Acute pancreatitis other diagnostic studies
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monish Thuvooru Muthu Kalyanaraman, M.B.B.S[2]
Other Diagnostic Studies
This microchapter covers diagnostic studies used in acute pancreatitis beyond standard laboratory testing (lipase, amylase, liver panel) and conventional imaging (CT, MRI/MRCP, ultrasound, chest radiograph). These include severity prediction scoring systems (modified Marshall, BISAP, Ranson, APACHE II, HAPS), CT-guided fine-needle aspiration (FNA) of pancreatic necrosis, genetic testing for hereditary pancreatitis, secretin-stimulated MRCP, duodenal bile crystal analysis, and sphincter of Oddi evaluation. The emphasis is on when each study is indicated, its diagnostic performance, and how it influences clinical decision-making.
Severity Prediction Scoring Systems
Multiple scoring systems have been developed to predict severity in acute pancreatitis. No single system has proven clearly superior, and clinical judgment remains essential.
Modified Marshall Scoring System
The modified Marshall score is the foundation of the revised Atlanta classification for defining organ failure. It assesses three organ systems — respiratory (PaO₂/FiO₂), renal (serum creatinine), and cardiovascular (systolic blood pressure despite fluid resuscitation) — each scored 0–4. A score ≥2 in any system defines organ failure. Persistent organ failure (>48 hours) defines severe acute pancreatitis.[1][2]
BISAP Score (Bedside Index for Severity in Acute Pancreatitis)
Developed in 2008 and validated by Wu et al., the BISAP score uses five variables obtainable within 24 hours of admission:
- BUN >25 mg/dL
- Impaired mental status (GCS <15)
- ≥2 SIRS criteria
- Age >60 years
- Pleural effusion on imaging
A BISAP score ≥3 is associated with increased mortality (AUC for mortality prediction ~0.87).[1] The BISAP is recommended by the ACG 2024 guidelines as a simple, practical bedside tool.[3]
Ranson Criteria
The Ranson score uses 11 variables — 5 measured at admission (age, WBC, glucose, LDH, AST) and 6 at 48 hours (hematocrit fall, BUN rise, calcium, PaO₂, base deficit, fluid sequestration). A score ≥3 predicts severe disease.
Limitations: Requires 48 hours for completion, making it less useful for early triage. Uses variables not routinely obtained in non-ICU patients. A 2024 meta-analysis (Zhu et al.) found the Ranson score had high sensitivity for severity (0.95) but moderate specificity (0.74), with AUC comparable to BISAP for mortality prediction (~0.91 vs 0.92).[4]
APACHE II
Originally designed for ICU patients, APACHE II uses 12 physiologic variables plus age and chronic health status. An APACHE II score ≥8 predicts severe acute pancreatitis with sensitivity 0.83 and specificity 0.59. It can be calculated within 24 hours but is cumbersome and not specific to pancreatitis.[1]
HAPS (Harmless Acute Pancreatitis Score)
HAPS identifies patients with mild, self-limiting disease at admission using three criteria: absence of rebound/guarding, normal hematocrit, and normal creatinine. When all three are present, the score predicts a harmless course with high negative predictive value (~98%), allowing safe early discharge or step-down decisions.[5]
Comparison of Scoring Systems
No scoring system has demonstrated consistent superiority across all outcomes. A 2025 retrospective study of 463 patients found CTSI and BISAP had the best diagnostic accuracy for severe acute pancreatitis (AUC 0.931 and 0.895, respectively).[6] In the 2024 Zhu meta-analysis, Ranson and BISAP had comparable AUC values for severity and mortality prediction.[4]
The ACG 2024 guidelines recommend using SIRS criteria and BUN as the simplest early bedside predictors of severity, while the modified Marshall score should be used to formally classify organ failure.[3]
CT-Guided Fine-Needle Aspiration (FNA)
The role of CT-guided FNA of pancreatic necrosis has declined substantially. The AGA 2020 Clinical Practice Update states that FNA is unnecessary in the vast majority of cases. The ACG 2024 guidelines acknowledge that FNA should be considered when infection is suspected but note that in many patients it will not influence management.[3][7]
Rationale for declining use:
- Infected necrosis can often be presumed clinically (persistent fevers, elevated inflammatory markers, clinical deterioration) or by gas on CT, without FNA confirmation.
- FNA has a false-negative rate of approximately 25%.[8]
- Broad-spectrum antibiotics are typically started empirically on clinical suspicion, and a negative FNA would not necessarily change management.
- There is a theoretical risk of introducing infection into sterile necrosis.
Remaining indications:
- Guidance of antibiotic selection in patients with suspected infected necrosis who deteriorate despite empiric antibiotic therapy.[7]
- When the delayed intervention approach is used (antibiotics alone without drainage), FNA may help confirm infection and guide targeted antimicrobial therapy. A 2025 Dutch post hoc analysis found that 18% of culture-positive percutaneous FNA samples grew pathogens resistant to the administered empiric regimen.[9]
- Percutaneous FNA is preferred over endoscopic FNA due to lower contamination rates (endoscopic FNA had 100% polymicrobial cultures in that series, versus 27% for percutaneous).[9]
Genetic Testing
Genetic testing is indicated for patients with idiopathic acute pancreatitis, recurrent acute pancreatitis without identifiable cause, or a family history of pancreatitis.
Indications (ACG 2020 Chronic Pancreatitis Guidelines, AGA 2022):
- Idiopathic recurrent acute pancreatitis (especially onset before age 35)
- Family history of pancreatitis or chronic pancreatitis
- Early-onset pancreatitis without alcohol or biliary cause
- Evaluation for hereditary pancreatitis syndromes
Genes tested: At minimum, testing should include PRSS1, SPINK1, CFTR, and CTRC. Extended panels incorporating CPA1, CASR, CEL, and other susceptibility genes are increasingly available.[10][11]
- PRSS1 mutations (p.R122H, p.N29I, p.R122C) — cause autosomal dominant hereditary pancreatitis with ~80% penetrance.[12]
- SPINK1 mutations — act as disease modifiers, increasing risk 5–20-fold.
- CFTR mutations — associated with idiopathic pancreatitis; may also present with subtle features of cystic fibrosis.
- CTRC mutations — impair trypsinogen degradation, increasing susceptibility.
Diagnostic yield: A 2024 analysis of 2,468 individuals undergoing multigene panel testing found clinically meaningful pathogenic or likely pathogenic variants in 10.8% of patients under age 35 and 5.4% of those ≥35. Positive family history was the strongest predictor (OR 8.59).[11]
Practical considerations:
- Genetic counseling is recommended before and after testing.[10]
- Genetic testing does not diagnose chronic pancreatitis but identifies high-risk populations and underlying mechanisms.
- Identification of CFTR mutations may have therapeutic implications (CFTR modulator therapy).[10]
Secretin-Stimulated MRCP (S-MRCP)
Secretin-stimulated MRCP enhances visualization of the pancreatic ductal system by stimulating pancreatic fluid secretion, transiently dilating the main pancreatic duct and side branches.
Indications in acute pancreatitis:
- Evaluation of recurrent acute pancreatitis when standard MRCP and EUS are nondiagnostic.
- Detection of pancreas divisum, anomalous pancreaticobiliary junction, and Santorinicele.
- Assessment of pancreatic duct integrity (disconnected duct syndrome).
- Estimation of exocrine pancreatic reserve (duodenal filling grade).[13]
Diagnostic performance:
- S-MRCP has significantly higher sensitivity for detecting ductal abnormalities than standard MRCP (76% vs 56%; AUC 0.983 vs 0.760) in patients with recurrent acute pancreatitis.[14]
- A phase 3 multicenter trial confirmed that synthetic human secretin (RG1068) significantly improved pancreatic duct abnormality detection and reduced unnecessary diagnostic ERCPs.[15]
Limitations:
- Limited availability and variable expertise in acquisition/interpretation.
- Not widely recommended as a first-line test; the AGA 2022 Clinical Practice Update positions EUS as the preferred initial modality, with MRCP (including S-MRCP) as complementary.[16]
Duodenal Bile Crystal Analysis
Microscopic examination of aspirated duodenal bile for cholesterol monohydrate crystals, calcium bilirubinate granules, and calcium carbonate microspheroliths can identify occult microlithiasis in patients with idiopathic pancreatitis.
- Sensitivity approximately 65%, specificity 94–100%.[17]
- Ros et al. demonstrated that 67% of patients with idiopathic pancreatitis had biliary crystals, and cholecystectomy or ursodeoxycholic acid prevented recurrence.[18]
Current status:
- Largely supplanted by EUS, which has superior sensitivity for detecting microlithiasis and sludge and does not require bile aspiration.
- May still be considered in specialized centers when EUS and MRCP are nondiagnostic.[19]
- Not appropriate in patients who have had prior cholecystectomy.
Sphincter of Oddi Evaluation
Sphincter of Oddi manometry has been essentially abandoned as a diagnostic tool for pancreatic sphincter of Oddi dysfunction. The Rome V criteria removed the requirement for abnormal manometry due to its lack of sensitivity, reproducibility, and association with high complication rates (post-ERCP pancreatitis).[20]
The diagnosis of pancreatic sphincter of Oddi disorder now relies on:
- Documented recurrent episodes of acute pancreatitis
- Exclusion of other etiologies (including by EUS)
- Clinical judgment regarding empiric biliary sphincterotomy
EUS has replaced manometry as the principal diagnostic modality in the evaluation of unexplained recurrent pancreatitis.[20]
Clinically Actionable Recommendations
- Use the modified Marshall score to formally classify organ failure and define disease severity per the revised Atlanta classification.
- BISAP and SIRS criteria are the most practical early bedside predictors of severity; calculate at admission.
- Do not routinely perform CT-guided FNA for suspected infected necrosis; start empiric antibiotics based on clinical suspicion. Reserve FNA for antibiotic guidance in patients who fail empiric therapy.
- Refer patients with idiopathic or recurrent acute pancreatitis (especially <35 years or with family history) for genetic counseling and multigene panel testing (PRSS1, SPINK1, CFTR, CTRC at minimum).
- Consider secretin-stimulated MRCP when standard EUS and MRCP are nondiagnostic in recurrent pancreatitis, particularly to evaluate ductal variants and exocrine reserve.
- Do not perform sphincter of Oddi manometry; it has been abandoned due to poor reproducibility and high complication rates.
References
- ↑ 1.0 1.1 1.2 Mederos MA, Reber HA, Girgis MD (2021). "Acute Pancreatitis: A Review". JAMA. 325 (4): 382–390. doi:10.1001/jama.2020.20317. PMID 33496779 Check
|pmid=value (help). - ↑ Trikudanathan G, Yazici C, Evans Phillips A, Forsmark CE (2024). "Diagnosis and Management of Acute Pancreatitis". Gastroenterology. 167 (4): 673–688. doi:10.1053/j.gastro.2024.02.052.
- ↑ 3.0 3.1 3.2 Tenner S, Vege SS, Sheth SG; et al. (2024). "American College of Gastroenterology Guidelines: Management of Acute Pancreatitis". Am J Gastroenterol. 119 (3): 419–437. doi:10.14309/ajg.0000000000002645.
- ↑ 4.0 4.1 Zhu J, Wu L, Wang Y; et al. (2024). "Predictive Value of the Ranson and BISAP Scoring Systems for the Severity and Prognosis of Acute Pancreatitis: A Systematic Review and Meta-Analysis". PLoS One. 19 (4): e0302046. doi:10.1371/journal.pone.0302046.
- ↑ Abu-Elfatth A, Osman AM, Mekky MA; et al. (2026). "Predictive Accuracy of Clinical, Laboratory, and Radiological Scores for Severe Acute Pancreatitis". Sci Rep. 16 (1): 10337. doi:10.1038/s41598-025-34077-1.
- ↑ Shi PN, Song ZZ, He XN, Hong JM (2025). "Evaluation of Scoring Systems and Hematological Parameters in the Severity Stratification of Early-Phase Acute Pancreatitis". World J Gastroenterol. 31 (15): 105236. doi:10.3748/wjg.v31.i15.105236.
- ↑ 7.0 7.1 Baron TH, DiMaio CJ, Wang AY, Morgan KA (2020). "American Gastroenterological Association Clinical Practice Update: Management of Pancreatic Necrosis". Gastroenterology. 158 (1): 67–75.e1. doi:10.1053/j.gastro.2019.07.064.
- ↑ Boxhoorn L, Voermans RP, Bouwense SA; et al. (2020). "Acute Pancreatitis". Lancet. 396 (10252): 726–734. doi:10.1016/S0140-6736(20)31310-6.
- ↑ 9.0 9.1 Pauw HS, Beij A, Timmerhuis HC; et al. (2025). "Fine-Needle Aspiration in Infected Necrotizing Pancreatitis in the Delayed Intervention Era: A Post Hoc Analysis of Safety, Microbiological Yield and Therapeutic Implications". J Antimicrob Chemother. doi:10.1093/jac/dkaf455.
- ↑ 10.0 10.1 10.2 Gardner TB, Adler DG, Forsmark CE; et al. (2020). "ACG Clinical Guideline: Chronic Pancreatitis". Am J Gastroenterol. 115 (3): 322–339. doi:10.14309/ajg.0000000000000535.
- ↑ 11.0 11.1 Ramsey ML, Heald B, Gokun Y; et al. (2024). "Germline Multigene Panel Testing in Acute and Chronic Pancreatitis". PLoS One. 19 (8): e0307076. doi:10.1371/journal.pone.0307076.
- ↑ Mayerle J, Sendler M, Hegyi E; et al. (2019). "Genetics, Cell Biology, and Pathophysiology of Pancreatitis". Gastroenterology. 156 (7): 1951–1968.e1. doi:10.1053/j.gastro.2018.11.081.
- ↑ Swensson J, Zaheer A, Conwell D; et al. (2021). "Secretin-Enhanced MRCP: How and Why—AJR Expert Panel Narrative Review". AJR Am J Roentgenol. 216 (5): 1139–1149. doi:10.2214/AJR.20.24857.
- ↑ Sandrasegaran K, Tahir B, Barad U; et al. (2017). "The Value of Secretin-Enhanced MRCP in Patients With Recurrent Acute Pancreatitis". AJR Am J Roentgenol. 208 (2): 315–321. doi:10.2214/AJR.16.16566.
- ↑ Sherman S, Freeman ML, Tarnasky PR; et al. (2014). "Administration of Secretin (RG1068) Increases the Sensitivity of Detection of Duct Abnormalities by Magnetic Resonance Cholangiopancreatography in Patients With Pancreatitis". Gastroenterology. 147 (3): 646–654.e2. doi:10.1053/j.gastro.2014.05.035.
- ↑ Strand DS, Law RJ, Yang D, Elmunzer BJ (2022). "AGA Clinical Practice Update on the Endoscopic Approach to Recurrent Acute and Chronic Pancreatitis: Expert Review". Gastroenterology. 163 (4): 1107–1114. doi:10.1053/j.gastro.2022.07.079.
- ↑ Draganov P, Forsmark CE (2005). ""Idiopathic" Pancreatitis". Gastroenterology. 128 (3): 756–763. doi:10.1053/j.gastro.2005.01.037.
- ↑ Ros E, Navarro S, Bru C, Garcia-Pugés A, Valderrama R (1991). "Occult Microlithiasis in 'Idiopathic' Acute Pancreatitis: Prevention of Relapses by Cholecystectomy or Ursodeoxycholic Acid Therapy". Gastroenterology. 101 (6): 1701–1709. doi:10.1016/0016-5085(91)90410-m.
- ↑ Chandrasekhara V, Chathadi KV, Acosta RD; et al. (2015). "The Role of Endoscopy in Benign Pancreatic Disease". Gastrointest Endosc. 82 (2): 203–214. doi:10.1016/j.gie.2015.04.022.
- ↑ 20.0 20.1 Elmunzer BJ, Winslow E, De Giorgio R; et al. (2026). "Gallbladder and Sphincter of Oddi Disorders". Gastroenterology. 170 (6): 1303–1317. doi:10.1053/j.gastro.2026.01.035.