Acute Pancreatitis

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Acute Pancreatitis written for patients
This is acute inflammation of the pancreas, releasing exocrine enzymes that cause autodigestion of the organ. There may be involvement of local tissues and distant organs.

It should not be confused with chronic pancreatitis. See separate article Chronic Pancreatitis for details on this condition.
  • The incidence of acute pancreatitis in the UK ranges from 150 to 420 cases per million population and is currently rising.[1]
  • There is considerable geographical variation. The incidence in the UK and the Netherlands is relatively low compared to Scandinavian countries and the USA.[2]
  • A Croatian study reported a mean age of 60 with roughly equal gender distribution.[2] However, the condition has been reported in children: the causes are more varied than in adults and include drugs, traumas, infections, multisystem disorders and biliary anomalies.[3]

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Gallbladder disease and excess alcohol consumption account for most cases and typically cause periductal necrosis.

  • Gallstones cause pancreatitis by blocking the bile duct, causing back pressure in the main pancreatic duct.
  • Perilobular necrosis is less common and usually found in those with hypothermia and gross hypotension.
  • Haemorrhagic, necrotic black discolouration is only found in the most severe cases.

Studies suggest that in countries with high prevalence the main cause is alcohol, whilst in low-prevalence countries it is mainly related to biliary disease.[4]

Less common causes include:

  • Injury - post-endoscopic retrograde cholangiopancreatography (ERCP), blunt trauma.
  • Viral - Coxsackie B, hepatitis and mumps (prodromal diarrhoea is indicative).
  • Metabolic - hyperlipoproteinaemia, hyperparathyroidism, hypothermia, uraemia, anorexia.
  • Drugs - thiazides, valproate, azathioprine, L-asparaginase, corticosteroids (all rare).
  • Malignancy - peri-ampullary tumour, pancreatic carcinoma, metastases to the pancreas.
  • Ischaemia - visceral thromboembolism, abdominal vascular surgery, cardiopulmonary bypass.
  • Inflammatory bowel disease - one UK study found a seven-fold increase in acute pancreatitis in patients with inflammatory bowel disease taking mesalazine, although it is not known whether this was due to the disease, the drug or a combination of both.[5]
  • Other rarities - alpha-1-antitrypsin deficiency, sclerosing cholangitis, duodenal re-duplication, annular pancreas, vasculitis.


Take careful history, including alcohol consumption and prodromal symptoms.

  • Most commonly, this presents as severe upper abdominal pain of sudden onset with vomiting.
  • Pain is focused in the left upper quadrant of the epigastrium and penetrates to the back. Occasionally, it encircles the abdomen.
  • Pain tends to decrease steadily over 72 hours.


  • Take the patient's temperature to exclude hypothermia; mild pyrexia is more common.
  • Look for evidence of hyperlipidaemia.
  • Probable tachycardia with the patient unwell and dehydrated.
  • Jaundice may be present in patients with common bile duct stones or, to a lesser degree, in those with alcohol-induced disease, compression of the lower bile duct, or hepatitis.
  • Epigastric or generalised abdominal tenderness, often with rigidity.
  • Bowel sounds are usually present in the early phase. Paralytic ileus, causing absent bowel sounds can last for >4 days and is a useful marker of disease severity.
  • In severe cases: gross hypotension, pyrexia, tachypnoea, acute ascites, pleural effusions, body wall staining around the umbilicus (Cullen's sign) or flanks (Grey Turner's sign).
  • Hypoxaemia is characteristic of acute pancreatitis.
  • Serum amylase 3 or more times normal is the traditional way of diagnosing acute pancreatitis. However, lipase levels are more sensitive and more specific.[1]
  • FBC, U&E, glucose and C-reactive protein (CRP) indicate prognosis. CRP value is significantly lower in drug-induced acute pancreatitis.[7]
    • Raised bilirubin and/or serum aminotransferase suggest gallstones.
    • Hypocalcaemia is relatively common.
  • Plain erect (if possible) abdominal X-ray:
    • This excludes some other causes (eg, intestinal obstruction and perforation) and may show calcification.
    • CXR may show elevation of one hemidiaphragm, infiltrates ± acute respiratory distress syndrome (ARDS) or pleural effusions in severe cases.
  • CT scan with contrast enhancement may be diagnostic where clinical and biochemical results are equivocal on admission. CT after four days can help in the assessment of complications.[8]
    • The CT severity index (CTSI), derived by Balthazar et al, has become widely used for description of CT findings in acute pancreatitis.
    • Contrast-enhanced CT scanning can identify pancreatic swelling, fluid collection and change in density of gland. Such criteria can have prognostic value and predict the need for surgery.[9] 
  • Ultrasound:
    • The pancreas is poorly visualised in 25-50% of cases.
    • Ultrasound can show a swollen pancreas, dilated common bile duct and free peritoneal fluid.
    • It is useful to detect the presence of gallstones.
    • Endoscopic ultrasound is a safe minimally invasive technique which is more accurate than transabdominal ultrasound and can accurately detect bile duct stones and other causes of recurrent acute pancreatitis.[10]
  • MRI may reveal acute abdominal wall oedema which may be a supplementary indicator of severity.[11]
  • Peritoneal aspiration of free fluid without bacterial contamination is a risk factor for mortality.[12]
  • Laparoscopy can reveal diagnosis where suspicion is high but tests are inconclusive.[13]

Other causes of raised amylase

Other causes of similar pain

  • Scoring systems increase accuracy of prognosis.
  • Use of the Glasgow Prognostic Score/Ranson's Criteria/Acute Physiology and Chronic Health Evaluation II (APACHE II) score can indicate prognosis, particularly if combined with measurement of CRP >150 mg/L.
Pancreatitis Prognostic Scores

Glasgow Prognostic Score

  • Age >55 years
  • WBC >15 x 109/L
  • Urea >16 mmol/L
  • Glucose >10 mmol/L
  • pO2 <8 kPa (60 mm Hg)
  • Albumin <32 g/L
  • Calcium <2 mmol/L
  • LDH >600 units/L
  • AST/ALT >200 units

Ranson's Criteria

Present on admission:

  • Age >55 years
  • WBC >15 x 109/L
  • Glucose >10 mmol/L
  • Serum AST >250 IU/L
  • Serum LDH >350 IU/L

Developing during the first 48 hours:

  • Haematocrit fall >10%
  • Urea increase ≥5 mg/dL (equivalent to ≥1.8 mmol/L)
  • Serum Ca <2.0 mmol/L
  • Hypoxaemia - arterial pO2 <60 mm Hg
  • Base deficit >4 meq/L
  • Estimated fluid sequestration >6 L
In either scoring system, the presence of three or more criteria indicates severe pancreatitis, which is associated with a higher mortality.

An APACHE II score of 8 or more is severe.[14]

The Atlanta Classification - revised in 2012 - allows comparison of these scoring systems and of clinical trials.[15][16]

  • The Classification identifies two phases - early (within the first two weeks) and late (thereafter).
  • Severity of disease is classified into three levels: mild (no complications), moderately severe (complications lasting for less than two days, local complications and/or recurrence of co-existing disease) and severe (organ failure lasting for more than two days).
  • Local complications are usually detected by CT and may include peripancreatic fluid collection, pseudocysts and necrosis.
  • Clinically apparent organ failure includes pulmonary, circulatory or renal insufficiency.

There has been criticism of current scoring systems as being unwieldy and difficult to interpret. Procalcitonin (PCT) and Bedside Index for Severity in Acute Pancreatitis (BISAP) have been mooted as possible candidates in the search for a more simplified approach.

Mild cases

  • Manage on a general ward.
  • Pain relief with pethidine or buprenorphine ± intravenous (IV) benzodiazepines. Morphine is relatively contra-indicated because of possible spastic effect on the sphincter of Oddi. Non-steroidal drugs may be effective during the recovery phase.
  • IV fluids with nil by mouth.
  • Nasogastric tube only for severe vomiting.
  • Antibiotics for specific infections.
  • No other treatment is necessary; no CT scan is necessary.
  • When pain and other symptoms have resolved and blood tests are normal, oral fluids and then solids, can be resumed. If gallstones are the cause then consider common bile duct clearance and cholecystectomy after recovery, preferably during original admission.

Severe case

  • Treat in ITU or a high dependency unit.
  • Where there is evidence of significant pancreatic necrosis, IV antibiotics should be given, preferably following percutaneous aspiration of peritoneal fluid for culture.[18] The role of routine prophylactic antibiotics for severe cases is less clear. A Cochrane review[19] found evidence of reduced incidence of superinfection of necrotic tissue, if given for 10-14 days in cases with CT-proven necrosis. However, the studies used differing agents and aetiology/use of surgical debridement may have influenced results; so, more research is needed to answer this question definitively.[20]
  • Feed with enteral nutrition (EN) via a nasogastric tube placed beyond the ligament of Treitz, provided there is no ileus (this ligament connects the duodenum to the diaphragm and feeding here is less likely to stimulate the pancreas). A Cochrane review found that EN significantly reduced mortality, multiple organ failure, systemic infections and the need for operative interventions and was associated with shorter hospital stays.[21]
  • A Cochrane review found no benefit in using antibiotics to prevent infection of pancreatic necrosis or mortality, except for when imipenem (a beta-lactam) was considered on its own, Further large-scale trials are needed.[22]
  • A Cochrane review supports early ERCP for patients with co-existing cholangitis or biliary obstruction.[23]
  • Surgery is only required where there is infection and necrosis. Open surgical debridement is being largely replaced by newer minimally invasive techniques such as transgastric endoscopy and video-assisted translumbar retroperitoneal necrosectomy followed by closed lavage of infected pancreatic necrosis.[24][25] 
  • Percutaneous catheter drainage with saline irrigation can sometimes avoid surgery.[26]
  • Hyperbaric oxygen therapy - administration of 100% oxygen at a pressure of 2.5 atmospheres for 90 minutes twice-daily for five days has been shown to improve APACHE II and CTSI grading scores.[27] Hyperbaric oxygen treatment acted by normalising the pancreatic microvasculature.[28]
  • Human adipose-derived stromal/stem cells may provide a valuable tool for cell-based therapy.[29] 
  • Pancreatic necrosis - if infected, this trebles mortality risk.
    • Rising CRP suggests necrosis and is confirmed by dynamic CT.
    • Infection occurs in 30-70% of cases of necrosis (the risk can be reduced by gut decontamination).[30] 
    • Take special care of aseptic technique with invasive procedures.
    • Where the patient suddenly deteriorates or worsens with intensive support, use CT-guided fine-needle aspiration for culture and microscopy.
  • Infected necrosis is almost always fatal without intervention.
    • The standard is IV antibiotics and aggressive surgical pancreatic debridement (necrosectomy) involving drain placement. In many cases, this can be accomplished using minimally invasive techniques, even if necrosis is severe.
  • Acute fluid collections are common in patients with severe pancreatitis (occurring in 30-50%).[31] 
    • The majority will resolve spontaneously and, in an otherwise stable patient, they do not require treatment.
    • Unnecessary percutaneous procedures risk introducing infections.
  • Pancreatic abscess is a collection of pus adjacent to the pancreas, presenting several months after an attack.
    • It requires surgery.
  • Acute pseudo-cyst contains pancreatic juice in a wall of fibrous or granulation tissue.
    • it arises four weeks after attack.
    • It can rupture or haemorrhage.
    • It requires surgery.
  • Pancreatic ascites occurs when a pseudo-cyst collapses into the peritoneal cavity or major pancreatic duct breaks down and releases pancreatic juices into the peritoneal cavity.
    • Treat with IV feeding plus synthetic somatostatin or surgical excision of the segment of pancreas drained by the broken duct.
  • Acute cholecystitis complicates approximately 10% of patients with severe acute pancreatitis in the late stage.[32] 

Systemic complications

  • Respiratory:
  • Cardiovascular:
    • Hypovolaemia
    • Shock
  • Disseminated intravascular coagulopathy (DIC).
  • Renal dysfunction due to hypovolaemia, intravascular coagulation. Usually avoided by adequate fluid replacement plus/minus low-dose dopamine; however, acute tubular or cortical necrosis can follow.
  • Metabolic:
  • Gastrointestinal:
    • Haemorrhage
    • Ileus
  • Weber-Christian disease:
    • Subcutaneous fat necrosis - relapsing febrile nodular nonsuppurative panniculitis. Recurring crops of tender nodules in the skin and subcutaneous fat of the trunk, thighs and buttocks, which is more common in middle-aged women.
    • These often ulcerate and scar on healing.
    • Difficult to treat - try prednisolone or immunosuppressives.
  • Splenic vein thrombosis.
  • 80% of patients have mild disease and recover without complications.[8]
  • An American study found that 22% of patients admitted with a first attack of pancreatitis subsequently had one or more attacks. However, progression to chronic pancreatitis occurred in only 6% of patients and this was normally against a background of recurrent attacks, alcohol or smoking.[4]
  • 5% mortality in mild cases; up to 30% mortality in severe cases.
  • Severe cases may be deficient in pancreatic enzymes for up to two years but only those with steatorrhoea and weight loss need treatment.
  • Subtle glucose intolerance is common but diabetes is uncommon.
  • Avoid alcohol.
  • Treat gallstones in patients who present with acute pancreatitis.
  • Plasmapheresis may help to reduce the incidence of acute pancreatitis in patients with severe hypertriglyceridaemia.

Further reading & references

  • Vaz J, Akbarshahi H, Andersson R; Controversial role of toll-like receptors in acute pancreatitis. World J Gastroenterol. 2013 Feb 7;19(5):616-30. doi: 10.3748/wjg.v19.i5.616.
  • Ewald N, Kloer HU; Treatment options for severe hypertriglyceridemia (SHTG): the role of apheresis. Clin Res Cardiol Suppl. 2012 Jun;7(Suppl 1):31-5.
  • Solanki NS, Barreto SG; Fluid therapy in acute pancreatitis. A systematic review of literature. JOP. 2011 Mar 9;12(2):205-8.
  • de Vries AC, Besselink MG, Buskens E, et al; Randomized controlled trials of antibiotic prophylaxis in severe acute pancreatitis: relationship between methodological quality and outcome. Pancreatology. 2007;7(5-6):531-8. Epub 2007 Sep 27.
  1. Gomez D, Addison A, De Rosa A, et al; Retrospective study of patients with acute pancreatitis: is serum amylase still required? BMJ Open. 2012 Sep 21;2(5). pii: e001471. doi: 10.1136/bmjopen-2012-001471. Print 2012.
  2. Stimac D, Mikolasevic I, Krznaric-Zrnic I, et al; Epidemiology of Acute Pancreatitis in the North Adriatic Region of Croatia during the Last Ten Years. Gastroenterol Res Pract. 2013;2013:956149. doi: 10.1155/2013/956149. Epub 2013 Feb 14.
  3. Minen F, De Cunto A, Martelossi S, et al; Acute and recurrent pancreatitis in children: exploring etiological factors. Scand J Gastroenterol. 2012 Dec;47(12):1501-4. doi: 10.3109/00365521.2012.729084. Epub 2012 Sep 28.
  4. Yadav D, O'Connell M, Papachristou GI; Natural history following the first attack of acute pancreatitis. Am J Gastroenterol. 2012 Jul;107(7):1096-103. doi: 10.1038/ajg.2012.126. Epub 2012 May 22.
  5. Ham M, Moss AC; Mesalamine in the treatment and maintenance of remission of ulcerative colitis. Expert Rev Clin Pharmacol. 2012 Mar;5(2):113-23. doi: 10.1586/ecp.12.2.
  6. Freedman S; Acute Pancreatitis, Merck Manual, 2012
  7. Mennecier D, Pons F, Arvers P, et al; Incidence and severity of non alcoholic and non biliary pancreatitis in a gastroenterology department. Gastroenterol Clin Biol. 2007 Aug-Sep;31(8-9):664-7.
  8. Frossard JL, Steer ML, Pastor CM; Acute pancreatitis. Lancet. 2008 Jan 12;371(9607):143-52.
  9. Alhajeri A, Erwin S; Acute pancreatitis: value and impact of CT severity index. Abdom Imaging. 2008 Jan-Feb;33(1):18-20.
  10. Albashir S, Stevens T; Endoscopic ultrasonography to evaluate pancreatitis. Cleve Clin J Med. 2012 Mar;79(3):202-6. doi: 10.3949/ccjm.79a.11092.
  11. Yang R, Jing ZL, Zhang XM, et al; MR imaging of acute pancreatitis: correlation of abdominal wall edema with severity scores. Eur J Radiol. 2012 Nov;81(11):3041-7. doi: 10.1016/j.ejrad.2012.04.005. Epub 2012 May 7.
  12. Busquets J, Fabregat J, Pelaez N, et al; Factors Influencing Mortality in Patients Undergoing Surgery for Acute Pancreatitis: Importance of Peripancreatic Tissue and Fluid Infection. Pancreas. 2013 Jan 25.
  13. Peris A, Matano S, Manca G, et al; Bedside diagnostic laparoscopy to diagnose intraabdominal pathology in the intensive care unit. Crit Care. 2009;13(1):R25. doi: 10.1186/cc7730. Epub 2009 Feb 25.
  14. Papachristou GI, Muddana V, Yadav D, et al; Comparison of BISAP, Ranson's, APACHE-II, and CTSI scores in predicting organ Am J Gastroenterol. 2010 Feb;105(2):435-41; quiz 442. Epub 2009 Oct 27.
  15. Sarr MG; 2012 Revision of the Atlanta Classification of Acute Pancreatitis. Pol Arch Med Wewn. 2013 Feb 11. pii: AOP_13_010.
  16. Carroll JK, Herrick B, Gipson T, et al; Acute pancreatitis: diagnosis, prognosis, and treatment. Am Fam Physician. 2007 May 15;75(10):1513-20.
  17. Banks PA, Conwell DL, Toskes PP; The management of acute and chronic pancreatitis. Gastroenterol Hepatol (N Y). 2010 Feb;6(2 Suppl 3):1-16.
  18. No authors listed; UK guidelines for the management of acute pancreatitis. Gut. 2005 May;54 Suppl 3:iii1-9.
  19. Villatoro E, Bassi C, Larvin M; Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD002941.
  20. de Vries AC, Besselink MG, Buskens E, et al; Randomized controlled trials of antibiotic prophylaxis in severe acute pancreatitis: relationship between methodological quality and outcome. Pancreatology. 2007;7(5-6):531-8. Epub 2007 Sep 27.
  21. Al-Omran M, Albalawi ZH, Tashkandi MF, et al; Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev. 2010 Jan 20;(1):CD002837.
  22. Villatoro E, Mulla M, Larvin M; Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev. 2010 May 12;(5):CD002941. doi: 10.1002/14651858.CD002941.pub3.
  23. Tse F, Yuan Y; Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis. Cochrane Database Syst Rev. 2012 May 16;5:CD009779. doi: 10.1002/14651858.CD009779.pub2.
  24. Ulagendra Perumal S, Pillai SA, Perumal S, et al; Outcome of video-assisted translumbar retroperitoneal necrosectomy and closed lavage for severe necrotizing pancreatitis. ANZ J Surg. 2013 Mar 4. doi: 10.1111/ans.12107.
  25. Rische S, Riecken B, Degenkolb J, et al; Transmural endoscopic necrosectomy of infected pancreatic necroses and drainage of infected pseudocysts: a tailored approach. Scand J Gastroenterol. 2013 Feb;48(2):231-40. doi: 10.3109/00365521.2012.752029. Epub 2012 Dec 27.
  26. Babu RY, Gupta R, Kang M, et al; Predictors of surgery in patients with severe acute pancreatitis managed by the step-up approach. Ann Surg. 2013 Apr;257(4):737-50. doi: 10.1097/SLA.0b013e318269d25d.
  27. Christophi C, Millar I, Nikfarjam M, et al; Hyperbaric oxygen therapy for severe acute pancreatitis. J Gastroenterol Hepatol. 2007 Nov;22(11):2042-6.
  28. Cuthbertson CM, Su KH, Muralidharan V, et al; Hyperbaric oxygen improves capillary morphology in severe acute pancreatitis. Pancreas. 2008 Jan;36(1):70-5. doi: 10.1097/mpa.0b013e3181485863.
  29. Wen Z, Liao Q, Hu Y, et al; Human adipose-derived stromal/stem cells: A novel approach to inhibiting acute pancreatitis. Med Hypotheses. 2013 Feb 16. pii: S0306-9877(13)00057-1. doi: 10.1016/j.mehy.2013.01.034.
  30. O'Connor OJ, McWilliams S, Maher MM; Imaging of acute pancreatitis. AJR Am J Roentgenol. 2011 Aug;197(2):W221-5. doi: 10.2214/AJR.10.4338.
  31. Beger H et al; The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, 2009
  32. Tong Z, Yu W, Ke L, et al; Acute Cholecystitis in the Late Phase of Severe Acute Pancreatitis: A Neglected Problem. Pancreas. 2013 Apr;42(3):531-536.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Hayley Willacy
Current Version:
Peer Reviewer:
Dr Helen Huins
Document ID:
626 (v24)
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