What is acute pancreatitis?

Acute pancreatitis refers to acute inflammation of the pancreas. The acute inflammation is typically caused by hypersecretion or backflow (due to obstruction) of exocrine digestive enzymes, which results in autodigestion of the pancreas.

Pancreatic damage can be classified into two major categories:

  • Interstitial oedematous pancreatitis – most common, better prognosis
  • Necrotising pancreatitis – less common, around 5-10%, more severe1

The damage that occurs during acute pancreatitis is potentially reversible (to varying degrees), whereas chronic pancreatitis involves ongoing inflammation of the pancreas that results in irreversible damage. Chronic pancreatitis is associated with endocrine and exocrine dysfunction, as well as chronic abdominal pain.


Why is it significant?

In the UK, the prevalence of pancreatitis is around 56 cases per 100,000 annually.2 All patients with suspected pancreatitis require urgent surgical review and admission if diagnosed. Though it is mild in the majority of people (mortality <1%), patients can deteriorate quickly. There is a high case fatality rate (~15%) in patients with severe pancreatitis.


Aetiology and Risk Factors

Aetiology

The vast majority of pancreatitis cases in the UK are caused by gallstones or alcohol.

A commonly used mnemonic to help remember the less common causes is ‘I GET SMASHED’:

  • Idiopathic
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps/Malignancy
  • Autoimmune disease
  • Scorpion sting
  • Hypertriglycerides/Hypercalcaemia
  • ERCP (endoscopic retrograde cholangiopancreatography)
  • Drugs –commonly azathioprine, thiazides, septrin, tetracyclines

Risk factors

Risk factors for pancreatitis include:

  • Male gender
  • Increasing age
  • Obesity
  • Smoking

History and Examination

History

Typically, acute pancreatitis presents as severe, sudden onset epigastric pain. Below, are important things to ask about in the context of suspected pancreatitis.

History of Presenting Complaint

It is important to ask for further details about the pain. The SOCRATES mnemonic can be useful in this scenario:

  • Site – epigastric
  • Onset – sudden onset
  • Character – sharp, stabbing
  • Radiation – through to the back, may radiate around sides to back if cholecystitis/cholangitis is present
  • Associated symptoms – recurrent vomiting
  • Timing – sudden onset that rapidly crescendos, likely duration of less than 1 day (if gallstone-related, may be preceded with a history of biliary colic)
  • Exacerbating features – exacerbated by movement, alleviated partially by leaning forward or adopting the fetal position
  • Severity – most patients experience severe abdominal pain

Past Medical History

  • History of biliary disease or pancreatitis (including results of investigations)
  • Recent illness
  • Surgery or other interventions (e.g. ERCP)

Medication History

  • Regular medications (including any recent additions)
  • Over the counter medications
  • Allergies

Family History

  • Gallstones
  • Biliary pathology
  • Malignancy

Social History

  • Smoking history
  • Alcohol history
  • Recreational drug use
  • Foreign travel

Examination

A thorough abdominal examination should be performed on all patients with suspected acute pancreatitis. See the Geeky Medics guide here.

Clinical signs relevant to pancreatitis include:

  • Tenderness in the epigastrium
  • Abdominal distention (due to local reactive ileus or retroperitoneal fluid)
  • Cullen’s sign (peri-umbilical bruising) and Grey-Turner’s sign (flank bruising)  are important to be aware of, but these are LATE signs of severe intra-abdominal and retroperitoneal haemorrhage, respectively.
  • Systemic inflammatory response syndrome (SIRS) is indicative of severe pancreatitis. If febrile and hypotensive on admission the patient is more likely to develop organ failure during their hospital stay. Tachycardia is a less helpful sign, as the adrenergic response can be driven by pain and stress.
Grey turner and Cullen's sign
Figure 1A. Cullen’s sign (periumbilical bruising)18 | Figure 1B. Grey-Turner’s sign (flank bruising)19

Diagnosis

The International Pancreatic Association criteria state that two of three criteria must be satisfied for a diagnosis of acute pancreatitis to be made: 4

  1. Abdominal pain plus a history suggestive of acute pancreatitis
  2. Serum amylase/lipase of over three times the upper limit of normal
  3. Imaging findings characteristic of acute pancreatitis

If a patient has a typical history of acute pancreatitis and a serum lipase in the thousands, consider the diagnosis made. It is crucial to note that any abdominal pathology may cause irritation of the pancreas and a rise in lipase, therefore it is often necessary to obtain imaging.


Differential Diagnoses

Severe, sudden onset epigastric pain has a number of extremely important differential diagnoses including a leaking abdominal aortic aneurysm, aortic dissection, myocardial infarction, perforated gastric/duodenal ulcer and oesophageal rupture. For this reason, all patients presenting with acute abdominal pain should have a serum lipase included in their panel of investigations (which if raised, would be highly suggestive of a diagnosis of pancreatitis). Ultimately, imaging (e.g. CT) is often required to rule out alternate pathology.


Investigations

Bloods

  • FBC – anaemia (may increase cardiovascular strain), raised WCC (part of the SIRS response)
  • CRP – non-specific, however high levels at admission can be used as an indicator of severity
  • U&Es – fluid depletion is extremely common in pancreatitis, so pay close attention to urea and eGFR
  • LFTs – may be deranged, more commonly (but not exclusively) in obstructive causes of pancreatitis (e.g. gallstone disease)
  • Lipase – very specific, normally 15-60 U/L, greater than 3x the upper limit is highly suggestive of pancreatitis 5
  • Venous blood gas (VBG) – a quick way to assess pH, electrolytes, Hb and lactate
  • Arterial blood gas (ABG) – essential for prognostic scoring in acute pancreatitis, provides a more accurate acid-base balance and true PaO2/CO2 (compared to a VBG)
  • beta-hCG – should be checked in all women of childbearing age, not only to rule out ectopic pregnancy but also to permit investigations such as x-ray and CT safely

Miscellaneous

  • ECG – a baseline investigation that should be performed for all patients presenting with epigastric pain (to avoid missing the myocardial infarction masquerading as epigastric pain)
  • Urinalysis – a routine investigation in acute abdominal pain (however, the urological system is unlikely to be the cause of sudden onset epigastric pain)

Imaging

As mentioned previously, the diagnosis of acute pancreatitis can and should be made clinically, however, imaging is sometimes used to support the diagnosis or rule out other pathology.

Erect chest x-ray (CXR)

  • Commonly used to look for free gas under the diaphragm (pneumoperitoneum) in patients who present with epigastric tenderness.

Abdominal ultrasound (USS)

  • Abdominal USS is a useful investigation to assess the biliary tree for evidence of obstruction (e.g. biliary dilatation).
  • The pancreas can sometimes be assessed using abdominal USS (e.g. evidence of oedema may be noted), however, the presence of bowel gas often obscures the pancreas, making assessment difficult or impossible.

CT abdomen and pelvis (CT-AP)

  • CT-AP is not normally necessary for immediate assessment of people with acute pancreatitis unless:
    • Alternative pathology needs to be ruled out to narrow the differential diagnosis.
    • There is suspicion is of a complication of previous pancreatitis (such as a pseudocyst or infected collection).
  • CT-AP provides optimum imaging of the pancreas and is typically performed at 48-72 hours after the initial presentation if patients do not clinically improve (to assess for evidence of pancreatic necrosis or other complications).6

Classification of Acute Pancreatitis

Classification of acute pancreatitis is governed by the Atlanta Criteria:7

  • Mild – most common, no organ dysfunction/complications, resolves normally within a week
  • Moderate – initially some evidence of organ failure which improves within 48 hours
  • Severe – persistent organ dysfunction for greater than 48 hours, together with local or systemic complications

Prognosis

Various tools exist for the prognostication of acute pancreatitis, with each aiming to identify those at higher risk of acute deterioration.

Predicting Severity

Glasgow-Imrie8

Commonly used for patients at admission, this severity score can be easily remembered using the mnemonic PANCREAS. Each criterion met, gets one point, and severe pancreatitis is indicated by a score of 3 or more:

  • PaO2 <7.9
  • Age >55
  • Neutrophils (really WCC) >15
  • Calcium <2.0
  • Renal function – Urea >16mmol/L
  • Enzymes – LDH >600 IU/L
  • Albumin <32 g/L
  • Sugar >10mmol

CRP

If CRP is over 150mg/L on admission, pancreatitis is likely to be severe.

APACHE II9

Used to estimate the mortality of patients deemed unwell enough (and suitable for) admission to ITU. It is based on a range of factors including past medical and surgical history, clinical observations and biochemical markers. These factors are then combined to generate a score that is used to predict the likely mortality rate of a patient if they were admitted to ITU.

Predicting Mortality

Ranson’s Criteria10

Uses a smaller range of clinical and biochemical markers; first at admission then again at 48 hours, to generate a predictive score of mortality.

Admission:

  • WCC >16
  • Age >55
  • Glucose > 10
  • AST >250
  • LDH >350

48-hour review:

  • HCT drop >10%
  • Urea increase >1.8mmol/L
  • Calcium <2 at any point
  • PaO2 <60mmHg at any point
  • Base deficit >4 at any point
  • Requiring over 6L fluid in 48 hours

The patient gets a point for each of the above criterion:

  • 1-2 – 1%
  • 3-4 – 15%
  • 5-6 – 40%
  • 7 or over – 100%

*Note, there is a second Ranson’s score for those in who there is confirmed gallstone disease, but the broad demographics are similar.

Balthazar Index11

This is a severity index based upon CT findings. It uses the grade of inflammation and the percentage of necrosis to generate predictions of morbidity and mortality.


Management

Once a patient has a confirmed diagnosis of pancreatitis, treatment is largely supportive.  Interventional treatments are sometimes used if deemed necessary for severe cases (e.g. necrosing pancreatitis). Below is a very useful treatment algorithm from BMJ Best Practice on how to manage early phases of pancreatic inflammation.12

Fluid Resuscitation

  • Crystalloid Hartmann’s, with an initial bolus of 1L (decrease if high risk of fluid overload e.g.), with 3ml/kg resus for the first 24 hours.
  • After the initial bolus, the IV fluids should continue at a rate of 0.5-1 ml/kg/hr to ensure urinary output over 0.5ml/kg/hr.

Analgesia

  • IV paracetamol
  • IV opioids (switched to the oral route when appropriate)
  • *Consult your local BNF for appropriate dosages

Nutrition

  • Nil by mouth (NBM) until initial pain improves (with gradual re-introduction of feeding via the oral route)
  • If the oral route is not tolerated, consider nasojejunal (NJ) feeding
  • If enteral feeding is not possible, total parenteral nutrition (TPN) should be considered in people with ongoing lack of nutrition, though keep in mind enteral feeding is associated with better outcomes.

Antiemetics

  • IV ondansetron

Correct Electrolyte Derangement

  • Calcium derangement (due to saponification), should be corrected via whatever route is available.

Control Glucose

  • Particularly important in diabetics, but anyone with ongoing hyperglycaemia should be considered for insulin therapy with a variable rate infusion.

Antibiotics

  • Current evidence suggests that routine antibiotic use for acute pancreatitis does not provide any benefit to patients and therefore should be avoided.
  • In the context of pancreatic necrosis, antibiotics are often used prophylactically due to the increased risk of infection.

Managing Underlying Disease

The two most common causes of acute pancreatitis are gallstone disease and alcohol excess, so these will be discussed.

Gallstone pancreatitis

Specific interventions include:13,14

  • Obstructed bile duct – needs ERCP to relieve obstruction, with or without sphincterotomy to dilate the sphincter of Oddi. This allows ductal stones to be removed, biliary sludge to be cleared, and relief of the obstructed biliary tree driving pancreatitis.
  • Cholecystectomy – should be performed on all patients with gallstone pancreatitis during the same admission as the acute episode. Delay is associated with a high chance of disease recurrence and readmission. The bile duct should be explored during this procedure to rule out ductal stones.

Alcoholic Pancreatitis

Prescribe according to local guidelines in keeping with severity scores, for example, the CIWA score. The general principles are ubiquitous:

  • Benzodiazepines to treat withdrawal agitation and seizures
  • Thiamine, folate, and B12 replacement

Infected Pancreatic Necrosis

Infected necrotic pancreatic tissue needs removing. This is managed via a step-up approach, aimed at minimal intervention:15

  • Percutaneous drainage
  • If this fails, may need larger percutaneous drain insertion, or potentially endoscopic approach to access the pancreas via the stomach.
  • If this fails, consider surgical necrosectomy. If such invasive methods are needed, try to defer intervention until 4 weeks after an acute presentation to allow collections to become walled off.

Complications

Early16

  • Necrotising pancreatitis – continue supportive management, aiming to avoid intervention if possible
  • Infected pancreatic necrosis – when necrosing pancreatic tissue becomes infected, patients require IV antibiotics and necrosectomy
  • Pancreatic abscess:
    • Occurs when peripancreatic collections of fluid become infected.
    • Needs IV antibiotics and urgent drainage, without which the mortality is very high.
  • Acute respiratory distress syndrome (ARDS):
    • Associated with the SIRS response of acute pancreatitis
    • Typical CXR appearance of widespread bilateral pulmonary infiltrates
    • Urgent critical care input required for consideration of admission to ITU

Late17

  • Pancreatic pseudocysts:
    • Collections of fluid that are not surrounded by epithelium.
    • They are typically amylase-rich and can become infected, rupture or bleed.
    • Typically accumulate within four weeks after acute pancreatitis.
    • Only 40% resolve spontaneously, therefore intervention is usually advised (drainage/excision).
  • Portal vein/splenic thrombosis – secondary to ongoing inflammation, anticoagulation required
  • Chronic pancreatitis – repeated attacks of acute pancreatitis can lead to ongoing inflammation and fibrosis of the pancreas
  • Pancreatic insufficiency:
    • The exocrine function of the pancreas is more commonly affected (whilst the endocrine function is typically maintained).
    • Supplement exocrine activity with Creon at meals
    • Supplement endocrine activity with insulin (less commonly required and endocrinology input essential)

References

  1. International Pancreatic Association/American Pancreatic Association. Evidence-based guidelines for the management of acute pancreatitis. Published in 2013. [LINK]
  2. BMJ Best Practice. Acute Pancreatitis. Last updated in 2013. [LINK]
  3. Van Brummelen SE et al. Acute idiopathic pancreatitis: does it really exist or is it a myth? Published in 2003. [LINK]
  4. International Pancreatic Association/American Pancreatic Association. Evidence-based guidelines for the management of acute pancreatitis. Published in 2013. [LINK]
  5. Rompianesi G et al. Serum amylase and lipase and urinary trypsinogen and amylase for diagnosis of acute pancreatitis. Published in 2017. [LINK]
  6. Balthazar EJ et al. Acute pancreatitis: value of CT in establishing prognosis. Published in 1990. [LINK]
  7. Banks PA et al; Acute Pancreatitis Classification Working Group. Classification of acute pancreatitis – 2012: revision of the Atlanta classification and definitions by international consensus. Published in 2013. [LINK]
  8. Imrie CW et al. A single-centre double-blind trial of Trasylol therapy in primary acute pancreatitis. Published in 1978. [LINK]
  9. Knaus WA et al. APACHE II: a severity of disease classification system. Published in 1985. [LINK]
  10. Ranson JH, Rifkind KM, Turner JW. Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. Published in 1976. [LINK]
  11. Balthazar EJ et al. Acute pancreatitis: value of CT in establishing prognosis. Published in 1990. [LINK]
  12. BMJ Best Practice. Acute Pancreatitis. Last updated in 2013. [LINK]
  13. Kimura Y. JPN Guidelines 2010. Gallstone-induced acute pancreatitis. Published in 2010. [LINK]
  14. BMJ Best Practice. Acute Pancreatitis. Last updated in 2013. [LINK]
  15. International Pancreatic Association/American Pancreatic Association. Evidence-based guidelines for the management of acute pancreatitis. Published in 2013. [LINK]
  16. Way LW, Doherty GM. Chapter 27: Pancreas. In: Current surgical diagnosis & treatment. Published in 2003. [LINK]
  17. BMJ Best Practice. Acute Pancreatitis. Last updated in 2013. [LINK]
  18. Herbert L. Fred and Hendrik A. van Djik. Cullen’s sign. [CC BY-SA] [LINK]
  19. Herbert L. Fred and Hendrik A. van Djik. Hemorrhagic pancreatitis. [CC BY-SA] [LINK]

Reviewer

Mr Martyn Stott

HPB Registrar


Editor

Hannah Thomas


 

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