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Research Article | Volume 11 Issue 5 (May, 2025) | Pages 804 - 809
Risk Stratification and Clinical Outcomes in Gallstone-Related Acute Pancreatitis: A Prospective Observational Analysis from a Tertiary Centre
 ,
1
Associate Professor, Department of General Surgery, Mulugu Medical College, Mulugu, Telangana, India
2
Associate Professor, Department of General Surgery, Bhupalpally Medical College, Bhupalpally, Telangana, India
Under a Creative Commons license
Open Access
Received
May 1, 2025
Revised
May 8, 2025
Accepted
May 20, 2025
Published
May 30, 2025
Abstract

Background: Gallstone pancreatitis is a leading cause of acute pancreatitis, marked by substantial morbidity and variable clinical outcomes. Identifying specific risk factors influencing disease severity can guide therapeutic decisions and prognostication. Materials and Methods: This prospective observational study was conducted over 12 months at a tertiary care center, enrolling 162 adult patients diagnosed with gallstone-induced acute pancreatitis. Patients were stratified into mild, moderately severe, and severe pancreatitis groups per the Revised Atlanta Classification. Baseline demographic, clinical, biochemical, and imaging data were collected. Key risk factors analyzed included age, BMI, comorbidities, leukocytosis, CRP, serum amylase, lipase, and imaging features. Outcomes assessed were ICU stay, necrosis, organ failure, and mortality. Chi-square and logistic regression analyses were performed. Results: Among 162 patients (mean age 46.2 ± 13.4 years; 57.4% female), 53.1% had mild, 30.2% moderately severe, and 16.7% severe disease. Age >60 years (OR 3.4; 95% CI: 1.6–7.1; p=0.002), BMI ≥30 (OR 2.8; p=0.008), elevated CRP >150 mg/L (OR 4.5; p<0.001), and CT-documented necrosis >30% (p<0.001) were significantly associated with severe pancreatitis. Overall mortality was 6.2%, exclusively in the severe group. ICU admission and multiorgan failure were independently associated with CRP >150 and necrosis. Conclusion: Older age, obesity, elevated inflammatory markers, and imaging-detected necrosis were significant predictors of adverse outcomes in gallstone pancreatitis. Early risk stratification using these parameters can optimize management and reduce complications.

Keywords
INTRODUCTION

Acute pancreatitis is an inflammatory condition of the pancreas with varying clinical presentations and outcomes. Gallstones represent the most common identifiable etiology globally, accounting for nearly 40–60% of cases [1]. Gallstone pancreatitis occurs when gallstones or biliary sludge transiently obstruct the ampulla of Vater, initiating enzymatic activation and inflammatory responses within the pancreas. While most cases resolve with conservative management, a subset progresses to severe disease involving necrosis, systemic inflammation, and multiorgan failure [2].

 

Clinical prediction of disease severity at presentation remains a formidable challenge. Although several scoring systems—such as BISAP, APACHE II, and Ranson’s criteria—exist, their utility in gallstone-specific pancreatitis has been variably validated [3]. Early identification of patients at risk for severe complications is crucial to improve outcomes, reduce ICU burden, and guide decisions regarding interventions such as early ERCP, cholecystectomy, or intensive supportive care.

 

The Revised Atlanta Classification stratifies disease into mild, moderately severe, and severe forms based on the presence and persistence of organ failure and local/systemic complications [4]. In gallstone pancreatitis, certain clinical and laboratory parameters have been proposed as potential predictors of severity—such as leukocytosis, elevated CRP, BMI, hyperglycemia, and radiological evidence of necrosis [5]. However, the predictive performance of these markers in routine clinical settings, especially in resource-limited environments, is inconsistent [6].

 

Moreover, while outcomes such as mortality and ICU admission have been linked to disease severity, few studies have prospectively evaluated gallstone pancreatitis in terms of both risk factors and clinical outcomes using standardized classifications [7-9]. In many tertiary centers in developing countries, delays in diagnosis, referral, and access to endoscopic/surgical services may further influence outcomes [10].

 

This study aims to evaluate key demographic, clinical, biochemical, and radiological risk factors influencing the severity and outcomes of gallstone-induced acute pancreatitis. By prospectively analyzing a cohort of patients presenting with this condition, we seek to develop a clearer understanding of predictors of complications such as necrosis, organ failure, ICU stay, and mortality.

MATERIALS AND METHODS

Study Design and Setting

A prospective observational study was conducted at the Department of Surgery, Mulugu Medical College a tertiary care referral center, from December 2024 to January 2025.

 

Study Population

All adult patients (>18 years) admitted with a diagnosis of acute pancreatitis were screened. Inclusion criteria comprised: (1) acute abdominal pain consistent with pancreatitis, (2) serum amylase or lipase ≥ 3 times the upper normal limit, and (3) imaging-confirmed pancreatitis (USG/CT). Only patients with gallstone etiology (confirmed by USG or MRCP showing cholelithiasis or choledocholithiasis) were included. Exclusion criteria were: (a) alcohol-related pancreatitis, (b) hypertriglyceridemia (>1000 mg/dL), (c) post-ERCP pancreatitis, (d) known pancreatic malignancy, and (e) incomplete data.

 

Sample Size

A total of 162 patients fulfilled eligibility and were included after informed consent.

 

Data Collection

Demographics (age, gender, BMI), comorbidities (diabetes, hypertension), symptom duration, lab values (WBC, CRP, amylase, lipase, creatinine, bilirubin), and imaging (CECT abdomen at 72 hours) were recorded. Severity was classified per Revised Atlanta Criteria into mild, moderately severe, and severe [4].

 

Outcomes Assessed

Primary outcomes included severity classification, necrosis extent, ICU admission, and in-hospital mortality. Secondary outcomes involved duration of stay and need for interventions (ERCP, drainage). Complications like pseudocyst, infected necrosis, and persistent organ failure were documented.

 

Statistical Analysis

Data were analyzed using SPSS v26. Continuous variables were expressed as mean ± SD and compared using ANOVA or t-test. Categorical variables were analyzed using chi-square or Fisher’s exact test. Logistic regression identified independent predictors of severe pancreatitis. A p-value <0.05 was considered statistically significant.

 

Ethical Considerations

The study was approved by the Institutional Ethics Committee. Written informed consent was obtained from all participants.

RESULTS

Table 1: Demographic and Clinical Profile

Parameter

Mild (n=86)

Moderate (n=49)

Severe (n=27)

p-value

Age (years, mean ± SD)

42.8 ± 12.6

47.3 ± 13.1

59.4 ± 11.2

<0.001

Female (%)

48 (55.8%)

30 (61.2%)

15 (55.6%)

0.84

BMI ≥30 (%)

11 (12.7%)

10 (20.4%)

10 (36.4%)

0.003

Diabetes Mellitus (%)

17 (19.8%)

11 (22.4%)

9 (33.3%)

0.11

Hypertension (%)

21 (24.4%)

15 (30.6%)

10 (37.0%)

0.17

 

Table 2: Severity-wise Distribution of Risk Factors

Risk Factor

Mild

Moderate

Severe

p-value

CRP >150 mg/L (%)

9 (10.4%)

21 (42.9%)

24 (88.9%)

<0.001

WBC >15000 (/mm³)

12 (14.0%)

18 (36.7%)

21 (77.8%)

<0.001

Serum Creatinine >1.5 mg/dL

4 (4.7%)

8 (16.3%)

17 (63.0%)

<0.001

Necrosis >30% on CT (%)

2 (2.3%)

10 (20.4%)

20 (74.1%)

<0.001

Persistent Organ Failure (%)

0 (0.0%)

5 (10.2%)

17 (63.0%)

<0.001

 

Table 3: Outcomes and Complications by Severity

Outcome

Mild

Moderate

Severe

p-value

ICU Admission (%)

0 (0.0%)

4 (8.2%)

20 (74.1%)

<0.001

Multiorgan Failure (%)

0 (0.0%)

2 (4.1%)

10 (37.0%)

<0.001

Length of Stay (days, mean ± SD)

4.2 ± 1.5

7.4 ± 2.2

12.6 ± 3.7

<0.001

In-hospital Mortality (%)

0 (0.0%)

0 (0.0%)

6 (22.2%)

<0.001

ERCP Needed (%)

13 (15.1%)

16 (32.7%)

19 (70.4%)

<0.001

 

Table 4: Predictors of Severe Pancreatitis (Logistic Regression)

Predictor

Odds Ratio (OR)

95% Confidence Interval

p-value

Age >60 years

3.4

1.6–7.1

0.002

BMI ≥30

2.8

1.3–6.1

0.008

CRP >150 mg/L

4.5

2.1–9.7

<0.001

WBC >15000

1.9

0.9–3.9

0.07

Necrosis >30%

5.8

2.7–12.3

<0.001

 

Table 5: Comparison of ICU Admission and Mortality Based on Risk Markers

Parameter

ICU Admission (%)

Mortality (%)

p-value (ICU)

p-value (Mortality)

CRP >150 mg/L

22/54 (40.7%)

6/54 (11.1%)

<0.001

0.002

Necrosis >30%

21/32 (65.6%)

5/32 (15.6%)

<0.001

<0.001

Age >60 years

15/42 (35.7%)

4/42 (9.5%)

0.01

0.04

WBC >15000

16/51 (31.4%)

3/51 (5.9%)

0.04

0.06

BMI ≥30

12/31 (38.7%)

3/31 (9.7%)

0.03

0.07

 

In this prospective cohort of 162 patients with gallstone pancreatitis, the majority had mild disease (53.1%), while 30.2% were moderately severe and 16.7% had severe pancreatitis. Age showed a significant association with severity, increasing from a mean of 42.8 ± 12.6 years in the mild group to 59.4 ± 11.2 years in the severe group (p < 0.001). Similarly, the proportion of patients with BMI ≥30 rose from 12.7% in mild to 36.4% in severe cases (p = 0.003), indicating obesity as a contributing risk factor.

 

Inflammatory markers were strongly predictive of severity. CRP >150 mg/L was observed in 88.9% of severe cases compared to 10.4% in mild cases (p < 0.001). WBC >15,000/mm³ was present in 77.8% of severe patients versus 14.0% of mild cases (p < 0.001). CT-detected pancreatic necrosis >30% occurred in 74.1% of severe cases (p < 0.001), and 63.0% of these patients developed persistent organ failure. ICU admission rates escalated with severity: 0% in mild, 8.2% in moderate, and 74.1% in severe pancreatitis (p < 0.001). In-hospital mortality was 0% for both mild and moderate cases but reached 22.2% in severe cases (p < 0.001). Patients with CRP >150 mg/L and necrosis >30% had the highest ICU admission rates (40.7% and 65.6%, respectively) and mortality rates (11.1% and 15.6%, respectively). Logistic regression identified CRP >150 mg/L (OR 4.5, p<0.001), age >60 years (OR 3.4, p=0.002), and necrosis >30% (OR 5.8, p<0.001) as independent predictors of severe pancreatitis. Although WBC >15000 and BMI ≥30 showed elevated odds, they did not reach statistical significance in multivariate analysis (p=0.07 and p=0.008, respectively).

 

These findings underscore the importance of inflammatory markers and imaging in early risk assessment and outcome prediction.

DISCUSSION

Gallstone pancreatitis represents a prevalent form of acute pancreatitis with variable clinical progression, ranging from self-limiting inflammation to life-threatening systemic complications. This prospective observational study aimed to identify and evaluate key clinical, biochemical, and radiological predictors of disease severity and their association with outcomes such as ICU admission and mortality.

 

The rationale for this investigation was grounded in the need for improved early risk stratification in gallstone pancreatitis. Despite multiple severity scoring systems, their predictive reliability in gallstone-specific cases remains inconsistent in daily clinical use. Our findings reinforce that simple, readily available clinical markers—particularly age >60 years, CRP >150 mg/L, BMI ≥30, and CT-proven necrosis >30%—serve as strong indicators of severe disease and adverse outcomes.

 

When compared with existing literature, our results demonstrate both concordance and clinical utility. The Revised Atlanta Classification [11] effectively stratified our cohort, with 16.7% falling into the severe category, aligning with global severity distribution trends [12]. CRP >150 mg/L, found in 88.9% of severe cases in our study, has been repeatedly validated in prior works as a reliable inflammatory predictor [13,14]. Moreover, the presence of necrosis >30% was strongly associated with both ICU requirement and mortality (65.6% and 15.6%, respectively), echoing findings from Bollen et al. [11] and Singh et al. [15].

 

Our study’s observation that age >60 years significantly correlates with worse outcomes (OR 3.4, p=0.002) mirrors previous studies highlighting age-related immune dysregulation and comorbidity burden as contributors to disease escalation [16]. Additionally, the association between obesity (BMI ≥30) and disease severity (36.4% in severe group, p=0.003) supports existing evidence linking visceral adiposity with heightened inflammatory responses in acute pancreatitis [17].

 

Clinical implications of these findings are considerable. Prompt CRP measurement and early cross-sectional imaging in high-risk individuals can facilitate triage decisions and inform the need for intensive monitoring or escalation of care. Furthermore, our results underscore the necessity for early cholecystectomy and ERCP in select cases to prevent recurrence and mitigate complications, particularly in moderate to severe disease. Nonetheless, certain limitations must be acknowledged. The study was conducted at a single tertiary center, which may limit generalizability. Additionally, long-term outcomes such as readmission and recurrence were not assessed due to the focus on in-hospital metrics. Despite these constraints, the prospective nature, consistent data acquisition, and focused gallstone-only population enhance the study’s internal validity. Future research should expand on these findings through multicentric studies and explore composite scoring systems incorporating CRP, BMI, and imaging features for rapid bedside application. Integration with AI-based prediction tools may further enhance early severity assessment in diverse clinical settings.

CONCLUSION

This prospective study highlights that gallstone pancreatitis exhibits a diverse clinical course, with severity influenced by identifiable risk factors. Our findings confirm that age above 60 years, obesity, elevated CRP (>150 mg/L), and extensive pancreatic necrosis (>30%) are significant predictors of severe disease and adverse outcomes, including ICU admission and mortality.

 

These parameters, available early during hospitalization, offer practical value for risk stratification. Incorporating such markers into routine assessment protocols may guide clinicians in making timely decisions regarding monitoring intensity, imaging, and therapeutic interventions.

Given the potential for rapid deterioration in high-risk individuals, a structured approach based on these findings can improve triage efficiency, optimize critical care resources, and enhance patient outcomes. Future multicenter studies are warranted to validate these predictors and develop simplified severity prediction models specific to gallstone pancreatitis.

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