Acute pancreatitis overview
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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] Raviteja Guddeti, M.B.B.S. [4] Tarek Nafee, M.D. [5]
Overview
Acute pancreatitis is an acute inflammatory injury of the pancreas that ranges from a mild, self-limited illness to necrotizing disease with persistent organ failure. The diagnosis requires at least 2 of 3 features: characteristic abdominal pain, serum lipase or amylase at least 3 times the upper limit of normal, or characteristic imaging findings; imaging is not routinely required when the clinical and biochemical criteria are already met.[1][2]
Gallstone disease and prolonged heavy alcohol exposure are the leading causes. Initial care focuses on determining the etiology, identifying patients at risk for deterioration, goal-directed intravenous hydration, analgesia, early oral or enteral nutrition, and treatment of complications. Prophylactic antibiotics, routine early CT, routine urgent ERCP in the absence of cholangitis or persistent biliary obstruction, prolonged fasting, and early open necrosectomy are not recommended.[3][4][5]
| Clinical dimension | Quick-glance summary |
|---|---|
| Diagnosis | At least 2 of 3: characteristic pain, lipase or amylase ≥3 times the upper limit of normal, or characteristic imaging |
| Most common causes | Gallstones and prolonged heavy alcohol exposure; evaluate triglycerides, calcium, medications, recent ERCP, structural disease, autoimmune disease, tumors, trauma, infection, and genetic susceptibility when appropriate |
| Severity | Mild: no organ failure or local/systemic complications; moderately severe: transient organ failure and/or local or systemic complications; severe: persistent organ failure for more than 48 hours |
| Initial priorities | Determine etiology, monitor for organ dysfunction, provide goal-directed lactated Ringer's solution and analgesia, initiate early feeding as tolerated, and arrange cause-specific treatment |
| Major complications | Pancreatic or peripancreatic necrosis and collections, infection, hemorrhage, venous thrombosis, biliary or gastric obstruction, exocrine insufficiency, diabetes, recurrent acute pancreatitis, and chronic pancreatitis |
Historical Perspective
Acute pancreatitis was established as a distinct clinicopathologic entity by Reginald H. Fitz in 1889, when he organized the clinical and postmortem findings from 53 patients and described hemorrhagic, suppurative, and gangrenous forms.[6] Subsequent advances shifted care from early operative exploration and prolonged pancreatic rest toward standardized severity classification, early nutrition, selective imaging, and delayed minimally invasive treatment of necrosis.
| Year | Milestone | Clinical importance |
|---|---|---|
| 1889 | Fitz's clinicopathologic description | Established acute pancreatitis as a recognizable disease and described major morphologic patterns.[6] |
| 1974 | Ranson prognostic signs | Introduced a structured clinical approach to early severity prediction.[7] |
| 1992–1993 | Original Atlanta Classification | Standardized clinical definitions and terminology for severity and complications.[8] |
| 2012–2013 | Revised Atlanta Classification | Defined early and late phases, organ-failure-based severity, interstitial edematous and necrotizing subtypes, and four standardized collection types.[1] |
| 2010s–2020s | Evidence-based supportive and step-up care | Established early feeding, avoidance of indiscriminate antibiotics and ERCP, moderate rather than aggressive hydration, and delayed minimally invasive intervention for necrosis.[4][5] |
Classification
Acute pancreatitis is classified by clinical phase, clinical severity, morphologic subtype, and the type of pancreatic or peripancreatic collection. The early phase usually encompasses the first week and is dominated by the systemic inflammatory response and organ dysfunction; the late phase may persist for weeks to months and is characterized by ongoing organ failure and local complications. Morphologically, acute pancreatitis is classified as interstitial edematous pancreatitis or necrotizing pancreatitis.[1]
| Revised Atlanta severity | Definition | Typical clinical implication |
|---|---|---|
| Mild | No organ failure and no local or systemic complications | Usually self-limited, with recovery during the first week |
| Moderately severe | Transient organ failure that resolves within 48 hours and/or local or systemic complications without persistent organ failure | Requires closer monitoring and may require treatment of local complications |
| Severe | Persistent organ failure lasting more than 48 hours; may involve one or multiple organ systems | High risk of critical illness, prolonged hospitalization, and death |
Local collections are classified as acute peripancreatic fluid collections, pancreatic pseudocysts, acute necrotic collections, or walled-off necrosis according to the underlying morphologic subtype, contents, encapsulation, and time from symptom onset. Organ failure is defined using the modified Marshall score; a score of at least 2 in the respiratory, renal, or cardiovascular system indicates organ failure.[1][9]
Pathophysiology
Acute pancreatitis begins when an initiating insult disrupts pancreatic acinar and ductal cell homeostasis. Sustained intracellular calcium elevation, premature digestive-enzyme activation, mitochondrial dysfunction, impaired autophagy, endoplasmic-reticulum stress, ductal bicarbonate failure, lipotoxicity, and regulated cell-death pathways interact to produce local pancreatic injury.[10]
Key steps include:
- Acinar-cell injury and intra-acinar zymogen activation
- Mitochondrial ATP depletion and failure of calcium homeostasis
- Impaired autophagic clearance of damaged organelles and activated enzymes
- Acinar necrosis with release of damage-associated molecular patterns
- Neutrophil, macrophage, complement, inflammasome, and cytokine activation
- Endothelial injury, capillary leak, pancreatic microcirculatory failure, and thrombosis
- Progression from local inflammation to systemic inflammatory response syndrome, shock, respiratory failure, acute kidney injury, and multiorgan failure
Gallstone obstruction, alcohol toxicity, hypertriglyceridemia-related lipotoxicity, hypercalcemia, ductal obstruction, medications, and genetic variants initiate injury through partly distinct upstream pathways but converge on common inflammatory and cell-death mechanisms.
Causes
Acute pancreatitis is most commonly caused by gallstones or prolonged heavy alcohol exposure, but a systematic etiologic evaluation is required because prevention of recurrence depends on correcting the underlying cause.[11]
| Etiologic category | Examples | Important clinical points |
|---|---|---|
| Biliary | Gallstones, biliary sludge, microlithiasis | The most common cause; evaluate with transabdominal ultrasound and liver biochemical tests |
| Alcohol associated | Prolonged heavy alcohol exposure, often with tobacco and genetic cofactors | Alcohol should not be assigned as the cause solely because a patient reports moderate use; alternative etiologies still require evaluation |
| Metabolic | Severe hypertriglyceridemia, hypercalcemia | A triglyceride level above 1,000 mg/dL is strongly suggestive when gallstones and alcohol are absent; identify the cause of hypercalcemia |
| Iatrogenic or traumatic | Post-ERCP pancreatitis, abdominal trauma, postoperative or ischemic injury | Timing and procedural or injury history are central to diagnosis |
| Drug induced | Selected medications with a credible temporal relationship and published evidence | A diagnosis of exclusion; review latency, competing causes, and improvement after withdrawal rather than relying on an uncritical medication list |
| Autoimmune | Type 1 IgG4-related autoimmune pancreatitis, type 2 autoimmune pancreatitis | Often has characteristic imaging or systemic features; autoimmune pancreatitis more often presents as a chronic or mass-forming process but can mimic acute pancreatitis |
| Obstructive or anatomic | Pancreas divisum, ampullary or pancreatic tumor, ductal stricture, choledochocele | Consider particularly in recurrent disease or in patients older than 40 years with otherwise unexplained pancreatitis |
| Genetic | Pathogenic or susceptibility variants involving PRSS1, SPINK1, CFTR, CTRC, CPA1, and other genes | Consider in early-onset, recurrent, familial, or otherwise unexplained pancreatitis |
| Infectious and other uncommon causes | Selected viral, bacterial, fungal, or parasitic infections; vascular and systemic inflammatory disorders | Require compatible clinical context; avoid attributing nonspecific enzyme elevation to pancreatitis without meeting diagnostic criteria |
| Idiopathic | No cause identified after standard evaluation | Repeat ultrasound, MRI/MRCP, and/or endoscopic ultrasound can reveal occult biliary, ductal, or neoplastic disease |
Differentiating Acute Pancreatitis from other Conditions
Acute pancreatitis should be differentiated from other causes of acute epigastric or upper abdominal pain, systemic inflammation, and elevated pancreatic enzymes. Lipase elevation is not specific when the clinical presentation is discordant, and myocardial, vascular, gastrointestinal, hepatobiliary, renal, metabolic, and pulmonary emergencies must not be missed.
| Condition | Features that favor the alternative diagnosis |
|---|---|
| Acute cholecystitis or acute cholangitis | Right upper-quadrant predominance, sonographic gallbladder inflammation, jaundice, cholestatic laboratory pattern, or biliary sepsis; these disorders may coexist with biliary pancreatitis |
| Perforated peptic ulcer | Sudden severe pain, peritoneal signs, and free intraperitoneal air |
| Mesenteric ischemia | Pain out of proportion to examination, vascular risk factors, elevated lactate, and vascular or bowel abnormalities on CT angiography |
| Bowel obstruction | Colicky pain, obstipation, marked distension, transition point, and dilated bowel loops |
| Acute coronary syndrome or pericarditis | Ischemic or positional symptoms, diagnostic ECG changes, and a compatible troponin pattern |
| Aortic aneurysm, dissection, or other vascular catastrophe | Abrupt pain, pulse or blood-pressure asymmetry, hemodynamic instability, and diagnostic vascular imaging |
| Diabetic ketoacidosis | Hyperglycemia, anion-gap metabolic acidosis, ketosis, and improvement with metabolic treatment; lipase may be elevated without pancreatitis |
| Renal colic or pyelonephritis | Flank-predominant pain, hematuria or pyuria, urinary symptoms, and urinary-tract imaging findings |
| Lower-lobe pneumonia or pulmonary embolism | Respiratory symptoms, hypoxemia, pleuritic pain, and diagnostic chest or pulmonary vascular imaging |
Epidemiology and Demographics
Acute pancreatitis is one of the most common gastrointestinal causes of acute hospitalization, and its incidence has increased globally over recent decades.[12]
- In 2021, an estimated 2.75 million cases and 122,420 deaths occurred worldwide, with substantial geographic and socioeconomic variation.[13]
- Reported incidence in high-income countries is approximately 34 cases per 100,000 person-years, although estimates vary by case definition, population, and etiology.[9]
- The United States records approximately 300,000 hospital admissions for acute pancreatitis each year, with substantial health-care utilization and cost.[2]
- Gallstone-related disease becomes more common with increasing age and is more frequent among women in many populations; alcohol-associated disease is more frequent among men, although these patterns vary.
- Obesity, metabolic disease, alcohol exposure, tobacco use, medication patterns, access to care, and diagnostic practices contribute to temporal and geographic variation.
- Racial and ethnic differences reported in United States cohorts should be interpreted in the context of structural inequities, comorbidities, environmental exposures, and access to timely care rather than as evidence of biologic racial causation.[4]
Risk Factors
Acute pancreatitis is more likely to occur in patients with gallstones, prolonged heavy alcohol exposure, tobacco use, severe hypertriglyceridemia, hypercalcemia, obesity or metabolic syndrome, selected medication exposures, recent ERCP, structural pancreaticobiliary disease, or genetic susceptibility.
Risk factors for a more severe course include:
- Persistent systemic inflammatory response syndrome
- Older age, frailty, and clinically important comorbidities
- Obesity
- Altered mental status
- High or rising blood urea nitrogen and hematocrit
- Pleural effusion, pulmonary infiltrates, and extensive extrapancreatic collections
- Early or evolving respiratory, renal, or cardiovascular dysfunction[2]
Risk factors for recurrence or progression to chronic pancreatitis include an untreated biliary cause, continued heavy alcohol exposure, tobacco smoking, severe hypertriglyceridemia, genetic susceptibility, structural ductal disease, and a prior necrotizing or recurrent episode.[4]
Natural History, Complications and Prognosis
Acute pancreatitis is mild and self-limited in approximately 80% of patients, but a minority develop transient or persistent organ failure, necrosis, infection, or other local complications.[14]
The clinical course is often biphasic:
- Early phase: Systemic inflammation, capillary leak, and organ failure drive morbidity and early deaths. Morphologic changes may still be evolving, so early CT can underestimate necrosis.
- Late phase: Persistent organ failure and local complications become dominant. Infected necrosis often becomes clinically apparent after the first 1–2 weeks, although the timing varies.[15][16]
Major complications include:
- Acute peripancreatic fluid collection, acute necrotic collection, pseudocyst, and walled-off necrosis
- Sterile or infected pancreatic and peripancreatic necrosis
- Acute respiratory failure, acute kidney injury, shock, and multiorgan failure
- Splanchnic venous thrombosis, pseudoaneurysm, hemorrhage, and bowel ischemia or fistula
- Biliary, gastric-outlet, or intestinal obstruction
- Abdominal compartment syndrome
- Pancreatic duct disruption and disconnected pancreatic duct syndrome
- Malnutrition, pancreatic exocrine insufficiency, and pancreatogenic diabetes
- Recurrent acute pancreatitis and progression to chronic pancreatitis
Overall mortality is approximately 1–2%, but it rises substantially with persistent organ failure and infected necrosis.[17] Recurrent acute pancreatitis develops in a clinically important minority of patients, and approximately 10% progress to chronic pancreatitis after a first episode, with a markedly greater risk after recurrent episodes.[18][4] Unexplained acute pancreatitis, particularly in a patient older than 40 years, should prompt consideration of an occult pancreatic tumor.
Diagnosis
Acute pancreatitis is diagnosed when at least 2 of the following 3 criteria are present:
- Characteristic acute upper abdominal pain
- Serum lipase and/or amylase at least 3 times the upper limit of normal
- Characteristic findings on cross-sectional imaging[1]
When characteristic pain and enzyme elevation are both present, CT is generally unnecessary solely to establish the diagnosis. Diagnostic evaluation should simultaneously identify the etiology and detect organ dysfunction or complications.
History and Symptoms
Acute pancreatitis typically presents with acute, persistent epigastric or upper abdominal pain that often radiates to the back and may be accompanied by nausea and vomiting.
Important history includes:
- Onset, severity, character, radiation, and progression of pain
- Nausea, vomiting, inability to tolerate oral intake, fever, dyspnea, oliguria, confusion, or syncope
- Prior pancreatitis, gallstones, biliary colic, jaundice, or cholecystectomy
- Amount and duration of alcohol use and tobacco exposure
- Recent ERCP, abdominal trauma, surgery, or ischemic event
- New or recently changed medications
- Hypertriglyceridemia, hypercalcemia, autoimmune disease, infection, or malignancy
- Family history and age at first episode, particularly in recurrent or early-onset disease
Physical Examination
Acute pancreatitis most commonly causes epigastric tenderness, which may be accompanied by guarding, abdominal distension, or decreased bowel sounds from ileus.
Examination should assess:
- Temperature, heart rate, blood pressure, respiratory rate, oxygen saturation, mental status, and urine output
- Volume depletion, capillary refill, and peripheral perfusion
- Peritoneal signs suggesting severe inflammation or an alternative surgical emergency
- Jaundice or right upper-quadrant findings suggesting biliary obstruction or cholangitis
- Respiratory distress, pleural effusion, or pulmonary edema
- Rare flank or periumbilical ecchymosis; Grey Turner and Cullen signs indicate retroperitoneal or intraperitoneal bleeding but are neither sensitive nor specific
Laboratory Findings
Acute pancreatitis is supported by a serum lipase or amylase concentration at least 3 times the upper limit of normal. Lipase is preferred because it remains elevated longer and performs better in delayed presentation, alcohol-associated pancreatitis, and hypertriglyceridemia-associated pancreatitis; the magnitude of elevation does not reliably indicate severity.[2][4]
Additional studies should be selected to determine etiology and assess severity:
- Complete blood count, electrolytes, glucose, blood urea nitrogen, creatinine, liver biochemical tests, calcium, and triglycerides
- Arterial or venous blood gas and lactate when shock, respiratory failure, or severe metabolic derangement is suspected
- C-reactive protein as a delayed inflammatory marker; it is not required to establish the diagnosis
- Blood cultures when sepsis, cholangitis, or infected necrosis is suspected
- Immunoglobulin G4 only when the clinical and imaging pattern suggests type 1 autoimmune pancreatitis
Electrocardiogram
Acute pancreatitis has no diagnostic electrocardiographic pattern. An ECG and cardiac biomarkers should be obtained when the presentation could represent acute coronary syndrome; nonspecific ST-segment or T-wave abnormalities may occur during acute pancreatitis and should not be assumed benign without appropriate clinical evaluation.
Chest X Ray
Acute pancreatitis has no specific diagnostic chest radiograph finding. Chest radiography may demonstrate a left-sided or bilateral pleural effusion, basilar atelectasis, pulmonary infiltrates, or acute respiratory distress syndrome and can help identify alternative diagnoses such as pneumonia or perforated viscus.
CT Scan
Acute pancreatitis may be characterized on contrast-enhanced CT by pancreatic enlargement, altered or absent pancreatic enhancement, peripancreatic inflammatory change, fluid collections, and local vascular or gastrointestinal complications. CT should be reserved for diagnostic uncertainty, failure to improve or clinical deterioration after approximately 48–72 hours, suspected necrosis or another complication, or procedural planning; CT performed during the first 24–48 hours may underestimate evolving necrosis.[19][2]
Echocardiography or Ultrasound
Acute pancreatitis should generally be evaluated with transabdominal ultrasound to identify gallstones, biliary sludge, and common bile duct dilation, although bowel gas frequently limits visualization of the pancreas. Repeat ultrasound, endoscopic ultrasound, or MRI/MRCP may identify occult microlithiasis, choledocholithiasis, structural disease, or small tumors in otherwise unexplained pancreatitis.[2][5]
Other Imaging Findings
Acute pancreatitis can be further evaluated with MRI/MRCP when CT is contraindicated or when ductal, biliary, or collection characterization is required. Secretin-enhanced MRCP and endoscopic ultrasound are especially useful in selected patients with recurrent or idiopathic disease. ERCP is primarily therapeutic rather than a routine diagnostic test and should not be performed solely to confirm acute pancreatitis.
| Test | Principal role | Main limitation or caution |
|---|---|---|
| Serum lipase | Supports diagnosis when ≥3 times the upper limit of normal | Elevation is not fully specific, and the degree of elevation does not grade severity |
| Transabdominal ultrasound | First-line assessment for gallstones and biliary dilation | Limited pancreatic visualization because of bowel gas and body habitus |
| Contrast-enhanced CT | Evaluates uncertain diagnosis, necrosis, collections, vascular complications, deterioration, and procedural anatomy | Routine early CT adds radiation and contrast exposure and may underestimate early necrosis |
| MRI/MRCP | Characterizes ducts, biliary disease, necrosis, and collections without ionizing radiation | Longer examination, reduced availability, and less suitability for some unstable patients |
| Endoscopic ultrasound | Detects microlithiasis, small common bile duct stones, small tumors, and subtle structural causes | Invasive and operator dependent; generally used after the acute presentation or when standard evaluation is unrevealing |
| ERCP | Therapeutic biliary decompression in cholangitis or selected cases of persistent obstruction | Can cause or worsen pancreatitis and is not a routine diagnostic test |
Treatment
Acute pancreatitis is treated with early supportive care, close reassessment for organ dysfunction, cause-specific therapy, and selective intervention for biliary disease, infected necrosis, symptomatic collections, or other complications.
Medical Therapy
Acute pancreatitis requires individualized fluid therapy, analgesia, nutrition, and organ support rather than a disease-specific medication for the inflammatory process.
- Monitoring: Reassess vital signs, urine output, mental status, oxygenation, blood urea nitrogen, creatinine, and hematocrit frequently during the first 6–24 hours; admit high-risk patients to a monitored or intensive-care setting.
- Fluids: Use goal-directed, moderately aggressive crystalloid resuscitation, with lactated Ringer's solution generally preferred. Avoid fixed aggressive hydration, particularly in patients with cardiac or renal disease. The WATERFALL trial found more fluid overload without improved outcomes from aggressive compared with moderate resuscitation.[20]
- Analgesia and antiemetics: Provide adequate pain and nausea control; opioid analgesia may be used when clinically appropriate.
- Nutrition: Begin a low-fat solid oral diet within 24–48 hours as tolerated. If oral intake is not tolerated, use enteral rather than parenteral nutrition; nasogastric feeding is generally acceptable.[21]
- Antibiotics: Do not administer prophylactic antibiotics for predicted severe disease or sterile necrosis. Give therapeutic antibiotics for cholangitis, infected necrosis, or another proven or strongly suspected infection.
- Organ support: Treat hypoxemia, shock, acute kidney injury, electrolyte abnormalities, hyperglycemia, and other organ dysfunction according to critical-care principles.
Surgery
Acute pancreatitis rarely requires immediate open surgery; endoscopic, radiologic, laparoscopic, and minimally invasive surgical procedures are selected according to etiology, complications, and timing.
- ERCP: Perform urgent ERCP for acute biliary pancreatitis complicated by cholangitis. In the absence of cholangitis, routine urgent ERCP is not recommended; persistent common bile duct obstruction requires individualized evaluation.
- Cholecystectomy: Perform same-admission laparoscopic cholecystectomy for mild gallstone pancreatitis when the patient is fit for surgery. In necrotizing pancreatitis, delay cholecystectomy until inflammation and collections have resolved or stabilized. A 2026 nationwide Swedish cohort found recurrent pancreatitis in 3.4% after index-admission cholecystectomy, 4.9% after ERCP alone, and 17.5% after no index intervention; other gallstone complications remained substantially more common after ERCP alone than after cholecystectomy.[22]
- Necrosis and collections: Observe asymptomatic sterile necrosis and collections. Intervene for infected necrosis or persistent symptoms and complications such as obstruction, nutritional failure, fistula, bleeding, or ongoing organ dysfunction.
- Step-up approach: When intervention is required, begin with endoscopic or percutaneous drainage and proceed to endoscopic or minimally invasive necrosectomy only if necessary. Delay intervention until the collection is walled off, usually approximately 4 weeks, when the patient's condition permits.[23][24]
Prevention
Acute pancreatitis is not a vaccine-preventable disease, and no vaccine is applicable. Prevention depends on reducing modifiable exposures, preventing post-ERCP pancreatitis, identifying the cause of every episode, and avoiding ineffective or harmful interventions.
| Prevention level | Strategies |
|---|---|
| Primary | Avoid prolonged heavy alcohol exposure and tobacco; treat severe hypertriglyceridemia and hypercalcemia; maintain a healthy weight; use ERCP only when indicated and apply evidence-based post-ERCP prophylaxis in appropriate patients |
| Secondary | Determine and correct the cause after the first episode; perform same-admission cholecystectomy for mild gallstone pancreatitis; stop a credible offending medication; support alcohol and smoking cessation; control triglycerides; evaluate recurrent, early-onset, familial, or idiopathic pancreatitis for structural and genetic causes |
| Tertiary | Prevent disability from established disease by treating infected necrosis and symptomatic collections with a multidisciplinary step-up approach, supporting nutrition and rehabilitation, and screening for pancreatic exocrine insufficiency, diabetes, and recurrent or chronic pancreatitis |
| Quaternary | Avoid routine early CT when diagnostic criteria are already met, prophylactic antibiotics for sterile disease, routine urgent ERCP without cholangitis or persistent obstruction, prolonged fasting, overly aggressive fluid resuscitation, and premature open necrosectomy |
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Banks PA, Bollen TL, Dervenis C; et al. (2013). "Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus". Gut. 62 (1): 102–111. doi:10.1136/gutjnl-2012-302779.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Tenner S, Vege SS, Sheth SG; et al. (2024). "American College of Gastroenterology Guidelines: Management of Acute Pancreatitis". The American Journal of Gastroenterology. 119 (3): 419–437. doi:10.14309/ajg.0000000000002645.
- ↑ Mederos MA, Reber HA, Girgis MD (2021). "Acute Pancreatitis: A Review". JAMA. 325 (4): 382–390. doi:10.1001/jama.2020.20317.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 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.
- ↑ 5.0 5.1 5.2 IAP/APA/EPC/IPC/JPS Working Group (2025). "International Association of Pancreatology Revised Guidelines on Acute Pancreatitis 2025: Supported and Endorsed by the American Pancreatic Association, European Pancreatic Club, Indian Pancreas Club, and Japan Pancreas Society". Pancreatology. 25 (6): 770–814. doi:10.1016/j.pan.2025.04.020.
- ↑ 6.0 6.1 Leach SD, Gorelick FS, Modlin IM (1990). "Acute pancreatitis at its centenary: the contribution of Reginald Fitz". Annals of Surgery. 212 (1): 109–113. doi:10.1097/00000658-199007000-00014.
- ↑ Ranson JH, Rifkind KM, Roses DF; et al. (1974). "Prognostic signs and the role of operative management in acute pancreatitis". Surgery, Gynecology & Obstetrics. 139 (1): 69–81.
- ↑ Bradley EL III (1993). "A clinically based classification system for acute pancreatitis: summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992". Archives of Surgery. 128 (5): 586–590. doi:10.1001/archsurg.1993.01420170122019.
- ↑ 9.0 9.1 Boxhoorn L, Voermans RP, Bouwense SA; et al. (2020). "Acute Pancreatitis". The Lancet. 396 (10252): 726–734. doi:10.1016/S0140-6736(20)31310-6.
- ↑ Saluja A, Dudeja V, Dawra R, Sah RP (2019). "Early intra-acinar events in pathogenesis of pancreatitis". Gastroenterology. 156 (7): 1979–1993. doi:10.1053/j.gastro.2019.01.268.
- ↑ Wang F, Görgülü K, Algül H, Hu LH (2026). "The Role of Alcohol in Pancreatic Diseases: A Comprehensive Perspective". Gastroenterology. 170 (2): 268–286. doi:10.1053/j.gastro.2025.08.025.
- ↑ Iannuzzi JP, King JA, Leong JH; et al. (2022). "Global incidence of acute pancreatitis is increasing over time: a systematic review and meta-analysis". Gastroenterology. 162 (1): 122–134. doi:10.1053/j.gastro.2021.09.043.
- ↑ Danpanichkul P, Pang Y, Diaz LA; et al. (2026). "Global, Regional, and National Disparities in the Burden of Acute Pancreatitis and Alcohol-Related Pancreatitis From 2000 to 2021". Mayo Clinic Proceedings. 101 (7): 1151–1162. doi:10.1016/j.mayocp.2025.06.026.
- ↑ Forsmark CE, Vege SS, Wilcox CM (2016). "Acute Pancreatitis". The New England Journal of Medicine. 375 (20): 1972–1981. doi:10.1056/NEJMra1505202.
- ↑ Oppenlander KE, Chadwick C, Carman K (2022). "Acute Pancreatitis: Rapid Evidence Review". American Family Physician. 106 (1): 44–50.
- ↑ Trikudanathan G, Wolbrink DRJ, van Santvoort HC; et al. (2019). "Current concepts in severe acute and necrotizing pancreatitis: an evidence-based approach". Gastroenterology. 156 (7): 1994–2007. doi:10.1053/j.gastro.2019.01.269.
- ↑ Wu BU, Banks PA (2013). "Clinical management of patients with acute pancreatitis". Gastroenterology. 144 (6): 1272–1281. doi:10.1053/j.gastro.2013.01.075.
- ↑ 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.
- ↑ Porter KK, Zaheer A, Kamel IR; et al. (2019). "ACR Appropriateness Criteria Acute Pancreatitis". Journal of the American College of Radiology. 16 (11S): S316–S330. doi:10.1016/j.jacr.2019.05.017.
- ↑ de-Madaria E, Buxbaum JL, Maisonneuve P; et al. (2022). "Aggressive or moderate fluid resuscitation in acute pancreatitis". The New England Journal of Medicine. 387 (11): 989–1000. doi:10.1056/NEJMoa2202884.
- ↑ Crockett SD, Wani S, Gardner TB, Falck-Ytter Y, Barkun AN (2018). "American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis". Gastroenterology. 154 (4): 1096–1101. doi:10.1053/j.gastro.2018.01.032.
- ↑ Selin D, Oskarsson V, Maret-Ouda J; et al. (2026). "Cholecystectomy vs Endoscopic Retrograde Cholangiopancreatography or No Intervention After Gallstone-Related Acute Pancreatitis". JAMA Surgery. doi:10.1001/jamasurg.2026.2168.
- ↑ 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.
- ↑ Masood M, Vedamurthy A, Krishnamoorthi R; et al. (2025). "Interventional Management of Acute Pancreatitis and Its Complications". Journal of Clinical Medicine. 14 (18): 6683. doi:10.3390/jcm14186683.