Acute pancreatitis CT

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2]; Monish Thuvooru Muthu Kalyanaraman, M.B.B.S[3]

Overview

In acute pancreatitis, contrast-enhanced CT (CECT) is most useful when the diagnosis is uncertain, the patient fails to improve or deteriorates after 48–72 hours, necrosis or another local complication is suspected, or an intervention is being planned.[1][2] CT is not routinely required when acute pancreatitis has already been established by characteristic abdominal pain and pancreatic enzyme elevation and the patient is improving clinically.

The principal CT findings of acute pancreatitis are pancreatic enlargement, altered pancreatic enhancement, peripancreatic inflammation, pancreatic or peripancreatic necrosis, fluid collections, and local vascular or gastrointestinal complications. The timing of CT must be matched to the clinical question because CT performed during the first 24–48 hours may underestimate or fail to demonstrate evolving necrosis.

Key CT Findings in Acute Pancreatitis

Indications and Timing

Acute pancreatitis is diagnosed when at least 2 of the following 3 criteria are present:

  • Characteristic abdominal pain
  • Serum lipase or amylase at least 3 times the upper limit of normal
  • Characteristic imaging findings[1]
Clinical situation Role of CT Practical interpretation
Diagnostic uncertainty CECT may help confirm acute pancreatitis or identify another intra-abdominal diagnosis. CT is appropriate when the symptoms or laboratory findings are equivocal or when bowel perforation, mesenteric ischemia, obstruction, or another emergency is possible.[2]
Typical presentation with clear enzyme elevation and clinical improvement Routine early CT is not indicated. Transabdominal ultrasound is the preferred initial imaging study for evaluating gallstones and biliary etiology.[1][2]
Failure to improve after 48–72 hours CECT may assess necrosis and local complications. Early CT can underestimate necrosis; imaging should be performed when its result is expected to affect management.[1][3]
Clinical deterioration CECT is indicated to assess for necrosis, infection, hemorrhage, vascular complications, bowel complications, or another cause of deterioration. Arterial-phase imaging or CT angiography should be added when active hemorrhage or pseudoaneurysm is suspected.
Suspected infected necrosis CECT may identify gas, fistulization, collection maturation, and other findings that guide intervention. Absence of gas does not exclude infected necrosis.
Pre-procedural planning CECT defines the location, extent, wall maturity, solid debris, and relationship of collections to adjacent structures. MRI or endoscopic ultrasound may better demonstrate occult solid debris within a predominantly fluid collection.[4]

The cited 2019 ACR Appropriateness Criteria describe five clinical variants:[2]

ACR variant Clinical scenario Imaging emphasized by the ACR
1 First presentation with typical pain and elevated amylase/lipase, less than 48–72 hours after symptom onset Abdominal ultrasound is usually appropriate to assess for gallstones; routine early CECT is generally unnecessary.
2 Critically ill patient with systemic inflammatory response syndrome or severe clinical scores, more than 48–72 hours after symptom onset CECT is usually appropriate; contrast-enhanced MRI with MRCP is a reasonable alternative when feasible.
3 Continued systemic inflammatory response syndrome, severe clinical scores, leukocytosis, or fever, 7–21 days after symptom onset CECT is usually appropriate to reassess necrosis and collections.
4 Atypical presentation, equivocal pancreatic enzyme values, or possible alternative diagnosis CECT is usually appropriate as a rapid comprehensive examination.
5 Known necrotizing pancreatitis with significant clinical deterioration CECT is usually appropriate; the protocol should be tailored when hemorrhage or another specific complication is suspected.
  • A normal or near-normal CT during the first 24–48 hours does not exclude acute pancreatitis or later necrosis.
  • When the purpose of CT is to evaluate pancreatic necrosis, delayed imaging at approximately 72–96 hours or later is generally more informative than immediate admission CT.[3][5]
  • Collections persisting beyond approximately 4 weeks should be characterized for encapsulation and for the presence or absence of necrotic debris.
  • There is no role for routine serial CT in a patient who is improving clinically. Repeat CT should be prompted by a clinical question rather than a fixed schedule.

CT Protocol

The CT protocol for acute pancreatitis should be tailored to the clinical indication:

Protocol component Role Important limitation or qualification
Portal venous phase CECT Usually sufficient for routine assessment of pancreatic enhancement, peripancreatic inflammation, necrosis, collections, and most complications. A 2024 retrospective study found that a single portal venous phase provided severity scores equivalent to a triple-phase protocol while reducing radiation exposure.[6]
Arterial-phase imaging or CT angiography Evaluates suspected pseudoaneurysm, active hemorrhage, or another arterial complication. Timing should follow the institution's angiographic protocol; routine multiphase CT is not necessary for uncomplicated severity assessment.
Non-contrast CT May identify calcification, hemorrhage, or another diagnosis when intravenous contrast cannot be administered. Non-contrast CT cannot reliably assess pancreatic parenchymal necrosis.
Pediatric CT When CT is necessary in children, intravenous contrast and a dose-optimized single-phase examination are generally preferred. Pediatric imaging recommendations should not be directly generalized to adult protocol selection.[7]

Intravenous iodinated contrast is important when the purpose of CT is to evaluate pancreatic enhancement or necrosis. The historical concern that iodinated contrast worsens acute pancreatitis has not been confirmed in human clinical studies and is not a reason to withhold clinically indicated CECT, although standard assessment of renal function and contrast-related risk remains necessary.[8]

Interstitial Edematous and Necrotizing Acute Pancreatitis

Acute pancreatitis is divided morphologically into interstitial edematous pancreatitis and necrotizing pancreatitis.[9]

Feature Interstitial edematous pancreatitis Necrotizing pancreatitis
Pancreatic parenchyma Focal or diffuse enlargement with preserved, relatively homogeneous enhancement Focal or diffuse hypoenhancing or non-enhancing parenchyma when pancreatic necrosis is present
Peripancreatic tissue Fat stranding, inflammatory change, and simple fluid Heterogeneous peripancreatic inflammation or necrosis containing nonliquid material; necrosis may be pancreatic, peripancreatic, or both
Fluid distribution May extend through the lesser sac, anterior pararenal spaces, fascial planes, or paracolic gutters May evolve into acute necrotic collections and subsequently walled-off necrosis
Fascial findings Thickening of the anterior renal fascia may be present More extensive retroperitoneal inflammation and collections may be present
Distinguishing feature Preserved pancreatic enhancement Non-enhancing pancreatic parenchyma and/or morphologic evidence of peripancreatic necrosis

Interstitial edematous pancreatitis accounts for most cases of acute pancreatitis. Necrotizing pancreatitis is less common but is associated with substantially greater morbidity. Reported estimates vary according to the population and whether isolated peripancreatic necrosis is included in the definition.[10][11][4]

Important points when evaluating necrotizing pancreatitis include:

  • Pancreatic parenchymal necrosis appears as focal or diffuse non-enhancement on CECT.
  • Peripancreatic necrosis may occur without pancreatic parenchymal necrosis and can be missed if interpretation is limited to pancreatic enhancement.
  • Isolated peripancreatic necrosis accounts for a substantial proportion of necrotizing pancreatitis.[1][12]
  • Early CECT may underestimate the final extent of necrosis.
  • Quantitative necrosis volume and mean attenuation have shown prognostic value in research cohorts but remain investigational and are not part of routine guideline-based assessment.[13]

Emerging CT Techniques

Emerging techniques for acute pancreatitis include subtraction CT and CT perfusion:

  • A subtraction color-map technique improved early detection of pancreatic necrosis compared with conventional CECT in one study, with reported sensitivity of 82–100% and specificity of 92–100%.[14]
  • A systematic review of CT perfusion reported sensitivity of 71–100% and specificity of 74–100% for predicting necrosis.[15]
  • These techniques remain investigational or limited to specialized centers and are not recommended as routine imaging by current acute pancreatitis guidelines.[1]

Pancreatic and Peripancreatic Collections

In acute pancreatitis, pancreatic and peripancreatic collection terminology should follow the Revised Atlanta Classification. The terms "phlegmon" and "pancreatic abscess" are obsolete and should not be used.[9]

Approximate timing Collection Associated morphologic subtype CT characteristics
Less than 4 weeks Acute peripancreatic fluid collection Interstitial edematous pancreatitis Homogeneous fluid attenuation; no definable wall; no solid component; conforms to normal fascial planes
Acute necrotic collection Necrotizing pancreatitis Heterogeneous fluid and nonliquid material; no definable wall; may involve the pancreas, peripancreatic tissues, or both
Usually 4 weeks or later Pancreatic pseudocyst Interstitial edematous pancreatitis Homogeneous fluid attenuation; well-defined wall; round or oval; no solid necrotic component
Walled-off necrosis Necrotizing pancreatitis Encapsulated collection with a well-defined enhancing wall and variable amounts of fluid, fat, or necrotic debris

Important interpretive points include:

  • The distinction between a pseudocyst and walled-off necrosis is based primarily on the presence or absence of necrotic material, not on wall formation alone.
  • The presence of solid debris influences the feasibility and complexity of drainage or debridement, but walled-off necrosis does not automatically require necrosectomy.
  • CECT may miss small amounts of solid debris within a fluid-predominant collection. MRI and endoscopic ultrasound are more sensitive for this purpose.[10]
  • A collection should not be labeled a pseudocyst merely because it appears cystic. A pseudocyst occurs in interstitial edematous pancreatitis and contains no solid necrotic material.
  • Although encapsulation generally develops after approximately 4 weeks, substantial encapsulation may occur earlier. The time threshold is a guide and should be interpreted together with morphology.[16][10]

CT Severity Scoring

In acute pancreatitis, the Balthazar CT grade and pancreatic necrosis score are combined to produce the CT Severity Index (CTSI).[17]

Balthazar CT grade Pancreatic necrosis score
Grade CT appearance Points Extent of necrosis Points
A Normal pancreas 0 None 0
B Focal or diffuse pancreatic enlargement 1 30% or less 2
C Pancreatic abnormality with peripancreatic inflammatory change 2 More than 30% to 50% 4
D Single peripancreatic fluid collection 3 More than 50% 6
E Two or more fluid collections and/or retroperitoneal gas 4

CTSI = Balthazar CT grade points + pancreatic necrosis points.

  • CTSI ranges from 0 to 10.
  • In the original 1990 cohort of 88 patients, CTSI 0–3 was associated with approximately 8% morbidity and 3% mortality; CTSI 4–6 with 35% morbidity and 6% mortality; and CTSI 7–10 with 92% morbidity and 17% mortality.[17]
  • These historical estimates should not be presented as contemporary individual risk estimates because the original cohort was small and clinical and interventional management has changed substantially.[18]

The Modified CT Severity Index (MCTSI) simplifies the assessment of pancreatic inflammation and necrosis and adds extrapancreatic complications.[19]

MCTSI component Finding Points
Pancreatic inflammation Normal pancreas 0
Intrinsic pancreatic abnormality with or without peripancreatic inflammation 2
Pancreatic or peripancreatic fluid collection or peripancreatic fat necrosis 4
Pancreatic necrosis None 0
30% or less 2
More than 30% 4
Extrapancreatic complications One or more pleural effusions, ascites, vascular complications, gastrointestinal complications, or extrapancreatic parenchymal abnormalities 2

MCTSI ranges from 0 to 10. The original validation study reported improved correlation with several clinical outcomes compared with CTSI. Subsequent comparative studies and meta-analysis have not consistently demonstrated that either index is superior, although MCTSI explicitly incorporates extrapancreatic complications.[20][21][22]

A 2026 meta-analysis of 5,419 patients found that the predictive performance of CTSI varied with imaging time: earlier assessment was more sensitive for predicting clinical severity, whereas assessment after 72 hours performed better for detecting pancreatic necrosis.[23]

The Extrapancreatic Inflammation on CT score is another CT-based prognostic score and has been compared with CTSI, MCTSI, and clinical scoring systems.[24]

CT severity scores:

  • Provide standardized radiologic descriptions
  • Support risk stratification and prognostication
  • Complement but do not replace clinical assessment
  • Do not replace the Revised Atlanta clinical severity categories, which are based on organ failure and local or systemic complications

Vascular and Hemorrhagic Complications

Acute pancreatitis may cause venous thrombosis, arterial pseudoaneurysm, and active hemorrhage.

Complication CT finding Clinical relevance
Splenic, portal, or superior mesenteric vein thrombosis Partial or complete venous filling defect, venous non-opacification, collateral vessels, or findings of left-sided portal hypertension Splanchnic vein thrombosis is more common in necrotizing pancreatitis and becomes more frequent as the disease evolves.[25][26][27]
Pseudoaneurysm Focal intensely enhancing arterial structure within or adjacent to an inflammatory or necrotic collection The splenic and gastroduodenal arteries are commonly involved; rupture may cause life-threatening hemorrhage.[28][29]
Active hemorrhage Active contrast extravasation, enlarging hematoma, or high-attenuation blood products Urgent arterial-phase imaging or CT angiography is appropriate when hemorrhage is suspected.
  • A sudden decrease in hemoglobin, hypotension, or otherwise unexplained deterioration should prompt evaluation for active bleeding or pseudoaneurysm.
  • A routine portal venous study may miss an arterial lesion; arterial-phase imaging should be added when hemorrhage is the clinical question.
  • In one cohort of patients with necrotizing pancreatitis and visceral artery pseudoaneurysm, CT identified approximately 84% of pseudoaneurysms. This cohort-specific figure should not be interpreted as universal CT sensitivity.[29]
  • When clinical suspicion remains high despite a negative CT, further evaluation should be determined with interventional radiology according to the patient's presentation and the adequacy of the CT protocol.

Infection and Other CT-Identifiable Complications

In acute pancreatitis, gas within a necrotic collection is strongly suggestive of infected necrosis when there has been no prior drainage or instrumentation and no gastrointestinal fistula. Gas is not present in every case of infected necrosis, and its absence does not exclude infection.[12][30][16][10]

Additional CT-identifiable complications include:

  • Gastric outlet or duodenal obstruction from inflammation or a mature collection
  • Distal common bile duct compression
  • Colonic inflammation, ischemia, necrosis, fistula, or perforation
  • Pancreatic ascites or pleural effusion
  • Pancreatic duct disruption or disconnected pancreatic duct syndrome, although MRCP is generally better for ductal characterization
  • Pancreatic or gastrointestinal fistula
  • Extrapancreatic organ inflammation or infarction

CT may show findings associated with intra-abdominal hypertension or abdominal compartment syndrome, such as bowel wall thickening, venous compression, and extensive ascites. These findings are nonspecific, and CT does not diagnose abdominal compartment syndrome; diagnosis requires the appropriate clinical setting and measurement of intra-abdominal pressure.[31]

CT-guided fine-needle aspiration is not routinely required to diagnose infected pancreatic necrosis because clinical and imaging findings usually guide management and false-negative cultures may occur. Selective aspiration may be considered when diagnostic uncertainty would change treatment.[4][1][12][30]

Common CT Interpretation Pitfalls

In acute pancreatitis, common CT interpretation pitfalls include:

Pitfall Correct interpretation
Excluding acute pancreatitis because an early CT is normal CT may be normal or near-normal early in the disease and may underestimate evolving necrosis.
Calling every mature collection a pseudocyst A pseudocyst contains fluid without necrotic debris and follows interstitial edematous pancreatitis; a mature necrotic collection is walled-off necrosis.
Assessing only pancreatic parenchymal enhancement Necrotizing pancreatitis may consist of isolated peripancreatic necrosis without pancreatic parenchymal necrosis.
Interpreting gas as proof of infection in every case Gas strongly suggests infection but may also follow intervention or result from fistulization.
Using portal venous imaging alone when hemorrhage is suspected Add arterial-phase imaging or CT angiography to assess for pseudoaneurysm or active bleeding.
Treating a CT severity score as the clinical severity classification CTSI and MCTSI complement clinical assessment; the Revised Atlanta clinical classification is based principally on organ failure and complications.

CT Examples of Acute Pancreatitis

The following CT example demonstrates acute pancreatitis with extensive peripancreatic fluid:

File:Akute exsudative Pankreatitis - CT axial.jpg
Contrast-enhanced axial CT of acute interstitial edematous pancreatitis demonstrating extensive peripancreatic fluid without diminished pancreatic enhancement. Image by Hellerhoff, available from Wikimedia Commons under the CC BY-SA 3.0 license.

The example demonstrates:

  • Extensive fluid surrounding the pancreas
  • Peripancreatic inflammatory change
  • Preserved pancreatic enhancement without a visible non-enhancing area of pancreatic necrosis

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Tenner S, Vege SS, Sheth SG, et al. American College of Gastroenterology Guidelines: Management of Acute Pancreatitis. Am J Gastroenterol. 2024;119(3):419-437. doi:10.14309/ajg.0000000000002645.
  2. ↑ 2.0 2.1 2.2 2.3 Expert Panel on Gastrointestinal Imaging, Porter KK, Zaheer A, et al. ACR Appropriateness Criteria® Acute Pancreatitis. J Am Coll Radiol. 2019;16(11S):S316-S330. doi:10.1016/j.jacr.2019.05.017.
  3. ↑ 3.0 3.1 IAP/APA Working Group. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013;13(4 Suppl 2):e1-e15. doi:10.1016/j.pan.2013.07.063.
  4. ↑ 4.0 4.1 4.2 Baron TH, DiMaio CJ, Wang AY, Morgan KA. American Gastroenterological Association Clinical Practice Update: Management of Pancreatic Necrosis. Gastroenterology. 2020;158(1):67-75.e1. doi:10.1053/j.gastro.2019.07.064.
  5. ↑ Leppäniemi A, Tolonen M, Tarasconi A, et al. 2019 WSES guidelines for the management of severe acute pancreatitis. World J Emerg Surg. 2019;14:27. doi:10.1186/s13017-019-0247-0.
  6. ↑ Ansel-Wallois W, Assako P, Yzet T, Bouzerar R. Acute pancreatitis and computed tomography: interest of portal venous phase alone in the initial phase. Acta Radiol. 2024;65(8):889-897. doi:10.1177/02841851241260874.
  7. ↑ Trout AT, Anupindi SA, Freeman AJ, et al. North American Society for Pediatric Gastroenterology, Hepatology and Nutrition and the Society for Pediatric Radiology joint position paper on noninvasive imaging of pediatric pancreatitis. J Pediatr Gastroenterol Nutr. 2021;72(1):151-167. doi:10.1097/MPG.0000000000002964.
  8. ↑ Hwang TL, Chang KY, Ho YP. Contrast-enhanced dynamic computed tomography does not aggravate the clinical severity of patients with severe acute pancreatitis. Arch Surg. 2000;135(3):287-290.
  9. ↑ 9.0 9.1 Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62(1):102-111. doi:10.1136/gutjnl-2012-302779.
  10. ↑ 10.0 10.1 10.2 10.3 Trikudanathan G, Wolbrink DRJ, van Santvoort HC, et al. Current concepts in severe acute and necrotizing pancreatitis: an evidence-based approach. Gastroenterology. 2019;156(7):1994-2007.e3. doi:10.1053/j.gastro.2019.01.269.
  11. ↑ Trikudanathan G, Yazici C, Evans Phillips A, Forsmark CE. Diagnosis and management of acute pancreatitis. Gastroenterology. 2024;167(4):673-688. doi:10.1053/j.gastro.2024.02.052.
  12. ↑ 12.0 12.1 12.2 Boxhoorn L, Voermans RP, Bouwense SA, et al. Acute pancreatitis. Lancet. 2020;396(10252):726-734. doi:10.1016/S0140-6736(20)31310-6.
  13. ↑ Liu N, He J, Hu X, et al. Acute necrotising pancreatitis: measurements of necrosis volume and mean CT attenuation help early prediction of organ failure and need for intervention. Eur Radiol. 2021;31(10):7705-7714. doi:10.1007/s00330-021-07840-x.
  14. ↑ Tsuji Y, Takahashi N, Fletcher JG, et al. Subtraction color map of contrast-enhanced and unenhanced CT for the prediction of pancreatic necrosis in early stage of acute pancreatitis. AJR Am J Roentgenol. 2014;202(4):W349-W356. doi:10.2214/AJR.13.10957.
  15. ↑ Smeets XJNM, Litjens G, Gijsbers K, et al. The accuracy of pancreatic perfusion computed tomography and angiography in predicting necrotizing pancreatitis: a systematic review. Pancreas. 2018;47(6):667-674. doi:10.1097/MPA.0000000000001067.
  16. ↑ 16.0 16.1 van Grinsven J, van Brunschot S, van Baal MC, et al. Natural history of gas configurations and encapsulation in necrotic collections during necrotizing pancreatitis. J Gastrointest Surg. 2018;22(9):1557-1564. doi:10.1007/s11605-018-3792-z.
  17. ↑ 17.0 17.1 Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990;174(2):331-336.
  18. ↑ Simchuk EJ, Traverso LW, Nukui Y, Kozarek RA. Computed tomography severity index is a predictor of outcomes for severe pancreatitis. Am J Surg. 2000;179(5):352-355. doi:10.1016/s0002-9610(00)00375-5.
  19. ↑ Mortele KJ, Wiesner W, Intriere L, 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. doi:10.2214/ajr.183.5.1831261.
  20. ↑ Bollen TL, Singh VK, Maurer R, et al. Comparative evaluation of the modified CT severity index and CT severity index in assessing severity of acute pancreatitis. AJR Am J Roentgenol. 2011;197(2):386-392. doi:10.2214/AJR.09.4025.
  21. ↑ Mikó A, Vigh É, Mátrai P, et al. Computed tomography severity index vs. other indices in the prediction of severity and mortality in acute pancreatitis: a predictive accuracy meta-analysis. Front Physiol. 2019;10:1002. doi:10.3389/fphys.2019.01002.
  22. ↑ Parmar G, Noronha GP, Poornima V. Comparative analysis of computed tomography severity indices in predicting the severity and clinical outcome in patients with acute pancreatitis. F1000Res. 2022;11:1272. doi:10.12688/f1000research.125896.2.
  23. ↑ Huang S, Liu X, Zhu L, Ai K. Comparison of the predictive value of different assessment times in the severity and prognostic outcomes of CTSI in patients with acute pancreatitis: a systematic review and meta-analysis. Abdom Radiol (NY). 2026;51(6):2879-2893. doi:10.1007/s00261-025-05296-x.
  24. ↑ Bollen TL, Singh VK, Maurer R, 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. doi:10.1038/ajg.2011.438.
  25. ↑ Borbély RZ, Szalai EÁ, Philip BM, et al. The risk of developing splanchnic vein thrombosis in acute pancreatitis increases 3 days after symptom onset: a systematic review and meta-analysis. United European Gastroenterol J. 2024;12(6):678-690. doi:10.1002/ueg2.12550.
  26. ↑ Anis FS, Adiamah A, Lobo DN, Sanyal S. Incidence and treatment of splanchnic vein thrombosis in patients with acute pancreatitis: a systematic review and meta-analysis. J Gastroenterol Hepatol. 2022;37(3):446-454. doi:10.1111/jgh.15711.
  27. ↑ Wu BU, Banks PA. Clinical management of patients with acute pancreatitis. Gastroenterology. 2013;144(6):1272-1281. doi:10.1053/j.gastro.2013.01.075.
  28. ↑ Maatman TK, Heimberger MA, Lewellen KA, et al. Visceral artery pseudoaneurysm in necrotizing pancreatitis: incidence and outcomes. Can J Surg. 2020;63(3):E272-E277. doi:10.1503/cjs.009519.
  29. ↑ 29.0 29.1 Abdallah M, Vantanasiri K, Young S, et al. Visceral artery pseudoaneurysms in necrotizing pancreatitis: risk of early bleeding with lumen-apposing metal stents. Gastrointest Endosc. 2022;95(6):1150-1157. doi:10.1016/j.gie.2021.11.030.
  30. ↑ 30.0 30.1 Maurer LR, Fagenholz PJ. Contemporary surgical management of pancreatic necrosis. JAMA Surg. 2023;158(1):81-88. doi:10.1001/jamasurg.2022.5695.
  31. ↑ Oppenlander KE, Chadwick C, Carman K. Acute pancreatitis: rapid evidence review. Am Fam Physician. 2022;106(1):44-50.
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