN Guidelines for the management of acute pancreatitis: medical management of acute pancreatitis. J Hepatobiliary Pancreat Surg. 2006;13(1):42-47.
11. Bollen TL, Besselink MG, van Santvoort HC, Gooszen HG, van Leeuwen MS. Toward an update of the Atlanta classification on acute pancreatitis: review of new and abandoned terms. Pancreas. 2007;35(2):107-113.
12. Meyers MA, Evans JA. Effects of pancreatitis on the small bowel and colon: spread along mesenteric planes. AJR Am J Roentgenol. 1973;119(1):151-165.
13. Petrov MS, Pylypchuk RD, Emelyanov NV. Systematic review: nutritional support in acute pancreatitis. Aliment Pharmacol Ther. 2008;28(6):704-712.
14. Singh VK, Bollen TL, Wu BU, Repas K, Maurer R, Yu S, et al. An assessment of the severity of interstitial pancreatitis. Clin Gastroenterol Hepatol. 2011;9(12):1098-1103.
15. Wang M, Wei A, Guo Q, Zhang Z, Lu H, Li A, et al. Clinical outcomes of combined necrotizing pancreatitis versus extrapancreatic necrosis alone. Pancreatology. 2016;16(1):57-65.
16. Schmid SW, Uhl W, Friess H, Malfertheiner P, Büchler MW. The role of infection in acute pancreatitis. Gut. 1999;45(2):311-316.
17. Thandassery RB, Yadav TD, Dutta U, Appasani S, Singh K, Kochhar R. Hypotension in the first week of acute pancreatitis and APACHE II score predict development of infected pancreatic necrosis. Dig Dis Sci. 2015;60(2):537-542.
18. Isenmann R, Rau B, Beger HG. Bacterial infection and extent of necrosis are determinants of organ failure in patients with acute necrotizing pancreatitis. Br J Surg. 1999;86(8):1020-1024.
19. Beger HG, Rau BM. Severe acute pancreatitis: clinical course and management. World J Gastroenterol. 2007;13(38):5043-5051.
20. Bollen TL, Singh VK, Maurer R, Repas K, van Es HW, Banks PA, et al. A comparative evaluation of radiologic and clinical scoring systems in the early prediction of severity in acute pancreatitis. Am J Gastroenterol. 2012;107(4):612-619.
21. De Waele JJ, Delrue L, Hoste EA, De Vos M, Duyck P, Colardyn FA. Extrapancreatic inflammation on abdominal computed tomography as an early predictor of disease severity in acute pancreatitis: evaluation of a new scoring system. Pancreas. 2007;34(2):185-190.
22. Papachristou GI, Muddana V, Yadav D, O’Connell M, Sanders MK, Slivka A, et al. Comparison of BISAP, Ranson’s, APACHE-II, and CTSI scores in predicting organ failure, complications, and mortality in acute pancreatitis. Am J Gastroenterol. 2010;105(2):435-441.
23. Tenner S, Baillie J, DeWitt J, Vege SS. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013;108(9):1400-1415.
24. Thoeni RF. The revised Atlanta classification of acute pancreatitis: its importance for the radiologist and its effect on treatment. Radiology. 2012;262(3):751-764.
25. Freeman ML, Werner J, van Santvoort HC, Baron TH, Besselink MG, Windsor JA, et al. Interventions for necrotizing pancreatitis: summary of a multidisciplinary consensus conference. Pancreas. 2012;41(8):1176-1194.
26. Garip G, Sarandöl E, Kaya E. Effects of disease severity and necrosis on pancreatic dysfunction after acute pancreatitis. World J Gastroenterol. 2013;19(44):8065-8070.
27. Laukkarinen JM, Kemppainen EA, Leppäniemi AK, Puolakkainen PA, Haapiainen RK, Hietaranta AJ, et al. Pancreatic necrosis in acute pancreatitis: evaluation with contrast-enhanced computed tomography. Pancreas. 2007;35(2):96-103.
28. Gurusamy KS, Belgaumkar AP, Haswell A, Pereira SP, Davidson BR. Interventions for necrotising pancreatitis. Cochrane Database Syst Rev. 2016;4(4):CD011383.