Suggestive Presentation
• Upper or generalised abdominal pain, often radiating through to the back
• Unable to get comfortable
• Associated sympathetic discharge, e.g. diaphoresis
• Distended, tender abdomen
• Shock, Cullen’s (haemorrhagic blueish tracking around umbilicus), and Grey-Turner’s (haemorrhagic blueish tracking along the loin), signs in severe disease
Is the Patient stable?
- ABCs, especially fluid resuscitation
- Emergent differentials to consider and act upon
» ACS
» Aortic Dissection
» Perforated Viscus e.g. PUD
» Oesophageal Rupture
» AAA
» Ectopic Pregnancy
Place the patient NBM, starting intravenous fluids, and consider a NGT. No routine prophylactic antibiotics needed if a perforated viscus has been excluded. Consider, however, PPI prophylaxis. Do not overlook VTE prophylaxis, assuming there is no contraindication, of which severe haemorrhagic pancreatitis may, in fact, constitute.
Initial Workup
• FBC
• EUC
• LFTs
• Lipase (+/- Amylase)
• BSL
• ECG
• CXR: free air +/- collapse / consolidation / pleural effusion / ARDS
• AXR: sentinel loop (of small or occasional large (so-called “colon cut-off” sign) intestine)
• +/- β-HCG
A Lipase that is 3 x the normal has a sensitivity of 80-100%. Lipase has a longer half-life and is more specific, for acute pancreatitis, than is serum Amylase. A person can, however, have a normal serum lipase and still have acute pancreatitis, especially recurrent acute pancreatitis.
I do not, as a rule, use scores in primary care—if, all things being equal, someone has a PO2 from acute pancreatitis of less than 60, for instance, then for all intents and purposes you have one shocked patient who is at risk of multi-organ failure, whether you add up their MGS or not—but some people seem to rely on them. I think they serve a mostly academic interest.
Modified Glasgow Score (MGS) conveniently utilises a “P-A-N-C-R-E-A-S” mnemonic:
HDU / ICU admission for scores ≥ 3
• PaO2 < 60 mmHg
• Age > 55 years
• Neutrophilia > 15
• Calcium < 2 mmol/L
• Renal: Urea > 16 mmol/L
• Enzymes: LDH > 600 IU/L / AST > 200 IU/L
• Albumin < 32 g/L
• Sugar: Glucose > 10 mmol/L
Ultrasonography (USS)
» Pancreatitis confirmed
» Gallstones
» Fatty liver
About ¼ to 1/3 are non-diagnostic, often because sentinel loop/ileus obstructs imaging of pancreas and hepatobiliary system, in which case a non-contrast Abdominal CT scan might be helpful, though it can often wait for the patient to settle a few days and then performed with contrast. IV contrast is best avoided in acute situation as it will only likely add to the patient’s misery. As pancreatic inflammation resolves, contrast-enhanced scans importantly may show evidence of necrosis in the early post-acute setting as well as other early complications in the post-acute setting (pseudocyst / collection / abscess).
Once the patient is stable and the diagnosis essentially confirmed, consider possible causes:
» Gallstones (50%)
» Alcohol (25%)
» Iatrogenic—e.g. complicates up to 10% of ERCPs
» Hyperlipidaemia—especially hypertriglyceridemia
» Hypercalcaemia
» Infection—especially viral
» Autoimmune disease, including vasculitis
» Ischaemic: thrombotic or embolic phenomena
» Genetic predisposition
» Idiopathic (10-30%)
Thankfully, most acute pancreatitis cases are mild and resolve with supportive care: conferring a mortality of less than 1%. Haemorrhagic/necrotic pancreatitis, on the other hand, has a mortality of 1 in 5 despite the best of care.
If alcohol use and gallstone disease has been excluded as a cause of Recurrent Acute Pancreatitis (RAP), further imaging modalities, such as endoscopic ultrasonography (EUS) and magnetic-resonance cholangiopancreatography (MRCP), may yield more information regarding cause, otherwise leaving Idiopathic Recurrent Acute Pancreatitis (IRAP) as the diagnosis of exclusion.
• microlithiasis (sludge)
• sphincter of Oddi dysfunction (SOD)
• pancreas divisum
• hereditary pancreatitis
• cystic fibrosis
• choledochocele
• annular pancreas
• anomalous pancreatobiliary junction
• pancreatobiliary tumors
• chronic pancreatitis
References
- Acute Pancreatitis, Emergency Care Institute NSW. Available at https://www.aci.health.nsw.gov.au/networks/eci/clinical/clinical-resources/clinical-tools/abdominal-emergencies/acute-pancreatitis. Accessed 23 May 2020.
- Lara Luis and Michael Levy. Idiopathic Recurrent Acute Pancreatitis. Medscape. Available at https://www.medscape.com/viewarticle/487185. Accessed 23 May 2020.
Further Reading
- Recurrent Acute Pancreatitis: An Algorithmic Approach to Identification and Elimination of Inciting Factors. Lehel Somogyi, Stephen P Martin, Thangham Venkatesan, and Charles D Ulrich II. gastroenterology, 2001; 120:708-717.
- Idiopathic recurrent acute pancreatitis. The Lancet Gastroenterology and Hepatology. Oct 2018. DOI: https://doi.org/10.1016/S2468-1253(18)30211-5.
- Hereditary pancreatitis. UpToDate. Available at https://www.uptodate.com/contents/hereditary-pancreatitis. Accessed 23 May 2020.
- Genetics of acute pancreatitis. F Ulrich Weiss and Markus M Lerch. Pancreapedia. American Pancreatic Association. DOI: 10.3998/panc.2016.22
- Acute recurrent pancreatitis: Etiopathogenesis, diagnosis
and treatment. Pier Alberto Testoni. World J Gastroenterol 2014 December 7; 20(45): 16891-16901. DOI: 10.3748/wjg.v20.i45.16891.
