Highlights & Basics
- Acute pancreatitis most commonly presents as severe mid-epigastric or left upper quadrant pain that radiates to the back. Epigastric tenderness is typical.
- Symptoms often include nausea and vomiting. A history of cholelithiasis or alcohol intake may be present.
- Signs of hypovolemia (including decreased skin turgor, dry mucous membranes, hypotension, and sweating) are common. In more severe cases, the patient may be tachycardic and/or tachypneic.
- In most patients who present with typical clinical signs, the diagnosis is confirmed by elevated serum lipase or amylase (>3 times upper limit of normal).
- Treatment includes early hydration with intravenous fluids, analgesia, and nutritional support, with early oral feeding favored if tolerated.
- Treatment of severe acute pancreatitis includes support of end organ failure, most commonly of respiratory, renal, and circulatory systems. Local complications that may develop later include sterile or infected pancreatic necrosis and pseudocysts.
- The presence of cholangitis in a patient with acute pancreatitis, characterized by an elevated bilirubin, warrants early endoscopic retrograde cholangiopancreatography (ERCP), typically within 24 hours from diagnosis.
Quick Reference
History & Exam
Key Factors
abdominal pain
nausea and vomiting
anorexia
signs of hypovolemia
Other Factors
signs of organ dysfunction
Grey-Turner sign
Cullen sign
Fox sign
Chvostek sign
abdominal distention
Diagnostics Tests
1st Tests to Order
serum lipase or amylase
liver function tests
CBC and differential
hematocrit
BUN and serum electrolytes
arterial blood gas
CRP
transabdominal ultrasound
chest x-ray
ratio of serum lipase:amylase
Other Tests to consider
abdominal CT scan
magnetic imaging/magnetic resonance cholangiopancreatography (MRI/MRCP)
endoscopic ultrasound (EUS)
Emerging Tests
procalcitonin
Treatment Options
acute
all patients
all patients
with gallstones; without cholangitis
with gallstones; with concurrent cholangitis
ongoing
deteriorating or failing to improve
deteriorating or failing to improve
with infected pancreatic necrosis
with sterile pancreatic necrosis
with symptomatic uninfected pseudocyst
with infected pseudocyst (abscess)
Definition
Classifications
Revised Atlanta classification
- Mild acute pancreatitis: the most common form, has no organ failure or local or systemic complications, and usually resolves in the first week.
- Moderately severe acute pancreatitis: presence of transient organ failure (resolves within 48 hours), and/or local complications or exacerbation of comorbid disease.
- Severe acute pancreatitis: persistent organ failure (>48 hours). Local complications are common and include peripancreatic fluid collections, pancreatic and peripancreatic necrosis (sterile or infected), pseudocyst, and walled-off necrosis (sterile or infected).
Balthazar classification
- A: Normal
- B: Focal or diffuse gland enlargement; small intrapancreatic fluid collection
- C: Any of the above plus peripancreatic inflammatory changes and <30% gland necrosis
- D: Any of the above plus single extrapancreatic fluid collection and 30% to 50% gland necrosis
- E: Any of the above plus extensive extrapancreatic fluid collection, pancreatic abscess, and >50% gland necrosis.
General pathologic classification
Vignette
Common Vignette 1
Common Vignette 2
Other Presentations
Epidemiology
Etiology
- Hypercalcemia
- Post-endoscopic retrograde cholangiopancreatography (2% to 3%)
- Trauma
- Infections (mumps, mycoplasma, Epstein-Barr virus, Ascaris lumbricoides, HIV-related coinfections)
- Autoimmune conditions (collagen vascular diseases)
- Pancreas divisum
- Intraductal papillary mucinous neoplasm
- Sphincter of Oddi dysfunction
- Autoimmune (immunoglobulin G4-related) sclerosing acute pancreatitis.
Pathophysiology
Images
Diagnostic Approach
- Pain consistent with the disease (e.g., epigastric pain of acute onset)
- Elevated serum lipase or amylase (>3 times the upper limit of normal)
- Imaging study (computed tomography [CT] or magnetic resonance imaging/magnetic resonance cholangiopancreatography [MRI/MRCP]) consistent with acute pancreatitis.
- Signs of hypovolemia may include hypotension, oliguria, dry mucous membranes, and decreased skin turgor. The patient may appear tachycardic, tachypneic, and sweating, particularly in more severe cases.
- The definition of SIRS is met by the presence of at least two of the following:[50]
- Pulse >90 beats per minute
- Respiratory rate >20 per minute or partial pressure of carbon dioxide (PaCO₂) <32 mmHg
- Temperature >100.4°F or <96.8ºF
- WBC count >12,000 or <4000 cells/mm³, or >10% immature neutrophils (bands).
History
Physical exam
Laboratory workup
Imaging
Emerging tests
Risk Factors
History & Exam
Tests
Differential Diagnosis
Peptic ulcer disease
Differentiating Signs/Symptoms
- Longstanding epigastric pain, which does not generally radiate to the back; reflux; heartburn; and anorexia. Identifiable causes such as nonsteroidal anti-inflammatory drug use, Helicobacter pylori, Zollinger-Ellison syndrome may be present.
Differentiating Tests
- May improve with proton pump inhibitors, lifestyle modifications, and H pylori treatment.
- Normal or low lipase and amylase.
- Endoscopic evaluation will be diagnostic after visualizing erosions, erythema, or ulcers, and allows biopsies to be performed.
Differentiating Signs/Symptoms
- Will present with acute abdomen, peritoneal signs, tachycardia, and sepsis. Generally the abdomen is rigid and tender in all 4 quadrants, with guarding.
Differentiating Tests
- Normal or slightly elevated lipase or amylase.
- Plain films show subdiaphragmatic air.
Differentiating Signs/Symptoms
- Dysphagia, odynophagia, weight loss, history of retrosternal pain. Physical exam may be normal.
Differentiating Tests
- A swallow study may demonstrate a contracted and abnormal-appearing esophagus. Patients may have increased wall pressure on esophageal manometry.
Intestinal obstruction
Differentiating Signs/Symptoms
- History of abdominal surgeries (especially colon resection, cesarean sections, and aortic procedures).
- Hernias, usually with incarcerated bowel, in the physical exam.
- Presents with abdominal distention (depends on the level of obstruction), tympanism, decreased bowel sounds, anorexia, emesis (quality depends on location of obstruction), obstipation, or constipation.
Differentiating Tests
- Normal or slightly elevated lipase and amylase.
- Acute abdominal series will show air-fluid levels, distended bowel loops, absence of distal gas, pneumatosis.
- An abdomen/pelvic CT scan may be more diagnostic, and will show point of transition and potentially identify etiology (such as volvulus, hernias, intussusception, masses).
Abdominal aorta aneurysm
Differentiating Signs/Symptoms
- Cardiovascular risk factors: hyperlipidemia, tobacco, diabetes mellitus, homocystinemia.
- Acute tearing-like abdominal pain, pulsating abdominal mass, hypotension, and mottled lower extremities with decreased pulses and abdominal distention.
Differentiating Tests
- High index of suspicion is necessary to make a rapid diagnosis and improve outcomes. In stable patients, where history and physical exam are equivocal, a CT angiography may be useful as a rapid way to make diagnosis.
- If too unstable for radiographic evaluation, patients usually go directly to surgery.
Cholangitis
Differentiating Signs/Symptoms
- Charcot's triad (jaundice, right upper quadrant pain, and fever) present in 70% of patients, altered mental status, and hypotension indicate biliary sepsis, usually caused by gram-negative bacteria.
- Patient may have a history of gallstones, periampullary neoplasms, or biliary manipulation such as endoscopic retrograde cholangiopancreatography.
Differentiating Tests
- Several clinical findings are present more frequently in cholangitis, such as fever (95%), right upper quadrant pain (90%), and jaundice (80%).
- Normal lipase and amylase.
- Blood cultures are usually positive, especially during episodes of chills, with Escherichia coli and Klebsiella as the most common microorganisms isolated from infected bile.[20]
Choledocholithiasis
Differentiating Signs/Symptoms
- Severe right upper quadrant pain of sudden onset, jaundice, acholia, choluria, and history of cholelithiasis. May occlude the common bile duct and cause pancreatitis.
Differentiating Tests
- Normal or slightly elevated lipase and amylase.
- Ultrasound will show gallstones, stones within the common bile duct with extrahepatic and/or intrahepatic duct dilatation.
- Chemistry will show biochemical obstruction, with increased levels of total and direct bilirubin, alkaline phosphatase, gamma glutamyl transpeptidase, and a slight increase in alanine aminotransferase/aspartate aminotransferase but normal levels of pancreatic enzymes (especially lipase).
Cholecystitis
Differentiating Signs/Symptoms
- Pain is generally triggered after a fatty meal and localized in the right upper quadrant. More common in overweight females between 40 and 50 years of age.
- Anorexia, nausea, and vomiting may be present. May show a positive Murphy sign and low-grade fever.
Differentiating Tests
- Normal or slightly elevated lipase and amylase.
- A right upper quadrant ultrasound will show thickened gallbladder wall, stones with acoustic shadows, biliary sludge, pericholecystic fluid, and sonographic Murphy sign, and allows evaluation of the duct system. Can suggest pancreatic head inflammation. May show mild leukocytosis and a very mild elevation of liver enzymes.
- A hepatobiliary iminodiacetic acid scan is diagnostic when there is no filling of the gallbladder or with delayed emptying of the radiotracer.
Viral gastroenteritis
Differentiating Signs/Symptoms
- Generalized nonspecific abdominal pain, anorexia, nausea, emesis, diarrhea, and dehydration.
- Is usually a self-limited viral infection but if fever is documented, bacterial and invasive organisms should be suspected.
- Consider in travelers and immunosuppressed patients.
- Consider osmotic and secretory diarrhea from history.
Differentiating Tests
- Normal or slightly elevated lipase and amylase.
- Important to obtain serum electrolytes and a complete blood count.
- Hypokalemia and alkalosis may be seen secondary to diarrhea, vomiting, and dehydration.
- Stool examination for microscopy, culture, osmolality, ova, parasites, Clostridium difficile toxin, and white blood cells may help in identifying the causative factor.
Differentiating Signs/Symptoms
- Jaundice, right upper quadrant pain, anorexia, and general malaise. Choluria and acholia may be seen.
- Exam: tenderness to palpation over the right upper quadrant and enlarged liver.
Differentiating Tests
- Normal lipase and amylase.
- Elevated liver function tests are characteristic. Aspartate aminotransferase/alanine aminotransferase in the range of the 1000 units/L is not rare. Serologic titers can make diagnosis of etiologic cause.
- Radiographic studies not important for its diagnosis.
Differentiating Signs/Symptoms
- Patients are usually older, may have a history of atrial fibrillation and risk factors for peripheral vascular disease.
- Hypercoagulable states may lead to bowel necrosis. Pain is usually out of proportion to the finding of the physical exam.
Differentiating Tests
- High index of suspicion of diagnosis is necessary. Angiography and CT scan may be useful in diagnosis as well as lactic acid levels.
- Normal lipase. May have elevated amylase (usually less marked than that seen in acute pancreatitis).
Myocardial infarction
Differentiating Signs/Symptoms
- Pain is usually retrosternal with radiation to jaw, neck, and left upper extremity. Associated with shortness of breath, nausea, vomiting, and diaphoresis. Cardiovascular risk factors in the history.
Differentiating Tests
- Elevated cardiac enzymes (creatine kinase or creatine phosphokinase, troponins), ECG changes, and clinical scenario make the diagnosis.
- Normal lipase and amylase.
- Cardiac catheterization, perfusion scans, and echocardiograms are useful during the workup of cardiac ischemia.
Criteria
- Clinical (upper abdominal pain)
- Laboratory (serum lipase or amylase >3 upper limit of normal)
- Imaging (computed tomography [CT], magnetic resonance [MR], ultrasound) criteria.
- Pulse >90 beats per minute
- Respiratory rate >20 per minute or partial pressure of carbon dioxide (PaCO₂) <32 mmHg
- Temperature >100.4°F or <96.8ºF
- WBC count >12,000 or <4000 cells/mm³, or >10% immature neutrophils (bands).
- Age >55 years
- Obesity (body mass index >30 kg/m²)
- Altered mental status
- Comorbid disease
- BUN >20 mg/dL
- Rising BUN
- Hematocrit (HCT) >44%
- Rising HCT
- Elevated creatinine
- Pleural effusions
- Pulmonary infiltrates
- Multiple or extensive extrapancreatic collections
- No organ failure
- No local or systemic complications
- Transient organ failure (<48 hours)
- Local or systemic complications without persistent organ failure
- Persistent single or multiple organ failure (>48 hours)
Treatment Approach
Initial management
- Pulse >90 beats per minute
- Respiratory rate >20 per minute or partial pressure of carbon dioxide (PaCO₂) <32 mmHg
- Temperature >100.4°F or <96.8ºF
- WBC count >12,000 or <4000 cells/mm³, or >10% immature neutrophils (bands).
- Shock: systolic blood pressure ≤90 mmHg
- Pulmonary insufficiency: partial pressure of oxygen (PaO₂) ≤60%
- Renal failure: creatinine ≥2 mg/dL
- Gastrointestinal bleeding: >500 mL blood loss in 24 hours.
Nutrition
Infectious complications
Pancreatic necrosis
Pseudocysts
Treatment Options
all patients
intravenous fluids
Comments
- All patients need to be treated with intravenous hydration for the first 24 hours and monitored closely for early fluid losses, hypovolemic shock, and symptoms suggestive of organ dysfunction in the first 48 to 72 hours from presentation.[17]
- Initial treatment of acute pancreatitis requires early intravenous hydration.[1] [5] [70] [73] [74] [75] [76] Clinicians should focus on a steady rate of initial resuscitation (no more than 1.5 mL per kg of body weight per hour) and should administer a bolus of 10 mL per kg, only if there are signs of initial hypovolemia.[71] A balanced crystalloid (such as Ringer's lactate [Hartmann solution] or Plasma-Lyte®) may have benefits compared with normal saline.[17] [48] Early intravenous hydration should be guided by close observation of clinical parameters such as heart rate, blood pressure, and urine output, with measurement of blood urea nitrogen and hematocrit within 6 to 12 hours. Although American College of Gastroenterology (ACG) guidelines from 2013 recommended aggressive early rehydration for all patients with acute pancreatitis, subsequent evidence supports a moderate approach.[17] [70] One multicenter randomized controlled trial published in 2022 showed that aggressive early hydration resulted in a higher incidence of fluid overload compared with moderate hydration, without improvement in clinical outcomes.[70]
- No patient should be classified as having mild disease until at least 48 hours after symptom onset as some patients who go on to develop severe disease present without signs of organ failure or local complications.[17]
- It is critical to recognize the paramount importance of organ failure in determining disease severity.[17] In the presence of systemic inflammatory response syndrome (SIRS)-associated organ dysfunction, additional monitoring and organ support may be necessary (e.g., oxygen supplementation and/or ventilatory support for respiratory failure). Signs of cardiovascular, respiratory, or renal dysfunction may be present. Patients with organ failure and/or persisting SIRS should be admitted to an intensive care unit whenever possible.[17] [27]
- The definition of SIRS is met by the presence of at least two of the following criteria: pulse >90 beats per minute; respiratory rate >20 per minute or partial pressure of carbon dioxide (PaCO₂) <32 mmHg; temperature >100.4°F or <96.8ºF; WBC count >12,000 or <4000 cells/mm³, or >10% immature neutrophils (bands).[50]
- The presence of persistent (>48 hours) single- or multi-organ failure defines acute pancreatitis as severe according to the revised Atlanta criteria.[17] [27] In everyday clinical practice, the following parameters (from the original Atlanta Criteria) may be used to establish organ failure: shock: systolic blood pressure ≤90 mmHg; pulmonary insufficiency: partial pressure of oxygen (PaO₂) ≤60%; renal failure: creatinine ≥2 mg/dL; gastrointestinal bleeding: >500 mL blood loss in 24 hours.[17]
analgesia
Primary Options
- morphine sulfate
2.5 to 10 mg intravenously/intramuscularly/subcutaneously every 2-6 hours when required
- morphine sulfate
- fentanyl
50-100 micrograms intravenously/intramuscularly every 1-2 hours when required
- fentanyl
- ketorolac
consult specialist for guidance on dose
- ketorolac
Comments
- Pain control with opioids may reduce the need for multimodal analgesia.[86]
- Fentanyl or morphine can be used, either for breakthrough pain or as patient-controlled analgesia. In mild cases, the standard World Health Organization pain ladder can be used to inform the selection, monitoring, and adjustment of analgesia.
- Ketorolac, a nonsteroidal anti-inflammatory drug, can be used in patients with intact renal function. It should not be used in older patients because of the risk of adverse gastrointestinal effects.[87]
nutritional support
Comments
- Enteral tube nutrition should be used for patients who are unable to feed orally; parenteral nutrition should be avoided.[91] Continuous enteral infusion is preferred over cyclic or bolus administration.[17] Small peptide-based medium chain triglyceride formulas can be used if standard formulas are not tolerated.[91]
- Nasogastric tube feeding is recommended in preference to the nasojejunal route for most patients.[17] [91] Patients at increased risk of aspiration should be put in a more upright position and placed on aspiration precautions.[17] Nasojejunal tube placement requires interventional radiology or endoscopy and thus has resource implications.[17]
- No specific enteral nutrition formulation has been proven to be better than another in patients with acute pancreatitis.[97] The recommended nutrient requirements in severe acute pancreatitis are as follows: energy 25 to 35 kcal/kg/day, protein 1.2 to 1.5 g/kg/day, carbohydrates 3 to 6 g/kg/day, and lipids 2 g/kg/day.[93] [98] [99]
antiemetic
Primary Options
- ondansetron
8 mg intravenously every 8 hours when required
- ondansetron
Comments
- Nausea and/or vomiting is a presenting symptom in 70% to 80% of patients. Ondansetron is the most commonly used antiemetic.
empiric intravenous antibiotics (if infection is confirmed or strongly suspected)
Primary Options
Secondary Options
- ciprofloxacin
400 mg intravenously every 12 hours
- ciprofloxacin
- metronidazole
15 mg/kg intravenously as a loading dose, followed by 7.5 mg/kg every 6 hours, maximum 4000 mg/day
- metronidazole
Comments
- When an infection is suspected, antibiotics should be given while the source of the infection is being investigated.
- Fever, tachycardia, tachypnea, and leukocytosis are associated with the systemic inflammatory response syndrome (SIRS) that may occur early in the course of acute pancreatitis. This clinical picture may be indistinguishable from sepsis.
- Other infectious complications of acute pancreatitis include cholangitis, urinary tract infections, infected pseudocysts, fluid collections, and infected pancreatic necrosis.
- If blood and other cultures are found to be negative and no source of infection is identified, antibiotics should be discontinued.
- Choose an antibiotic that has good pancreatic penetration, such as a carbapenem (e.g., imipenem/cilastatin), a fluoroquinolone (e.g., ciprofloxacin), or metronidazole.[17] [27] Imipenem/cilastatin is usually the first-line choice because it has good pancreatic penetration. Check local guidance on antibiotic stewardship. Fluoroquinolones have been associated with serious, disabling, and potentially irreversible adverse effects, including tendonitis, tendon rupture, arthralgia, neuropathies, and other musculoskeletal or nervous system effects.[102] Warnings have also been issued about the increased risk of aortic dissection, significant hypoglycemia, and mental health adverse effects in patients taking fluoroquinolones.[103] [104]
with gallstones; without cholangitis
cholecystectomy
Comments
- Patients with mild gallstone pancreatitis should have a cholecystectomy during the initial admission, after the acute symptoms have resolved. Cholecystectomy is typically delayed for patients with severe disease; these patients require complex decision-making between the surgeon and gastroenterologist.[17] [48]
with gallstones; with concurrent cholangitis
endoscopic retrograde cholangiopancreatography (ERCP)
Comments
- Patients with gallstone pancreatitis and concurrent cholangitis benefit from early ERCP. The benefit is seen in patients with sepsis complicated by organ failure who undergo the procedure within the first 24 hours from admission.[17] [48] [84] [85] Although gallstones in the common bile duct are a common cause of acute pancreatitis, most gallstones readily pass to the duodenum and are lost in the stool. Persistent choledocholithiasis can lead to persistent pancreatic duct and/or biliary tree obstruction, leading to necrosis and/or cholangitis. Removal of obstructing gallstones from the biliary tree in patients with acute pancreatitis should reduce the likelihood of complications.
deteriorating or failing to improve
ongoing supportive treatment
Comments
- American College of Gastroenterology guidelines recommend computed tomography (CT) or magnetic resonance imaging/magnetic resonance cholangiopancreatography (MRI/MRCP) after 48 hours in patients who do not improve or whose symptoms worsen, to assess for necrosis.[17] Other guidelines recommend a delay of 72 to 96 hours after symptom onset before contrast-enhanced CT or MRI.[27] [48]
ongoing nutritional support
Comments
- In patients who are unable to feed orally, enteral tube nutrition should be used; parenteral nutrition should be avoided.[91]
with infected pancreatic necrosis
intravenous antibiotics
Primary Options
Secondary Options
- ciprofloxacin
400 mg intravenously every 12 hours
- ciprofloxacin
- metronidazole
15 mg/kg intravenously as a loading dose, followed by 7.5 mg/kg every 6 hours, maximum 4000 mg/day
- metronidazole
Comments
- Fluoroquinolones have been associated with serious, disabling, and potentially irreversible adverse effects, including tendonitis, tendon rupture, arthralgia, neuropathies, and other musculoskeletal or nervous system effects.[102] Warnings have also been issued about the increased risk of aortic dissection, significant hypoglycemia, and mental health adverse effects in patients taking fluoroquinolones.[103] [104]
catheter drainage (endoscopic or radiologic)
Comments
- Once the inflammatory reaction has become better organized (i.e., fully walled off), a decision can be made regarding the preferred method of drainage. This may include endoscopic or radiologic approaches.
necrosectomy/debridement
Comments
- If there is no prompt response to antibiotics or if the clinical situation deteriorates, necrosectomy/debridement should be performed.[17]
with sterile pancreatic necrosis
catheter drainage or necrosectomy/debridement
Comments
- Prophylactic antibiotics to prevent infection are not recommended for patients with sterile necrosis (even for those predicted as having severe disease).[17]
- After approximately 4 weeks, a fibrous wall develops around the necrotic area, making it easier to remove with drainage or necrosectomy/debridement.[48]
with symptomatic uninfected pseudocyst
drainage (endoscopic, radiologic, or surgical)
Comments
- Pseudocysts do not appear until 2 to 4 weeks after the onset of an episode of acute pancreatitis.
with infected pseudocyst (abscess)
drainage (endoscopic, radiologic, or surgical) and intravenous antibiotics
Primary Options
Secondary Options
- ciprofloxacin
400 mg intravenously every 12 hours
- ciprofloxacin
- metronidazole
15 mg/kg intravenously as a loading dose, followed by 7.5 mg/kg every 6 hours, maximum 4000 mg/day
- metronidazole
Comments
- Pseudocysts do not appear until 2 to 4 weeks after the onset of an episode of acute pancreatitis.
- If a pseudocyst becomes infected, it is best described as an abscess, which requires antibiotics and drainage.
- Choose an antibiotic that has good pancreatic penetration, such as a carbapenem (e.g., imipenem/cilastatin), a fluoroquinolone (e.g., ciprofloxacin), or metronidazole.[17] [27] Imipenem/cilastatin is usually the first-line choice because it has good pancreatic penetration. Check local guidance on antibiotic stewardship.
- Fluoroquinolones have been associated with serious, disabling, and potentially irreversible adverse effects, including tendonitis, tendon rupture, arthralgia, neuropathies, and other musculoskeletal or nervous system effects.[102] Warnings have also been issued about the increased risk of aortic dissection, significant hypoglycemia, and mental health adverse effects in patients taking fluoroquinolones.[103] [104]
Emerging Tx
Gastric antisecretory agents
CM4620
Prevention
Secondary Prevention
Follow-Up Overview
Prognosis
Monitoring
Complications
Citations
Tenner S, Baillie J, DeWitt J, et al. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013 Sep;108(9):1400-15.[Abstract]
Leppäniemi A, Tolonen M, Tarasconi A, et al. 2019 WSES guidelines for the management of severe acute pancreatitis. World J Emerg Surg. 2019 Jun 13;14:27.[Abstract][Full Text]
Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013 Jul-Aug;13(4 Suppl 2):e1-15.[Abstract][Full Text]
American College of Radiology. ACR appropriateness criteria: acute pancreatitis. 2019 [internet publication].[Full Text]
Crockett SD, Wani S, Gardner TB, et al. American Gastroenterological Association Institute guideline on initial management of acute pancreatitis. Gastroenterology. 2018 Mar;154(4):1096-101.
Crockett SD, Wani S, Gardner TB, et al. American Gastroenterological Association Institute guideline on initial management of acute pancreatitis. Gastroenterology. 2018 Mar;154(4):1096-101.[Abstract]
1. Nirula R. Chapter 9: Diseases of the pancreas. High yield surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2000.
2. Banks PA, Bollen TL, Dervenis C, et al; Acute Pancreatitis Classification Working Group. Classification of acute pancreatitis - 2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013 Jan;62(1):102-11.[Abstract][Full Text]
3. Balthazar EJ, Robinson DL, Megibow AJ, et al. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990 Feb;174(2):331-6.[Abstract]
4. Doherty GM, Meko JB, Olson JA, et al. Chapter 17: Pancreas. In: The Washington manual of surgery. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999.
5. Way LW, Doherty GM. Chapter 27: Pancreas. In: Current surgical diagnosis & treatment. 11th ed. New York, NY: McGraw-Hill; 2003.
6. Raghu MG, Wig JD, Kochhar R, et al. Lung complications in acute pancreatitis. JOP. 2007 Mar 10;8(2):177-85.[Abstract]
7. Kingsnorth A, O'Reilly D. Acute pancreatitis. BMJ. 2006 May 6;332(7549):1072-6.[Full Text]
8. Xiao AY, Tan ML, Wu LM, et al. Global incidence and mortality of pancreatic diseases: a systematic review, meta-analysis, and meta-regression of population-based cohort studies. Lancet Gastroenterol Hepatol. 2016 Sep;1(1):45-55.[Abstract]
9. GBD 2017 Pancreatic Cancer Collaborators. The global, regional, and national burden of pancreatic cancer and its attributable risk factors in 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol. 2019 Dec;4(12):934-47.[Abstract][Full Text]
10. Munoz A, Katerndahl DA. Diagnosis and management of acute pancreatitis. Am Fam Physician. 2000 Jul 1;62(1):164-74.[Abstract][Full Text]
11. Peery AF, Crockett SD, Murphy CC, et al. Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: update 2018. Gastroenterology. 2019 Jan;156(1):254-72.e11.[Abstract][Full Text]
12. Brindise E, Elkhatib I, Kuruvilla A, et al. Temporal trends in incidence and outcomes of acute pancreatitis in hospitalized patients in the United States from 2002 to 2013. Pancreas. 2019 Feb;48(2):169-75.[Abstract]
13. Whitcomb DC. Clinical practice: acute pancreatitis. N Engl J Med. 2006 May 18;354(20):2142-50.
14. Mederos MA, Reber HA, Girgis MD. Acute pancreatitis: a review. JAMA. 2021 Jan 26;325(4):382-90.[Abstract]
15. Roberts SE, Morrison-Rees S, John A, et al. The incidence and aetiology of acute pancreatitis across Europe. Pancreatology. 2017 Mar - Apr;17(2):155-65.[Abstract]
16. van Brummelen SE, Venneman NG, van Erpecum KJ, et al. Acute idiopathic pancreatitis: does it really exist or is it a myth? Scand J Gastroenterol Suppl. 2003;(239):117-22.[Abstract]
17. Tenner S, Baillie J, DeWitt J, et al. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013 Sep;108(9):1400-15.[Abstract]
18. Hines OJ, Pandol SJ. Management of severe acute pancreatitis. BMJ. 2019 Dec 2;367:l6227.[Abstract]
19. Brunicardi FC, Andersen DK, Billiar TR. Chapter 32: Pancreas. In: Schwartz's principles of surgery. 8th ed. New York, NY: McGraw-Hill; 2005.
20. Underwood TW, Frye CB. Drug-induced pancreatitis. Clin Pharm. 1993 Jun;12(6):440-8.[Abstract]
21. Gelrud A, Sheth S, Banerjee S, et al. Analysis of cystic fibrosis gener product (CFTR) function in patients with pancreas divisum and recurrent acute pancreatitis. Am J Gastroenterol. 2004 Aug;99(8):1557-62.[Abstract]
22. Maxson CJ, Greenfield SM, Turner JL. Acute pancreatitis as a common complication of 2',3'-dideoxyinosine therapy in the acquired immunodeficiency syndrome. Am J Gastroenterol. 1992 Jun;87(6):708-13.[Abstract]
23. Tenner S. Drug induced acute pancreatitis: does it exist? World J Gastroenterol. 2014 Nov 28;20(44):16529-34.[Abstract][Full Text]
24. Sah RP, Saluja A. Molecular mechanisms of pancreatic injury. Curr Opin Gastroenterol. 2011 Sep;27(5):444-51.[Abstract][Full Text]
25. Townsend C. Chapter 53: exocrine pancreas. In: Sabiston textbook of surgery board review. 17th ed. Philadelphia, PA: Saunders; 2004.
26. Carr RA, Rejowski BJ, Cote G2, et al. Systematic review of hypertriglyceridemia-induced acute pancreatitis: A more virulent etiology? Pancreatology. 2016 Jul-Aug;16(4):469-76.[Abstract]
27. Leppäniemi A, Tolonen M, Tarasconi A, et al. 2019 WSES guidelines for the management of severe acute pancreatitis. World J Emerg Surg. 2019 Jun 13;14:27.[Abstract][Full Text]
28. Bálint ER, Fűr G, Kiss L, et al. Assessment of the course of acute pancreatitis in the light of aetiology: a systematic review and meta-analysis. Sci Rep. 2020 Oct 21;10(1):17936.[Abstract][Full Text]
29. Frick TW, Wiegand D, Bimmler D, et al. A rat model to study hypercalcemia-induced acute pancreatitis. Int J Pancreatol. 1994 Apr;15(2):91-6.[Abstract]
30. Frick TW, Spycher MA, Heitz PU, et al. Hypercalcaemia and pancreatic ultrastructure in cats. Eur J Surg. 1992 May;158(5):289-94.[Abstract]
31. Juang P, Page RL, Zolty R. Probable loop diuretic-induced pancreatitis in a sulfonamide-allergic patient. Ann Pharmacother. 2006 Jan;40(1):128-34.[Abstract]
32. Akshintala VS, Sperna Weiland CJ, Bhullar FA, et al. Non-steroidal anti-inflammatory drugs, intravenous fluids, pancreatic stents, or their combinations for the prevention of post-endoscopic retrograde cholangiopancreatography pancreatitis: a systematic review and network meta-analysis. Lancet Gastroenterol Hepatol. 2021 Sep;6(9):733-42.[Abstract]
33. Akbar A, Abu Dayyeh BK, Baron TH, et al. Rectal nonsteroidal anti-inflammatory drugs are superior to pancreatic duct stents in preventing pancreatitis after endoscopic retrograde cholangiopancreatography: a network meta-analysis. Clin Gastroenterol Hepatol. 2013 Jul;11(7):778-83.[Abstract]
34. Yaghoobi M, Rolland S, Waschke KA, et al. Meta-analysis: rectal indomethacin for the prevention of post-ERCP pancreatitis. Aliment Pharmacol Ther. 2013 Nov;38(9):995-1001.[Abstract][Full Text]
35. Elmunzer BJ, Higgins PD, Saini SD, et al; United States Cooperative for Outcomes Research in Endoscopy. Does rectal indomethacin eliminate the need for prophylactic pancreatic stent placement in patients undergoing high-risk ERCP? Post hoc efficacy and cost-benefit analyses using prospective clinical trial data. Am J Gastroenterol. 2013 Mar;108(3):410-5.[Abstract][Full Text]
36. Márta K, Gede N, Szakács Z, et al. Combined use of indomethacin and hydration is the best conservative approach for post-ERCP pancreatitis prevention: a network meta-analysis. Pancreatology. 2021 Oct;21(7):1247-55.[Abstract][Full Text]
37. American Society for Gastrointestinal Endoscopy guideline on post-ERCP pancreatitis prevention strategies: summary and recommendations. Feb 2023 [internet publication].[Full Text]
38. Buxbaum J, Yan A, Yeh K, et al. Aggressive hydration with lactated Ringer's solution reduces pancreatitis after endoscopic retrograde cholangiopancreatography. Clin Gastroenterol Hepatol. 2014 Feb;12(2):303-7.e1.[Abstract][Full Text]
39. Wu D, Wan J, Xia L, et al. The efficiency of aggressive hydration with lactated ringer solution for the prevention of post-ERCP pancreatitis: a systematic review and meta-analysis. J Clin Gastroenterol. 2017 Sep;51(8):e68-76.[Abstract]
40. Heyries L, Barthet M, Delvasto C, et al. Long-term results of endoscopic management of pancreas divisum with recurrent acute pancreatitis. Gastrointest Endosc. 2002 Mar;55(3):376-81.[Abstract]
41. Strand DS, Law RJ, Yang D, et al. AGA clinical practice update on the endoscopic approach to recurrent acute and chronic pancreatitis: expert review. Gastroenterology. 2022 Oct;163(4):1107-14.[Abstract]
42. Spicak J. Etiological factors of acute pancreatitis [in Czech]. Vnitr Lek. 2002 Sep;48(9):829-41.[Abstract]
43. Guda NM, Muddana V, Whitcomb DC, et al. Recurrent acute pancreatitis: international state-of-the-science conference with recommendations. Pancreas. 2018 Jul;47(6):653-66.[Abstract]
44. Vitone LJ, Greenhalf W, Howes NR, et al. Hereditary pancreatitis and secondary screening for early pancreatic cancer. Rocz Akad Med Bialymst. 2005;50:73-84.[Abstract]
45. Whitcomb DC. Genetic risk factors for pancreatic disorders. Gastroenterology. 2013 Jun;144(6):1292-302.[Abstract][Full Text]
46. Whitcomb DC. Genetic aspects of pancreatitis. Annu Rev Med. 2010;61:413-24.[Abstract]
47. Giefer MJ, Lowe ME, Werlin SL, et al. Early-onset acute recurrent and chronic pancreatitis is associated with PRSS1 or CTRC gene mutations. J Pediatr. 2017 Jul;186:95-100.[Abstract][Full Text]
48. Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013 Jul-Aug;13(4 Suppl 2):e1-15.[Abstract][Full Text]
49. National Institute for Health and Care Excellence. Pancreatitis. Dec 2020 [internet publication].[Full Text]
50. Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS international sepsis definitions conference. Crit Care Med. 2003 Apr;31(4):1250-6.[Abstract]
51. Bass G, Gilani SN, Walsh TN. Validating the 5Fs mnemonic for cholelithiasis: time to include family history. Postgrad Med J. 2013 Nov;89(1057):638-41.[Abstract]
52. Stinton LM, Shaffer EA. Epidemiology of gallbladder disease: cholelithiasis and cancer. Gut Liver. 2012 Apr;6(2):172-87.[Abstract][Full Text]
53. Zuo L, Wang CH, Yang JL, et al. The role of a workflow in diagnosing biliary causes for acute pancreatitis [in Chinese]. Zhonghua Nei Ke Za Zhi. 2012 Feb;51(2):104-7.[Abstract]
54. Hujoel IA. The association between serum calcium levels and Chvostek sign: a population-based study. Neurol Clin Pract. 2016 Aug;6(4):321-8.[Abstract][Full Text]
55. Rompianesi G, Hann A, Komolafe O, et al. Serum amylase and lipase and urinary trypsinogen and amylase for diagnosis of acute pancreatitis. Cochrane Database Syst Rev. 2017 Apr 21;(4):CD012010.[Abstract][Full Text]
56. Choosing Wisely. American Society for Clinical Pathology: testing for amylase. Sep 2016 [internet publication].[Full Text]
57. Steinberg WM, Nauck MA, Zinman B, et al. LEADER 3--lipase and amylase activity in subjects with type 2 diabetes: baseline data from over 9000 subjects in the LEADER Trial. Pancreas. 2014 Nov;43(8):1223-31.[Abstract][Full Text]
58. Brown A, Orav J, Banks PA. Hemoconcentration is an early marker for organ failure and necrotizing pancreatitis. Pancreas. 2000 May;20(4):367-72.[Abstract]
59. Tenner S, Dubner H, Steinberg W. Predicting gallstone pancreatitis with laboratory parameters: a meta-analysis. Am J Gastroenterol. 1994 Oct;89(10):1863-6.[Abstract]
60. Khanna AK, Meher S, Prakash S, et al. Comparison of Ranson, Glasgow, MOSS, SIRS, BISAP, APACHE-II, CTSI scores, IL-6, CRP, and procalcitonin in predicting severity, organ failure, pancreatic necrosis, and mortality in acute pancreatitis. HPB Surg. 2013;2013:367581.[Abstract][Full Text]
61. Komolafe O, Pereira SP, Davidson BR, et al. Serum C-reactive protein, procalcitonin, and lactate dehydrogenase for the diagnosis of pancreatic necrosis. Cochrane Database Syst Rev. 2017 Apr 21;(4):CD012645.[Abstract][Full Text]
62. Ranson JH, Rifkind KM, Turner JW. Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. Surg Gynecol Obstet. 1976 Aug;143(2):209-19.[Abstract]
63. American College of Radiology. ACR appropriateness criteria: acute pancreatitis. 2019 [internet publication].[Full Text]
64. Frossard JL, Steer ML, Pastor CM. Acute pancreatitis. Lancet. 2008 Jan 12;371(9607):143-52.
65. Fogel EL, Sherman S. ERCP for gallstone pancreatitis. N Engl J Med. 2014 Jan 9;370(2):150-7.
66. ASGE Standards of Practice Committee; Muthusamy VR, Chandrasekhara V, Acosta RD, et al. The role of endoscopy in the diagnosis and treatment of inflammatory pancreatic fluid collections. Gastrointest Endosc. 2016 Mar;83(3):481-8.[Full Text]
67. Simundic AM, Bölenius K, Cadamuro J, et al. Joint EFLM-COLABIOCLI recommendation for venous blood sampling. Clin Chem Lab Med. 2018;56(12):2015-38.[Abstract]
68. McPherson RA, Pincus MR. Henry's clinical diagnosis and management by laboratory methods. 21st ed. Philadelphia, PA: Saunders; 2006.
69. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992 Jun;101(6):1644-55.[Abstract]
70. de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or moderate fluid resuscitation in acute pancreatitis. N Engl J Med. 2022 Sep 15;387(11):989-1000.[Abstract]
71. Gardner TB. Fluid resuscitation in acute pancreatitis - going over the WATERFALL. N Engl J Med. 2022 Sep 15;387(11):1038-9.
72. Baillie J, ed. Advances in endoscopy: current developments in diagnostic and therapeutic endoscopy. Gastroenterol Hepatol (N Y). 2010 Jan;6(1):16-8.[Full Text]
73. Darvas K, Futo J, Okros I, et al. Principles of intensive care in severe acute pancreatitis in 2008 [in Hungarian]. Orv Hetil. 2008 Nov 23;149(47):2211-20.[Abstract]
74. Curtis CS, Kudsk KA. Nutrition support in pancreatitis. Surg Clin North Am. 2007 Dec;87(6):1403-15.[Abstract]
75. Thomson A. Nutritional support in acute pancreatitis. Curr Opin Clin Nutr Metab Care. 2008 May;11(3):261-6.[Abstract]
76. Marik PE. What is the best way to feed patients with pancreatitis? Curr Opin Crit Care. 2009 Apr;15(2):131-8.[Abstract]
77. Choosakul S, Harinwan K, Chirapongsathorn S, et al. Comparison of normal saline versus Lactated Ringer's solution for fluid resuscitation in patients with mild acute pancreatitis, a randomized controlled trial. Pancreatology. 2018 Jul;18(5):507-12.[Abstract]
78. Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018 Mar 1;378(9):829-39.[Abstract][Full Text]
79. Zampieri FG, Machado FR, Biondi RS, et al. Effect of intravenous fluid treatment with a balanced solution vs 0.9% saline solution on mortality in critically ill patients: the BaSICS randomized clinical trial. JAMA. 2021 Aug 10;326(9):1-12.[Abstract][Full Text]
80. Finfer S, Micallef S, Hammond N, et al. Balanced multielectrolyte solution versus saline in critically ill adults. N Engl J Med. 2022 Jan 18 [Epub ahead of print].[Abstract]
81. Crockett SD, Wani S, Gardner TB, et al. American Gastroenterological Association Institute guideline on initial management of acute pancreatitis. Gastroenterology. 2018 Mar;154(4):1096-101.
82. Buxbaum JL, Quezada M, Da B, et al. Early aggressive hydration hastens clinical improvement in mild acute pancreatitis. Am J Gastroenterol. 2017 May;112(5):797-803.[Abstract]
83. Fisher JM, Gardner TB. The "golden hours" of management in acute pancreatitis. Am J Gastroenterol. 2012 Aug;107(8):1146-50.[Abstract]
84. van Dijk SM, Hallensleben NDL, van Santvoort HC, et al. Acute pancreatitis: recent advances through randomised trials. Gut. 2017 Nov;66(11):2024-32.[Abstract]
85. Moretti A, Papi C, Aratari A, et al. Is early endoscopic retrograde cholangiopancreatography useful in the management of acute biliary pancreatitis? A meta-analysis of randomized controlled trials. Dig Liver Dis. 2008 May;40(5):379-85.[Abstract]
86. Basurto Ona X, Rigau Comas D, Urrútia G. Opioids for acute pancreatitis pain. Cochrane Database Syst Rev. 2013 Jul 26;(7):CD009179.[Abstract][Full Text]
87. American Geriatrics Society 2012 Beers Criteria Update Expert Panel. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2012 Apr;60(4):616-31.[Abstract][Full Text]
88. Ramírez-Maldonado E, López Gordo S, Pueyo EM, et al. Immediate oral refeeding in patients with mild and moderate acute pancreatitis: a multicenter, randomized controlled trial (PADI trial). Ann Surg. 2021 Aug 1;274(2):255-63.[Abstract]
89. Vaughn VM, Shuster D, Rogers MAM, et al. Early versus delayed feeding in patients with acute pancreatitis: a systematic review. Ann Intern Med. 2017 Jun 20;166(12):883-92.[Abstract]
90. Bakker OJ, van Brunschot S, van Santvoort HC, et al. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med. 2014 Nov 20;371(21):1983-93.[Abstract][Full Text]
91. Arvanitakis M, Ockenga J, Bezmarevic M, et al. ESPEN guideline on clinical nutrition in acute and chronic pancreatitis. Clin Nutr. 2020 Mar;39(3):612-31.[Abstract][Full Text]
92. Yi F, Ge L, Zhao J, et al. Meta-analysis: total parenteral nutrition versus total enteral nutrition in predicted severe acute pancreatitis. Intern Med. 2012;51(6):523-30.[Abstract][Full Text]
93. Mirtallo JM, Forbes A, McClave SA, et al. International consensus guidelines for nutrition therapy in pancreatitis. JPEN J Parenter Enteral Nutr. 2012 May;36(3):284-91.[Abstract]
94. Petrov MS, Zagainov V. Influence of enteral versus parenteral nutrition on blood glucose control in acute pancreatitis: a systematic review. Clin Nutr. 2007 Oct;26(5):514-23.[Abstract]
95. Petrov MS, Kukosh MV, Emelyanov NV. A randomized controlled trial of enteral versus parenteral feeding in patients with predicted severe acute pancreatitis shows a significant reduction in mortality and in infected pancreatic complications with total enteral nutrition. Dig Surg. 2006;23(5-6):336-44; discussion 344-5.[Abstract]
96. Dutta AK, Goel A, Kirubakaran R, et al. Nasogastric versus nasojejunal tube feeding for severe acute pancreatitis. Cochrane Database Syst Rev. 2020 Mar 26;(3):CD010582.[Abstract][Full Text]
97. Poropat G, Giljaca V, Hauser G, et al. Enteral nutrition formulations for acute pancreatitis. Cochrane Database Syst Rev. 2015 Mar 23;(3):CD010605.[Abstract][Full Text]
98. Meier R, Beglinger C, Layer P, et al; European Society of Parenteral and Enteral Nutrition. ESPEN guidelines on nutrition in acute pancreatitis. Clin Nutr. 2002 Apr;21(2):173-83.
99. Gianotti L, Meier R, Lobo DN, et al; ESPEN. ESPEN guidelines on parenteral nutrition: pancreas. Clin Nutr. 2009 Aug;28(4):428-35.[Abstract]
100. Dellinger EP, Tellado JM, Soto NE, et al. Early antibiotic treatment for severe acute necrotizing pancreatitis: a randomized, double-blind, placebo-controlled study. Ann Surg. 2007 May;245(5):674-83.[Abstract][Full Text]
101. Jiang K, Huang W, Yang XN, et al. Present and future of prophylactic antibiotics for severe acute pancreatitis. World J Gastroenterol. 2012 Jan 21;18(3):279-84.[Abstract][Full Text]
102. European Medicines Agency. Quinolone- and fluoroquinolone-containing medicinal products. Mar 2019 [internet publication].[Full Text]
103. US Food and Drug Administration. FDA reinforces safety information about serious low blood sugar levels and mental health side effects with fluoroquinolone antibiotics; requires label changes. Jul 2018 [internet publication].[Full Text]
104. US Food and Drug Administration. FDA warns about increased risk of ruptures or tears in the aorta blood vessel with fluoroquinolone antibiotics in certain patients. Dec 2018 [internet publication].[Full Text]
105. Boxhoorn L, van Dijk SM, van Grinsven J, et al. Immediate versus postponed intervention for infected necrotizing pancreatitis. N Engl J Med. 2021 Oct 7;385(15):1372-81.[Abstract]
106. Gurusamy KS, Belgaumkar AP, Haswell A, et al. Interventions for necrotising pancreatitis. Cochrane Database Syst Rev. 2016 Apr 16;(4):CD011383.[Abstract][Full Text]
107. Gluck M, Ross A, Irani S, et al. Endoscopic and percutaneous drainage of symptomatic walled-off pancreatic necrosis reduces hospital stay and radiographic resources. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1083-8.[Abstract][Full Text]
108. Vitas GJ, Sarr MG. Selected management of pancreatic pseudocysts: operative versus expectant management. Surgery. 1992 Feb;111(2):123-30.[Abstract]
109. Chathadi KV, Chandrasekhara V, Acosta RD, et al; ASGE Standards of Practice Committee. The role of ERCP in benign diseases of the biliary tract. Gastrointest Endosc. 2015 Apr;81(4):795-803.[Full Text]
110. Sankaran SJ, Xiao AY, Wu LM, et al. Frequency of progression from acute to chronic pancreatitis and risk factors: a meta-analysis. Gastroenterology. 2015 Nov;149(6):1490-500.[Abstract][Full Text]
111. Herrera ME, Seller G, de la Rubia C, et al. Hemofiltration in acute pancreatitis [in Spanish]. Med Intensiva. 2003;27:137-43.
112. Sainio V, Kemppainen E, Puolakkainen P, et al. Early antibiotic treatment in acute necrotising pancreatitis. Lancet. 1995 Sep 9;346(8976):663-7.[Abstract]
113. Hernandez-Aranda JC, Gallo-Chico B, Ramirez-Barba EJ. Nutritional support in severe acute pancreatitis. Controlled clinical trial [in Spanish]. Nutr Hosp. 1996 May-Jun;11(3):160-6.[Abstract]
114. Kotani J, Usami M, Nomura H, et al. Enteral nutrition prevents bacterial translocation but does not improve survival during acute pancreatitis. Arch Surg. 1999 Mar;134(3):287-92.[Abstract]
115. Ammori BJ. Role of the gut in the course of severe acute pancreatitis. Pancreas. 2003 Mar;26(2):122-9.[Abstract]
116. Hart PA, Bradley D, Conwell DL, et al. Diabetes following acute pancreatitis. Lancet Gastroenterol Hepatol. 2021 Aug;6(8):668-75.[Abstract]
117. Crockett SD, Wani S, Gardner TB, et al. American Gastroenterological Association Institute guideline on initial management of acute pancreatitis. Gastroenterology. 2018 Mar;154(4):1096-101.[Abstract]
118. Bråthen G, Ben-Menachem E, Brodtkorb E, et al. Chapter 29: alcohol-related seizures. EFNS guidelines of alcohol-related seizures. In: Gilhus NE, Barnes MP, Brainin M, eds. European handbook of neurological management. 2nd ed, v1. Oxford, UK: Blackwell Publishing; 2011:429-36.
119. Preiss D, Tikkanen MJ, Welsh P, et al. Lipid-modifying therapies and risk of pancreatitis: a meta-analysis. JAMA. 2012 Aug 22;308(8):804-11.[Abstract][Full Text]
120. Andriulli A, Leandro G, Niro G, et al. Pharmacologic treatment can prevent pancreatic injury after ERCP: a meta-analysis. Gastrointest Endosc. 2000 Jan;51(1):1-7.[Abstract]
121. Venneman NG, van Erpecum KJ. Gallstone disease: primary and secondary prevention. Best Pract Res Clin Gastroenterol. 2006;20(6):1063-73.[Abstract]
Key Articles
Referenced Articles
Guidelines
Diagnostic
Summary
This guideline provides a comprehensive overview of the diagnosis and assessment of this disease.Published by
American College of Gastroenterology
Published
2013
Summary
Overview of which radiologic test to choose to make the diagnosis. An appropriateness scale is derived.Published by
American College of Radiology
Published
2019
Summary
These guidelines provide recommendations regarding the appropriate use of endoscopy for the diagnosis of inflammatory pancreatic fluid collections.Published by
American Society for Gastrointestinal Endoscopy
Published
2016
Treatment
Summary
Addresses management of acute pancreatitis within the first 48 to 72 hours of admission.Published by
American Gastroenterological Association
Published
2018
Summary
These guidelines provide recommendations regarding the appropriate use of endoscopy for the treatment of inflammatory pancreatic fluid collections.Published by
American Society for Gastrointestinal Endoscopy
Published
2016
Summary
Evidence-based guidelines on therapeutic use of endoscopic retrograde cholangiopancreatography in benign diseases of the biliary tract.Published by
American Society for Gastrointestinal Endoscopy
Published
2015
Summary
This guideline provides a comprehensive overview of the management of this disease.Published by
American College of Gastroenterology
Published
2013
Summary
Provides evidence-based international consensus statements on the management of severe acute pancreatitis.Published by
World Society of Emergency Surgery
Published
2019
Summary
Provides recommendations concerning key aspects of medical and surgical management of acute pancreatitis based on currently available evidence.Published by
International Association of Pancreatology; American Pancreatic Association
Published
2013
Summary
Provides an evidence-based approach for strategies to prevent post-ERCP pancreatitis.Published by
American Society for Gastrointestinal Endoscopy
Published
2023