Pancreatitis

Pancreatitis is inflammation of the pancreas, and the single most important thing to understand before anything else in this chapter is that acute and chronic pancreatitis are not two severities of the same illness — they are two genuinely different disease processes that happen to share an organ. Acute pancreatitis is a sudden, usually self-limited inflammatory insult in a previously normal (or previously damaged) gland, diagnosed using the internationally adopted revised Atlanta classification's "2 of 3" rule and staged by a severity grade that drives nearly every decision that follows.^[1] Chronic pancreatitis is irreversible fibro-inflammatory destruction of pancreatic tissue, developing over years, that eventually fails at both of the gland's core jobs: the exocrine function of secreting digestive enzymes (lipase, amylase, protease) into the duodenum, and the endocrine function of insulin and glucagon secretion from the islets of Langerhans.

The pancreas's two jobs in one gland — exocrine acinar cells (roughly 98% of pancreatic tissue) produce digestive enzymes, while endocrine islets of Langerhans produce insulin and glucagon. Chronic pancreatitis eventually damages both. (OpenStax College, CC BY 3.0, Wikimedia Commons)

Why acute pancreatitis matters

Acute pancreatitis is one of the most common reasons for gastrointestinal hospitalization worldwide. The great majority of cases are mild and self-limited, but a substantial minority — roughly 20-30% — develop moderately severe or severe disease with local complications or organ dysfunction, and severe disease carries real mortality, concentrated in patients who develop infected pancreatic necrosis.^[2] Gallstones and alcohol together account for the large majority of cases in most populations; hypertriglyceridemia, ERCP, drugs, and a genuinely long list of rarer causes make up the rest, and roughly 10-15% remain idiopathic even after a reasonable workup (see Risk Factors).^[3]

Why chronic pancreatitis matters

Chronic pancreatitis's damage is cumulative and permanent — nothing in this chapter reverses established fibrosis or restores destroyed acinar or islet tissue. The clinical goal is instead to control pain, replace what the gland can no longer make (enzymes, and eventually insulin), prevent malnutrition and its downstream complications (fat-soluble vitamin deficiency, metabolic bone disease), and remove the ongoing insult — alcohol and tobacco chief among them — that keeps driving further damage.^[4] This chapter is authored primarily from the International Association of Pancreatology's 2025 revised guidelines on acute pancreatitis — the newest and most comprehensive international synthesis available, spanning 18 domains and 96 clinical questions — cross-checked against the foundational revised Atlanta classification, the WSES 2019 severe-pancreatitis guidelines, the HaPanEU chronic pancreatitis guideline, and a genuinely Canadian consensus guideline on pancreatic exocrine insufficiency in primary care.^[3][5]

Acute pancreatitis

The classic presentation is severe, constant epigastric pain, often radiating straight through to the back, that characteristically improves when the patient leans forward or curls into a fetal position and worsens lying flat — though this "pancreatic posture" is a supportive clue, not a requirement. Nausea and vomiting are common, and low-grade fever, tachycardia, and epigastric or diffuse abdominal tenderness are typical on exam. Bowel sounds may be reduced from an associated ileus.

Two rare but classic physical findings signal a hemorrhagic, necrotizing course rather than routine interstitial pancreatitis: Cullen's sign (periumbilical ecchymosis, from retroperitoneal blood tracking along the falciform ligament) and Grey Turner's sign (flank ecchymosis, from retroperitoneal hemorrhage tracking laterally). Either finding should prompt reassessment for severe, necrotizing, or hemorrhagic disease rather than being treated as an incidental bruise.

Chronic pancreatitis

Recurrent or persistent epigastric pain, often radiating to the back and sometimes provoked by eating, is the most common presenting symptom, though a meaningful minority of patients — particularly later in the disease course — have little or no pain despite advanced structural damage ("burnout"), which does not mean the exocrine and endocrine failure have also stabilized. Steatorrhea (bulky, greasy, malodorous, difficult-to-flush stools) and unintentional weight loss are classic but genuinely late findings — clinically overt steatorrhea does not appear until pancreatic lipase output has fallen below roughly 10% of normal, meaning substantial, often clinically silent exocrine damage has already occurred by the time steatorrhea is the presenting complaint (see Assessment & Diagnosis for earlier-detection testing).^[5] New-onset or difficult-to-control diabetes in a patient with a pancreatitis history — pancreatogenic (type 3c) diabetes — is itself a recognition clue, not only a late complication (see Special Populations).

The relationship between the two

Recurrent acute pancreatitis is itself one of the recognized pathways into chronic pancreatitis (see the TIGAR-O classification in Risk Factors) — a patient's second or third "acute" episode, particularly with a persistent etiology such as ongoing heavy alcohol use, deserves a structural and functional workup for evolving chronic disease rather than being treated as an isolated, unrelated event each time.

Acute pancreatitis

• Gallstones — the single most common cause in most populations, including small stones and microlithiasis/biliary sludge too small to reliably see on standard ultrasound; obstruction at the ampulla is the presumed mechanism.
• Alcohol — typically heavy, sustained use rather than a single binge in a previously abstinent person; the second leading cause in most Western series.
• Hypertriglyceridemia — triglycerides above roughly 1000 mg/dL (11.3 mmol/L) carry a meaningfully increased risk, rising further above 2000 mg/dL (22.6 mmol/L); an under-recognized and often reversible cause (see Choose Initial Treatment and Special Populations).^[6]
• Post-ERCP pancreatitis — the most common serious complication of ERCP itself; risk factors include difficult cannulation, pancreatic duct injection/instrumentation, and suspected sphincter of Oddi dysfunction (see Choose Initial Treatment for prophylaxis).^[7]
• Drug-induced — a genuinely long list, including azathioprine/mercaptopurine, valproic acid, thiazide diuretics, mesalamine/sulfasalazine, didanosine, pentamidine, estrogens, and sulfonamide antibiotics; GLP-1 receptor agonists (semaglutide, liraglutide, dulaglutide, tirzepatide) carry a reported but not definitively causal association and should remain on the differential in a patient taking one who develops otherwise-unexplained pancreatitis.
• Trauma (including post-surgical), scorpion sting (rare outside endemic regions), and viral infection (mumps, coxsackievirus).
• Autoimmune pancreatitis — an IgG4-related systemic disease (type 1) or an idiopathic duct-centric process (type 2); consider specifically when imaging shows a diffusely enlarged, "sausage-shaped" gland or when pancreatitis coexists with other IgG4-related organ involvement.
• Genetic — hereditary pancreatitis (PRSS1 gain-of-function mutations), SPINK1, and CFTR mutations (see the Cystic Fibrosis chapter for CFTR-related exocrine disease) predispose to recurrent acute and eventual chronic pancreatitis, particularly with recurrent episodes at a young age or a strong family history.
• Idiopathic — roughly 10-15% even after a reasonable initial workup; pursue endoscopic ultrasound for occult microlithiasis or a structural anomaly (see Treatment Failure/Next Step) before permanently labelling a case idiopathic.

Chronic pancreatitis — the TIGAR-O framework

The TIGAR-O classification organizes chronic pancreatitis etiology into six categories and is a genuinely useful structure for a systematic workup rather than anchoring on "probably alcohol" alone.^[4]

Alcohol and tobacco are by far the most common drivers in most populations, and — critically for counselling — their effects are synergistic, not simply additive: a patient who both smokes and drinks heavily faces a materially higher risk than either exposure alone.^[4]

Diagnosing acute pancreatitis — the revised Atlanta "2 of 3" rule

The internationally adopted diagnostic standard requires 2 of the following 3 criteria: (1) abdominal pain consistent with acute pancreatitis, (2) serum lipase or amylase activity greater than 3 times the upper limit of normal, and (3) characteristic findings on cross-sectional imaging.^[1][9] Lipase is preferred over amylase where both are available — it rises and stays elevated longer, and it is more specific, since amylase is also produced by the salivary glands and elevated in a wider range of non-pancreatic conditions. A patient with classic pain and a lipase over 3x the upper limit of normal does not routinely need a CT scan to confirm the diagnosis — 2 of 3 criteria are already met, and CT is reserved for diagnostic uncertainty, an atypical presentation, or assessing complications in a patient who is not improving as expected (see Imaging below).

Contrast-enhanced axial CT in acute exudative (interstitial) pancreatitis, showing extensive fluid tracking around the pancreas. CT is not required to make the diagnosis when pain and a lipase >3x the upper limit of normal already satisfy 2 of the revised Atlanta's 3 criteria. (Hellerhoff, CC BY-SA 3.0, Wikimedia Commons)

Severity classification — the revised Atlanta 3-tier grade

^[1] Local complications, also defined by the revised Atlanta classification, are distinguished by content (fluid alone versus necrotic debris) and by timing (before versus after 4 weeks, by which point a collection typically develops a defined wall):

^[1] This vocabulary matters clinically, not just academically — timing (before or after the collection is "walled off") is exactly what governs whether and when to intervene on infected necrosis (see Choose Initial Treatment).

Severity prediction — BISAP

The Bedside Index for Severity in Acute Pancreatitis (BISAP) is a simple, 5-variable score calculable from data available in the first 24 hours, without needing 48 hours of data collection the way older scores (Ranson's criteria, APACHE II) require — a genuine practical advantage that has made it the platform's preferred bedside tool, while Ranson's and APACHE II remain in wider legacy use and are referenced in some regional protocols.

A score of 3 or higher is associated with a substantially increased risk of in-hospital mortality (sensitivity approximately 56%, specificity approximately 91% in the original validation) and should prompt closer monitoring, a lower threshold for escalating the level of care, and reassessment of the fluid and nutrition plan below.^[10] Trending hematocrit (hemoconcentration suggests inadequate resuscitation; a falling hematocrit with clinical worsening suggests hemorrhage) and C-reactive protein at 48 hours (a value over 150 mg/L is a well-validated marker of severe disease) are useful complementary bedside markers.

Imaging

Diagnosing chronic pancreatitis

Axial CT in chronic pancreatitis showing coarse pancreatic parenchymal calcifications (arrow) — a near-pathognomonic finding in advanced disease, though its absence does not exclude earlier-stage chronic pancreatitis. (Hellerhoff, CC BY-SA 3.0, Wikimedia Commons; arrow annotation added by Doc James)

Cross-sectional imaging (CT or MRI/MRCP) findings — parenchymal calcifications (near-pathognomonic in advanced disease), pancreatic duct dilation or an irregular "chain of lakes" appearance, ductal strictures, and parenchymal atrophy — support the diagnosis, with EUS the most sensitive modality for earlier, minimal-change disease before calcifications or overt ductal changes have developed. Diagnostic ERCP has been largely superseded by MRCP and EUS given its own procedural risk, including a real risk of provoking acute pancreatitis.

Assessing exocrine function — do not wait for steatorrhea

Fecal elastase-1 is the standard, non-invasive first-line test for pancreatic exocrine insufficiency (PEI) — a low result (commonly under 200 mcg/g, with under 100 mcg/g suggesting more severe insufficiency) supports the diagnosis, but a single abnormal fecal elastase, on its own, should never be treated as diagnostic of PEI in isolation, and a predisposing condition such as chronic pancreatitis should never be treated as proof of PEI without actually testing — both are genuine, well-documented pitfalls.^[5] The secretin-stimulated pancreatic function test is more sensitive and considered a reference standard where available, but it is invasive and not widely accessible. A 72-hour quantitative fecal fat collection is rarely used today given the burden on the patient and the lab. Blood levels of the fat-soluble vitamins (A, D, E, K) are a genuinely useful complementary marker — a deficiency associated with an underlying condition such as chronic pancreatitis is highly suggestive of clinically significant malabsorption even before overt steatorrhea appears.^[5]

• Confirm the diagnosis efficiently using the revised Atlanta 2-of-3 rule, and grade severity (mild, moderately severe, severe) — grade drives fluid rate, level of care, and how closely to monitor for complications.
• Resuscitate with a moderate, goal-directed fluid strategy — not the older default of maximal early hydration, which current trial evidence shows causes harm without benefit.
• Control pain effectively with scheduled multimodal analgesia, including opioids where needed, without withholding effective analgesia over outdated sphincter-of-Oddi concerns.
• Feed early, by mouth as tolerated, rather than defaulting to prolonged bowel rest or reflexively placing a feeding tube.
• Identify the etiology specifically (biliary ultrasound in every patient, triglycerides, calcium, medication review) since etiology changes management — same-admission cholecystectomy for gallstones, insulin/fibrate for hypertriglyceridemia, drug discontinuation for a drug cause.
• Reserve antibiotics for confirmed or strongly suspected infected necrosis — not as prophylaxis against it.
• For necrotizing pancreatitis needing intervention, use a minimally invasive step-up approach and delay intervention until the collection is walled off wherever the patient's clinical trajectory allows.
• For chronic pancreatitis: control pain via a genuine stepwise ladder; correct exocrine insufficiency with correctly dosed and correctly counselled PERT; identify and treat pancreatogenic diabetes; prevent and correct fat-soluble vitamin deficiency and malnutrition; and remove the ongoing insult (alcohol, tobacco) driving further damage.

Acute pancreatitis

• Early oral feeding as tolerated, generally within 24-72 hours — not prolonged NPO/bowel rest (see Choose Initial Treatment).^[11]
• Enteral (oral or tube) nutrition in preference to parenteral nutrition when tube feeding is genuinely needed.
• Same-admission cholecystectomy for mild gallstone pancreatitis once the patient is recovering.^[14]
• ERCP with sphincterotomy, reserved for concurrent cholangitis or persistent biliary obstruction.^[13]
• Step-up drainage and, if needed, minimally invasive necrosectomy for infected pancreatic necrosis, delayed until walled off where the clinical course allows.^[12]
• Alcohol cessation counselling for alcohol-related pancreatitis, and smoking cessation counselling regardless of etiology, given tobacco's independent contribution to recurrence and progression.

Chronic pancreatitis

• Alcohol and tobacco cessation — the single most disease-modifying non-pharmacologic intervention available, altering the trajectory of both pain and further gland destruction, not just a general health recommendation.^[4] Consider pharmacotherapy for alcohol use disorder (e.g., naltrexone) alongside counselling and, where available, addiction medicine referral.
• Do not routinely recommend a low-fat diet as the primary fix for malabsorption — patients with chronic pancreatitis are already at risk of malnutrition, and the correct first response to persistent steatorrhea is adequate PERT dosing (see Choose Initial Treatment), not fat restriction; an important exception is a patient with coexisting obesity, where some fat moderation may be reasonable alongside optimized PERT.^[5]
• Small, more frequent meals may be better tolerated than three large meals.
• Registered dietitian referral for individualized nutritional counselling and monitoring.^[5]
• Bone density (DEXA) screening given cumulative risk factors — malabsorption, chronic vitamin D/K deficiency, alcohol use, and reduced activity in more advanced disease.
• Psychosocial support — chronic pain and, often, coexisting substance use create a genuinely high treatment burden; involve psychology/psychiatry and social work proactively rather than only after adherence visibly breaks down.

Pregnancy

Gallstone disease is the most common cause of acute pancreatitis in pregnancy, typically presenting in the second or third trimester. General management principles are unchanged — moderate fluid resuscitation, adequate analgesia, early oral feeding as tolerated — with acetaminophen and opioids preferred for analgesia and NSAIDs avoided, particularly in the third trimester. MRCP (no ionizing radiation) is preferred over CT when duct imaging is needed. ERCP with appropriate fetal shielding is safe when genuinely indicated (concurrent cholangitis or persistent obstruction) and should not be withheld on the basis of pregnancy alone; laparoscopic cholecystectomy is likewise considered safe in any trimester where expertise is available, with elective/interval timing preferentially in the second trimester when surgery is not urgent.

Breastfeeding

Short-acting opioids are preferred where analgesia is needed, with monitoring for infant sedation; acetaminophen and pancrelipase (not systemically absorbed) are compatible. Confirm specific antibiotic and PPI compatibility against each drug's own Drug Database entry.

Pediatrics

Causes differ meaningfully from adults — trauma, biliary anomalies, systemic illness, drugs, and idiopathic disease are proportionally more common than gallstones or alcohol. The same revised Atlanta diagnostic and severity framework applies, adapted to paediatric norms. Consider hereditary pancreatitis (PRSS1) specifically in a child with recurrent acute pancreatitis and a strong family history; cystic fibrosis-related exocrine pancreatic insufficiency is covered in detail in this platform's Cystic Fibrosis chapter.

Older adults

Gallstone etiology and biliary complications are proportionally more common, presentation is more often blunted, and mortality from severe disease is higher — maintain a lower threshold for imaging and escalation, and review the full medication list specifically for a drug-induced contributor given the cumulative polypharmacy burden common in this population.

Pancreatogenic (type 3c) diabetes in chronic pancreatitis

This is mechanistically distinct from type 1 or type 2 diabetes — concurrent glucagon deficiency from islet destruction produces genuinely brittle glucose control with a materially higher hypoglycemia risk at any given insulin dose than typical type 2 diabetes. A trial of metformin is reasonable in earlier, milder pancreatogenic diabetes with preserved insulin secretion, but insulin (e.g., insulin glargine basal, insulin aspart prandial) becomes necessary once beta-cell reserve is inadequate, and should not be delayed simply because the patient does not fit a typical type 2 diabetes profile. As with cystic fibrosis-related diabetes, do not impose calorie or fat restriction to manage pancreatogenic diabetes — the malnutrition risk from underlying exocrine insufficiency takes priority, and insulin dosing should support adequate intake rather than restrict it.

Alcohol use disorder

Alcohol cessation is the single highest-yield intervention for both acute recurrence and chronic disease progression. Consider pharmacotherapy (e.g., naltrexone) alongside counselling and addiction medicine referral, and provide genuine psychosocial support for the behaviour change being asked of the patient rather than treating a single cessation discussion as sufficient.

Renal impairment

Dose-adjust meropenem, imipenem-cilastatin, piperacillin-tazobactam, gabapentin, and pregabalin for reduced renal function; use ketorolac (see the Cholecystitis chapter's drug table) cautiously if at all given nephrotoxicity risk during a period of ongoing volume shifts.

Hepatic impairment

Relevant particularly in alcohol-related chronic pancreatitis with coexisting liver disease — reduce the acetaminophen maximum daily dose, use duloxetine cautiously (avoid in significant hepatic impairment), and note that mild transaminase elevation can occur in acute pancreatitis itself and does not automatically indicate drug-related hepatotoxicity.

Acute pancreatitis

• Serial vital signs, urine output, and abdominal exam, particularly through the first 48-72 hours while severity is still evolving.
• Trend BUN and hematocrit as resuscitation-adequacy markers, and CRP at 48 hours as a severity marker.^[10]
• Reassess the BISAP score and overall clinical trajectory rather than relying on a single admission snapshot.
• Reimage only for a genuine clinical indication — failure to improve by about 72 hours, or new deterioration — not on a routine fixed schedule.
• Confirm the etiology workup was actually completed before discharge (biliary ultrasound, triglycerides, calcium, medication review) since it directly determines follow-up (same-admission cholecystectomy, fibrate initiation, drug discontinuation).

Chronic pancreatitis

• Reassess PERT dosing, timing, and adherence at every visit — persistent symptoms are more often a dosing/adherence/acid-suppression problem than a true treatment failure (see Treatment Failure/Next Step).^[5]
• Annual (or more frequent, per symptoms) fat-soluble vitamin levels (A, 25-hydroxyvitamin D, E) and coagulation status if vitamin K status or liver disease is a concern.^[5]
• Weight, BMI, and nutritional status trend at every visit.
• Bone density (DEXA) screening starting once cumulative risk factors are present.
• Glucose/HbA1c monitoring for pancreatogenic diabetes, recognizing the higher hypoglycemia risk at any given insulin dose.
• Reinforce alcohol and tobacco cessation at every visit — a single early discussion is not sufficient given how disease-modifying ongoing abstinence is.
• Maintain awareness of the elevated pancreatic cancer risk in chronic pancreatitis (particularly hereditary pancreatitis) and evaluate promptly, rather than reflexively, for any new red-flag symptom (see Red Flags & Refer).

1. Acute pancreatitis not improving by about 72 hours despite appropriate supportive care: obtain contrast-enhanced CT to look for necrosis or a local complication rather than simply continuing the same supportive measures unchanged.
2. New fever or clinical deterioration after an initial period of improvement (classically week 2 or later): treat as suspected infected necrosis — pursue CT-guided FNA culture where genuinely uncertain, start empiric carbapenem therapy, and plan a step-up drainage approach rather than reflexive early necrosectomy.^[12]
3. Persistent organ failure beyond 48 hours: this reclassifies the episode as severe under the revised Atlanta system and warrants critical-care-level monitoring and support.^[1]
4. Recurrent acute pancreatitis with no clear etiology identified on initial workup: pursue EUS for occult microlithiasis, pancreas divisum, or another structural cause, and consider genetic testing (PRSS1, SPINK1, CFTR) in a younger patient or one with a strong family history, before permanently labelling the case idiopathic.
5. Chronic pancreatitis pain refractory to the stepwise pharmacologic ladder: escalate to endoscopic (stricture/stone therapy) or surgical referral — and do so genuinely early, rather than cycling through additional endoscopic attempts or simply escalating opioid dose indefinitely.^[4]
6. Persistent steatorrhea or inadequate nutritional response despite PERT: confirm the dose is actually being taken with every fat-containing meal and snack (not only "main meals"), confirm the enteric-coated formulation is not being crushed or chewed, add a trial of concomitant acid suppression, and only then consider a higher PERT dose — rather than assuming primary treatment failure or escalating the dose first.^[5]
7. Suspected pancreatic exocrine insufficiency not responding to an empiric PERT trial: reconsider the diagnosis — investigate for an alternative or coexisting cause of malabsorption such as giardiasis, small intestinal bacterial overgrowth, or celiac disease, rather than continuing to escalate enzyme dosing indefinitely.^[5]

• Defaulting to aggressive, high-volume fluid resuscitation instead of moderate, goal-directed resuscitation — current trial evidence shows this causes more fluid overload without benefit.
• Prolonged NPO/"bowel rest" instead of early oral refeeding once the patient is tolerating it.
• Giving prophylactic antibiotics for predicted severe or necrotizing pancreatitis without confirmed or strongly suspected infection.
• Ordering routine urgent ERCP for gallstone pancreatitis without confirmed cholangitis or ongoing biliary obstruction.
• Delaying cholecystectomy to "let inflammation settle" for mild gallstone pancreatitis, rather than proceeding during the same admission.
• Reflexively avoiding morphine for pancreatitis or biliary pain over outdated sphincter-of-Oddi-spasm concerns.
• Reaching for octreotide as a routine adjunct — evidence does not support it in acute pancreatitis.
• Choosing primary open necrosectomy over a minimally invasive step-up approach for infected necrosis, or intervening before a collection is walled off without a genuine indication to act sooner.
• Dosing pancreatic enzymes on a fixed clock schedule instead of with the first bite of every fat-containing meal and snack.
• Crushing or chewing enteric-coated PERT formulations.
• Recommending a routine low-fat diet as the primary fix for chronic pancreatitis malabsorption instead of adequately dosing PERT.
• Waiting for overt steatorrhea to suspect pancreatic exocrine insufficiency — it appears only after enzyme output has already fallen below roughly 10% of normal, so earlier detection (fecal elastase, fat-soluble vitamin levels) matters.
• Anchoring on gallstones or alcohol as the only possible causes and missing hypertriglyceridemia or a drug-induced etiology.
• Escalating to long-term full-agonist opioids for chronic pancreatitis pain by default, rather than working through the adjuvant and endoscopic/surgical steps of the pain ladder first.
• Treating a single abnormal fecal elastase, or the mere presence of a predisposing condition like chronic pancreatitis, as diagnostic of exocrine insufficiency without the accompanying clinical picture.

Acute Pancreatitis — Fluid Resuscitation, Analgesia, and Antiemesis

Moderate, goal-directed fluid resuscitation and scheduled multimodal analgesia are the evidence-based defaults — see Choose Initial Treatment for the WATERFALL trial rationale.

Confirmed or Strongly Suspected Infected Pancreatic Necrosis — Antibiotic Therapy

Not for prophylaxis in predicted severe or necrotizing disease — reserve strictly for confirmed or strongly suspected infection (see Choose Initial Treatment).

Hypertriglyceridemia-Induced Acute Pancreatitis

Insulin infusion is first-line during the acute episode; fibrate therapy is for secondary prevention once the episode resolves — see Choose Initial Treatment.

Chronic Pancreatitis — Pancreatic Enzyme Replacement Therapy and Fat-Soluble Vitamins

For every patient with confirmed pancreatic exocrine insufficiency. Dose PERT with the first bite of every fat-containing meal or snack, never crushed or chewed — see Choose Initial Treatment.

Chronic Pancreatitis Pain — Stepwise Adjuvant and Opioid Therapy

Follow the stepwise ladder in Choose Initial Treatment — adjuvant neuromodulators and a weak opioid (tramadol) before a full-agonist opioid.

Not Recommended in Routine Acute Pancreatitis Management

Included for teaching contrast — evidence-based guidelines do not support routine use.